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RAJIV GANDHI UNIVERSITY OF HEALTH SCIENCES,
BANGALORE, KARNATAKA
SYNOPSIS
OF
DISSERTATION
"STUDY OF SERUM SIALIC ACID AND
MICROALBUMINURIA IN DIABETIC NEPHROPATHY"
Submitted by
Dr. DIVIJA D.A.
POST GRADUATE STUDENT IN
BIOCHEMISTRY (M.D.)
DEPARTMENT OF BIOCHEMISTRY
ADICHUNCHANAGIRI INSTITUTE OF MEDICAL SCIENCES,
B.G.NAGARA-571448
RAJIV GANDHI UNIVERSITY OF HEALTH SCIENCES, BANGALORE, KARNATAKA
ANNEXURE – II
PROFORMA FOR REGISTRATION OF SUBJECTS FOR DISSERTATION
1 NAME OF THE CANDIDATE AND
ADDRESS
2 NAME OF THE INSTITUTION
3 COURSE OF STUDY AND SUBJECT
4 DATE OF ADDMISSION TO THE
COURSE
5 TITLE OF THE TOPIC
6 BRIEF RESUME OF INTENDED
WORK
DR. DIVIJA D. A.
P.G. IN (M.D) BIOCHEMISTRY
DEPT. OF BIOCHEMISTRY
A.I.M.S., B.G.NAGARA,
MANDYA DISTRICT-571448
ADICHUNCHANAGIRI INSTITUTE
OF MEDICAL SCIENCES,
B.G.NAGARA.
M.D. IN BIOCHEMISTRY
24TH MAY 2010
“STUDY OF SERUM SIALIC ACID AND
MICROALBUMINURIA IN DIABETIC
NEPHROPATHY”
APPENDIX-I
6.1 NEED FOR THE STUDY
APPENDIX-IA
6.2 REVIEW OF LITERATURE
APPENDIX-IB
6.3 OBJECTIVES OF THE STUDY
APPENDIX-IC
6.4 INCLUSION AND EXCLUSION
. CRITERIA
7 MATERIALS AND METHODS
APPENDIX-ID
APPENDIX-II
7.1 SOURCE OF DATA
APPENDIX-IIA
7.2 METHOD OF COLLECTION OF
DATA (INCLUDING SAMPLING
PROCEDURES ANY)
APPENDIX-IIB
7.3 DOES STUDY REQUIRED ANY
INVESTIGATIONS OR
INVESTIGATIONS TO BE
CONDUCTED ON PATIENTS OR
OTHER ANIMALS, IF SO PLEASE
DESCRIBE BRIEFLY
7.4 HAS ETHICAL CLEARANCE
BEEN OBTAINED FROM YOUR
INSTITUTION IN CASE OF 7.3
YES
APPENDIX –IIC
YES
APPENDIX –IID
8 PROFORMA AND LIST OF
REFERENCES
APPENDIX – III
9 SIGNATURE OF THE CANDIDATE
10 REMARKS OF THE GUIDE
THE ABOVE MENTIONED TOPIC IS
ACCEPTED TO GUIDE
11 11.1 NAME OF THE GUIDE
DR. RAJESHWARI.A., M.Sc , Ph.D
ASSISTANT PROFESSOR
DEPT. OF BIOCHEMISTRY
A.I.M.S., B.G.NAGARA
11.2 SIGNATURE OF THE GUIDE
11.3 CO-GUIDE
DR. ALIYA NUSRATH, M.D
ASSOCIATE PROFESSOR AND
INCHARGE HOD
DEPT. OF BIOCHEMISTRY
A.I.M.S., B.G.NAGARA
11.4 SIGNATURE OF CO-GUIDE
11.5 HEAD OF THE DEPARTMENT
11.6 SIGNATURE OF
HEAD OF
THE DEPARTMENT
12 12.1 REMARKS OF THE
CHAIRMAN
AND
PRINCIPAL
12.2 SIGNATURE
DR. ALIYA NUSRATH, M.D
ASSOCIATE PROFESSOR AND
INCHARGE HOD
DEPT. OF BIOCHEMISTRY
A.I.M.S., B.G. NAGARA
STUDY OF SERUM SIALIC ACID AND MICROALBUMINURIA IN
DIABETIC NEPHROPATHY
APPENDIX-I
6. BRIEF RESUME OF THE INTENDED WORK.
APPENDIX-IA
NEED FOR THE STUDY
Diabetes mellitus is the major healthcare problem worldwide. Diabetes mellitus, the
most common endocrine disorder is characterized by metabolic abnormalities due to relative
or absolute deficiency of insulin and or insulin resistance resulting in hyperglycemia and
associated with micro and macrovascular complications.
