Bancroftian filariasis in south east Madhya Pradesh: Pre-control epidemilogical observations

Lymphatic filariasis caused byWuchereria bancrofti is a major health problem next only to malaria. A study had been conducted to estimate the prevalence of microfilaraemia in a rural endemic community near Raipur. The incidence of microfilaramia in the community was found to be about 14% when studied by night finger prick method. The incidence appears to be more in males as compared to females. The infection rate in vector population i.e.,Culex quinquefasciatus was recorded at a rate of 10%. No relationship could be drawn between the rates of vector and human filarial infections or between the density of vector population and the rate of vector/human infection(s). Prior health education is essential before taking up control and preventive measures in given endemic zone.     

知识溢出效应测度的实证研究

通过构建计量经济模型,分析不同影响因子间知识溢出效应的差异,测度影响因子与知识溢出效应的关联度和有效性。研究表明:在企业知识溢出与模仿结构中存在向稳定性水平收敛的格局及模仿收益递减的趋势,形成创新与模仿的螺旋式演进模式。知识溢出效应除了与交易成本、时空间距有关外,与R&D投入总量、劳动力流动性、交易运输条件、知识溢出时滞、市场机制的灵活性、厂址变迁等因素密切相关。R&D投入总量与被解释变量呈显著正相关关系;经济差距、地区或企业之间的距离与知识溢出效应显著负相关;企业知识吸收能力与知识溢出效应成正比,当企业知识存量差距等于企业知识吸收能力时,知识溢出效应最大;知识溢出时滞、知识退化率与知识溢出效应成反比,而地区或行业的销售收入及该地区或行业的流动资产、固定资产之和对知识溢出效应和劳动生产率的提高无实质性的直接影响。知识溢出时滞是由知识本身特性和知识外部性内在化程度决定的,知识外部性内在化的实施方式主要取决于产权制度的安排、政府对创新主体的保护和道德约束等诸多因素。     

Hyperhomocysteinemia,MMPs and Cochlear Function: A Short Review

Hyperhomocysteinemia (HHCY) has been demonstrated to affect cochlear microvasculature as well as cochlear epithelial cells directly, with a resultant alteration of the expression of matrix metalloproteinases (MMPs) and their inhibitors, tissue inhibitors of metalloproteinases (TIMPs). Hence, ascertaining the optimum concentration of MMPs and TIMPs in the cochlea could help to inhibit hearing loss due to HHCY by the administration of appropriate MMP inhibitors, Since infections/inflammations as well as ototoxic antibiotics have a similar mechanism of otic pathology, the cochlear damage they cause could also be similarly prevented.     

Privacy,speech, and values: what we have no business knowing

In the United States the ascendancy of speech protection is due to an expansive and unjustified view of the value or primacy of free expression and access to information. This is perhaps understandable, given that privacy has been understood as a mere interest, whereas speech rights have been seen as more fundamental. I have argued elsewhere that the “mere interest” view of privacy is false. Privacy, properly defined, is a necessary condition for human well-being or flourishing. The opening section of this article will provide an overview of this theory. Next, after a few remarks on speech absolutism, privacy absolutism, and balancing theories, I will sketch several of the dominant argument strands that have been offered in support of presumptively weighty speech rights. While these arguments, taken together, establish that free speech is important, they do not support the view that speech should nearly always trump privacy. In final section I will present and defend a way to balance free speech and privacy claims.     

Superoxide dismutase and catalase activities and their correlation with malondialdehyde in schizophrenic patients

Free radical mediated pathological processes may have a role in schizophrenia. Free radicals (oxy radicals, such as superoxide, hydroxyl ions and nitric oxide) cause cell injury, when they are generated in excess or when the antioxidant defense is impaired. Both these processes seem to be affected in schizophrenia. In this study we investigated erythrocyte superoxide dismutase (SOD) and catalase (CAT) activities as antioxidant enzymes, malondialdehyde (MDA) as a sign of lipid peroxidation in schizophrenic patients. Activities of superoxide dismutase, catalase and malondialdehyde were greater in patients compared with the control group which may reflect increased oxidative stress in the brain tissue of schizophrenics. In the patient group erythrocyte SOD and CAT activities were weakly negative correlated with MDA concentration. These data reveal that antioxidant defense mechanisms might be impaired in schizophrenic patients. These findings also provide a theoretical basis for the development of novel therapeutic strategies, such as antioxidant supplementation.     

