Study Guide Cell Smstr I 20 Nov 2013

Study Guide The Cell as Biochemical Machinery

PREFACE

The Block “The Cell as Biochemical Machinery” (CBM) has been designed for students at the first semester in order to understand the concept about cells. Cell is the smallest unit of the body; grouping with other substances to represent its products to form a bigger unit, called body tissues. Cell is a protoplasm mass with a nucleus, which is lined by a membrane. In particular condition, cell can make assimilation, growth, and reproduction.

In this Block, there are three main areas that have to be understood:1. The structure and function of the cell including plasma membrane, transport of

various substances in cell membrane, receptors, organelles and inclusions, nucleus and chromosomes, cytoskeleton, and cell cycle.

2. Introduction to biology molecular and its application in medicine, gene expression, and signal transduction.

3. Cellular responses to injury and death (necrosis and apoptosis).

Beside these three areas, this Block also defines about the basic characteristics of cell, and describes about some prominent individuals who have done cell researches, given in the introductory lecture.

By understanding the concepts of cell, students are expected to have a sufficient basis for continuing medical studies to further extend their knowledge and skills in the medical sciences. By doing so, students will be able to keep update with the fast progressing medical sciences and technologies and apply them properly in their future medical practice.

This Study Guide of “The Cell as Biochemical Machinery” (CBM) contains learning tasks to be discussed by the students in the small group discussions and individually in order to achieve the block objectives. Other than that, there are overviews of lectures, student project to write and to present a paper, practice, items for self-assessment to evaluate students’ understanding on the concepts.

The Block “The Cell as Biochemical Machinery” (CBM) is undertaken 20 days including examination. Student-centered learning as the primary approach in the teaching-learning activities with dynamic group discussions are facilitated by tutors. Individual learning on campus and at home is also an important part of the learning process. To develop good understanding of the CBM, learning activities will also be carried out as lectures and practical works.

The Planner Team CBM

Faculty of MedicineUdayanaUniversity, MEU 1


TABLE OF CONTENTS

Preface.............................................................................................................Table of contents …………………………..……..................................................Learning outcome .................................................. ………………………………Curriculum content ...........................................................................................Planners Team ...................................................................................................Lectures ..............................................................................................................Facilitators ………………………………………………... ………...............................Time Table Class A ………………………………………………………....................

Time Table Class B……………………..……………………………………………….Meeting of students representatives …………………………………………….…….Plenary Session …………………………………………………………………………Assessment Method……………………………………………………………………..Student project ...................................................................................................Abstract ............................................................................................................Task 1 The Structure of the Plasma Membrane and The Transport Mechanism of

Various Substances ……………………………………………………………Task 2 Organelles and Inclusions.....………………………………… ………………

Task 3 Cytoskeleton................ ……… ……………………………………..……… Task 4 Nucleus and Chromosomes……………………………………………………. Task 5 Cell organization in Connective tissue ................................................... Task 6 Cell organization in Epithelial tissue Task 7 Introduction to Molecular Biology ………... …………………………………… Task 8 Gene expression ................................................................................. Task 9 Basic feature of enzyme ....................................................................... Task 10 Signal transduction.............................................................................. Task 11 Cell cycle............................................................................................. Task 12 Bioenergetics and oxidative metabolism ……….. ………………………..... Task 13 Cellular Responses to Injury and Death ……………………...…………… Task 14 Application of molecular biology in medicine ........................................ Task 15 Cellular intervention/therapies ............................................................

Practice………………………………………………………………………………….Self Assessment ………………………………………………………………………..

Curriculum Map………………………………………………………………………… References……………………………………………………………………………..

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~ CURRICULUM ~

THE CELL AS BIOCHEMICAL MACHINERY

UdayanaUniversity Faculty of Medicine, MEU 2


Aims: To comprehend the molecular mechanisms underlying normal cell function and

disorders To apply basic cellular and molecular concepts and principles in dealing with clinical

disorders

Learning Outcomes:

1. Explain the structure of the plasma membrane and differentiate the transport mechanism of various substances through plasma membrane.

2. Explain the general structure and function of cytoskeleton in relation to endocytosis, pinocytosis, and locomotion.

3. Differentiate functionally cytoplasmic organelles from cytoplasmic inclusions.

4. Explain the general functional structure of cell nucleus.

5. Explain the functional structure of cells organization in various tissues and its clinical implication.

6. Explain the principal mechanisms by which genes control general cell functions and gene expression in normal cells.

7. Explain the enzyme as a protein that regulates metabolism and its function in medical diagnostic.

8. Explain the energy metabolism of the cell and its clinical implications

9. Explain the signaling mechanism underlying cell to cell communication and its clinical or practical implications

10. Summarize cell cycle and its clinical implications.

11. Explain the cellular responses to injury and death (necrosis and apoptosis).

12. Explain applications of molecular biology in medicine

13. Explain pharmacology and pharmacodynamic (action of drugs to the body, mechanism of action)

CURRICULUM CONTENT



1. The Structure of the Plasma Membrane & the Transport Mechanism of Various Substancesa. The molecular structure of plasma membraneb. The transport mechanism of common substances (micro molecules) through the

plasma membranec. The practical and clinical implication of transport substances

2. Organelles and Inclusionsa. The basic concept of organelles & inclusion bodyb. The general principle of post translation modifications on Rough Endoplasmic

Reticulum and Golgi Apparatus c. The functional structure of the lysosomes, proteasomes, and peroxisomesd. The mitochondria function underlying energy metabolisme. The clinical implication of the function of proteasomes, peroxisomes, lysosomes,

and mitochondria3. Cytoskeleton

a. The components of cytoskeletonb. The mechanism of macromolecules crossing from extracellular to intracellularc. The mechanism of cells product release from intracellular to extracellulard. The common mechanisms of cell locomotione. The clinical implication of cytoskeleton disorders

4. Nucleus and Chromosomesa. The major components of the cell nucleusb. The structures that compose the nuclear pore complexc. The structures that compose the nucleosomed. The syndromes that has an association to the sex chromosome abnormalities

5. Cell organization in connective tissuea. The components of connective tissueb. The functional structures of connective tissuec. The classification of connective tissued. The clinical impication of connective tissue

6. Cell organization in epithelial tissuea. Cell-cell and cell-matrix adhesion in assembling into epithelial tissueb. Polarity of epitheliumc. The clasification of epithelial tisssued. The functional structures of epithelial tissuee. The clinical implication of epithelial tissue

7. Introduction to Molecular Biologya. The basic concept of gene, genome, and central dogmab. The functional structure of DNA & RNAc. The molecular mechanism of genetic inheritedd. The clinical implication of DNA mutatione. The various mechanism of DNA repair system

8. Gene expressiona. The function of three types of RNAb. The definition of genetic code and codonc. The mechanism of transcriptiond. The mechanism of translation

9. Basic feature of enzyme a. The concept of enzyme, apoenzyme, coenzyme, and holoenzymeb. The enzyme kinetics



10. Bioenergetics and oxidative metabolisma. Mitochondrial electron transport systemb. Mechanism of ATP synthasec. Oxidative phosphorylation inhibitors

11. Signal transductiona. The signaling molecules (ligand)b. The cell receptorsc. The variety pathways transduction signals from peripheral cytoplasm to the

nucleus by which stimulate inhibit.d. The function of secondary and the third messenger.

12. Cell Cyclea. The basic concept of the cell cycleb. The two major events in cell cyclec. The mechanism of the cell divisiond. The mitotic and the meiotic cell divisione. The process of cell differentiationf. The clinical implication of the cell division and cell differentiation disorders

13. Cellular Responses to Injury & Death a. The mechanisms and causes of cell injuryb. The cell adaptation to injury (atrophy, hypertrophy, hyperplasia & metaplasia,

sub cellular responses to injury, mechanism of intracellular accumulation and its morphologic and pathologic calcification.

c. The general pathways of cellular injury, mechanism of reversible and irreversible injury and its morphologic changes

d. The mechanism of apoptosis and its morphologic changes and some examplese. The differentiation necrosis from apoptosis in relation to their causes,

mechanisms, and morphologic changesf. The various forms of necrosis with their respective underlying mechanisms of

many kind of necrosis such as coagulative necrosis, caseous necrosis, liquifactive necrosis, enzymatic necrosis, fatty necrosis, and gangrenous necrosis.

g. The general mechanisms of cellular aging14. Applications of Molecular Biology in Medicine

a. The implications of gene testingb. The advantages of using recombinant vaccine compared with non-

recombinant/conventionalc. Reproductive cloning

15. Cellular Intervention/Therapiesa. The definition of a drugb. The common route of drugs administrationc. The fate of drugs in the body, if taken orallyd. The basic concept of pharmacology, Pharmacokinetic, Pharmacodynamic,

Volume of Distribution, Half life, Bioavaibility, Minimum Effective Concentration, Therapeutic window, First Pass Effect

e. Differences between drug elimination and drug excretionf. Differences between first order elimination and cero order eliminationg. The basic concept of agonist drug, antagonist drug, full agonist, partial agonist,

Pharmacologic antagonist, competitive, Physiologic antagonist, ED50, LD50, Therapeutic index, efficacy of drug, potency of drugs

~ PLANNERS TEAM ~



No Name Departement Phone

1 dr. IGN Ngr Mayun, Sp.HK (Head) Histology 08155715359

2 dr. I.A. Ika Wahyuniari, M.Kes (Secretary) Histology 08123614856

3 dr. Sri Widnyani,Sp.PA Pathology 08123925845

4 dr. Wayan Surudarma, M.Si Biochemistry 081338486589

5 Prof. dr. Gst Md Aman, PFK Pharmacology 081338770650

~ LECTURER ~

No Name Departement Phone

1 dr. IGN Ngr Mayun, Sp.HK Histology 08155715359

2 dr. I.A. Ika Wahyuniari, M.Kes Histology 08123614856

3 dr. Ni Putu Sri Widnyani, Sp.PA Pathology 081337115012

4 dr. Wayan Surudarma, M.Si Biochemistry 081338486589

5 dr. IGA Artini, M.Si Pharmacology 08123650481

6 Prof. dr. Bagiada, Sp.Biok Biochemistry 081338338611

7 dr. Desak Made Wihandani, M.Kes Biochemistry 081338776244

8 dr.Komang Januartha Putra Pinatih, M.Kes

Microbiology 08123831710

9 dr. IGK Nyoman Arijana, M.Si.Med Histology 085339644145

10 dr. Ni Made Linawati, M.Si Histology 03518617765

11 dr. IGA Dewi Ratnayanti, S.Ked Histology 03618550344

12 Prof.Dr.dr.I Nyoman Adiputra, MOH, PFK,Sp.Erg.

Physiology 0811397971

13 Ni Wayan Tianing, S.Si, M.Kes Biochemistry 08123982504

14 dr. Ni Nyoman Sri Budayanti, Sp.MK Microbiology 08553711398

15 Dr. rer. Nat. dr. Ni Nyoman Ayu Dewi, M.Si

Biochemistry 081337141506

~ FACILITATORS ~



Regular Class

NO NAME GROUP DEPT PHONE ROOM

1dr. Ni Kadek Mulyantari, Sp PK 1 Clinical

Pathology08123647413

3nd floor: R.3.01

2dr. Dewi Sutriani Mahalini, Sp.A 2

Pediatric08123641466 3nd floor:

R.3.02

3dr. Dudut Rustyadi , Sp.F 3

Forensic 08186510153nd floor: R.3.03

4dr. Nyoman Ratep, Sp.KJ (K) 4

Psychiatry 081236188613nd floor: R.3.04

5dr. Nyoman Sunerti, Sp.M 5

Opthalmology 081239826243nd floor: R.3.05

6dr. Putu Anda Tusta Adiputra, Sp.B(K)Onk

6Surgery 08123826430

3nd floor: R.3.06

7dr. Ayu Setyorini Mestika Mayangsari, M.Sc,Sp.A

7Pediatric 081353286780

3nd floor: R.3.07

8dr. Sianny Herawati, Sp.PK 8 Clinical

Pathology0818566411

3nd floor: R.3.08

9dr. A.A.Bagus Ngurah Nuartha, SpS.(K)