Serum sialic acid is a newly established potential risk factor for the development of
macro and microvascular complications of diabetes. (1) Serum sialic acid is a component of
glycoprotein such as acute phase proteins and several serum acute phase proteins are elevated
in diabetes. Serum sialic acid level is increased in both type 1 and type 2 diabetes mellitus
patients with albuminuria. The possible mechanism associated with the role of sialic acid is in
maintaining the negative charge of renal glomerular basement membrane which is one of the
main regulators of membrane permeability. Due to increased vascular permeability there is
shedding of vascular endothelial sialic acid into circulation. (2)
Diabetes mellitus is the leading cause of end stage renal disease (ESRD). It is
responsible for 30-40 % of all ESRD. Although type 1 and type 2 DM lead to ESRD, the
great majority of patients are those with type 2 DM.
Microalbuminuria is the earliest manifestation of diabetic nephropathy and it is the
predictor of incipient nephropathy in diabetic patients. Glycated hemoglobin is a standard
measure of severity of diabetes mellitus and gives an idea about long term glycemic control.
The current study was designed to investigate the role of serum sialic acid as a major
risk factor in the development of diabetic nephropathy and to correlate the clinical
relationship of serum sialic acid with glycated hemoglobin and marker of diabetic
nephropathy such as microalbuminuria.
APPENDIX-IB
REVIEW OF LITERATURE
Diabetes mellitus is not a single disease entity but rather a group of metabolic
disorders sharing the common underlying feature of hyperglycemia. Chronic hyperglycemia
and attendant metabolic dysregulation of diabetes mellitus may be associated with secondary
damage in multiple organ systems, especially kidneys, eyes, nerves and blood vessels.(3)
Diabetes mellitus tends to run in families. It is associated with dyslipidemia,
atherosclerosis and predispose to certain specific microvascular abnormality including
retinopathy, nephropathy and neuropathy. It increases the risk of stroke, myocardial
infarction, peripheral vascular diseases. It also decreases the resistance to infection, especially
if diabetes is poorly controlled.
CLASSIFICATION OF DIABETES MELLITUS (4)
1) Type 1 Diabetes mellitus (Insulin dependent diabetes mellitus)
Type 1 Diabetes mellitus is due to absolute deficiency of insulin caused by an
autoimmune attack on the β cells of the pancreas and its progressive destruction.
It is sub classified as
a) Immune mediated
b) Idiopathic
2) Type 2 Diabetes mellitus (Non insulin dependent diabetes mellitus)
It is due to insulin resistance and dysfunctional β cells. It is further classified as
a) Obese
b) Non-obese
c) Maturity onset diabetes of young
3) Diabetes Prone Status
a) Gestational diabetes mellitus
b) Impaired glucose tolerance (IGT)
c) Impaired fasting hyperglycemia (IGF)
4) Secondary to other known causes
a) Endocrinopathies :
Cushing’s disease, Thyrotoxicosis, Acromegaly
b) Drug induced:
Pentamidine, Nicotinic acid, Glucocorticoids,
BETA blockers
c) Diseases of exocrine pancreas:
Pancreatitis, Pancreatectomy, Neoplasia,
Cystic fibrosis, Hemochromatosis
d) Infections:
Congenital Rubella, Coxsackies,
Cytomegalo virus
e) Uncommon forms of immune mediated diabetes
-
Stiff man syndrome
-
Anti insulin receptor antibodies
f) Genetic syndrome associated with diabetes mellitus
-
Down’s syndrome
-
Klinefelter’s Syndrome
-
Turner’s Syndrome
-
Wolfram Syndrome
METABOLIC DERANGEMENTS IN DIABETES MELLITUS
CARBOHYDRATE METABOLISM
Insulin is a hypoglycemic hormone which lowers blood glucose level by promoting
utilization and storage of glucose. It stimulates glycolysis and inhibits gluconeogenesis and
glycogenolysis. In diabetes mellitus the release of insulin and the cellular response to insulin
are decreased which leads to inhibition of glycolysis and stimulation of gluconeogenesis and
glycogenolysis resulting in hyperglycemia. (4)
LIPID METABOLISM
Normally insulin inhibits lipolysis which is evidenced by fall in circulating plasma
free fatty acid levels. It enhances lipogenesis and the synthesis of triacyl glycerols by
providing more acetyl coA and NADPH. The principle action of insulin in adipose tissue is
