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Biomedical subjects

M Venugopal

Publications and source records attributed to M Venugopal.

14 recordsLinked to original sources
PubMed2004

Leprosy case detection using schoolchildren.

An innovative method that combined awareness creation with screening of high school students by their peers was undertaken in 26 randomly selected schools in the project area of the Schieffelin Leprosy Research and Training Center, Karigiri, Vellore, India. This method entailed educating teachers and student leaders in grades 8-12 about leprosy and how to suspect leprosy among their peers. The student leaders in turn conducted a similar awareness programme for their peers and encouraged them to report if they suffered from any skin problem or skin lesion. Based on the reporting by their peers, the class leaders prepared a 'suspect list'. Within a fortnight of the awareness program, a trained leprosy worker visited the school and examined all the students on the 'suspect list'. Those diagnosed to have leprosy were referred to a medical officer, who then confirmed the diagnosis and initiated treatment. Among the 23,125 students enrolled in the 26 randomly selected schools, 234 student leaders were educated about leprosy and trained to detect suspect lesions among their peers. A total of 2200 (9.5%) children reported with skin lesions to their leaders and after screening by a leprosy supervisor and confirmation by a medical officer, 14 new cases (NCDR 6.05/10,000) were detected. This rate was found to be comparable with case detection rates of annual school surveys done during the National Leprosy Eradication Programme (NLEP), when all schoolchildren were examined. The paper suggests that schoolchildren can be used effectively in leprosy case detection and this method has the additional advantage of creating awareness among them, their teachers and communities.

Adolescent↗
PubMed2000

The organization and distribution of patient education materials in family medicine practices.

BACKGROUND: Millions of dollars are spent annually on the production and distribution of patient education materials; however, there are no studies describing their actual use by physicians. Using qualitative data from a large comparative case study, our analysis evaluates how patient education materials are organized and used in family practices. METHODS: Eighteen purposefully selected family medicine practices were directly observed for 4 to 12 weeks each. A total of 57 providers were shadowed by a research nurse, and detailed field notes on 1600 patient encounters were recorded. A 3-member analysis team reviewed the qualitative data and identified emergent patterns. RESULTS: Clinics' use of patient education materials fell mostly into 2 distinct patterns. "Stockpilers" were providers who relied on the clinic staff to develop and organize a common library of patient education handouts. Providers with a "personal stash" collected much smaller numbers of materials that they personally maintained. Providers in the latter group had a known repertoire of a limited amount of educational material and used it more often than providers with access to a greater variety and number of handouts. In all practices, providers distributed most handouts; staff and self-selection by patients played a minor role. CONCLUSIONS: It appears that provider involvement and familiarity with patient education materials are key to their use in clinical practice. Clinicians use written patient education materials most efficiently by personally selecting and maintaining a small number of handouts that address topics most relevant to their practice.

Family Practice↗
PubMed1999

Inhibition of cell death in human mammary epithelial cells by the cooked meat-derived carcinogen 2-amino-1-methyl-6-phenylimidazo[4, 5-b]pyridine.

2-Amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) is a mammary gland carcinogen present in the human diet in cooked meat. To examine if PhIP and its reactive metabolite N-hydroxy-PhIP inhibit apoptosis in human mammary epithelial MCF-10A cells, confluent cultures deprived of serum and growth factors were incubated for 24 h with either compound. The percentages of dead cells (mean +/- SEM, n = 3) as measured by trypan blue exclusion were 5.7 +/- 0.6, 3.4 +/- 0.3, 2.7 +/- 0.3, and 0.2 +/- 0.003%, in control, 1 microM N-hydroxy-PhIP-, 5 microM N-hydroxy-PhIP-, and 100 microM PhIP-treated dishes, respectively. The expression of Bcl-2 and Bcl-x(L) as quantitated by Western blotting was 1.2- to 1.9-fold higher in the treated groups. PhIP-DNA adducts induced by N-hydroxy-PhIP in MCF-10A cells measured by the (32)P-postlabeling assay were low (<1 x 10(7), relative adduct labeling). No adducts were detected after incubation with PhIP. Western blot analysis indicated that PhIP increased ERK2 phosphorylation concomitant with Bcl-2. The results suggest that the inhibition of cell death in mammary epithelial cells by PhIP occurs independently of PhIP-DNA adducts and may involve enhanced signaling through the MAP kinase pathways.

Apoptosis↗
PubMed1999

2-Amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) retards mammary gland involution in lactating Sprague-Dawley rats.

