Biomedical subjects
Publications and source records attributed to S Agarwal.
Bilateral testicular biopsies from 202 infertile males were examined to ascertain the differences in the degree of damage to the germinal epithelium on both sides. Depending on the histologic changes, the biopsies were divided into six groups. A significant difference in the morphology on both sides was seen only in 3% cases. The left and the right testes were equally damaged in cases with similar morphology.
Testicular biopsies of 38 infertile males with varicocele were examined for vascular changes. Endothelial prominence, intimal fibrosis and increased amount of collagen in the media were present in veins, venules and capillaries. The small vessels were thickened with the deposition of homogeneous bluish pink material. The material stained green on Van Geison stain. The vascular changes were bilateral even in patients of unilateral varicocele. The severity of these changes was not related to tubular morphology.
Drug sensitivity of Salmonella typhi isolated from 25 blood culture positive cases of typhoid fever who presented between May and July 1990 was tested to determine their in vitro susceptibility to various antimicrobials. Twenty-one of them (84%) showed resistance to chloramphenicol and 24 (96%) to cotrimoxazole. All the 25 cases were sensitive to norfloxacin, gentamicin and cephalexin. Sixteen of 21 chloramphenicol resistant typhoid cases in whom chloramphenicol was initially started failed to respond to this drug even after 5 to 7 days, thereby indicating that in vivo response matched with the in vitro sensitivity. Clinical response to norfloxacin, whether given initially or following chloramphenicol failure, was prompt and satisfactory. Norfloxacin thus appears to be a good choice in such cases.
Sera and leukaemic cell extracts from patients of acute leukaemia were evaluated for their effect on the repopulating ability of the pluripotent stem cells and erythroid differentiation by an in vivo splenic colony count (CFU-S) technique. Normal donor marrow cells of mice were treated with sera and cell extracts from patients of acute leukaemic and healthy controls and injected in the recipient mice. The CFU-S performed on the seventh day to assess repopulating ability of the stem cell showed consistently lower CFU-S counts in the test groups, with leukaemic sera (P less than 0.01) as well as leukaemic cell-extracts (P less than 0.001). The erythroid differentiation assessed by 59Fe uptake by the spleens also showed significantly reduced counts in the two test groups (P less than 0.01 and less than 0.001 respectively). The results indicate that both leukaemic sera and cell-extracts exert a significant suppressive effect on the repopulating ability of the stem cells and on their erythroid differentiation.
Bull horn injury is not uncommon, and during a 12 year period from 1977 to 1988, 101 patients required inpatient treatment at the Christian Medical College Hospital, a teaching hospital at Vellore in South India. The ages of these patients ranged from two years to 90 years and the male to female ratio was 4:1. Sixty-one per cent of the injuries occurred either to the perineum or abdomen and wounds were directed obliquely upward. Thirty-five per cent required extensive surgical intervention. The over-all wound infection rate was 12.9 per cent. Of wounds that were primarily closed, 42.9 per cent had wound infection, while only 6.3 per cent that were secondarily closed developed infection. Two patients died as a consequence of the injury. Based on the results of this study, we recommend that a careful evaluation of the injury and timely and appropriate management of each patient must be done to reduce morbidity and mortality. Primary closure of wounds must be avoided even when surgical intervention is possible soon after injury.
Infection after arthroplasty is a serious complication associated with a high incidence of morbidity. A 24-year-old woman developed brucella septic arthritis in both knees following bilateral total knee arthroplasty. This complication appears not to have been previously reported in the literature.
The effect of primaquine enantiomers on cell membranes of glucose-6-phosphate (G-6PD)-deficient erythrocytes was studied in vitro. Staining with merocyanine (Mc-540) showed that exposure to primaquine enantiomers produces significant fluorescence in G-6PD-deficient erythrocytes, indicating marked drug-induced alterations in membrane fluidity. Scanning electron microscopy (SEM) studies confirmed that primaquine enantiomers altered membrane morphology (by producing stomatocytes) in both normal and G-6PD-deficient cells. The concentration-dependent effect, however, was more pronounced with MC-540, a lipophylic dye, than with SEM (an expensive technique).