to inhibit the activity of hormone sensitive lipase reducing the release not only of free fatty
acid but also of glycerol. (5)
In diabetes mellitus, due to insulin deficiency there is increased lipolysis with
increased plasma free fatty acids. This causes increased uptake and oxidation of free fatty
acid, releasing more of acetyl CoA. The acetyl CoA cannot be completely oxidized in TCA
cycle, as the availability of oxaloacetate is limited. Hence excess of acetyl CoA is diverted to
ketogenesis causing Ketonemia and Ketosis. (4)
PROTEIN MATABOLISM
Insulin is an anabolic hormone. It stimulates entry of amino acids into the cells,
enhances protein synthesis and reduces protein degradation. In diabetes mellitus there will be
absence of anabolic effects of insulin which leads to increased catabolism of proteins and
amino acids providing substrates for gluconeogenesis. (4)
DIABETIC NEPHROPATHY
Diabetic nephropathy is characterized clinically as a triad of hypertension, proteinuria
(>300 mg/24 hrs) and progressive decline in renal function. (8)
The term diabetic nephropathy is applied to the conglomerate of lesions that often
occur concurrently in the diabetic kidney. (3)
Morphologic changes in the glomeruli include (3)
a) Capillary basement membrane thickening
b) Diffuse mesangial sclerosis
c) Nodular glomerulosclerosis
Diabetic nephropathy is separated into 4 classes, based on biopsy findings. They
range from the least severe (class 1) to the most severe ( class 1V) (6)
Class I : Glomerular basement membrane thickening. No mesangial expansion, nodular
increase in the mesangial matrix or global glomerulosclerosis of more than half of the
glomeruli.
Class II: Mesangial expansion, mild (IIa) or severe (IIb)
Class III : Nodular sclerosis (Kimmelstiel-Wilson lesions); The presence of atleast one strong
Kimmelstiel-Wilson lesion but no more than 50% global glomerulosclerosis.
Class IV : Advanced diabetic glomerulosclerosis. Biopsies with more than 50% global
glomerulosclerosis.
Diabetic nephropathy, leading cause of ESRD remains a major cause of morbidity and
mortality for persons with either type 1 or type 2 DM. Nephropathy if suboptimally managed
follows a predictable course, starting with microalbuminuria through proteinuria, azotemia
and culminating in end stage renal disease.
PATHOGENESIS OF DIABETIC NEPHROPATHY :
Tissue injury caused by diabetic vascular complications stimulates local cytokine
secretion from cells such as endothelium and macrophages which are the major sources of
cytokine production, this stimulates an acute phase response. Sialic acid being a component
of acute phase glycoprotein if increases before microangiopathy develops, it may be an early
signal of process such as hypercytokinemia that cause or drastically increase the risk of renal
failure. (1)
The reason for increased incidence of microalbuminuria in diabetic nephropathy is
probably the result of widespread endothelial dysfunction arising from the effects of
cytokines and other inflammatory mediators, released during the intense inflammatory
responses that are associated with critical illnesses. (7)
The effects of disruption of the integrity of the endothelial barriers is manifested as
altered glomerular endothelial permeability in the kidneys, allowing increased amounts of
albumin to escape into the glomerular ultrafiltrate. The tubular reabsorptive mechanism for
albumin from the ultrafiltrate is exceeded beyond its threshold capacity, leading to increased
excretion of albumin in the urine. (7)
Other causes for diabetic nephropathy include (8)

Generation of mitochondrial ROS (Reactive Oxygen species)

Accumulation of AGE’s (Advanced Glycation End Products)

Activation of intracellular signalling molecules such as PKC (Protein Kinase C)
SERUM SIALIC ACID
Serum sialic acid (N-acetyl neuraminic acid) an inflammatory marker, is a protein
bound carbohydrate and occurs in combination with other monosaccharides like galactose,
mannose, glucosamine, galactosamine and fructose. Sialic acid is the group name for the
acetylated neuraminic acids such as N -acetyl neuraminic acid, N-glycol neuraminic acid and
Di-acetyl neuraminic acid. Only N- acetyl neuraminic acid has been isolated from human
serum.
