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Infants of HIV-infected mothers are at great risk of becoming infected with HIV during childbirth. Many infants acquire HIV during labor and delivery. Others can acquire HIV through the mixing of fetal and maternal blood as the placenta separates. The duration of membrane rupture, acute chorioamnionitis and invasive delivery techniques that increase the baby's contact with the mother's blood have been associated with higher risks of MTCT during labor and delivery. HIV is present in breast milk and risk of its transmission during breastfeeding depends on several factors, including: infant age, pattern of breastfeeding, breastfeeding duration, breast health, maternal viral load and maternal immune status. Infants born to HIV infected mothers carry their mother's antibodies in their blood into the second year of life, even if the infants themselves are not infected. For this reason, standard HIV antibody tests cannot reliably confirm HIV infection in infants until after the maternal antibodies have disappeared. Tests that can diagnose pediatric HIV infection accurately during the first year of life include HIV-PCR, CD4/CD8 counts, P24 antigen tests, and viral cultures. PCR offers an effective tool to reliably diagnose HIV in a pediatric age group. Nineteen infants born by normal delivery to HIV-1 seropositive mothers were studied by PCR for the HIV1 env gene. Thirteen babies (68.5%) were negative whereas 6 babies were found to be positive (31.5%). Although PCR is one of the most useful tests for this clinical situation, it is not definitive. Therefore, PCR should be interpreted with caution and repeated at regular defined intervals, preferably lasting until the HIV antibody status of the infant is resolved.

One hundred four Rheumatoid factor (RF) positive Rheumatoid Arthritis (RA) patients fulfilling ARA criteria were screened for extraarticular manifestations. Rheumatoid nodules were present in 2.8% cases. Other extraarticular manifestations such as pulmonary, cardiac, occular, renal or GI involvement were absent in these cases. However, circulating immune complexes (CICs) were highly significantly raised in all the RA patients (P < 0.001). From amongst these cases a limited number (8 cases) have been subjected to qualitative and quantitative analysis of CICs to look for whether there could be any relationship between these and mild extraarticular manifestations that were being noticed in our groups of patients. Finding showed IgG-IgG CICs in five, IgG-IgM in two and IgG-IgA in one case. Quantitative analysis revealed mean IgG 4.97 +/- 1.7 IU/ml, IgM 14.58 +/- 5.53 IU/ml and IgA 5.08 +/- 1.53 IU/ml on LD Solugen plates. Serum concentration of C3 was not reduced (94.1 +/- 8.9 mg/dl). Low IgM contents of CICs and no reduction in complement level is the likely explanation for less severe inflammatory manifestations seen in our study. The conclusion and findings have been discussed in the light of observation reported by the Western workers.

Clinical presentation of rheumatoid arthritis (RA) and its severity differs in different races. Genetic factors play a significant role in its predeliction. The present study was undertaken to find out association of HLA class I and class II antigens with rheumatoid arthritis prevalent in Asian Indians residing at Varanasi. Ninety rheumatoid arthritis patients strictly fulfilling American Rheumatism Association criteria were screened for prevalent HLA class I and class II antigen by Terasaki Microlympho-cytotoxicity test. Results were compared with 100 healthy controls and 35 Seronegative Spondyloarthritides cases (SSA). Rheumatoid arthritis patients showed increased frequency of HLA-A2 and B40 antigens compared to healthy controls (p < .001). SSA patients showed significantly increased Phenotype frequency (PF) of HLA-B27 (p < .0001) and B40 (p < .001). Significant detection of HLA-A2 exclusively in RA patients suggests a more positive association of A2 in rheumatoid arthritis at Varanasi. HLA-B40 could not be attributed absolute significance of association with SSA or RA as it showed increased frequency in both diseases.

Twenty diabetic uraemics and twenty two healthy matched controls comprised the material for this study. Cell mediated immunity was assessed by estimation of T-cell rosette percentage and cutaneous response to recall antigens--purified protein derivative, candida antigen and 2:4 dinitrochlorobenzene. Results analysis revealed depressed cell mediated immunity in diabetic uraemics in the form of impaired cutaneous response to recall antigens and reduction in T cell rosette percentage, in comparison to controls.

Both cell mediated immunity and humoral immunity was assessed in 16 patients of hydatidiform mole and 6 patients of choriocarcinoma. Fifty percent patients of choriocarcinoma and 11 patients of vesicular mole were given levamisole (LVM) trial and were followed for 2 months. Absolute lymphocyte count (ALC) was significantly increased in vesicular mole after levamisole treatment but in choriocarcinoma no effect was obtained. Marked improvement of T cell rosette count was also seen in LVM treated patient of both vesicular mole (p < 0.001) and choriocarcinoma. Cutaneous DTH response to 2:4 DNCB in vesicular mole was also increased after LVM. Before treatment only 31.25% patients had strong cutaneous response but after treatment 53.35% patients had strong response, while cases of choriocarcinoma were unaffected. LVM also raised all the serum immunoglobulins (IgG, IgM, IgA) in both vesicular mole and choriocarcinoma. Hence, levamisole therapy was found to have a beneficial effect on both cellular and humoral immunity in the lesions of trophoblasts.

Total 39 cases of carcinoma stomach were noticed out of 142 malignant tumours of GIT (27.46 percent). Histologically maximum cases were of diffuse type (56.41 percent) followed by intestinal type (35.89 percent) and indolent mucoid carcinoma (7.69 percent) of the stomach. The surrounding epithelium showed lot of changes in the intestinal type of carcinoma stomach. About 78.57 percent showed intestinal metaplasia, 14.28 percent of these cases showed chronic gastric ulcer and severe dysplasia (carcinoma in situ) and another 14.28 percent revealed villous adenoma with carcinoma in situ. In contrast to this, in diffuse variety, only 13.63 percent cases revealed intestinal metaplasia, 27.27 percent showed basal cell hyperplasia, stratification of the epithelium of crypts and diffuse infiltration of mucosa by malignant cells and 4.54 percent showed atrophic gastritis also. In mucoid carcinoma all cases had basal cell hyperplasia and stratification of crypts. Hence these conditions should be taken as premalignant lesions of stomach and should be cured in proper time.