Ozone (O3) is a powerful oxidizing component of air pollution that may react with other air pollutants before or after inhalation. Because ozonized compounds can be mutagenic to bacteria, we examined whether ambient O3 levels can transform tobacco smoke arylamines into products that are genotoxic to human lung cells. To test this possibility, aqueous solutions of 1-naphthylamine (1-NA) were first exposed to air or O3 in the absence of cells and then used to treat cultured human lung cells, i.e., the diploid fibroblasts CCD-18Lu and the transformed type II epithelial cells A549. DNA single-strand breaks were assayed by DNA alkaline elution. Neither air-exposed 1-NA nor O3-exposed buffer or water were DNA-damaging. However, exposure of 1-NA (15 microM) to O3 (0.1 ppm; 1 h) produced 400 rad equivalents of DNA breaks in either cell type. Although maximal induction of DNA breaks depended upon arylamine concentration, the rates at which DNA-damaging products were formed (activated) and subsequently deactivated depended upon O3 concentration. O3-activated 1-NA was stable for at least 4 h and could damage cellular DNA at 4 degrees C. During ozonization, hydroperoxides were formed at levels equivalent to between 2 and 20 microM of hydrogen peroxide and were eliminated by treatment with catalase. However, failure of catalase and superoxide dismutase to block formation of DNA breaks indicated that neither hydrogen peroxide nor superoxide anions were involved in breaking DNA.(ABSTRACT TRUNCATED AT 250 WORDS)
Analyses of DNA from 64 patients with thalassemia major using the hybridization technique of amplified DNA with radiolabeled synthetic oligonucleotide probes identified 13 different beta-thalassemia mutations. The codon 39 (C----T) and IVS-I-110 (G----A) mutations occurred most frequently but seven additional mutations were observed which were present at frequencies of 3.9 to 10.2%. This broad spectrum of beta-thalassemia alleles complicates the analyses for institutions involved in prenatal diagnosis. Promoter mutations were rare and the frequencies of two other mild mutations [IVS-I-6 (T----C) and the poly A mutation] were relatively low indicating that beta-thalassemia is a severe disease among Bulgarians. The high frequencies of 4.7-5.5% for the four frameshifts at codons 5, 6, 8, and 8/9 may be specific for this population.
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Tissues for 74 uterine cervical lesions including 64 invasive squamous cell carcinomas, 4 adenocarcinomas and 6 cervical intraepithelial neoplasia (CIN) were studied by peroxidase-antiperoxidase (PAP) method for presence of carcinoembryonic antigen (CEA). CEA was absent in normal squamous and endocervical epithelium. The antigen was demonstrated in all the cases of CIN (100%) and in 48 invasive carcinomas (70.6%). A heterogeneous pattern of staining was noted in different cases and also within a tumour. None of the 6 endometrial carcinomas showed CEA reactivity while all sections from endocervical carcinomas were positive for CEA. Carcinoembryonic antigen may be a useful tumour marker in the diagnosis of cervical neoplasia and helpful in differentiating endocervical carcinoma from endometrial carcinoma.
Seventy-five cases of tibial condylar fractures irrespective of type of fractures were treated on a purely conservative line of management, consisting of traction and early mobilisation. The follow-up ranged from 6 months to 10 years; 67 cases had satisfactory results. Causes of unsatisfactory results were stiff knee, flexion deformity, osteo-arthritis and ligamentous instability.