Normal range of total sialic acid level in serum plasma is (9)
Men
:
1.57 – 2.63 mmol / l
Women
:
1.69 – 2.64 mmol / l
There is only a minute amount of free SA in tissues and body fluids, and no direct
biological role has been identified for this unbound SA. Bound sialic acid is of major
importance in cell biology because of the external position of SA on glycoproteins and
glycolipids and on the outer cell membranes. (10) The unique structural feature of sialic acid
is the negative charge present in it, which enables it to take part in binding and transport of
positively charged molecules, and in the attraction and repulsion of cells and molecules. SA
also contributes to the regulation of the permeability of the basement membranes in
glomeruli. Sialic acid is released from the terminal oligosaccharide chains of some
glycoproteins and glycolipids in the acute phase of inflammation.
GLYCATED HEMOGLOBLIN (4)
It is one of the best index of long term control of blood glucose level. When there is
hyperglycemia proteins in the body undergo glycation. Glycation is a non enzymatic process
where the glucose after entering RBC forms a Schiff’s base with N terminal amino group of
protein by an aldimine linkage which changes to a ketamine linkage by an irreversible
Amadori rearrangement. It remains inside the erythrocytes throughout its life span. (4)
Normal level of glycated hemoglobin (HbA1c) is about 4-7%. Elevated glycated
hemoglobin indicates poor control of diabetes mellitus. The risk of retinopathy and renal
complications are proportionately increased with elevated glycated hemoglobin value and
also with increase in age and duration of diabetes mellitus. HbA1c level reveals mean glucose
level over previous 8-10 weeks. (4)
BLOOD SUGAR LEVEL :
FASTING BLOOD GLUCOSE (11)
FBS is directly proportional to the severity of diabetes mellitus and the most
commonly used marker for DM. In general FBS levels greater than 126mg/ dl on more than
one occasion are diagnostic of diabetes mellitus, provided that drugs such as glucocorticoids
are not being administered.
POSTPRANDIAL BLOOD GLUCOSE (11)
Two consecutive post prandial tests are recommended for diagnosis. Blood is drawn
at 2 hrs after ingestion of the meal or glucose load. Two post prandial tests with glucose
levels of 200 mg/dl or higher at 2 hours are suggestive of diabetes.
BLOOD UREA
Urea is the major nitrogen containing metabolic product of protein catabolism in
humans accounting for > 75% of the non protein nitrogen eventually excreted. An increase in
plasma urea concentration characterizes uremic (Azotemic) state. Measurement of blood and
plasma urea has been widely used as an indicator of kidney function. (11).
Normal range of Blood urea is 20-40 mg/dl. (4)
Blood urea concentration in patient with untreated ESRD typically reach 108-135 mg/dl.
SERUM CREATININE : (11)
Creatinine is the cyclic anhydride of creatine that is produced as the final product of
decomposition of phosphocreatine. Plasma creatinine is measured as a test of kidney
function.
Normal range of serum creatinine; 0.9 – 1.3 mg/dl in men
0.6 – 1.1 mg/dl in women
Plasma Creatinine concentration in patients with untreated end stage renal disease may
exceed 11mg /dl (11)
MICROALBUMINURIA (11), (12)
Microalbuminuria is defined as the excretion of 30 to 300 mg of albumin per
day in urine. It is not a different form or fraction of albumin but just a very small amount of
albumin. Albumin molecule is relatively small and it is often the first protein to enter the
urine after the kidney is damaged.
Normoalbuminuria:
< 30 mg/24 hrs or <20 µg/min
Microalbuminuria :
30-300 mg/24 hrs or 20-200 µg/min
Macroalbuminuria :
>300 mg/24 hrs or >200 µg/min
APPENDIX-IC
6.3. OBJECTIVES OF THE STUDY
-
To estimate the serum sialic acid levels in diabetic nephropathy patients.
-
To know the correlation between serum sialic acid and microalbuminuria in
diabetic nephropathy patients.
-
To know the correlation between serum sialic acid and glycated hemoglobin in
diabetic nephropathy patients.
APPENDIX-ID
6.4 INCLUSION AND EXCLUSION CRETERIA
INCLUSION CRITERIA
50 clinically diagnosed cases of diabetic nephropathy who will attend out patient
department and also who are admitted in wards will be taken for case study and 50 numbers
of age and sex matched healthy persons will be taken as control.
EXCLUSION CRITERIA
Patients with acute and chronic inflammatory conditions, other metabolic conditions
like ketoacidosis, cerebrovascular accidents, patients with pregnancy, pre-existing chronic
Kidney disease, previously undiagnosed chronic renal failure, chronic glomerulonephritis,
Nephrotic syndrome and alcoholics will be excluded from the study.
