Biomedical subjects
Publications and source records attributed to K Rao.
In vivo bioassay-guided fractionation of the aqueous alcohol extract of the aerial parts of Teramnus labialis (Roxb.) Benth. (Fabaceae), using C57BL/Ks-db/db mice as a model for type 2 diabetes, yielded an active fraction containing a mixture of coumarins. The major coumarin present in the active fraction was identified as fraxidin.
This study examined the factor structure of the Mental Health Professionals Stress Scale (MHPSS) and its reliability and validity in a sample of 116 clinical psychologists in India. Principal component analysis of the MHPSS identified four factors that accounted for 42.2% of the total variance. These 4 factors reflected 6 of the 7 original subscales. The subscale 'Client-related difficulties' did not emerge as a distinct factor. The authors attribute this to cultural differences in the therapist-patient relationship. The MHPSS correlated negatively with measures of professional role satisfaction and subjective well being. It was concluded that the MHPSS is a reliable and valid tool to measure sources of occupational stress experienced by mental health professionals.
OBJECTIVE: To explore the methods to select population-based controls in a pair-matched case-control study of risk factors for lung cancer and to lay foundation for development of their monitoring in urban areas. METHODS: Data of cases of lung cancer and their three different groups of pair-matched control based on population from the "Study on surveillance for incidence and mortality of common malignant tumor and their risk factors" in Beijing, Tianjin, Shanghai and Chongqing were personally-interviewed and analyzed with conditional multivariate logistic regression using STATA software involving 1 312 pairs aged 35 - 74. RESULTS: Odds ratios for main risk factors were consistent with the three groups of controls, and there was certain difference in ORs for dietary factor, etc. between the studies with three difference control groups. There was little differences in frequencies of exposure to risk factors between studies with neighbor-controls and normal-controls. Cigarette smoking, lower body mass index, long-time depressed mood, lower capability of emotion regulation, previous respiratory diseases, family history of cancer in the first-degree relatives significantly increased the risk for lung cancer after adjusted for age, education level, family average income and other risk factors. CONCLUSION: It was feasible to use population-based controls instead of neighbor controls in surveillance for risk factors of lung cancer.
OBJECTIVE: To analysis the risk factors of lung cancer and determine the surveillance index in urban areas in four metropolises in China. METHODS: The paper used the data from the in-person interviews of National Research on Malignant Tumor Morbidity, Mortality and Surveillance Methods in 1996. We carried out a 1:1 matched case-control study based on population involving 1 312 cases and 1 312 neighborhood controls aged 35 - 74 from Beijing, Tianjin, Shanghai, Chongqing urban areas. The relationships between risk factors and lung cancer were analyzed by conditional univariant and multivariate logistic regression on the computer package, STATA. RESULTS: Cigarette smoking, lower body mass index, longtime depressed mood, lower capability of emotion regulation, previous respiratory diseases, family history of cancer in first-degree relatives significantly increased the risk of lung cancer after adjusted by age, education, family average income and other risk factors. The odds ratios of these risk factors were 3.46 (95% CI 2.70 - 4.45), 1.18 (95% CI 1.22 - 1.40), 2.64 (95% CI 1.95 - 3.57), 2.71 (95% CI 2.02 - 3.65), 2.28 (95% CI 1.81 - 2.88), 1.79 (95% CI 1.38 - 2.32), respectively. The odds ratio associated with the highest quartile of fresh vegetables consumption compared with the lowest was 0.75 (95% CI 0.65 - 0.87), showed an inverse relationship. Exercising more often had a significant inverse association between cases and controls, and its odds ratio was 0.81 (95% CI 0.74 - 0.89). CONCLUSION: Cigarette smoking, psychological factor, previous respiratory diseases and family history of cancer were the main risk factors of lung cancer in four cities. They were the important surveillance index of lung cancer. The relation between lung cancer and environmental tobacco smoke, dietary factors and the factors related with female etc. should conduct further studies or special studies which defined the exposures carefully and exactly.
Based on the 145-site Disease Surveillance Point System (DSP) of the Ministry of Health in conjunction with 600-site Urban/Rural Household Socio-economic Survey System of State Statistic Bureau carried out by the Urban Household Socio-Economic Survey Team and Rural Household Socio-Economic Survey Team. Three strata including urban, general rural and less-developed rural were defined. Sample size of 16,000 children was designed according to the estimate of 5% underweight prevalence of children under 6 years of age. 40 sites were sampled by stratified random sampling, involving 14 urban sites, 17 general rural sites and 9 poor rural sites in 26 provinces. The total population of the 40 sites is 20.678 million, which is 1.7% of whole population of the country. 400 children under 6 years of age were sampled by Multi-stage Cluster Sampling at each site. The consistency of age distribution of children between the sample and the National Population Census data in 1990 by Goodness of Fit Test indicated the representativeness of the sample is reliable.