9Neurology 08179782240

3nd floor: R.3.19

10I.D.A. Pt Rasmika Dewi, S.Si, Apt 10 Clinical

Pathology081558914941

3nd floor: R.3.20

11dr. Ni Made Linawati , MSi 11

Anatomy 036186177653nd floor: R.3.21

12dr. Anak Agung Mas Putrawati Triningrat, Sp.M

12Opthalmology 08123846995

3nd floor: R.3.22

English Class

NO NAME GROUP DEPT PHONE ROOM

1dr. Anak Agung Sagung Sawitri, MPH

1Public Health 0817340145

3nd floor: R.3.01

2dr. Anak Agung Wiradewi Lestari , Sp PK

2 ClinicalPathology

081552379373nd floor: R.3.02

3dr. I A. Ika Wahyuniari, M.Kes 3

Histology 081236148563nd floor: R.3.03

4dr. Dewa Made Artika , Sp.P 4

Pulmonology 081238758753nd floor: R.3.04

5Dr. dr. Ketut Suega, Sp.PD-KHOM

5Interna 081338728421

3nd floor: R.3.05

6Dr. dr. Bagus Komang Satriyasa , M.Repro

6Pharmacology 081805368922

3nd floor: R.3.06

7Dr. dr. I Dewa Made Sukrama, MSi, Sp.MK(K)

7Microbiology 081338291965

3nd floor: R.3.07

8Dr. dr. I Wayan Suranadi , Sp.An.KIC

8Anesthesi 08223847675

3nd floor: R.3.08

9Dr. dr. Wayan Sudana, Sp.THT-KL(K)

9ENT 08123987001

3nd floor: R.3.19

10dr Ni Nyoman Metriani Nesa, M.Sc.,Sp.A

10Pediatric 081337072141

3nd floor: R.3.20

11dr. Elysanti Dwi Martadiani, Sp.Rad.

11Radiology 081805673099

3nd floor: R.3.21

12dr. Anak Agung Gde Yuda Asmara, Sp.OT

12Orthopaedi 081337870347

3nd floor: R.3.22

TIME TABLECLASS A (Regular)



Day/date

Time ActivityVenue

Lecturers

1Wed

20Nov 13

08.00 – 08.30 Introductory block C A.Bagiada08.30 – 09.00 Lecture 1. The Structure of

plasma membrane & transport mechanism of various substances

C Adiputra

09.00 – 10.30 Independent learning10.30 – 11.30 PPKN C Lecture11.30 – 12.00 Break12.00 – 13.30 SGD DR Facilitators13.30 – 14.00 Student project14.00 – 15.00 Plenary Session C Adiputra

2Thur

21Nov 13

08.00 – 09.00 Lecture 2. Organelles and Inclusions

C Linawati

09.00 – 10.30 Independent learning10.30 – 12.00 Student project12.00 – 13.30 SGD DR Facilitators13.30 – 14.00 Break14.00 – 15.00 Plenary Session C Linawati

3Fri

22Nov 13

08.00 – 09.00 Lecture 3. Cytoskeleton C Arijana09.00 – 10.30 Independent learning10.30 – 11.30 PPKN C Lecture11.30 – 12.00 Break12.00 – 13.30 SGD DR Facilitators13.30 – 14.00 Student project14.00 – 15.00 Plenary Session C Arijana

4Mon

25 Nov 13

08.00 – 09.00 Lecture 4. Cell organization in connective tissue

C Ratnayanti

09.00 – 10.30 Independent learning10.30 – 11.30 PPKN C Lecture11.30 – 12.00 Break12.00 – 13.30 SGD DR Facilitators13.30 – 14.00 Student project14.00 – 15.00 Plenary Session C Ratnayanti

5Tues

26 Nov 13

08.00 – 09.00 Lecture 5. Cell organization in epithelial tissue

C Wahyuniari

09.00 – 10.30 Independent learning10.30 – 12.00 Student project12.00 – 13.30 SGD DR Facilitators13.30 – 14.00 Break14.00 – 15.00 Plenary Session C Wahyuniari

6Wed

08.00 – 09.00 Lecture 6. Nucleus and Chromosome

C Mayun

09.00 – 10.30 Independent learning



27Nov13

10.30 – 11.30 PPKN C Lecture11.30 – 12.00 Break12.00 – 13.30 SGD DR Facilitators13.30 – 14.00 Student project14.00 – 15.00 Plenary Session C Mayun

7Thur

28Nov13

Practicum08.00 – 08.30 Explanation of microscopic

structure of connective tissue C Ratnayanti

08.30 – 09.30 Discussion about microscopic structure of connective tissue

DR

09.30 – 11.00 Microscopic structure of connective tissue (A1 – A6) LB Ratnayanti

11.00 – 12.30 Microscopic structure of connective tissue (A7 – A12)

12.30 – 13.00 Break13.00 – 15.00 Student Presentation C Adiputra

ArijanaLinawati

8Fri

29Nov 13

08.00 – 09.00 Lecture 7. Introduction to molecular biology

C Ayu Dewi

09.00 – 10.30 Independent learning10.30 – 11.30 PPKN C Lecture11.30 – 12.00 Break12.00 – 13.30 SGD DR Facilitators13.30 – 14.00 Student project14.00 – 15.00 Plenary Session C Ayu Dewi

9Mon

2 Dec13

08.00 – 09.00 Lecture 8. Gene expression C Ayu Dewi09.00 – 10.30 Independent learning10.30 – 11.30 PPKN C Lecture11.30 – 12.00 Break12.00 – 13.30 SGD DR Facilitators13.30 – 14.00 Student project14.00 – 15.00 Plenary Session C Ayu Dewi

10Tues

3Dec 13

08.00 – 08.30 Explanation of microscopic structure of epithelial tissue

C Wahyuniari

08.30 – 09.30 Discussion about microscopic structure of epithelial tissue

DR

09.30 – 11.00 Microscopic structure of epithelial tissue (A7 – A12) LB Wahyuniari

11.00 – 12.30 Microscopic structure of epithelial tissue (A1 – A6) LB Wahyuniari

12.30 – 13.00 Break13.00 – 15.00 Student Presentation C Linawati

MayunRatnayanti



11Wed

4Dec13

08.00 – 09.00 Lecture 9. Enzyme C Tianing09.00 – 10.30 Independent learning10.30 – 11.30 PPKN C Lecture11.30 – 12.00 Break12.00 – 13.30 SGD DR Facilitators13.30 – 14.00 Student project14.00 – 15.00 Plenary Session C Tianing

12Thur

5Dec13

08.00 – 09.00 Lecture 10. Signal Transduction

C Wihandani

09.00 – 11.00 Independent learning11.00 – 12.00 Student Presentation C Ratnayanti

Wahyuniari12.00 – 13.30 SGD DR Facilitators13.30 – 14.00 Break14.00 – 15.00 Plenary Session C Wihandani

13Fri

6Dec13

08.00 – 09.00 Lecture 11. Cell Cycle C Mayun09.00 – 10.30 Independent learning10.30 – 11.30 PPKN C Lecture11.30 – 12.00 Break12.00 – 13.30 SGD DR Facilitators13.30 – 14.00 Student project14.00 – 15.00 Plenary Session C Mayun

14Mon

9 Dec13

08.00 – 09.00 Lecture 12. Bioenergetics and Oxidative metabolism

C Surudarma

09.00 – 10.30 Independent learning10.30 – 11.30 PPKN C Lecture11.30 – 12.00 Break12.00 – 13.30 SGD DR Facilitators13.30 – 14.00 Student project14.00 – 15.00 Plenary Session C Surudarma

15Tues

10 Dec13

08.00 – 09.00 Lecture 13. Cellular Responses to Injury/Death

C Sri Widnyani

09.00 – 10.00 Independent learning10.00 – 11.30 Meeting of student

representativesC Planners

team, Facilitators

11.30 – 12.00 Independent learning12.00 – 13.30 SGD DR Facilitators13.30 – 14.00 Break14.00 – 15.00 Plenary Session C Sri Widnyani

16

Wed

08.00 – 09.00 Clinical application of molecular biology laboratory

C Budayanti

09.00 – 10.30 Student Presentation C Ayu Dewi10.30 – 11.30 PPKn C Lecture11.30 – 12.00 Break



11Dec13

12.00 – 13.00 Discussion about clinical application of molecular laboratory

13.00 – 14.00 Student Presentation C Wihandani14.00 – 15.00 Plenary session C Budayanti

17

Thur

12Dec13


structure of cell injury CSri Widnyani

08.30 – 09.30 Discussion about microscopic structure of cell injury

DR

09.30 – 11.00 Microscopic structure of cell injury (A1 – A6) LB Sri Widnyani

11.00 – 12.30 Microscopic structure of cell injury (A7 – A12)

12.30 – 13.00 Break13.00 – 15.00 Student Presentation C Mayun

Surudarma Bagiada

18

Fri

13Dec13

08.00 – 09.00 Lecture 14. Application of molecular biology in medicine

C Januartha

09.00 – 10.30 Independent learning10.30 – 11.30 PPKN C Lecture11.30 – 12.00 Break12.00 – 13.30 SGD DR Facilitators13.30 – 14.00 Break14.00 – 15.00 Plenary Session C Januartha

19Mon

16Dec 13

08.00 – 10.30 Isolation of DNA C Tianing10.30 – 11.30 PPKn C Lecture 11.30 – 12.30 Break12.30 – 15.00 Student Presentation C Sri Widnyani

JanuarthaArtini

20Tues

17Dec 13

08.00 – 09.00 Lecture 15. Cellular intervention/Therapies

C Artini

09.00 – 10.30 Independent learning10.30 – 12.00 Student project12.00 – 13.30 SGD DR Facilitators13.30 – 14.00 Break14.00 – 15.00 Plenary Session C Artini

Wed18

Dec 13

Preparation for Final Test

Thur19

Dec 10.00 – 14.00

AssessmentC Team



13

Notes: C : Class room (4.014thfloor)DR : Discussion RoomSGD : Small Group DiscussionLB : Lab Bersama (4th floor)

TIME TABLECLASS B (English Class)

Day/date

Time ActivityVenue

Lecturers

1 09.00 – 09.30 Introductory block C A.Bagiada



Wed

20Nov 13

09.30 – 10.00 Lecture 1. The Structure of plasma membrane & transport mechanism of various substances

C Adiputra

10.00 – 11.30 Independent Learning11.30 – 12.30 PPKn C Lecture12.30 – 13.00 Break13.00 – 13.30 Student Project13.30 – 15.00 SGD DR Facilitators15.00 – 16.00 Plenary Session C Adiputra

2Thur

21Nov 13

09.00 – 10.00 Lecture 2. Organelles and Inclusions

C Linawati

10.00 – 11.30 Student project11.30 – 12.00 Break12.00 – 13.30 Independent Learning13.30 – 15.00 SGD DR Facilitators15.00 – 16.00 Plenary Session C Linawati

3Fri

22Nov 13

09.00 – 10.00 Lecture 3. Cytoskeleton C Arijana10.00 – 11.30 Independent Learning11.30 – 12.30 PPKn C Lecture12.30 – 13.00 Break13.00 – 13.30 Student Project13.30 – 15.00 SGD DR Facilitators15.00 – 16.00 Plenary Session C Arijana

4Mon

25 Nov 13

09.00 – 10.00 Lecture 4. Cell organization in connective tissue

C Ratnayanti

10.00 – 11.30 Independent Learning11.30 – 12.30 PPKn C Lecture12.30 – 13.00 Break13.00 – 13.30 Student Project13.30 – 15.00 SGD DR Facilitators15.00 – 16.00 Plenary Session C Ratnayanti