2-Amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP), a compound from cooked meat, is an established mammary gland carcinogen in female rats. Four doses of PhIP (150 mg/kg, p.o., once per day) were given to lactating Sprague-Dawley rats separated from their 10-day-old pups to initiate involution of the gland. Twenty-four hours after the last dose, apoptotic index in the mammary gland, as measured by the TUNEL assay, was significantly higher in the gland from control rats than in the PhIP-treated rats (4.757 +/- 1.066 versus 1.905 +/- 0.248%; P < 0.05). In comparison with controls, alveoli in the mammary gland of PhIP-treated rats were also visibly larger and contained more secretory epithelial cells. The expression of Bax, a stimulator of apoptosis, and Bcl-2, an inhibitor of apoptosis, were quantitated by western blotting. Accordingly, Bax expression was 2.7-fold higher in control rats, whereas Bcl-2 expression was 3.1-fold higher in PhIP-treated rats, both changes being statistically different (Student's t-test, P < 0.05). Immunohistochemistry further confirmed a lower expression of Bax and higher expression of Bcl-2 in secretory alveolar epithelial cells of the PhIP-treated mammary gland. The findings are consistent with the notion that exposure to PhIP retarded involution via partial inhibition of programmed cell death. To investigate possible mechanisms for the inhibitory effects of PhIP on mammary gland involution, serum levels of prolactin, an important hormone for the maintenance of lactation, were measured in virgin rats with regular estrous cycles given PhIP (150 mg/kg, p.o.) on the morning of diestrous. After one estrous cycle, on proestrous morning, serum prolactin levels were 1.3-fold higher after PhIP than after control vehicle (one-way ANOVA, Fisher LSD multiple comparison test, P < 0. 05). PhIP exposure during involution was associated with the induction of benign mammary tumors. Seven out of 12 rats developed fibroadenomas, and one developed a tubulopapillary carcinoma within 1 year of receiving PhIP administration during involution (150 mg/kg, p.o., once per day for 5 days), and a high-fat diet (23.5% corn oil). An increase in serum prolactin level and the effects on mammary gland apoptosis seen with PhIP may have implications for the mechanisms of carcinogenic targeting of PhIP to the mammary gland.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1999

Intraocular gnathostomiasis.

We report a rare case of intraocular Gnathostomiasis, where a live worm, intracameral in location, was successfully removed. Its identity was confirmed by microscopy.

Adult↗
PubMed1998

Mammary gland carcinogenicity of 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine in Sprague-Dawley rats on high- and low-fat diets.

2-Amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) is a carcinogenic heterocyclic amine derived from cooked meat. Mammary gland tumors were induced in female Sprague-Dawley rats given 10 doses of PhIP (75 mg/kg po) once per day from 43 days of age and then placed on a defined high-fat (23.5% corn oil) or low-fat (5% corn oil) diet for 25 weeks. Mammary tumor incidence was 49% (44 of 90 rats) and 31% (27 of 88 rats) in the high- and low-fat groups, respectively. No tumors were found in vehicle control rats on the high-or the low-fat diet (n = 44 and 43, respectively). The higher tumor incidence in the high-fat group was due to an increase specifically in carcinomas (classified as tubulopapillary carcinomas) rather than benign tumors (tubular adenomas and fibroadenomas). The incidence of carcinomas was 45% and 24% in PhIP-treated rats on the high- and low-fat diets, respectively. In addition, the percentage of carcinomas showing stromal invasion was highest in the high-fat diet group (22% vs. 8%, high- vs. low-fat diet). Proliferating cell nuclear antigen immunostaining (PCNA) index revealed six times more proliferation in carcinomas from rats on the high-fat diet than in rats on the low-fat diet. Adenomas from rats on different diets had similar PCNA indexes. The tumor apoptotic index, quantitated by immunohistochemical detection (terminal deoxynucleotidyl transferase nick end labeling), was twice as high in carcinomas from rats on the high-fat diet as in carcinomas from rats on the low-fat diet but was similar between the two groups of adenomas. The PCNA-to-apoptosis ratio was 43 and 17 in carcinomas from rats on the high- and low-fat diets, respectively, indicating that the growth rate of carcinomas was greater in rats on the high-fat diet. The results from this study show that the high-fat diet increases the incidence, invasiveness, and growth of PhIP-induced mammary gland carcinomas.

Animals↗
PubMed1996

Synergistic antitumour activity of vitamins C and K3 against human prostate carcinoma cell lines.

Vitamins C, K3 (VC, VK3) and a VC/VK3 combination with a VC:VK3 ratio of 100:1 were assayed for their antitumour activity against two human prostatic carcinoma cell lines. Co-administration of the vitamins enhanced the antitumour activity 5- to 20-fold even with a 1 h exposure time. While exogenous catalase destroyed the antitumour activity, hydrogen peroxide-induced lipid peroxidation was negligible. Analysis of cellular ATP and thiol levels as well as DNA and protein synthesis revealed: a transient increase in ATP production, a decrease in DNA synthesis, an increase in protein synthesis and a decrease in thiol levels. These results suggested that the increased cytotoxicity of the vitamin combination was due to redox cycling and increased oxidative stress.

Adenosine Triphosphate↗
PubMed1996

Synergistic antitumor activity of vitamins C and K3 on human urologic tumor cell lines.