APPENDIX-II
7. MATERIALS AND METHODS
APPENDIX-IIA
7.1 SOURCE OF DATA
All clinically diagnosed cases of diabetic nephropathy irrespective of age and sex who
attend out patient department and admitted cases of Adichunchanagiri hospital and research
centre will be included in the study. Age and sex matched healthy individuals will be taken as
control group. Study span is about 18 months.
APPENDIX-IIB
7.2 METHOD OF COLLECTION OF DATA
LABORATORY INVESTIGATION IN DIABETIC NEPHROPATHY
Blood samples will be collected in fasting state and will be analyzed for fasting blood
glucose, serum sialic acid, blood urea, serum creatinine and glycated hemoglobin. Again
blood sample will be collected from the same patient at 2 hrs after meal for post prandial
sugar level estimation.
10ml of blood will be drawn under aseptic precautions from clinically diagnosed
cases of diabetic nephropathy and healthy controls and divided into 4 test tubes, marked as 1,
2, 3 and 4.
1. Test tube 1 Contains 2 ml of blood with anticoagulant, which is used for estimation of
FBS ( Glucose oxidase method )
2. Test tube 2 contains 4 ml of blood with no anticoagulant that is allowed to clot and
serum is separated. Serum is used for measurement of
a) Blood Urea – ( Glutamate dehydrogenase– Urease method )
b) Serum creatinine ( Jaffe’s method )
c) Serum Sialic acid ( Modified Thiobarbituric acid assay of Warren )
3. Test tube 3 contains whole blood that is used for estimation of glycated hemoglobin
(Ion exchange Resin method )
4. Test tube 4 contains 2 ml of blood which will be collected with anticoagulant after 2
hrs of meals, which is used for estimation of PPBS.
5. URINE – Microalbumin
Random midstream urine samples (10ml) were collected in a sterile container without
preservative and assayed for microalbumin (Immunoturbidimetric assay).
STATISTICAL ANALYSIS
Statistical analysis will be done using student‘t’ test and relevant statistical test and
statistical significance will be compared between cases and control group.
APPENDIX-IIC
7.3 DOES THE STUDY REQUIRE ANY INVESTIGATIONS OR
INTERVENTION TO BE CONDUCTED ON PATIENTS OR OTHER
ANIMALS, IF SO PLEASE DESCRIBE BRIEFLY
YES, the patient will require the following blood and urine investigations
1. Blood sugar level (FBS and PPBS)
2. Blood urea
3. Serum creatinine
4. Serum sialic acid
5. Glycated hemoglobin
6. Microalbuminuria
APPENDIX-IID
7.4 HAS THE ETHICAL CLEARANCE BEEN OBTAINED FROM
YOUR INSTITUTION IN CASE OF 7.3?
YES, the investigations are carried out after the ethical clearance from the institution.
All investigations are carried out after taking the written consent from the patients.
-: LIST OF REFERENCES :1) Syed Muhammad Shahid, Tabassum Mahaboob. “Clinical correlation between frequent
risk factors of diabetic nephropathy and serum sialic acid”. Int J. Diabetes Metab 14:138-142,
2006.
2) Mohammad J.S, Muhammad T.M, Mukhtar Ahmad, Muhammad Riaz, Muhammad
Umair. “ Serum Sialic acid concentration and type 2 DM”. Professional Med J Dec 2006;
13(4): 508-510.
3) Raminder Kumar, Ann Abbas, Nelson Fausto, Jon C. Aster, Robbins and cotron
“Pathologic basis of disease” 8th Ed. Saunders Elsevier Publishing Division; 2010. 934-935,
1131-1146.
4) Vasudevan D.M and Srekumari S “Text book of Biochemistry for Medical Students”. 5th
Ed. Jaypee brother’s medical publishers (P) Ltd: 2007.
5) Robert K. Murray., Daryle K Granner, Peter A Mayer, Victor M Rodwell. Harpers
Illustrated Biochemistry 26th Ed. Mc.Graw-Hill Publisher; 2003.
6) Nancy Fowler Larson Authors and Disclosures; “Classification systems for Diabetic
Nephropathy may advance patient care”. The Journal of the American Society of Nephrology
Feb 18, 2010.
7) S. Basu, S. Chaudhuri, M. Bhattacharyya, T.K Chatterjee, S. Todi and A Majumdar.
“Microalbuminuria ; An inexpensive, non invasive bedside tool to predict outcome in
critically ill patients.” Indian journal of clinical Biochemistry, Vol 25, Number 2. April 2010
146-152.
