Ethical Publications in Medical Research

Ethics in medical sciences research may not always translate into ethical publications. Unfortunately due to lack of regulatory bodies, publication misconduct is now a global menace for the scientific community. Publication misconducts are not only restricted to research fraud or data manipulations alone but also seriously include plagiarism, duplicate publications especially on figures and tables, authorship disputes and conflict of interests. As global scientific research is expanding particularly in the field of health sciences hence possibilities of more rise of unethical practices from research to publications are very high, authors suggest a strong peer-reviewing system, use latest technological support, strong publication ethics policies, active monitoring, protection of whistle blowers and more liaisons between journals and research institutions or universities possibly to prevent publication misconduct effectively. This chapter discusses how medical publications might have abused various ethical norms not only while conducting research but also during the publication process. The review also discusses the possible preventive measures against unethical practices of research publications

Tissue Specific Effects of Chronic Sustained Hypoxia on Oxidative Stress: Role of Cilnidipine, a Dual L/N Type Calcium Channel Blocker

Background: Blood flow, metabolic rate and oxygen requirements of an organ guide the extent of oxidative stress experienced by any tissue in response to chronic hypoxia. Currently cilnidipine is used in the management of hypertension and its antioxidant actions are gaining wide interest. Aim and Objectives: To evaluate the tissue specific effects of chronic sustained hypoxia with regards to oxidative stress in the context of cilnidipine. Material and Methods: Twenty four adult male Wistar strain albino rats were randomly assigned into four groups: group 1, control, normoxia (21% O ); group 2, chronic hypoxia (CH) (10% O) for 21 days; group 3, normoxia + cilnidipine (Cil) for 21 days; group 4, chronic hypoxia + cilnidipine (CH+Cil) for 21 days. Following 21 days of intervention blood was collected and animals were sacrificed and liver,lung and heart were collected. Serum MDA and MDA in tissue homogenate of liver, lung and heart were estimated. Results: Our results demonstrate the elevated serum MDAlevels in chronic hypoxia exposed rats (group 2). We also observed increased MDA in liver followed by lung and least in the heart in chronic hypoxia exposed rats (group 2). Treatment with cilnidipine reduced serum MDA and heart MDA levels in cilnidipine treated chronic hypoxia exposed rats (group 4). However cilnidipine did not have any influence on MDA levels in the liver and lung in same group of rats. Conclusion: The results demonstrate tissue specific effects of chronic sustained hypoxia with the highest oxidative stress observed in the liver followed by the lung. Although oxidative stress is also observed in the heart it is the least in comparison to the liver and the lung. Cilnidipine, a dual L/N type calcium channel blocker demonstrated beneficial antioxidant actions only in the heart supporting the cardioprotective role of cilnidipine

Effect of 1,25-dihydroxy vitamin D3 (1,25(OH)2D3 ) on hexavalent chromium (Cr (VI)) induced alteration of glucose homeostasis in Wistar rats

Background: 1,25-dihydroxy vitamin D3(1,25(OH)2D3) is a fat-soluble known antioxidant vitamin to protect cardiovascular health. Hexavalent chromium (Cr (VI)) as a heavy metal has adverse effects on vascular system. Aim and Objectives: To evaluate the possible protective effects of 1,25(OH)2D3 supplementation on Cr (VI) induced altered glucose regulation. Materials and Methods: Twenty-four adult Wistar male rats were divided into four groups (n=6 in each group) as following: Group-1 (control); Group-2 received K2Cr2O7 5.0 mg/kg body weight intraperitoneally for 10 dosages on every alternate day for 20 days; Group-3 received 1,25(OH)2D3 12.5μg/kg/d, orally daily till 20 days; and Group-4 received both K2Cr2O7 and 1,25(OH)2D3 with dosages as above. At the end of 10th dosage after overnight fasting i.e. (on day 21) blood samples were collected from tail vein of all the rats. Oral Glucose Tolerance Test (OGTT), serum glucose and insulin concentrations were estimated. Insulinogenic index was also calculated. Liver glycogen concentrations were assessed after sacrificing the animals. Results: OGTT showed an increase of fasting blood glucose levels in Cr (VI) treated Group-2 rats till at the end of 2.0 hrs. The Cr (VI) treated and simultaneously supplemented with 1,25(OH)2D3 Group-4 rats showed lesser elevation of blood glucose level till 2.0 hrs. A decrease in plasma insulin level and increase in insulinogenic index were also found in Cr (VI) treated Group-2 rats but in case of vitamin D supplemented Group-4 rats, both plasma insulin levels and insulinogenic index were found to be improved remarkably. Liver glycogen concentrations in K2Cr2O7 treated rats were also found to be reduced significantly but 1,25(OH)2D3 supplemented Group-4 rats showed improvement in liver glycogen concentrations. Conclusion: 1,25(OH)2D3 is found to be beneficial against hexavalent chromium induced alteration of glucose homeostasis

Hypoglycemic activity of curcumin synthetic analogues in alloxan-induced diabetic rats.

The currently available therapies for type 2 diabetes have been unable to achieve normoglycemic status in the majority of patients. The reason may be attributed to the limitations of the drug itself or its side effects. In an effort to develop potent and safe oral antidiabetic agents, we evaluated the in vitro and in vivo hypoglycemic effects of 10 synthetic polyphenolic curcumin analogues on alloxan-induced male diabetic albino rats. In vitro studies showed 7-bis(3,4-dimethoxyphenyl)hepta-1,6-diene-3,5-dione (4) to be the most potential hypoglycemic agent followed by 1,5-bis(4-hydroxy-3-methoxyphenyl)penta-1,4-dien-3-one (10). Structure activity relationship (SAR) of the tested compounds was elucidated and the results were interpreted in terms of in vitro hypoglycemic activities. Furthermore, oral glucose tolerance test (OGTT) with compounds 4, 10 and reference hypoglycemic drug glipizide showed that compound 4 and glipizide had relatively similar effects on the reduction of blood glucose levels within 2 h. Thus, compound 4 might be regarded as a potential hypoglycemic agent being able to reduce glucose concentration both in vitro and in vivo