5Tues

26 Nov 13

09.00 – 10.00 Lecture 5. Cell organization in epithelial tissue

C Wahyuniari

10.00 – 11.30 Student project11.30 – 12.00 Break12.00 – 13.30 Independent Learning13.30 – 15.00 SGD DR Facilitators15.00 – 16.00 Plenary Session C Wahyuniari

6Wed

27Nov13

09.00 – 10.00 Lecture 6. Nucleus and Chromosome

C Mayun

10.00 – 11.30 Independent Learning11.30 – 12.30 PPKn C Lecture12.30 – 13.00 Break13.00 – 13.30 Student Project13.30 – 15.00 SGD DR Facilitators



15.00 – 16.00 Plenary Session C Mayun

7Thur

28Nov13


structure of connective tissue CRatnayanti

09.30 – 11.30 Student Presentation C Adiputra Arijana

Linawati11.30 – 12.30 Discussion about microscopic

structure of connective tissue DR

12.30 – 13.00 Break13.00 – 14.30 Microscopic structure of

connective tissue (B1-B6) LB Ratnayanti14.30 – 16.00 Microscopic structure of

connective tissue (B7-B12) LB Ratnayanti

8Fri

29Nov13

09.00 – 10.00 Lecture 7. Introduction to molecular biology

C Ayu Dewi

10.00 – 11.30 Independent Learning11.30 – 12.30 PPKn C Lecture12.30 – 13.00 Break13.00 – 13.30 Student Project13.30 – 15.00 SGD DR Facilitators15.00 – 16.00 Plenary Session C Ayu Dewi

9Mon

2 Dec13

09.00 – 10.00 Lecture 8. Gene expression C Ayu Dewi10.00 – 11.30 Independent Learning11.30 – 12.30 PPKn C Lecture12.30 – 13.00 Break13.00 – 13.30 Student Project13.30 – 15.00 SGD DR Facilitators15.00 – 16.00 Plenary Session C Ayu Dewi

10Tues

3Dec13

09.00 – 09.30 Explanation of microscopic structure of epithelial tissue C

Wahyuniari

09.30 – 11.30 Student Presentation C Linawati Mayun

Ratnayanti11.30 – 12.30 Discussion about microscopic

structure of epithelial tissue DR

12.30 – 13.00 Break13.00 – 14.30 Microscopic structure of

epithelial tissue (B1-B6) LB Wahyuniari14.30 – 16.00 Microscopic structure of

epithelial tissue (B7 – B12) LB Wahyuniari

11Wed

09.00 – 10.00 Lecture 9. Enzyme C Tianing10.00 – 11.30 Independent Learning11.30 – 12.30 PPKn C Lecture



4Dec13

12.30 – 13.00 Break13.00 – 13.30 Student Project13.30 – 15.00 SGD DR Facilitators15.00 – 16.00 Plenary Session C Tianing

12Thur

5Dec13

09.00 – 10.00 Lecture 10. Signal Transduction

C Wihandani

10.00 – 11.00 Student Presentation C RatnayantiWahyuniari

11.00 – 12.00 Break12.00 – 13.30 Independent Learning13.30 – 15.00 SGD DR Facilitators15.00 – 16.00 Plenary Session C Wihandani

13Fri

6Dec13

09.00 – 10.00 Lecture 11. Cell Cycle C Mayun10.00 – 11.30 Independent Learning11.30 – 12.30 PPKn C Lecture12.30 – 13.00 Break13.00 – 13.30 Student Project13.30 – 15.00 SGD DR Facilitators15.00 – 16.00 Plenary Session C Mayun

14Mon

9 Dec13

09.00 – 10.00 Lecture 12. Bioenergetics and Oxidative Metabolism

C Surudarma

10.00 – 11.30 Independent Learning11.30 – 12.30 PPKn C Lecture12.30 – 13.00 Break13.00 – 13.30 Student Project13.30 – 15.00 SGD DR Facilitators15.00 – 16.00 Plenary Session C Surudarma

15Tues

10 Dec13

09.00 – 10.00 Lecture 13. Cellular Responses to Injury/Death

C Sri Widnyani

10.00 – 11.30 Meeting of student representative

C Planners team,

Facilitators11.30 – 12.00 Break12.00 – 13.30 Independent Learning13.30 – 15.00 SGD DR Facilitators15.00 – 16.00 Plenary Session C Sri Widnyani

16

Wed

11Dec13

09.00 – 10.00 Clinical application of molecular laboratory

LB Budayanti

10.00 – 11.30 Student Presentation LB Ayu Dewi11.30 – 12.30 PPKn C Lecture12.30 – 13.00 Break DR13.00 – 14.00 Discussion about clinical

application of molecular laboratory

14.00 – 15.00 Student Presentation LB Wihandani



15.00 – 16.00 Plenary Session LB Budayanti

17

Thur

12Dec13


structure of cell injury CSri Widnyani

09.30 – 11.30 Student Presentation C SurudarmaBagiada

11.30 – 12.30 Discussion about microscopic structure of cell injury

DR

12.30 – 13.00 Break13.00 – 14.30 Microscopic structure of cell

injury (B1 - B5) LB Sri Widnyani

14.30 – 16.00 Microscopic structure of cell injury (B6 – B10)

18

Fri

13Dec13

09.00 – 10.00 Lecture 14. Application of molecular biology in medicine

C Januartha

10.00 – 11.30 Independent Learning11.30 – 12.30 PPKn C Lecture12.30 – 13.00 Break13.00 – 13.30 Student Project13.30 – 15.00 SGD DR Facilitators15.00 – 16.00 Plenary Session C Januartha

19Mon

16Dec 13

09.00 – 11.30 Student Presentation LB Sri WidnyaniJanuartha

Artini11.30 – 12.30 PPKn C Lecture12.30 – 13.30 Break13.30 – 16.00 Isolation of DNA LB Tianing

20Tues

17Dec 13

09.00 – 10.00 Lecture 15. Cellular intervention/Therapies

C Artini

10.00 – 11.30 Student project11.30 – 12.00 Break12.00 – 13.30 Independent Learning13.30 – 15.00 SGD DR Facilitators15.00 – 16.00 Plenary Session C Artini

Wed18

Dec 13

Preparation for Final Test

Thur19

Dec 13

10.00 – 14.00 Assessment C Team

Notes: C : Class room (4.014thfloor)DR : Discussion Room



SGD : Small Group DiscussionLB : Lab Bersama (4thfloor)

~ MEETING ~

Meeting of the Student Representatives and the facilitatorsThe meeting between block planners team and the student group representatives

will be held on Tuesday, 10th December 2013, at 10.00 until 11.30 am at Class room (4.01). In this meeting, all of the student group representatives (approximately 24 students) are expected to give suggestions and inputs or complaints to the team planners for improvement. For this purpose, every student group must choose one student as their representative to attend the meeting.

~ PLENARY SESSION ~



For each learning task, the student is requested to prepare a group report. The report will be presented in plenary session. Lecturer in charge will choose the group randomly. The aim of this presentation is to make similar perception about the topic that has been given.

~ ASSESSMENT METHOD ~

Assessment will be performed on Thursday, 19th December 2013, 09.00 until 13.00 a.m for both Regular class and English class. There are 100 questions for the examination that consist of Multiple Choice Question (MCQ).

The borderline to pass exam is 70. The proportion of examination score are:Small group discussion : 5%Paper (student project) : 15%Final exam (MCQ) : 80%

~ STUDENT PROJECT ~

Students have to write a paper with topics that has been given by lecturer. The topic will be chosen randomly on day 1. Each small group discussion is consist of 2 paper with different tittle. Therefore, 1 paper will be wrote by 5-7 students. Students can discuss about content of paper with relevant lecturer. Students can discuss about format of paper with respective facilitator. Students write a paper as student project and will be presented in front of the class. The paper and the presentation will be evaluated by respective facilitator and lecturer.

Format of the paper :1. Cover Tittle

Name Student Registration Number

Faculty of Medicine, Udayana University 2013

2. Introduction 3. Content 4. Conclusion5. References (minimal 3 references)

Example :Journal

Porrini M, Risso PL. 2011. Lymphocyte Lycopene Concentration and DNA Protection from Oxidative Damage is Increased in Woman. Am J Clin Nutr 11(1):79-84.Textbook

Abbas AK, Lichtman AH, Pober JS. 2011. Cellular and Molecular Immunology. 4th ed. Pennysylvania: WB Saunders Co. Pp 1636-1642.

Note.5-10 pages; 1,5 spasi; Times new roman 12

Paper Assessment FormBlock The Cell as Biochemical Machinery

Name : ...........................................



Student Reg. Number : ...........................................Facilitator : ...........................................Title : ...........................................

Supervisor’s (Facilitator) scoring with 60% qualification :

No Item Assessment Range Score (%) Score1. Ability to find the literature 0-202. Communication/Attitude 0-303 Quality of material 0-404 Student’s interest and

motivation0-10

TOTAL 100

Supervisor,

(...........................................)NIP.

Evaluator’sscoring (presentation) with 40% qualification :

No Item Assessment Range Score (%) Score1. Quality of material 0-602. Capability of information

searching0-10

3 Critical thinking 0-30TOTAL 100

Evaluator,

(................................................) NIP.

Topic of Student Project

Regular and English ClassNo SGD Title Evaluator Date of

presentation

1 The effect of free radical on cell membrane Adiputra 28 Nov2 Glial Fibrillary Acidic Protein in Stroke Patients Arijana 28 Nov3 Role of Vincristine in Treatment of Multiple

MyelomaArijana 28 Nov

4 Lysosomal disorders Linawati 28 Nov5 Ribosomal disorders Linawati 3 Dec



6 Abnormalities in number of sex chromosomes Mayun 3 Dec 7 Abnormalities in number of autosom Mayun 3 Dec 8 Connective Tissue Disorder Ratnayanti 3 Dec 9 Connective Tissue Disorder Ratnayanti 5 Dec

10 Endothelial function and dysfunction Wahyuniari 5 Dec11 The mutation of DNA Repair system and cancer Ayu Dewi 11 Dec12 Telomerase and aging Ayu Dewi 11 Dec13 Dogma central in molecular biology Ayu Dewi 11 Dec14 The role of calcium in nerve transmission Wihandani 11 Dec15 The role of DAG in signal transduction Wihandani 11 Dec16 The role of cyclin and CDKs in cell cycle Mayun 12 Dec17 Bacterial protein synthetic machinery inhibitors Surudarma 12 Dec18 Mithocondrial poisons Surudarma 12 Dec19 Enzyme serum in diagnose of diseases Bagiada 12 Dec20 Ischemic and hypoxic injury in myocardial

infarctionSri Widnyani 16 Dec

21 Free radicals and cancer Sri Widnyani 16 Dec22 PCR in diagnosis of infectious diseases Januartha 16 Dec23 Pharmacology changes in drug response due to

chronic drug useArtini 16 Dec

24 The role of genetic factor in the variation of drug response

Artini 16 Dec

~ LEARNING PROGRAMS ~

Lectures

Lecturer : Prof adiputraObjective : to understand the structure of plasma membraneAbstract :

UdayanaUniversity Faculty of Medicine, MEU

DAY 1: The Structure of the Plasma Membrane & the Transport Mechanism of Various Substances

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Every eukaryotic cell is covered by plasma membrane, which separates the extracellular from the intracellular fluid. Plasma membrane is mainly composed of phospholipids bilayer, protein and lesser amount of polysaccharide and cholesterol.The functions of plasma membrane are maintaining cell integrity, as a barrier at membrane-plasma and recognizing antigens.