A micro-tetrazolium assay was employed to evaluate vitamin C (VC), vitamin K3 (VK3) and vitamin C/vitamin K3 combinations (VC/VK3) for their antitumor activity against eight human urologic tumor cell lines. While the individual vitamins exhibited antitumor activity at high concentrations, co-administration of the vitamins in a VC : VK3 ratio of 100 : 1 potentiated antitumor activity 4- to 61-fold even when exposure times were as short as 1 hour. Administration of exogenous catalase destroyed the antitumor activity of the vitamins and suggested that hydrogen peroxide and perhaps other reactive oxygen species were involved in the antitumor mechanism of these vitamins. Electron micrographs taken in a previous study demonstrated that vitamin treatment damaged mitochondria and may have impaired ATP synthesis. Analysis of cellular ATP and thiol levels as well as DNA and protein synthesis during the first five hours following a one hour VC/VK3 treatment, revealed: a transient increase in ATP production, a substantial decrease in DNA synthesis, an increase in protein synthesis and a decrease in thiol levels. These results suggested that redox cycling of the vitamin combination increased oxidative stress until it surpassed the reducing ability of the cellular thiols and cellular or genetic damage ensued.

Adenosine Triphosphate↗
PubMed1996

Flow cytometric and ultrastructural aspects of the synergistic antitumor activity of vitamin C-vitamin K3 combinations against human prostatic carcinoma cells.

Transmission and scanning electron microscopy and flow cytometry were employed to characterize the cytotoxic effects of vitamin C (VC), vitamin K3 (VK3), or VC-VK3 combinations on a human prostate carcinoma cell line (DU145) following a 1-h vitamin treatment and a 24-h incubation in culture medium. Cells exposed to VC exhibited membranous blebs, aberrant microvillar morphology, mitochondria with swollen cristae and intramitochondrial deposits, as well as nucleoli with segregated components. VK3-treated cells displayed a damaged cytoskeleton and membranes, a cytoplasm which contained large lumen, condensed polysomes, and severely damaged mitochondria with residual bodies, and nuclei which exhibited chromatic condensation, pyknosis, and karyolysis. VC-VK3-treated cells exhibited characteristics consistent with necrosis, i.e. swollen mitochondria and swollen, achromatic nuclei with marginated chromatin and intact envelopes, while other cells displayed characteristics consistent with apoptosis, i.e. expulsion of organelle-containing blebs, margination of nuclear chromatin, and segregation of nucleolar components. Vitamin treatment also decreased DNA synthesis, induced a S/G2 block in the cell cycle, and resulted in the accumulation of fragmented DNA. These results suggested that increased oxidative stress, subsequent membrane damage, and DNA fragmentation were responsible for enhanced cytotoxicity of the vitamin combination.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1995

Scanning electron microscopy and transmission electron microscopy aspects of synergistic antitumor activity of vitamin C - vitamin K3 combinations against human prostatic carcinoma cells.

A MTT/formazan assay was used to evaluate the antitumor activity of vitamin C (Vit C), vitamin K3 (Vit K3), or vitamin C:vitamin K3 combinations against a human prostatic carcinoma cell line (DU145). Both Vit C and Vit K3 alone exhibited antitumor activity, but only at elevated doses. When Vit C and Vit K3 were combined at a C:K3 ratio of 100:1 and administered to the carcinoma cells, the 50% cytotoxic concentrations (CD50) of the vitamins decreased 10- to 60-fold. Subsequently, the DU145 cells were examined with transmission and scanning electron microscopy (TEM and SEM) following a 1 hour treatment with Vit C, Vit K3, or Vit C/K3 combined at their 50% cytotoxic dose. Our morphological data suggest that vitamin treatment with individual vitamins affects the cytoskeleton, the mitochondria, and other membranous components of the cell. Treatment with the vitamin combination appears to potentiate the effects of the individual vitamin treatment. Specifically, there are abundant necrotic cells. The surviving cells display morphological defects characteristic of cell injury.

Antineoplastic Agents↗
PubMed1988

Conditioned taste aversion is reduced in rats with a history of lithium/pilocarpine-induced limbic seizures.

Limbic seizures were evoked in rats by single subcutaneous injections of lithium and pilocarpine that are known to elicit severe damage to gustatory-affective centers in the brain. About two months later 12 of these rats and 12 control rats that received either lithium or pilocarpine (no seizures) were given free access to 10% sucrose solutions and then injected with 0.15 M LiCl (10 ml/kg). Whereas the control rats demonstrated the expected conditioned taste aversion (CTA) to later presentations of sucrose during single bottle drinking tests, the rats that had been seizured demonstrated a significant attenuation in CTA.

Animals↗
PubMedDate not supplied

Effectiveness of chemotherapy in melanotic neurectodermal tumor of infancy.

MNTI is an uncommon tumor mainly of infants. Surgery is the primary modality of treatment. Chemotherapy has been tried for recurrent/residual tumors. The chemotherapeutic response of 3 infants treated at a center is discussed here. All 3 infants showed good response to chemotherapy. In 2 of them complete residual tumor resection became possible; 2 of them are alive and tumor regression continues. One child had local recurrence later and was lost for follow-up.

Antineoplastic Combined Chemotherapy Protocols↗