A diagnosis of Pelizaeus-Merzbacher disease (MIM 312080) was made in a young boy. No mutation in the coding region of the proteolipid protein (PLP) gene had been found. The boy's maternal aunt came for prenatal diagnosis when 16+ weeks pregnant and carrying a male fetus. Samples were tested for duplication of the PLP gene, by interphase FISH, in lymphocyte preparations from the proband, his aunt and an amniotic fluid cell preparation from the fetus. The proband was found to carry the duplication, thus confirming the diagnosis of Pelizaeus Merzbacher disease, but neither the aunt nor the fetus carried a duplication.
Recently we described a block in bile acid synthesis in cerebrotendinous xanthomatosis (CTX), a lipid storage disease related to an inborn error of bile acid metabolism. In this disease a defect in hepatic microsomal (24S) hydroxylation blocks the transformation of 5beta-cholestane-3alpha,7alpha,12alpha,25-tetrol into (24S) 5beta-cholestane-3alpha,7alpha,12alpha,24,25- pentol and cholic acid. Mitochondrial cholesterol 27-hydroxylation has also been reported to be abnormal in CTX subjects, but the relative importance of the enzymatic defect in this alternative microsomal pathway (namely, the 24S hydroxylation of 5beta-cholestane-3alpha,7alpha, 12alpha,25-tetrol relative to the abnormality in mitochondrial 27-hydroxylase) has not been established in CTX. To delineate the sequence of side-chain hydroxylations and the enzymatic block in bile acid synthesis, we synthesized the (23R and 23S) 24-nor-5beta-cholestane-3alpha,7alpha, 12alpha,23,25-pentols utilizing a modified Sharpless asymmetric dihydroxylation reaction on 24-nor-5beta-cholest-23-ene-3alpha, 7alpha, 12alpha-triol, a C26 analog of the naturally occurring C27 bile alcohol, 5beta-cholest-24-ene-3alpha,7alpha,12alpha-triol . Stereospecific conversion of the unsaturated 24-nor triol to the corresponding chiral compounds (23R and 23S), 24-nor-5beta-cholestane-3alpha,7alpha,12alpha,23 ,25-pentols, was quantitative. However, conversion of the unsaturated 24-nor triol to the chiral nor-pentols had absolute stereochemistry opposite to the products predicted by the Sharpless steric model. The absolute configurations and enantiomeric excess of the C26 nor-pentols and the C27 pentols (synthesized from 5beta-cholest-24-ene-3alpha,7alpha,12alpha-triol for comparison) were confirmed by nuclear magnetic resonance and lanthanide-induced circular dichroism Cotton effect measurements. These results may contribute to a better understanding of the role of the 24S-hydroxylation vs. 27-hydroxylation step in cholic acid biosynthesis.
The disease visceral leishmaniasis is caused by a protozoan parasite, Leishmania donovani and is characterized by depressed cell-mediated immunity (CMI) and unhindered parasite growth in a susceptible host. The opposite trend is observed in a resistant host. However, the mechanism of this loss of CMI during the progressive disease is unknown as yet. In this report, we demonstrate that more than 40% of CD4+ T cells from a susceptible host undergo apoptosis resulting in a significant decrease in interleukin (IL)-2 and interferon (IFN)-gamma secretion, leaving IL-4 secretion unaffected. These changes are not apparent in the case of CD4+ T cells derived from a resistant host. The data reported here suggest that experimental Leishmania donovani infection leads to selective deletion of the IL-2 and IFN-gamma-secreting cells but not Th2-like cells in a susceptible but not a resistant host.