Phospholipid Bilayer MembraneDominant phospholipids component of plasma membrane are phosphatidylcholine, phosphatidylethanolamine, phosphate-dylserine and sphingomyelin. Other phopolipids e.g inositol phospholipids, arachidonic acid phospholipids are present in lesser amount, even though its have important functional value, phospholipids bilayer is said to be amphipathic because it has hydrophilic, hydrophobic nature. Small uncharged and lipid molecules can get through plasma membrane, it is called simple diffusion.

Protein MembraneProtein of plasma membrane consists of integral protein (transmembrane protein/multipass protein (fluid mosaic model) and peripheral protein. These proteins have role in selective permeability as facilitated diffusion. Integral protein may function as channel protein, carrier protein. Channel protein could adjust with the across hydrophilic molecule by forming polar inner lining channel, which could be gated channel (ligand-gated channels, voltage-gated channel and G-protein gated ion channel) and ungated channel.

Carbohydrate and Cholesterol MembranePolysaccharide molecule on the outer side of plasma membrane is called glycocalyx, can inform of glycoprotein and glycolipid. It functions in protection.

Lecturer : Prof AdiputraObjective: to understand the transport mechanism of various substances through

plasma membraneAbstract :

Cell membrane separates cytoplasm (intacellular fluid) from its environment (extracellular fluid). Both fluids consist of different substances which are maintained by the existence of cell membrane. Its structure makes the transport of spesific substances occur to support cell life.

There are two types of transport mechanism across the cell membrane i.e. passive transport (diffusion) and active transport. The diffusion itself can be differentiated into simple diffusion and facilitated diffusion, with its different mechanism. There are too many factors that can affect diffusion, each of which must be learnt by the students. Active transport can be divided inti primary active and with its own character including the substance to be transported and factors that involve.

Transport across cell membrane can describe many physiologic processes that take place in different parts of human cells such as intestine epithelium, renalis tubules epithelial, exocrine glands epithel, gall bladder epithel and membrane of choroideus plexus in the brain. All will be learnt in this topic.

Lecturer : dr. Ni Made Linawati, M.Si


DAY 2: Organelles & Inclusion

21


Objective: to differentiate functionally cytoplasmic organelles from cytoplasmic inclusions

Abstract :

The cytoplasm contains other organelles, which are better visualized with an electron microscope that can view components as small as 2 nm. The organelles include the nucleus, mitochondria, endoplasmic reticulum, Golgi apparatus, lysosomes, peroxisomes, proteasomes, cytoskeleton, and plasma membrane.Mitochondria contain a double membrane; with the inner membrane containing many infolds, referred to as the cristae that contain the machinery for cellular respiration. Mitochondria contain their own mitochondrial DNA and make proteins.The endoplasmic reticulum (ER) consists of flattened sheets, sacs, and tubes of membranes throughout the cytoplasm and is responsible for protein synthesis (rough ER) and lipid metabolism (smooth ER and rough ER). The Golgi apparatus is a stack of flattened membranous sacs involved in the modification and transport of molecules made in the endoplasmic reticulum. The membrane-enclosed Lysosome contains enzymes required for intracellular digestion. Peroxisomes are membrane-bound organelles in which hydrogen peroxide is generated and degraded. Proteasomes responsible for proteolysis of malformed and ubiquitin-tagged protein or antigenic protein have to be cleaved into epitopes.

Cytoplasmic inclusion is not always present in every cell. Glycogen is the polymer of simple glucose. Blood glucose metabolized within cell to produce ATP or stored in the glycogen vesicle.Lipid, stored in triacylglycerol form as various sizes of droplets whether as a single and hugedroplet (lipocytes), or small and multiple consisted of ester cholesterol (dominantly within cells that synthesized steroid hormones).Lipofuchsin pigmen is residual bodies that unable to be digested by lysosomes, permanently in nature. The amount become increasingly in number due to the increasing of life span and often existed in nervous cell.

Lecturer : dr. IGK Nym Arijana, M.Si.MedObjective : to understand the general structure and function of cytoskeleton in

relation to endocytosis, pinocytosis, and locomotionAbstract :

The cytoskeleton is a dynamic three-dimensional structure that fills the cytoplasm, acts as both muscle and skeleton. This structure maintains cell shape, protects the cell, enables cellular motion (using structures such as flagella, cilia and lamellipodia), and plays important roles in both intracellular transport (the movement of vesicles and organelles, for example) and cellular division.

The long fibers of the cytoskeleton are polymers of subunits. The primary types of fibers comprising the cytoskeleton are micro (thin) filaments, microtubules, and intermediate filaments.

Thin filaments are fine, thread-like protein fibers, 6 nm in diameter, composed of two intertwined chains of G-actin. Thin filaments are most concentrated just beneath the cell membrane, and are responsible for resisting tension and maintaining cellular shape, forming cytoplasmatic protuberances (pseudopodia and microvillus), and participation in some cell-to-cell or cell-to-matrix junctions. Thin filaments are also important for cytokinesis (formation of the cleavage furrow) and, association with myosin responsible for muscle contraction. Actin/Myosin interactions also help produce cytoplasmic streaming in most cells.


DAY 3: Cytoskeleton

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Microtubules are hollow-like cylindrical structure, 25 nm in diameter. They are composed of subunits of the protein tubulin--these subunits are termed alpha and beta. . They have a very dynamic behaviour, binding GTP for polymerization. They are commonly organized by the Centrosome. Microtubules act as a scaffold to determine cell shape, and provide a set of "tracks" for cell organelles and vesicles to move on. Microtubules also form the spindle fibers for separating chromosomes during mitosis (mitotic spindle). When arranged in geometric patterns inside flagella and cilia, they are used for locomotionIntermediate filaments are about 10 nm diameter and provide tensile strength for the cell. These filaments, are more stable (strongly bound) than actin filaments, and heterogeneous constituents of the cytoskeleton.]Like actin filaments, they function in the maintenance of cell-shape by bearing tension. Intermediate filaments organize the internal three-dimensional structure of the cell, anchoring organelles and serving as structural components of the nuclear lamina and sarcomere. They also participate in some cell-cell and cell-matrix junctions. Different types of intermediate filaments are: vimentin, keratin, neurofilaments, lamin, and desmin.

Lecturer : dr. IGA Dewi Ratnayanthi S.KedObjective : to understand the functional structure of cells organization in

connective tissues and its clinical implication. Abstract :

Most of the cells in multicellular organisms are organized into cooperative assemblies called tissues, which in turn are associated in various combinants to form larger functional units called organs. The four basic tissue types are nerve, muscle, epithelial tissue, and connective tissue. These tissues are found in most organs.

As one of the basic tissue, Connective tissue, as it’s name implies, is a structure that functions to relate and joint other tissue in our body. Therefore, it can be found in every organ or as an organ itself. Beside that bare in it’s name, connective tissue has many important function, such as support, protection, transportation, storage, and hormone production. As one of the basic tissue, connective tissue may vary in form depending on their components. Connective tissue generally consists of two components, which are cells and extracellular matrix. The main component is fibroblast cell, because it is the major source of the extracellular matrix. Histologically, connective tissue is classified into embryonal and proper connective tissue. Embryonal connective tissue is composed of mesenchym and mucous tissue. These tissues are only found in embryo or umbilical cord. The second type connective tissue is found in mature tissue or organ. It composed of four types, which are loose, dense, reticular and adipose tissue. Connective tissue can also be specialized into distinct types of tissue; bone, cartilage, and blood. These types of tissue will be independently discussed on the regard block.

Lecturer : dr. Ida Ayu Ika Wahyuniari, M.KesObjective : to understand the functional structure of cells organization in epithelial

tissues and its clinical implication.Abstract :


DAY 4: Cell organization in Connective tissue

DAY 5: Cell organization in Epithelial tissue

23


All tissues are composed of cells and an extracellular matrix. As one of the basic tissue, epithelial tissue, are principally cellular in composition, although a small amount of extracellular matrix is present, called basal lamina. Cells in epithelial tissues can adhere to one another (cell-cell adhesion) and adhere to components of extracellular matrix/basal lamina (cell-matrix adhesion) through specialized integral membrane proteins called cell-adhesion molecules (CAMs) that often cluster into specialized cell junctions, such as occluding junction (tight junction), anchoring junction (zonula adherens, desmosomes, hemidesmosomes), and communicating junction (gap junction).

Epithelial tissue is present in two forms : as sheets of contiguous cells (epithelia) and as glands. The function of epithelial tissues are protection, transcellullar transport, secretion, absorption, selective permeability, and detection of sensations. These function is related to the morphology of epithelial cells.

Lecturer : dr. IGN Mayun, Sp.HKObjective : to understand the general functional structure of cell nucleus and

chromosomeAbstract :The nucleus is the largest organelle of the cell. where the size, shape of the nucleus are generally constant for particular cell type. The nucleus is usually spherical and is centrally located in the cell. Each cell usually has a single nucleus, some cells possess several nuclei ( such as osteoclast) , where mature red blood cells have extruded nuclei. The nucleus contains nearly all of DNA (deoxyribonucleic acid) for RNA (ribonucleic acid) synthesis. It has nucleolus for the essembly of ribosomal subunits.The nucleus bounded by two lipid membranes, houses three major components:

- Chromatins. The genetic material of the cell- The nucleolus, the center for ribosomal RNA ( r RNA ) synthesis- Nucleoplasm, containing macromolecules and nuclear particles involved in the

maintenance of the cell.

Nuclear envelope is composed of two parallel unit membranes that fuse with each other at certain regions to form perforation known as nuclear pore.

Lecturer : Dr. rer. Nat. dr. Ni Nyoman Ayu Dewi, M.Si Objective : to understand the principles mechanisms by which genes control general

cell functions Abstract :

The term genome comes from gene and chromosome. Genome is the entire DNA of one species. Human Genome Project (HGP) is a project to find out the total DNA ofhuman.

Part of DNA in chromosome which has a special function is called gene. Recently, only about 5% of genome is identified as gene. According to their location, we identify 2


DAY 6: Nucleus & Chromosomes

DAY 7: Introduction to Molecular Biology

24


kinds of DNA i.e. nuclear DNA (n-DNA) and mitochondrial DNA (mt-DNA). Recent researches have focused on mtDNA because of its special characteristic (small molecule, prone to get mutation and its maternal inheritance characteristic).

Molecular mechanism of inheritance involves a process known as replication in which parental DNA is divided into two DNA progenies by semi conservative mechanism. An error which happens in replication process will repair through DNA repair system.

Central dogma explains how the DNA can act as a messenger molecule which carries the inheritance characteristic [DNA (replication) transcription translation]. Gene expression requires two processes i.e. transcription and translation. DNA is transcribed into 3 forms of RNA i.e. mRNA, tRNA, dan rRNA which involved in translation process (protein synthesis). mRNA will acts as a template for protein synthesis. tRNA contains the anticodon that recognizes the codon in mRNA corresponding to the amino acid it carries and several rRNA associate with a large number of proteins to form the small and large ribosomal subunits. Codon is a three-base sequence in mRNA, are arranged to form amino acid which sequence is inherited from the parental. As we know, there are 4 bases so we have 64 codons (43) consist of 61 generating codons and 3 stop codons. The genetic code stand for 20 amino acids, it means that 1 amino acid can be coded by more than 1 codon. Genetic code is almost universal for both nDNA inti and mtDNA, wirh several exception: AGA and AGG encode for arginin in nDNA but act as stop codon in mtDNA, UGA code for stop codon in nDNA but encode tryptophan in mtDNA.

Lecturer : Dr. rer. Nat. dr. Ni Nyoman Ayu Dewi, M.SiObjective : to understand the principles mechanisms of gene expression in normal

and abnormal cells Abstract :Gene expression is the process by which a gene is decoded and its information is used to produce polypeptide or RNA molecule. A cell uses some of the information encoded by DNA to manufacture protein. To do this, first the process of transcription copies a particular part of the DNA sequence of a chromosome into an RNA molecule that complement to one strand of the DNA double helix. Then the process of translation uses the information copied into messenger RNA (mRNA) to manufacture a specific protein by aligning and joining the specified amino acid. Messenger RNA is a template of protein synthesis where sequences of codon are present. There are 64 codons stand for 20 amino acids. The protein synthesis is started by initiating codon and will be lasted by stop codon. Many kind of protein are produced in our body. Each has a specific function.