8) Henry M. Kronerberg., Shlomo melmed, Kenneth S. Polonsky, P. Reed Larsen, “Williams
textbook of endocrinology” 11th edition Saunders Elsevier Publishing Division; 2008.
9) Lorentz K T, Weib, Krass. Sialic acid in Humans serum and CSF. J Clin Chem Biochem
1986: 24: 189-198.
10) Schauer R Achievements and challenges of Sialic acid research. Glycoconj. J. 2000: 17:
485-499
11) Carl A Burtis, Edward R. Ashwood., David E. Burns, “Teitz textbook of clinical
chemistry and molecular diagnosis.” 4th edition published by Elseveir, a division of Reed
Elsevier India Private Ltd; 2006.
12) Bilous R W. DM and the Kidney. In; warell DA, COX TM, Firth JD, Jr. Benz Edwards J,
editors, Oxford textbook of Med 4th edn: Newyork; Oxford University Press 2003; 374-380.
APPENDIX – IID
PROFORMA APPLICATION FOR ETHICS COMMITTEE APPROVAL
SECTION A
A.
Title of the study
B.
Principal investigator
DR. DIVIJA D. A.
P. G. IN (M.D) BIOCHEMISTRY
C.
Co-investigator
DR. RAJESHWARI.A M.Sc, Ph.D
ASSISTANT PROFESSOR
DEPT. OF BIOCHEMISTRY
A.I.M.S., B.G. NAGARA
GUIDE
D.
“ STUDY OF SERUM SIALIC ACID
AND MICROALBUMINURIA IN
DIABETIC NEPHROPATHY”.
Name of the collaborator
NA
Department / Institution
E.
Whether permission has been obtained
from the head of the collaborating
department and institution
NA
SECTION – B
APPENDIX-II
Summary of the project
SECTION - C
APPENDIX-IC
Objectives of the study
SECTION – D
APPENDIX-IIB
Methodology
A.
Where the proposed study will be undertaken
B.
Duration of the project
AH & RC, B.G.NAGARA.
18 MONTHS
C.
D.
Nature of the subject:
Does the study involve adult patients?
YES
Does the study involve children?
YES
Does the study involve normal volunteers?
YES
Does the study involve psychiatric patients?
NO
Does the study involve pregnant women?
NO
If the study involves healthy volunteers
1.
Will they be institute students?
NO
2. Will they be institute employees?
NO
3. Will they be paid?
NA
4. If they are to be paid, how much per person
NA
E.
Is the study multi central trial?
NO
F.
If yes, who is the coordinator?
(Name and designation)
NA
Has the trial been approved by the ethical
committee of other centers?
NA
If the study involves the usage of drugs:
Please indicate whether,
1. The drug is marketed in India for the
indication in which it will be used in the
study.
NA
2. The drug is marketed in India but not for
the indication in which it will be used in the
study.
NA
3. The drug is only used for experimental use
in humans.
NA
4. Clearance of the drug controller of India
has been obtained for:
-
Use of the drug in the healthy volunteers
NA
-
Use of drug in-patients for a new
indication.
NA
Phase one and two clinical trials
NA
-
G.
H.
Experimental use in-patients and healthy
volunteers.
How do you propose to obtain the drug to be used
in the study?
NA
NA
-
Gift from a drug company
NA
-
Hospital supplies
NA
-
Patients will be asked to purchase
NA
-
Other sources (Explain)
NA
Funding (if any) for the project.
Please state.
NONE
-None
-Amount
-Source
-To whom payable
I.
Does any agency have a vested interest in
NO
the outcome of the project?
J.
Will data relating to subjects/controls be
NO
stored in a computer?
K.
L.
Will the data analysis be done by
-The researcher?
YES
-The funding agency
NO
Will technical / nursing help be required for the
staff of hospital, if yes,
Will it interfere with their duties?
NO
Will you recruit other staff for the duration of the
study?
NO
If yes give details of
M.
I Designation
NA
II Qualification
NA
III Number
NA
IV Duration of employment
NA
Will informed consent be taken?
YES
If yes,
Will it be written informed consent?
YES
Will it be oral consent?
NO
Will it be taken from the subject
themselves?
YES
Will it be from the legal guardian?
YES
If no, give reason:
N.
Describe design, Methodology and
APPENDIX-II
Techniques
Ethical clearance has been accorded.
Date:
Place:
Chairman
PG Training-cum research committee
A.I.M.S., B.G.Nagara