OBJECTIVE: This study was aimed to evaluate the immuno-modulator role of homeopathic remedies in Human Immunodeficiency Virus (HIV) infection. METHODOLOGY: A randomised double blind clinical trial was conducted to compare the effect of homeopathic remedies with placebo, on CD4+ve T-lymphocytes in HIV infected individuals, conforming to Centres for Disease Control (CDC) stage II & III. 100 HIV+ve individuals between 18-50 y (71% males) were included in the study. 50 cases conformed to CDC stage II--Asymptomatic HIV infection, and 50 cases to CDC stage III--Persistent Generalised Lymphadenopathy (PGL). Cases were stratified according to their clinical status and CD4+ve lymphocyte counts. The randomisation charts were prepared much before the start of the trial by randomly assigning placebo and verum codes to registration numbers from 1 to 50. A single individualised homeopathic remedy was prescribed in each case and was followed up at intervals of 15 d to one month. A six months study was performed for each registered case. Assessment of progress was made by evaluation of CD+ve lymphocyte counts, which was the prospectively-defined main outcome measure of the study; the results were compared with the base line immune status. RESULTS: In PGL, a statistically significant difference was observed in CD+ve T-lymphocyte counts between pre and post trial levels in verum group (P < 0.01). In the placebo group a similar comparison yielded non-significant results. (P = 0.91). Analysis of change in the pre and post trial counts of CD4+ve cells between groups was also statistically significant (P = 0.04). In asymptomatic HIV infection, differences in absolute CD4+ve lymphocyte counts between pre and post trial levels were not significant. Analysis of changes in pre and post trial CD4 levels of placebo and verum groups for combined strata of asymptomatic and PGL groups was also not significant. CONCLUSION: The study suggests a possible role of homeopathic treatment in HIV infection in symptomatic phase, as evidenced by a statistically significant elevation of base line immune status in persistent generalised lymphadenopathy.
Meningiomas constitute 15% to 18% of all primary intracranial and intraspinal tumors. Distant extracranial metastases are reported to occur in fewer than 1 in 1000 cases. Of 1992 primary intracranial meningiomas seen at Mayo Clinic Rochester from 1972 through 1994, we identified 3 (0.15%) with documented extracranial metastasis. A review of the literature suggests that previous craniotomy, venous sinus invasion, local recurrences, histological malignancy, and papillary morphology may be risk factors for systemic spread, as demonstrated in our cases. Although rare, metastatic meningioma should be considered in the differential diagnosis of abnormal findings on chest radiography in patients with known or suspected intracranial meningioma.
Unlike wild-type mouse melanocytes, where melanosomes are concentrated in dendrites and dendritic tips, melanosomes in dilute (myosin Va-) melanocytes are concentrated in the cell center. Here we sought to define the role that myosin Va plays in melanosome transport and distribution. Actin filaments that comprise a cortical shell running the length of the dendrite were found to exhibit a random orientation, suggesting that myosin Va could drive the outward spreading of melanosomes by catalyzing random walks. In contrast to this mechanism, time lapse video microscopy revealed that melanosomes undergo rapid ( approximately 1.5 microm/s) microtubule-dependent movements to the periphery and back again. This bidirectional traffic occurs in both wild-type and dilute melanocytes, but it is more obvious in dilute melanocytes because the only melanosomes in their periphery are those undergoing this movement. While providing an efficient means to transport melanosomes to the periphery, this component does not by itself result in their net accumulation there. These observations, together with previous studies showing extensive colocalization of myosin Va and melanosomes in the actin-rich periphery, suggest a mechanism in which a myosin Va-dependent interaction of melanosomes with F-actin in the periphery prevents these organelles from returning on microtubules to the cell center, causing their distal accumulation. This "capture" model is supported by the demonstration that (a) expression of the myosin Va tail domain within wild-type cells creates a dilute-like phenotype via a process involving initial colocalization of tail domains with melanosomes in the periphery, followed by an approximately 120-min, microtubule-based redistribution of melanosomes to the cell center; (b) microtubule-dependent melanosome movement appears to be damped by myosin Va; (c) intermittent, microtubule-independent, approximately 0.14 microm/s melanosome movements are seen only in wild-type melanocytes; and (d) these movements do not drive obvious spreading of melanosomes over 90 min. We conclude that long-range, bidirectional, microtubule-dependent melanosome movements, coupled with actomyosin Va-dependent capture of melanosomes in the periphery, is the predominant mechanism responsible for the centrifugal transport and peripheral accumulation of melanosomes in mouse melanocytes. This mechanism represents an alternative to straightforward transport models when interpreting other myosin V mutant phenotypes.
Drawing on experiences from China and Russia (the world's two largest transitional economies), this paper empirically examines the impact of economic reforms on health status. While China's overall health status continued to improve after the economic reform, Russia experienced a serious deterioration in its population health. The observed differences in health performance between China and Russia can be explained by the different impacts of economic reforms on three major socioeconomic determinants of health. Depending on whether or not the reform improves physical environment (as reflected in income level and nutritional status), social environment (including social stability and security system), and health care, we would observe either a positive or a negative net effect on health. Despite remarkable differences in overall health development, China and Russia share some common problems. Mental and social health problems such as suicides and alcohol poisoning have been on the rise in both countries. These problems were much more serious in Russia, where political and social instability was more pronounced, associated with Russia's relatively radical reform process. With their economies moving toward a free market system, health sectors in China and Russia are undergoing marketization, which has had serious detrimental effect on the public health services.