Lecturer : Ni Wayan Tianing, S.Si., M.Kes Objective : to understand the enzyme as a protein that regulates metabolism and its function in medical diagnostic.Abstract :

Gene encodes the information that determines the structure of protein. In turned the protein structure determines its biological activity. Through the biological of protein inthe cells physiological role is determined. Protein are the most abundant and vital organic molecule of the cells. Why? Its cause by great variety of protein functions in the physiological activity of the cell. Protein are capable assuming so many roles, because their structure can vary enormously, depend on the variation of amino acids sequence of the


DAY 8: Gene Expression

DAY 9: Basic Feature of Enzyme

25


molecule. One of the important roles of protein is act as an enzyme. Another is receptor, and transport protein such as hemoglobin, transferin, immunoglobin, etc.

Thus enzyme is a specific protein catalyst, because its catalyst only limited, usually one kind of reaction. Non protein catalyst can catalyst many kind of reactions (H+, OH-). The complete enzyme called holoenzyme. Holoenzyme consists of apoenzyme and coenzyme. Some factors influencing the velocity of the reactin (such as enzyme concentration, substrate concentration, pH, temperature, some inhibitor substance, etc).Many drugs and poisons irreversibly inhibit enzymes. Measuring of activity level of enzyme in serum can help physician in more accurate diagnose of diseases. The nonfunctional of enzyme serum activity are more important for above purpose.

Lecturer : dr. Desak Made Wihandani, M Kes.Objective : to understand the signaling mechanism underlying cell to cell

communication & its clinical or practical implicationsAbstract :

Signal transduction pathways allow cells to respond to their environment and to change their behavior accordingly. Signals are sensed by a receptor and changed in their form so that they can exert their final effect on the cell.

Signals take a variety of forms, but for our purposes there only two. The first type are signals that go into the cell, bind to internal receptors and excert their effects.Steroid hormones, vitamin D, thyroid hormone, and retinoids are the only members of this class. All of the intracellular receptors ultimately activate the transcription of regulated genes. The common feature of signals that enter the cell is that they are small lipophilic molecules that can across the cell membrane. All the other signals exert their effects by binding to extracellular receptor and initiating a cascade of signaling events. They work by activating a phosphorylation cascade and/or the release of second messengers in the cell.

Receptors recognize a signal molecule and transmit the signal by activating a downstream signaling pathway. Cytosolic receptors are soluble, cytoplasmic proteins (signal must get inside). The signal grosses the membrane and activates gene transcription. Transmembrane receptors span a membrane (signal outside, response outside). This signal activates a channel, an enzyme, or a G-protein cascade.

Lecturer : dr. I G N Mayun, Sp.HKObjective : to understand normal and abnormal cell cycle and its clinical implicationsAbstract :

The cell cycle is a series of events within the cell that prepare the cell for dividing into two daughter cells. The cell cycle is divided into two major events: interphase and mitosis. Interphase period is a longer period of time and take place 95% of cycle, while mitosis, a shorter period of time and take place 5% of cycle. The capability of the cell to begin and


DAY 10: Signal Transduction

DAY 11: Cell Cycle

26


advance through the cell cycle is governed by the presence and interactions of a group of related proteins known as cyclin, with specific cyclin dependent kinase (CDKs).

In interphase period, occur replication of genetic material and the cell increases its size. Interphase is subdivided into three phases: G1 (Gap) phase, when the synthesis of macromolecule essential for DNA duplication begins; S (synthesis), when the DNA is duplicated; and G2 phase, when the cell undergoes preparations for mitosis. There are some cells able to undergo mitosis permanently (e.g., muscle cells, neurons), while temporarily (e.g., lymphocytes) will return to the cell cycle at a later time. Cell that have left the cell cycle are said to be in a resting stage, the G0 or the stable phase. Cell division can occur by mitosis and meiosis. Mitosis is cell division that result in the formation of two daughter cells whose chromosome number is equal from theparental chromosome number (diploid), while meiosis will give rise daughter cells whose chromosome number is reduced from the diploid (2n) to the haploid (1n) number (1/2 from mother chromosome number).

The process of mitosis is divided into five stage: prophase, prometaphase, metaphase, anaphase, an telophase; while in meiosis consist of two events: meiosis I and meiosis II. The last stage of cell division is cytokinesis.

Lecturer : dr. Wayan Surudarma, M.SiObjective : to understand the bioenergetics and oxidative metabolismAbstract :

Oxidation of metabolic fuels is essential to life. In higher organisms, fuels, such as carbohydrates and lipids are metabolized to carbon dioxide and water. Most metabolic energy is provided by oxidation-reduction reactions in mitochondria. This is no small feat, because warm-blooded animals have such variable demands for energy from such processes as thermogenesis at low temperatures, stimulation of ATP synthesis during stress, degradation of excess food, efficient use of nutrients during starvation, and coupling of ATP synthesis with the rate of respiration.

This topic will provide an introduction to the concept of free energy, oxidative phosphorylation and the transduction of energy from fuels into useful work. The pathways and specific molecules through which electrons are transported to oxygen and the mechanism of generation of ATP will be described and related to the structure of the mitochondrion, the powerhouse of the cell and the major source of cellular ATP. Lastly, these biochemical processes will be applied to human health and disease.

The electron transport system consists of at least eight major electron carriers that are located in the inner mitochondrial membrane, each of which is isolable as a complex or as a single molecule. Electrons from four major flavoproteins feed electrons to ubiquinone, the first member of the common pathway. Energy derived from the conductance of electrons through the electron transport system is used by three of the complexes to pump protons into the intermembrane space, creating an electrochemical gradient or proton motive force. The proton gradient is used to power ATP synthase for synthesis of ATP by rotary catalysis. Numerous toxins can severely impair the electron transport system, the ATP synthase and the translocase that exchanges ATP and ADP across the inner mitochondrial membrane. The rate of ATP production by the electron transport system is regulated by modulation of the proton gradient, by allosteric modification and phosphorylation-dephosphorylation and by thyroid hormones. At least five uncoupling proteins (UCP) with specific tissue distributions occur in the inner mitochondrial membrane, and they all regulate the membrane potential and thermogenesis. Chronic diseases or conditions, such as diabetes,


DAY 12 : Bioenergetics and Oxidative Metabolism

27


cancer, obesity, and aging all have metabolic links to dysregulation of oxidative phosphorylation through effects on electron transport system and ATP synthase.

Lecturer : dr. Sri Widnyani, Sp.PAObjective : to understand the cellular responses to injury and death (necrosis and

apoptosis)Abstract :

Cells are active participants in their environment, constantly adjusting structure and function to accommodate changing demands and extracellular stresses. Cells tend to preserve their immediate environment and intracellular milieu within relatively narrow range of physiologic parameters. As cells encounter physiologic stresses or pathologic stimuli, they can undergo adaptation, achieving a new steady state and preserving viability. If the adaptive capability is exceeded, cells injury develop. Within certain limits, injury is reversible, and cells return to a stable baseline; however with severe or persistent stress, irreversible injury results, and the effected cells die. In this topic, student will learn the causes of cell injury and the mechanisms by which they exert their effects, cellular and sub cellular adaptation to injury, morphology of injured cells, apoptosis, and cellular senescence.

Lecturer : dr. Komang Januartha, M.KesObjective : Explain applications of molecular biology in medicineAbstract :

Following the advancement of science and technology, medical science also reaches its molecular state. Genetic, genomic and proteomic open the way to a new deeper understanding about processes inside the human body, and provide more accurate intervention tools when disturbance in body function occur. Scientists believe that all diseases have genetic component, whether it is inherited or as a body response against environmental stress. Therefore, genetic plays an important role in prevention, diagnosis and therapy for infectious and non-infectious diseases.

Molecular medicine is the clinical application of molecular biology for prevention, diagnosis and treatment of diseases, both infectious and non-infectious. Molecular medicine can be used to increase the accuracy of diagnostic method, detection of predisposed genetic disorders, designing new drugs based on molecular information, gene therapy, and development of DNA-vaccine and also in forensic medicine.

Testing for inherited diseases and susceptibilities will become standard practice as health care becomes increasingly individualized. Tests that detect specific variations in genetic material will enable physicians to select treatments that a person can tolerate and that are the most likely to be effective. Genetics impacts our lives in diverse ways. Genetic tests serve many purposes. They are widely used to screen newborns for a variety of disorders. Often this information enables the doctors to minimize the damage caused by the mutation. In oncology, doctors use gene testing to diagnose cancer, to classify cancer into subtypes, or to predict a patient’s responsiveness to new treatments.

Much of the excitement today centers on gene expression profiling that use a technology called microarrays. A DNA microarray is a thin-sized chip that has been spotted


DAY 13: Cellular Responses to Injury & Death

DAY 14: Applications Of Molecular Biology In Medicine

28


at fixed locations with thousands of single-stranded DNA fragments corresponding to various genes of interest. A single microarray may contain 10,000 or more spots, each containing pieces of DNA from a different gene. Fluorescent-labeled probe DNA fragments are added to ask if there are any places on the microarray where the probe strands can match and bind. Complete patterns of gene activity can be captured with this technology.

Genes, which are carried on chromosomes, are the basic physical and functional units of heredity. Genes are specific sequences of bases that encode instructions on how to make proteins. Although genes get a lot of attention, it’s the proteins that perform most life functions and even make up the majority of cellular structures. When genes are altered so that the encoded proteins are unable to carry out their normal functions, genetic disorders can result. Gene therapy is a technique for correcting defective genes responsible for disease development. Researchers may use several approaches for correcting faulty genes.

Lecturer : dr. IGA Artini, M.SiObjective : to understand pharmacology, and pharmacodynamic (action of drugs to

the body, mechanism of action)

Abstract :Drugs are agents that are used for diagnosed diseases, prevent diseases, treat disease, rehabilitation, and prevent pregnant. The action of drugs on the body or the effects of drugs on biologic systems is call pharmacodynamic. Most drugs exert their specific effects in the body by forming a bound with some cellular constituent known as receptor. Drugs that interact with receptor and have intrinsic activity, and elicit a response are termed agonists, but drug that interact with receptor and has no intrinsic activity and preventing response are referred as antagonists. Not all drug actions are mediated by receptor. Volatile anesthetics, metal chelating agents, osmotic diuretic, allopurinol exert their effects that are not mediated by specific receptor.When the response is measured against increasing drug concentration, the graph of the response and concentration is called a graded dose-response curve. Increasing the dose, increasing the response, until some time the response can not increase although the dose is increased. This response is called maximal effect or maximal efficacy or efficacy. The smaller the dose to achieve the maximal efficacy, the greater the potency of the drug. Even all known source of variation are controlled, drug effects are never identical in all patients. The fact that a range of doses is required to produce a specified intensity of effect in all individual. The dose of a drug required to produce a specified effect in an individual is termed the individual effective dose. The dose of drug required to produce a specified intensity of effect in 50% of individuals is known as the Median effective dose (ED50). If death is the end point, the ED50 is termed the Median lethal dose (LD50). There are individuals who are unusually sensitive or unusually resistant to a drug or a drug produces an unusual effect. If a drug produces its usual effect at unexpected low dosage, the individual is said to be hyper reactive (not hypersensitive). If a drug produces its usual effect only at unusually large dosage, the individual is said hypo reactive. Decreased sensitivity is also described as tolerance. Tolerance that develops rapidly after administration of only a few doses of a drug is termed tachyphylaxis. An unusual effect of a drug (not dose dependence), that occurs in only a small percentage of individuals is often termed idiosyncracy.