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Transcription factor activator protein 1 (AP-1) is a protein fraction that contains c-fos, c-jun, and several other related proteins. Although this protein fraction can stimulate transcription in vitro, the relative contributions of c-fos and c-jun to the transcriptional effect of AP-1 are not clear. In order to approach this question, we have overexpressed both proteins using a baculovirus-mediated expression system and defined their DNA-binding and transcriptional enhancement activities in vitro. Gel mobility-shift and DNase 1 footprinting assays showed that c-jun protein specifically binds to DNA through an AP-1 binding site. Under the same conditions, no detectable binding of c-fos protein was observed. However, when the DNA binding assays were performed in the presence of both c-jun and c-fos, a marked increase in the affinity of c-jun for the AP-1 site was observed. An AP-1-dependent transcription assay was used to test the capability of both proteins to stimulate correctly initiated RNA synthesis in vitro. Under our conditions, c-jun protein was capable of stimulating specific RNA transcription in an AP-1 site-dependent manner. In contrast, c-fos protein showed no detectable transcriptional activation by itself. However, a transcription assay carried out in the presence of both c-fos and c-jun proteins showed that the c-fos/c-jun complex was more active as a transcriptional regulator than c-jun protein alone. These experimental results indicate that c-fos and c-jun proteins are required to reconstitute full AP-1-dependent transcriptional activation and directly demonstrate that c-fos is a regulator of gene expression.
The autologous mixed lymphocyte reaction is the in vitro expression of the regulation of the immune response. This article deals with the current knowledge of the subject and try to demonstrate that the mixed lymphocyte reaction is modified during some of the periodontal diseases.
Ultrasonic radiation produced a dose-dependent linear increase in lipid peroxidation in the liposomal membrane as reflected in the measurements of conjugated dienes, lipid hydroperoxides, and malondialdehydes (MDA). Production of MDA was confirmed by spectrophotometric and spectrofluorometric methods including the detection of excitation (360 nm) and emission (435 nm) maxima characteristic of the MDA-glycine adduct formed after addition of glycine in the system. Ultrasound of frequencies 20 kHz (used for laboratory purposes) and 3.5 MHz (used for clinical purposes) produced MDA in an identical manner. Ultrasound-induced lipid peroxidation was enhanced synergistically by 2.5 X 10(2) microM ascorbic acid but inhibited significantly by 10(4) microM ascorbic acid. Ultrasound-induced production of MDA could not be inhibited to any significant degree by superoxide dismutase, histidine, dimethylfuran, or beta-carotene but was very significantly inhibited by cholesterol (93%), butylated hydroxytoluene (88%), alpha-tocopherol (85%), sodium benzoate (80%), dimethyl sulfoxide (80%), sodium formate (64%), and EDTA (64%). The scavenger studies indicated the functional role of OH radicals in the initiation of ultrasound-induced lipid peroxidation.
The molecular basis of the sunlight-induced skin carcinogenesis has been elucidated. Of the two ultraviolet components of sunlight that reach the earth's surface the UV-B is known to be carcinogenic but the mode of action of UV-A, the predominant component of sunlight, is ill understood. Using the liposomes as a model system, it has been shown here that UV-A causes dose-dependent lipid peroxidation as estimated by measurements of conjugated dienes, lipid hydroperoxides, malondialdehydes and the fluorescent adducts (Schiff bases) produced by the reaction of MDA with glycine. Direct exposure to sunlight has also been shown to cause dose-dependent lipid peroxidation. The UV-A induced lipid peroxidation has also been shown to be dependent on dose rate. While the sodium formate, dimethyl sulphoxide, superoxide dismutase and EDTA do not have any significant effect, sodium azide, histidine, beta-carotene and dimethylfuran were shown to inhibit significantly the UV-A induced lipid peroxidation, thereby providing significant evidence of the involvement of singlet oxygen (1O2) as the initiating agent. The use of D2O in place of H2O as the liposome dispersing medium enhanced to great extent the UV-A induced lipid peroxidation, thereby lending additional support to the finding that singlet oxygen was the initiating agent. The possible mode of formation of 1O2 on exposure to UV-A was discussed. This study also highlighted the role of environmental factors on the sunlight-induced cutaneous damage. Finally, the relation between lipid peroxidation, DNA damage and carcinogenesis has been discussed in a way to suggest the possible link between sunlight exposure and causation of skin cancer.