Functionalized 2-alkyl derivatives of inosinic acid have been synthesized to serve as reversible as well as irreversible inhibitors of the human type II enzyme inosine monophosphate dehydrogenase. These compounds were designed to react with Cys-331 of the enzyme to form covalent bonds so as to interfere with the normal enzyme mechanism which involves attack of Cys-331 at C-2 of the substrate. Mass spectrometric analysis of the reaction products after enzymatic degradation confirmed the appropriateness of the inhibitor design.
Cytogenetic and molecular studies have implied the presence of tumor suppressor genes (TSGs) on chromosome 9p that are critical in the development of lung and other cancers. The p16/CDKN2 gene, a cyclin dependent kinase inhibitor, is a well-defined TSG on 9p21. Although the frequency of mutations in the p16/CDKN2 gene has been detected in approximately 30% of non-small cell lung cancer, loss of heterozygosity on 9p has been observed in greater than 70% of non-small cell lung cancers. These and other deletion mapping studies have suggested the existence of additional TSGs on 9p. This study examined chromosome 9p for TSG loci by analyzing 23 squamous cell carcinomas of the lung with 21 microsatellite markers. Loss of heterozygosity was detected in all of the tumors, and homozygous deletions of the p16/ CDKN2 locus were observed in 6 of the 23 tumors (26%). In addition, a novel region of homozygous deletion was detected in six tumors (26%) at D9S126, approximately 2.5 cM proximal to p16/CDKN2. A single tumor contained a homozygous deletion at both the p16/CDKN2 locus and the D9S126 locus. The possibility of homozygous loss was confirmed by multiplex PCR using both the D9S126 marker and a chromosome 9p control marker. Fluorescence in situ hybridization analysis with P1 and cosmid probes containing D9S126 also confirmed these data. The minimum region of homozygous deletion was determined by testing markers immediately proximal and distal to the D9S126 region. The data identify a homozygous loss on the short arm of chromosome 9 suggesting the presence of a novel TSG locus, proximal to p16/CDKN2 and located between D9S265 and D9S259.
In cultured rat pituitary cells, increases in the cytosolic calcium concentration ([Ca2+]i) and LH release are induced by activation of GnRH receptors as well as by nonreceptor-mediated stimuli. Treatment of pituitary cells with the myosin light chain kinase (MLCK) inhibitor, wortmannin, attenuated GnRH-induced LH release. Wortmannin also reduced the LH responses to nonreceptor-mediated elevation of [Ca2+]i by ionomycin and activation of voltage-sensitive Ca2+ channels by Bay K 8644 or high K+, as well as Ca2+-induced LH release in permeabilized pituitary cells. The [Ca2+]i responses to these stimuli were unaltered in wortmannin-treated pituitary cells, indicating that this compound inhibits a Ca2+-dependent step in exocytosis without affecting Ca2+ signaling. In perifused pituitary cells, the GnRH-induced early spike phase of LH release was not affected by wortmannin, whereas the subsequent plateau phase was almost completely inhibited. No significant changes in GnRH-induced phospholipase D activity and diacylglycerol production were observed in wortmannin-treated pituitary cells during the sustained phase of agonist stimulation. Wortmannin also had no effect on LH responses to the protein kinase C activator, phorbol 12-myristate 13-acetate, further indicating that the attenuation of agonist-induced LH release is not related to inhibition of the diacylglycerol/protein kinase C pathway. In addition, agonist-induced LH release was attenuated by two other MLCK inhibitors, MS-347a and KT5926. These data suggest that MLCK mediates the downstream effects of Ca2+ on exocytosis, an action supported by the finding of wortmannin-sensitive phosphorylation of a 20-kDa protein in pituitary cells and alphaT3-1 gonadotrophs treated with GnRH, K+, and Bay K 8644. This protein was coprecipitated from pituitary extracts with a specific antibody to nonmuscle myosin IIB and comigrated with 20-kDa smooth muscle myosin light chain on SDS-PAGE. These results demonstrate that Ca2+ controls exocytosis through an initial wortmannin-insensitive step and a sustained wortmannin-sensitive step and suggest that the latter event in the cascade of cellular responses is dependent on phosphorylation of nonmuscle myosin IIB light chain by MLCK.
Healthy life expectancy in some urban residents was analyzed with fundamental principles of Sullivan's method and mortality data in our residents and some data from national health service survey conducted in 1993 to assess their quality of life. Results showed that proportion of healthy to total life expectancy accounted for more in males than in females and in medium-sized and small cities than in large ones, and decreased with increase of age. It suggests that quality of life in some of our urban residents lowered with increase of age, was worse in women than in men and lower in large cities than in mediumsized and small ones.
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