DAY 15: Cellular intervention/therapies

29


Learning Task

THE STRUCTURE OF THE PLASMA MEMBRANE & THE TRANSPORT MECHANISM OF VARIOUS SUBSTANCES

Learning Task


LECTURE 1

30


(Fawcett & Gartner; Guyton & Ganong)1. Describe the structure and function of plasma membrane!2. The composition of intra-cellular fluid and extra-cellular fluid is different! Why it

happen? How cells regulate it?3. Describe the mechanism of types of diffusion and example of substances diffused

through cell membrane!4. Describe the mechanism of type of active transport, and example of substances

actively transported through cell membrane!5. Describe the difference between the co-transport and counter-transport!6. Describe the active transport through cellular sheets occurs at many places in the

body!

ORGANELLES AND INCLUSIONS

Learning task (Gartner)Vignette A new born baby was died because of deficiency in β-galactosidase enzyme.

1. Please describe the structure of organelle involved in this disorders.2. Please describe the structure of the organelles that involves in protein syntesize!3. Please describe the functional structure of the organelle that involve in post

translation modification !4. Please describe the structure of the organelle that involve in ATP synthesize and in

which part of the organelle the process of ATP occur ?

CYTOSKELETON

Learning task 3(Fawcett & Gartner; Guyton)

Vignette 1A woman, 40 years old come to Hospital complains with mass in her right breast. Anamnesis and physical examination is performed, supported by histopathology and


LECTURE3

LECTURE 2

31


laboratory test. Finally, the diagnosis is breast cancer but the cancer hasn’t yet disseminate into other organs (metastasis). In other to follow up the progression of the cancer, mRNA of keratin 19 in patient’s bloodd is monitored as a biomarker.

Learning Task1. Keratin 19 is a part of cytoskeleton, which one and what is the function?

(microfilaments, intermediate filaments, or microtubules)2. Keratin 19 is expressed in mainly epithelial cell as cytoskeleton, what is the logic

keratin 19 can be also used as biomarker for metastasis in breast cancer?

Vignette 2A man, 48 years old come to Hospital complains headache, vomiting since several months ago. Anamnesis and physical examination is performed, supported by histopathology and laboratory test. Using immunohistochemistry staining, it reveals that GFAP expression is increasing. Finally, the diagnosis is astrocytoma (a type of brain cancer).

Learning Task1. GFAP is a part of cytoskeleton, which one and what is the function? (microfilaments,

intermediate filaments, or microtubules)2. What is the logic GFAP expression is increasing in astrocytoma?

CELL ORGANIZATION IN CONNECTIVE TISSUE

Learning Task(Gartner)

A 7 year-old child is brought to the hospital for examination and visum et repertum due to several bone fractures found in his extremities. The parents refuse to admit of child abuse. They said that the child is very fragile, a slight bump or falling could made such fracture to


LECTURE 4

32


their son. These had been happened since he was a baby; therefore their son extremities were not as straight as normal children. From the examination it was found that the child was suffered from Osteogenesis Imperfecta. A low impact, which normally has no effect to non-sufferer, can cause fracture to this patient.

1. Explain about the component of connective tissue that secretes the fiber involved in the case above!

A 35 year-old man was submitted to the hospital due to abrupt thoracic pain. From the examination he was found to have a heart murmur and further investigation showed aortic dilatation and mitral valves prolapsed. The man had a tall-lean figure with pigeon chest, arachnodactily, positive thumb and wrist sign, and joint laxity. The patient finally passed away due to aortic dissection. He was diagnosed of having Marfan Syndrome.

2. Explain about the components of connective tissue involved in the case above!

A 55 year-old woman wanted to have a more youthful appearance and particularly complained about deep line that run along her nose and corner of her mouth, on her fore head, and eye tip. The aesthetic doctor suggested her to take dermal filler treatment. The procedure was done by injecting substance under the skin to fill the groove that resulted from loss of volume and elasticity due to aging. The substance is also used in osteoarthritis treatment to add on intra articular fluid.3. Explain about the components of connective tissue involved in the case above!4. Explain the other components of connective tissue!5. Please describe the functions of connective tissue and which component/s contributes

to each function!6. Describe the organization of cell into connective tissue!7. Describe the classification of connective tissue!8. Differentiate the following types of connective tissue, based on components (cells,

ground substance, fiber) and arrangement:a. Dense connective tissue and loose connective tissueb. Dense regular and dense irregular connective tissuec. Dense regular collagenous and elastic connective tissued. White adipose tissue and brown adipose tissue

CELL ORGANIZATION IN EPITHELIAL TISSUE

Vignette :A 60 year old man complained black lump at his right forehead that becomes larger and darker. The doctor diagnosed it as skin cancer from epithelial cells. Cancer has already metastasized to regional lymphnode from examination. A metastasize can occur if adhesion to neighboring cells in an epithelium is disrupted because of loss of E-chaderin expression. The ability to burrow through tissues seems to depend on the production of proteolytic enzymes that can break down basal lamina.


LECTURE 5

33


Learning Task (Gartner and Goodman)1. What is Cadherin? Explain its role in cell-cell adhesion of epithelium!2. Basal lamina is an extracellular matrix. Explain macromolecule components of the

extracellular matrix in epithelium!3. Summarize about cell-cell and cell-matrix adhesion in assembling into epithelium!4. Differentiate the structure and function of cell junctions in epithelium!5. Explain the classification of epithelium & glands and its sample location!6. Explain the clinical correlation of epithelial tissue!

rsday

NUCLEUS & CHROMOSOMES

Learning task (Gartner; Strachan & Read)

1. Describe the composition of the nucleus, and its envelope!2. Describe the nuclear pore, and its role in the cell!3. Describe the nuclear pore complex !4. Explain about the chromatin! How many types of chromatin that you know ?5. Describe about the sex chromatin !

INTRODUCTION TO MOLECULAR BIOLOGY

Researchers from German Cancer Research Centerand Essen University Hospital Germany unravelled the cause of malignant melanoma. They found an identical mutation in the gene for telomerase, an enzyme often called “immortality enzyme”. Telomerase protects the ends of chromosomes from being lost in the process of cell division and, thus, prevents that the cell ages and dies. The inherited gene mutation leads to the formation of a binding site for protein factors in the controlling region of the telomerase gene, causing it to become overactive. As a result, mutated cells overproduce telomerase and hence become virtually immortal.(Susanne Horn, Adina Figl, P. SivaramakrishnaRachakonda, Christine Fischer, Antje Sucker, Andreas Gast, Stephanie Kadel, Iris Moll, Eduardo Nagore, Kari Hemminki, Dirk Schadendorf and Rajiv Kumar: TERT Promoter Mutations in Familial and Sporadic Melanoma. Science 2013, DOI: 10.1126/science.1230062).

To have a better understanding on above information, you need to discuss the following tasks:1. Definition of chromosome, gene, genome, central dogma in molecular biology, and

mutation.2. Mechanism of DNA replication.


LECTURE 6

LECTURE 7

34


3. Role of telomerase in DNA replication process.4. Define about point mutations. Distinguish between transition and transversion. 5. Compare the differences between mutation caused by UV radiation and X-rays. How do

the DNA repair systems fix it?

GENE EXPRESSION

Learning Task (Baynes, J.W. and Dominiczak, M.H. Medical Biochemistry)

Thalassemias are common world-wide causes of anemia. Often, however, DNA sequencing of the exons of the ß-globin genes reveals no abnormal nucleotides, but the ß-globin mRNA is smaller than expected. The hemoglobin produced is defective.

1. How do you define gene expression?2. Explain about types of RNAs and their function.3. Describe major steps of transcription.4. Describe major steps of translation.5. Define codon, anticodon, stop codon and start codon.6. How might genetic mutations lead to such abnormal gene expression as the above

case?

BASIC FEATURE OF ENZYME

VignetteA sixty five years old woman came to doctor complaining pain on her left breast. She had her self breast examination (SADARI technique). After doctor examination she diagnosed as breast cancer stadium IIA. The doctor gave metrotrexate as one of the medicine for cancer.

Leraning Task1. What is plasma enzyme and what is functional and non functional plasma enzyme?2. What is coenzyme? Give some examples!3. What is an active site and function of active site?4. What is Michaelis constant. Give the reason about Michaelis Menten or Km!.5. What is competitive inhibitors and non competitive inhibitors. Give some examples

in an application!6. What is the role of metrotrexate in the case above?


LECTURE 8

LECTURE 10

LECTURE 9

35


SIGNAL TRANSDUCTION

Vignette:A 23 year-old man presents to the emergency room complaining severe diarrhea. Base on the result of the examination, the diagnose of that patient is Cholera. As the doctor known, cholera is caused by Vibrio Cholera that exert their toxin and bind covalently to the G-protein receptor. Learning Task

1. Explain about signals and its classification!2. Explain about receptors and its classification!3. Describe G-protein-coupled receptors!4. Outline the activation of downstream intracellular signaling cascades by

heterotrimetric G-proteins5. Explain the mechanism of diarrhea caused by V. cholera!6. Expalin about the role of calcium as a second messenger!

CELL CYCLE

Learning task(Gartner)

1. Describe about the cell cycle!2. How do you sub divided the interphase in cell cycle!3. Describe the role of the protein cyclin in continuing the cell cycle process!4. Describe about the mitosis!5. Compare the mitosis and meiosis cell division!6. Describe the clinical correlations of mitosis and the cell cycle!

BIOENERGETICS AND OXIDATIVE METABOLISM

VignetteA 16-year-old boy presented with headache, seizures and visual loss. There was a

long history of inability to exercise due to muscle weakness. There have been episodes of hemianopia and mild hemiparesis lasting several days. His maternal aunt had a similar illness. Accumulation of lactate during and after exercise suggested a defect in mitochondrial oxidative metabolism. Muscle mitochondria were isolated for study.


LECTURE 11

LECTURE 12

36


Respiratory Complex I activity was reduced. A point mutation in mitochondrial DNA was identified.Learning Task (Harper)1. What is the diagnosis of the patient above?2. Outline the mitochondrial electron transport system showing eight major electron

carriers.

VignetteAn unresponsive 25-year-old woman is carried into the emergency room by her

boyfriend, because after taking two doses of 'weight loss' pills, she complained of headache, fever, chest pain, profuse sweating, and weakness. Initial findings were: rectal temperature, 40.8 °C (105.5 °F), pulse 151 beats per minute, respiratory rate, 56 per minute, blood pressure 40/10. In 15 minutes she died and could not be resuscitated. After death, rigor mortis set in after 10 minutes and her temperature rose to 46 °C (115 °F) in 10 additional minutes. It was found that she was a body builder and that she took 'weight loss' capsules purchased from a friend, because she wanted to have a leaner body for a show. Among her personal effects, was a plastic bottle containing capsules that proved to contain 2,4-dinitrophenol.

Learning Task1. How does 2,4-dinitrophenol act as poisons? 2. Explain the mechanism of ATP synthase!3. What is the role of uncoupling proteins?4.

CELLULAR RESPONSES TO INJURY AND DEATH

VignetteA 60 year old man died after treated in intensive care unit because of hemorrhagic hypertensive encephalopathy. At autopsy, the heart weighted 580 gram and showed marked left ventricular hypertrophy, coronary arterial atherosclerosis, and focus scar in myocard. The brain showed massive bleeding in right temporal lobe and tonsilar herniation. The liver showed yellowish fatty liver and the prostate was enlarge about twice normal size.

Learning Task (Robbins & Kumar)

1. List abnormal adaptation process, cell injury, and abnormal material accumulation occurred in this patient

2. Describe their morphologic appearance.3. Explain pathogenesis of myocardial hypertrophy 4. Explain mechanisms of cell death in this condition5. Explain pathogenesis of fatty liver


LECTURE 13

LECTURE 14

37


APPLICATIONS OF MOLECULAR BIOLOGY IN MEDICINE

Learning Task(Gene Therapy and Genetic Counseling)

1. Describe the implications of gene testing regarding to social and ethical issues!2. What are the advantages of using recombinant vaccine compared with non-

recombinant/conventional one?3. What is your opinion about reproductive cloning? Is it legal or illegal?