Overexpression of Aldose Reductase Render Mouse Hepatocytes More Sensitive to Acetaminophen Induced Oxidative Stress and Cell Death

Acetaminophen (APAP) a commonly used drug for decrease the fever and pain but is capable to induced hepatotoxicity at over dose. This study was carried out to investigate the effect of APAP on the expression of anti-apoptotic and antioxidative defense genes, and whether aldose reductase over-expressing plasmid capable to protect against APAP-induced oxidative stress and cell death. APAP treatment induced oxidative stress and hepatotoxicity, and significantly increased aldose reductase mRNA and protein expression in mouse hepatocyte (AML-12). Unexpectedly, AML-12 cells over-expressing aldose reductase augmented APAP-induced reduction in cell viability, reactive oxygen species (ROS) production, glutathione (GSH) depletion and glutathione S-transferase A2 expression. Moreover, over-expression of aldose reductase potentiated APAP induced reduction on proliferating cell nuclear antigen, B cell lymphoma-extra large (bcl-x_L), catalase, glutathione peroxidase-1 (GPx-1) and abolished APAP-induced B-cell lymphoma 2 (bcl-2) inductions. Further, over-expression of aldose reductase significantly abolished AMP activated protein kinase (AMPK) activity in APAP-treated cells and induced p53 expression. This results demonstrate that APAP induced toxicity in AML-12, increased aldose reductase expression, and over-expression of aldose reductase render this cell more susceptible to APAP induced oxidative stress and cell death, this probably due to inhibition AMPK or bcl-2 activity, or may due to competition between aldose reductase and glutathione reductase for NADPH.     

Effect of <Emphasis Type="SmallCaps">l</Emphasis>-Thyroxine on Micronuclei Frequency in Peripheral Blood Lymphocytes in Clinical and Experimental Conditions

The aim was to study the genotoxic effect of high concentration of thyroxine (T₄) in vivo in peripheral blood lymphocytes (PBL) of the patients suffering from thyroid disorders. The effect was compared by performing in vitro experiments with addition of increasing concentration of T₄ (0.125–1 µM) in whole blood samples from healthy donors. Cytokinesis-blocked micronuclei (CBMN) assay method was used to assess the DNA damage in the PBL. The study included 104 patients which were grouped as control (n = 49), hyperthyroid (n = 31) and hypothyroid (n = 24). A significant increase in micronuclei (MN) frequency was observed in hyperthyroid patients when compared with the hypothyroid and euthyroid group thereby suggesting increased genotoxicity in hyperthyroidism (p < 0.001). A significant increase in MN frequency was observed at T₄ concentration of 0.5 µM and above when compared to lower T₄ concentrations (0.125 and 0.25 µM) and basal in in vitro experiments (p = 0.000). The results indicate that the T₄ in normal concentration does not exhibit the genotoxic effect, as observed in both the in vivo and in vitro experiments. The toxicity of T₄ increases at and above 0.5 μM concentration in vitro. Therefore acute T₄ overdose should be handled promptly and effectively so as to avoid the possible genotoxic effect of high concentration of T₄ in vivo.     

Age related changes in lipid peroxidation and antioxidants in elderly people

Advanced age is associated with an accumulation of free radical damage, which leads to physiological and clinical modifications. Age related changes resulting from free radical reactions include increasing levels of lipid peroxides, alterations in enzyme activities and greater osmotic fragility. The present study was conducted to estimate the level of lipid peroxidation product-Malondialdehyde and antioxidants Catalase and Glutathione in elderly people. An increase in lipid peroxidation and decrease in antioxidants was observed in normal elderly people. Highly significant increase in MDA and decrease in antioxidants was observed in elderly people when complicated with diabetes and hypertension. Supplementation of antioxidants may prevent further oxidative injury in elderly people.     

Status and Interrelationship of Zinc,Copper, Iron,Calcium and Selenium in Prostate Cancer

Deficiency or excess of certain trace elements has been considered as risk factor for prostate cancer. This study was aimed to detect differential changes and mutual correlations of selected trace elements in prostate cancer tissue versus benign prostatic hyperplasia tissue. Zinc, copper, iron, calcium and selenium were analysed in histologically proven 15 prostate cancer tissues and 15 benign prostatic hyperplasia tissues using atomic absorption spectrophotometer. Unpaired two tailed t test/Mann–Whitney U test and Pearson correlation coefficient were used to compare the level of trace elements, elemental ratios and their interrelations. As compared to benign prostatic tissue, malignant prostatic tissue had significantly lower selenium (p = 0.038) and zinc (p = 0.043) concentrations, a lower zinc/iron ratio (p = 0.04) and positive correlation of selenium with zinc (r = 0.71, p = 0.02) and iron (r = 0.76, p = 0.009). Considerably divergent interrelationship of elements and elemental ratios in prostate cancer versus benign prostatic hyperplasia was noted. Understanding of differential elemental changes and their interdependence may be useful in defining the complex metabolic alterations in prostate carcinogenesis with potential for development of element based newer diagnostic, preventive and therapeutic strategies. Further studies may be needed to elucidate this complex relationship between trace elements and prostate carcinogenesis.