CELLULAR INTERVENTION/THERAPIES

Learning task (Katzung & Trevor)

1. Learn the term: Receptor, Effector, Agonist drug, Full agonist, Partial agonist, Pharmacologic antagonist, Competitive antagonist, Irreversible antagonist (Non Competitive antagonist, Physiologic antagonist, Chemical antagonist, Graded dose-response curve, Quantal dose-response curve, ED50 (Effective Dose 50), LD50 (Lethal Dose 50), Therapeutic Index, Efficacy, Potency.

2. Compare the efficacy and the potency of two drugs on the basis of their dose-response curves.

3. Describe about tolerance, hyperreactive, hyporeactive, and idiosyncrasy!

VignetteThe trial of two antihypertensive drug (A & B) were studied in a group of population, and the percentage of the group showing a specific effect (can decrease 20 mmHg systolic pressure) were determined.

The results of the study are as below.

Dosage percentage responding percentage respondingto drug A to drug B------------------------------------------------------------------------------------------------------------12.5 mg 1 1025 mg 10 5037.5 mg 50 7050 mg 90 100

Can you define: Efficacy of drug A and B ED50 of drug A and B


DAY 15

38


LD50 of drug A and B Therapeutic index of drug A and B Potency of drug A and B



PRACTICE

Practice 1: Cell Organization in Connective Tissue

Objective : to increase understanding about Connective TissueDate and Place :

Thursday, 28th November 2013 Lab Bersama (4th floor)

Facilitator : dr. IGA Dewi Ratnayanti, S.KedMaterials : Microscope, Microscopic preparations about :

A. Embryonal connective tissuea. Mesenchymal connective tissueb. Mucoid connective tissue

B. Proper connective tissuea. Loose connective tissue

i. Adipose connective tissueii. Limphoreticular connective tissueiii. Areolar connective tissue

b. Dense connective tissuei. Elastic connective tissueii. Collagen connective tissue

Practice 2: Cell Organization in Epithelial Tissues

Objective : to increase understanding about Epithelial TissueDate and Place :

Tuesday, 3rd December 2013 Lab Bersama (4th floor)

Facilitator : dr. Ida Ayu Ika Wahyuniari, M.KesMaterials : Microscope, Microscopic preparations about :

A. Epitheliuma. Stratified epitheliumb. Simple epitheliumc. Pseudostratified epitheliumd. Transtitional epithelium

B. Glandsa. Serous glandsb. Mucous glandsc. Mixed glands



PRACTICE 3 : Cellular Responses to Injury and Death

Objective : to increase understanding about cellular responses to injury and death

Date and Place : Thursday, 12th December 2013 Lab bersama(4th floor)

Facilitator : dr. Sri Widnyani, Sp.PA (K)Materials : Microscope, Microscopic preparations about :

A. Cell Adaptation1. Atrophy2. Hypertrophy3. Hyperplasia4. Metaplasia

B. Reversible injury1. Cellular swelling2. Fatty change

C. Cell death1. Necrosis

a. Coagulative necrosisb. Liquefactive necrosisc. Caseous necrosisd. Enzymatic necrosis

2. Apoptosis

D. Intracellular & ekstracellular acummulation1. Lipids

a. Steatosisb. Cholesterol

2. Hyaline change3. Pigmen

a. Melaninb. Carbon

E. Pathologic calcification1. Dystrophic calcification2. Metastatic calcification



Practice 4: Isolation of DNA

Objective : to increase understanding about DNA isolationDate and Place :

Monday,16th December 2013 Lab bersama (4th floor)

Facilitator : Ni Wayan Tianing, S.Si, M.Kes.

DNA Isolation Procedure from Whole Blood (Genomic DNA Extraction)

1. Add 12 ml blood + 36 ml (3 times blood volume) 1X RBC solution to a 50 ml Falcon centrifuge tube. Invert the tube 2-3 times during the preparation. Incubate the sample for at least 10 minutes at room temperature. Do not allow the sample to sit in the RBC lysis solution for extended periods of time, this can be detrimental to the sample.

2. Centrifuge at room temperature at 1500 rpm for 10 minutes. Remove the supernatant leaving behind the visible layer of white blood cells pellet. Then repeat step 1 until virtually all of the red blood cells are gone. Then vortex the pellet to spread the cells into the remaining drops of supernatant.

3. Add 3 ml of cell lysis solution to the centrifuge tube and right away pipette up and down to lyse the cells (make sure the solution is homogenous).

4. Add 6 l of RNase A (10 mg/ml) to the centrifuge tube. Mix the solution by inverting it several times and then incubate in a 37 oC water bath for 15 minutes. This can be run longer.

5. For protein precipitation, add 2 ml of protein precipitation solution (5 M ammonium acetate) to the centrifuge tube and then vortex until the solution look milky.

6. Centrifuge at 3000 rpm at 4 oC 15 minutes. The precipitated proteins will from a light brown pellet. If a protein pellet is not visible, repeat step 5.

7. Then pour the supernatant containing the DNA into a clean 50 ml Falcon tube containing 9 ml of isopropanol, do this at room temperature.

8. Mix the tube by inverting 25-30 times until white DNA pellet becomes visible (make sure all the pellet becomes visible).

9. Centrifuge at 3000 rpm at 4 oC 15 minutes. The DNA should be visible as a small white pellet.

10. Pour the supernatant and add 10 ml of 70 % ethanol. Invert several times to wash the DNA.

11. Spin again and pour off the 70 % ethanol. Then left the DNA air dry. Use a cotton swab to remove the excess supernatant on the sides of the tube.

12. Rehydrate the DNA in 1-1.5 ml of TE. Placed in 37 oC water bath for 2 hours to get the DNA in solution. Make sure that it is a homogenous solution.

13. Store at – 20 oC.

Additional Lecture :Topic : Clinical Application of Molecular Biology Laboratory

Objective : to broden students’ horizon on the existing facilities of our molecular biology laboratory.

Date and Place : Wednesday,11th December 2013 Class room

Content : - Application of molecular biology technique in infectious diseases- Application of molecular biology technique in Forensic



~ SELF ASSESSMENT ~

The Structure of the Plasma Membrane & The Transport Mechanism of Various Substances

1. Describe structure and function of phospholipids membrane; which molecule can diffuse across the membrane without mediated by protein (channel or carrier protein)?

2. Describe the structure of protein membrane and function of each protein in transport mechanism and its example!

3. Explain the difference of content and composition between intracellular and extracellular fluids!

4. Describe the passive transport mechanism through cell membrane!5. Explain various substances which transported through passive process!6. Describe factors that determine diffusion process!7. Explain transport mechanism for molecule that soluble in lipid!8. Describe sodium channel mechanism!9. What is voltage gating channel?10. Explain the difference between primary and secondary transportation with its examples!11. What is co-transport?

Organelles & InclusionsComprehend the structure of the organelles that involve in drug and alkohol detoxication !

Cytoskeletons1. Mention three types of cytoskeleton!2. Mentions minimal 1 examples and its function of each type in cytoskeleton!

3.

Identify the structures labeled of an axoneme and explain the role of each cytoplasmic component in the generation of axoneme movement.

Cell Organization in Connective Tissue1. Explain about cells that synthesize elastic fiber!2. Explain and give examples of dense regular collagenous connective tissue! 3. Describe characteristic of loose connective tissue!



4. Describe cells in connective tissue that function as Antigen Presenting Cells and phagocytosis!

5. Describe ground substances that function as agent barrier! 6. Explain the consequences of severe vitamin C deficiency in connective tissue!7. Explain the histologic structure of mucoid tissue!

Cell Organization in Epithelial Tissue1. Describe three major type of cell junction and its function!2. Describe the function of epithelial tissue!3. Mention and give example every kind of epithelium!4. Describe the structure and function of basal lamina!5. Differentiate about cell polarity!

Nucleus & Chromosomes1. Describe all of the protein that found at nucleoplasm!2. Describe the definition and function of nucleoplasmic ring and nuclear basket!3. Describe the nucleosome! Mention the proteins that arranged them!4. Describe chromatin assembly factor!5. Describe the function of nuclear pores!6. Describe the X-machvation (lionization)!7. Describe the differences between chromosome 1 and 2!8. Describe the differences between chromosome X and Y!9. Describe monosomy and trisomy!10. Describe poliploidi, aneuploidi!

Introduction to Molecular Biology1. Describe about replication mechanism, and enzymes that are involved!2. Describe how to detect mutation in the gene.3. Describe about mutation, and its clinical implication4. Describe about DNA repair system!

Gene Expression1. In When considering the initiation of transcription one often finds consensus sequences

located in the region of the DNA where RNA polymerase(s) bind. Which are common consensusA. CAATB. TATAC. TTTTAAAAD. both B and CE. both A and B

2. Which of the following occurs when RNA polymerase attaches to the promoter DNA?A. elongation of the growing RNA moleculeB. initiation of a new polypeptide chainC. initiation of a new RNA moleculeD. termination of the RNA moleculeE. addition of nucleotides to the DNA template

3. When examining the genetic code it is apparent thatA. there can be more than one amino acid for a particular codon.



B. AUG is a terminating codonC. there can be more than one codon for a particular amino acidD. the code is ambiguous in that the same codon can code for two or more amino acidsE. there are 44 stop codons because there are only 20 amino acids.

4. A short segment of an mRNA molecule is shown below. The polypeptide it codes for is also shown:

5’-AUGGUGCUGAAG : methionine-valine-leucine-lysine

Assume that a mutation in the DNA occurs so that the fourth base (counting from the 5’ end) of the messenger RNA now reads A rather than G. What sequence of amino acids will the mRNA now code for? A. methionine-valine-leucine-lysineB. methionine-lysine-leucine-lysineC. methionine-leucine-leucine-lysineD. methionine-valine-methionine-lysineE. methionine-methionine-leucine-lysine

5. Which of the following takes place during translation?A. the conversion of genetic information from DNA nucleotides into RNA nucleotidesB. conversion of genetic information from the language of proteins to the language of

enzymesC. the conversion of genetic information from the language of nucleic acids to the

language of proteinsD. DNA replicationE. the addition of nucleotides to a DNA template

6. During the process of translation, which translation site on the ribosome is filled by the iniatortRNA moleculeA. AB. BC. PD. OE. E

7. Which of the following statements is true regarding gene expression?A. The 3' end of mRNA corresponds to the carboxyl terminus of the proteinB. The first step is the association of mRNA with an intact ribosomeC. Involves proof-reading of the mRNAD. Prokaryotic RNA usually undergoes nuclear processingE. Polypeptides are synthesized by addition of amino acids to the amino terminus

8. Which of the following best describes the relationship between genes and proteinsA. one gene: one enzymeB. one gene: two polypeptidesC. one gene: one polypeptideD. one gene: one proteinE. none of the above describe the relationship

9. To describe the genetic code as degenerate indicates that A. mRNA is rapidly degradedB. The code is not universal among organismsC. Some amino acids have more than one codonD. Frameshift mutations are toleratedE. Stop codons may have corresponding tRNA molecules

10. A peptide has the sequence NH2-phe-pro-lys-gly-phe-pro-COOH. What is the sequence in DNA that codes for this peptide? A. 3' UUU-CCC-AAA-GGG-UUU-CCC B. 3' AUG-AAA-GGG-TTT-CCC-AAA-GGG



C. 3' AAA-GGG-TTT-CCC-AAA-GGG D. 5' GGG-AAA-TTT-AAA-CCC-ACT-GGG E. 5' ACT-TAC-CAT-AAA-CAT-TAC-UGA

Basic Feature of Enzyme1. Explain about co-enzyme and apo enzyme2. Differentiate about protein and non protein catalyst3. Explain about production and function of CK, LDH, ALT, and AST!

Signal Transduction1. Explain the character of ligand/signaling molecules!2. Explain structure and function of each receptor type!3. Describe various second messengers forming process!4. Describe about phosphorylation protein kinase in the cytoplasm!5. Describe cell signaling mechanism until gene expression occurs!6. Describe the mechanism of action of drugs-receptors until biology’s responses occur!

Cell Cycle1. Cell cycle consists of several phases. Describe the events that occur during every

phase!2. Describe the type of cell division and its differences!3. Describe the phases in mitosis and the events that occur during every phases!

Bioenergetics and Oxidative Metabolism 1. Which one of the following is the correct sequence of stages in cellular respiration?

A. glycolysis, oxidative phosphorylation, and the citric acid cycle B. glycolysis, the citric acid cycle, and oxidative phosphorylation C. the citric acid cycle, oxidative phosphorylation, and glycolysis



D. oxidative phosphorylation, the citric acid cycle, and glycolysis E. oxidative phosphorylation, glycolysis, and the citric acid cycle

2. Complex II differs from the other three complexes of the electron transport chain in one major aspect. What is this aspect?

A. It is not located on the inner membrane of the mitochondriaB. It does not require cofactorsC. It does not pump protonsD. It requires ATP for its reaction.E. It contains no covalently-bound FAD

3. During oxidative phosphorylation, the proton motive force that is generated by electron transport is used to:

A. create a pore in the inner mitochondrial membrane.B. generate the substrates (ADP and Pi) for the ATP synthase.C. induce a conformational change in the ATP synthase.D. oxidize NADH to NAD+.E. reduce O2to H2O.

4. Almost all of the oxygen (O2) one consumes in breathing is converted to:

A. acetyl-CoA. B. carbon dioxide (CO2).

C. carbon monoxide and then to carbon dioxide. D. none of the above. E. water.

5. Cyanide, oligomycin, and 2,4-dinitrophenol (DNP) are inhibitors of mitochondrial aerobic phosphorylation. Which of the following statements correctly describes the mode of action of the three inhibitors?

A. Cyanide and 2,4-dinitrophenol inhibit the respiratory chain, and oligomycin inhibits the synthesis of ATP.

B. Cyanide inhibits the respiratory chain, whereas oligomycin and 2,4-dinitrophenol inhibit the synthesis of ATP.

C. Cyanide, oligomycin, and 2,4-dinitrophenol compete with O2 for cytochrome

oxidase (Complex IV). D. Oligomycin and cyanide inhibit synthesis of ATP; 2,4-dinitrophenol inhibits the

respiratory chain.E. Oligomycin inhibits the respiratory chain, whereas cyanide and 2,4-dinitrophenol

prevent the synthesis of ATP.

6. During chemiosmosis A. a concentration gradient is generated when large numbers of H+ ions are

passively transported from the matrix of the mitochondrion to the mitochondrion's intermembrane space.

B. energy is generated by coupling exergonic reactions with other exergonic reactions.

C. ATP is synthesized when H+ ions move through a protein port provided by ATP synthase.

D. H+ ions serve as the final electron acceptor. E. energy is released as H+ ions move freely across mitochondrial membranes



7. A drug is tested in the laboratory and is found to create holes in both mitochondrial membranes. Scientists suspect that the drug will be harmful to human cells because it will inhibit

A. glycolysis. B. the citric acid cycle. C. oxidative phosphorylation. D. Beta oxidation of fatty acids E. Oxidation of piruvate

8. Rotenone is a poison commonly added to insecticides. Insects exposed to rotenone will die because

A. high levels of fermentation products will build up. B. water will not be produced and dehydration will occur. C. anaerobic respiration can't occur. D. of inadequate ATP production. E. None of the choices are correct.

9. Uncoupling of mitochondrial oxidative phosphorylation: A. allows continued mitochondrial ATP formation, but halts O2 consumption.

B. halts all mitochondrial metabolism. C. halts mitochondrial ATP formation, but allows continued O2 consumption.

D. slows down the citric acid cycle. E. slows the conversion of glucose to pyruvate by glycolysis.

10. Antimycin A blocks electron transfer between cytochromes b and c1. If intact

mitochondria were incubated with antimycin A, excess NADH, and an adequate supply of O2, which of the following would be found in the oxidized state?

A. Coenzyme Q B. Cytochrome a3 C. Cytochrome b D. Cytochrome e E. Cytochrome f

Cellular Responses to Injury and Death1. Explain adaptations of cellular growth and differentiation2. List the causes of cell injury3. Explain the mechanisms of cells injury4. Explain clinico-pathologic correlations with some examples of cell injury and necrosis5. Explain the mechanisms of necrosis 6. Describe the morphology of necrosis7. Explain the mechanisms of apoptosis8. Describe the morphology of apoptosis 9. List some condition with pathologic calcification10. Explain the mechanisms of senescence11. Describe the morphology of cellular aging



Cellular Intervention/Therapies1. A 55-year-old woman with heart failure is to be treated with a diuretic drug. Drug X and

Y have the same mechanism of diuretic action. Drug X in a dose of 5 mg produces the same magnitude of diuresis as 500 mg of drug Y. This suggests that :a. Drug Y is less efficacious than drug Xb. Drug X is about 100 times more potent than drug Yc. Toxicity of drug X is less than that of drug Yd. Drug X is a safer drug than drug Ye. Drug X will have a shorter duration of action than drug Y because less of drug X is

present for a given effect

2. In the absence of other drugs, pindolol causes an increase in heart rate by activating beta adrenoceptors. In the presence of highly effective beta stimulants, however, pindolol causes a dose-dependent, reversible decrease in heart rate. Therefore, pindolol should be classified as:a. An irreversible antagonistb. A physiologic antagonistc. A chemical antagonistd. A partial agoniste. A spare receptor agonist

3. Which of the following provides information about the largest response a drug can produce, regardless of dose?a. Drug potencyb. Maximal efficacyc. Mechanism of receptor actiond. Therapeutic indexe. Therapeutic window



~ CURRICULUM MAP ~Smstr Program or curriculum blocks

10 Senior Clerkship

9 Senior Clerkship

8 Senior clerkship

7

Medical Emergency(3 weeks)

BCS (1 weeks)

Special Topic:-Travel medicine(2 weeks)

Elective Study III(6 weeks)

Clinic Orientation (Clerkship)(6 weeks)

6

The Respiratory System and Disorders(4 weeks)

BCS (1 weeks)

The Cardiovascular System and Disorders(4 weeks)

BCS (1 weeks)

The Urinary System and Disorders(3 weeks)

BCS (1 weeks)

The Reproductive System and Disorders (3 weeks)

BCS (1 weeks)

5

Elective Study II(1 weeks)

Alimentary & hepato-biliary systems& disorders(4 Weeks)

BCS (1 weeks)

The Endocrine System, Metabolism and Disorders(4 weeks)

BCS (1 weeks)

Clinical Nutrition and Disorders(2 weeks)

BCS (1 weeks)

Special Topic : - Palliative medicine-Complementary & Alternative Medicine - Forensic(3 weeks)

Elective Study II(1 weeks)

4

Musculoskeletal system &connectivetissue disorders(4 weeks)

BCS (1 weeks)

Neuroscienceandneurologicaldisorders(4 weeks)

BCS (1 weeks)

Behavior Changeand disorders(4 weeks)

BCS(1 weeks)

The Visualsystem &disorders(2 weeks)

BCS(1 weeks)

3

Hematologicsystem & disor-ders & clinical oncology(4 weeks)

BCS (1 weeks)

Immune system &disorders(2 weeks)

BCS(1 weeks)

Infection & infectiousdiseases(5 weeks)

BCS (1 weeks)

The skin & hearing system& disorders(3 weeks)

BCS(1 weeks)

2

Medical Professionalism(2 weeks)

BCS (1 weeks)

Evidence-based Medical Practice(2 weeks)

Health System-based Practice(3 weeks)

BCS (1 weeks)

Community-based practice(4 weeks)

Special Topic- Ergonomi- Geriatri(2 weeks)

Elective Study I(2 weeks)

1

StudiumGenerale and Humaniora(3 weeks)

Medicalcommunication(3 weeks)

BCS (1 weeks)

The cellas bioche-mical machinery(3 weeks)

BCS(1 weeks)

Growth&development(4 weeks)

BCS: (1 weeks)

Pendidikan Pancasila & Kewarganegaraan (3 weeks)

~ REFERENCES ~



Used in the Block The Cell as Biochemical Machinery

Student Standard References:

1. Gartner LP, Hiatt JL : Concise Histology, Philadelphia, W.B. Saunders, 2011, pp 8-73(H2)

2. Guyton AC, Hall JE : A Textbook of Medical Physiology, 11th ed., 2006, pp.1-51; 829-901 (PS1)

3. Baynes, J.W. and Dominiczak, M.H. Medical Biochemistry second edition.Elsevier London. 2005:p. 641 (B1)

4. Robbins SL, Kumar V : Basic Pathology, London, Saunders, 7th ed, 2003, pp.3-31 (BP)5. Strachan T & Read AP; Human Molecular Genetics, John Wiley & Sons (Asia) PTELTD

(HMG)6. Trevor AJ, Katzung BG, and MastersSB :Pharmacology Examination & Broad Review,

7th ed, 2005, pp. 10-19 (PH)7. Goodman SR : Medical Cell Biology, 2nd ed, pp. 195-202 (CB)8. Gene Therapy and Genetic Counseling

Additional recommended reading:

9. Fawcett DW, Jensh RP : Bloom & Fawcett’s Concise Histology, 2nd ed, London, Arnold, 2002, pp 1- 27(H1)

10. Ganong, WF: Review of Medical Physiology, 20thed, New York, Lange Medical Books/McGraw-Hill, 2001, pp 1-48 (PS2)

11. Murray RK, Granner DK, Mayes PA : Harper, s Illustrated Biochemistry,26 th ed, New York, Lange Medical Books / McGraw-Hill, 2003 , 314 – 373; 74-102 (B2)

12. Alberts B, Johnson A, Lewis J : Molecular Biology of THE CELL, 4TH ed , New York, Garland Science, 2002, pp 1010 – 1021 (MB2)

Paper Assessment Form



Block The Cell as Biochemical Machinery

Name : ...........................................Student Reg. Number : ...........................................Facilitator : ...........................................Title : ...........................................

Supervisor’s (Facilitator) scoring with 60% qualification :]


motivation0-10

TOTAL 100

Supervisor,

(...........................................)NIP.



Supervisor’s (Facilitator) scoring with 60% qualification :


motivation0-10

TOTAL 100

Supervisor,

(...........................................)NIP.

TIME TABLE REVISION :



1. Lecture 7. Introduction to Molecular Biology : 15 November 2011

2. Lecture 8. Gene expression : 17 November 2011

3. Practicum microscopic structure of connective tissue : 18 November 2011

4. Student project presentation yang tanggal 15 November pindah ke tanggal 18

November 2011






November 2011






November 2011






November 2011

Paper Assessment Form



Block The Cell as Biochemical Machinery

Name : ...........................................Student Reg. Number : ...........................................Facilitator : ...........................................Title : ...........................................Evaluator’sscoring (presentation) with 40% qualification :

No Item Assessment Range Score (%) Score1. Quality of material 0-60

2. Capability of information searching

0-10

3 Critical thinking 0-30

TOTAL 100

Evaluator,

(................................................) NIP.



Evaluator’sscoring (presentation) with 40% qualification :

No Item Assessment Range Score (%) Score1. Quality of material 0-60

2. Capability of information searching

0-10

3 Critical thinking 0-30

TOTAL 100

Evaluator,

(................................................) NIP.


Study Guide Cell Smstr I 20 Nov 2013

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