Malaria and ABO blood groups.

Subjects from Muria gond tribal community (n = 258) as well as from Delhi (n = 100) were classified according to ABO blood groups, and were also assayed for malarial antibodies by ELISA technique. The distribution of ABO blood groups did not differ significantly in Muria gonds and Delhi subjects. Within Muria gonds the observed frequency of ABO blood groups did not differ significantly from the expected values. No significant difference was observed in the rate of seropositivity for malarial antibodies among subjects with different blood groups. Malarial parasitaemia, although observed more in individuals with blood group A, did not differ significantly as compared with other blood groups. We conclude that ABO blood groups do not show differential susceptibility to malaria.     

Protection against 7,12-dimethylbenzanthracene-induced tumour initiation by protein A in mouse skin.

Protein A is an immunostimulating glycoprotein obtained from Staphylococcus aureus Cowan I. Its antitumour activity is proven in various tumour models. Its ability to provide protection against tumour initiation by the chemical carcinogen 7,12-dimethylbenzanthracene (DMBA) has been investigated in the present study using a mouse skin model of two-stage carcinogenesis. Protein A was administered intraperitoneally (1 microgram/animal 20 g body wt.) twice a week for 2 weeks, prior to initiation by DMBA. The promotion was performed by twice weekly applications of 12-O-tetradecanoyl phorbol-13-acetate (TPA) (3 or 5 micrograms/animal in 100 microliters acetone). Protein A provided significant protection to animals from DMBA-induced tumour initiation as was observed by the decrease in cumulative number of tumours, percent of animals developing tumours, number of tumours per animal and rate of tumour growth. Our data indicate that protein A has anticarcinogenic properties.     

Idiopathic hypertrophic cranial pachymeningitis: a case report

Hypertrophic pachymeningitis is a rare fibrosing inflamatory process involving dura mater and tentorium. In this report we are presenting contrast enhanced MRI findings of an unusual case of pachymeningitis which presented with a periorbital mass due to dural sinuses occlusion and retrograde filling of periorbital veins through superior sagittal sinus.     

Thymic function in HIV infection

Current models hold that CD4+ depletion occurs as a result of direct and indirect effects of HIV, which both kill peripheral CD4+ cells and prevent adequate regeneration. Although age-associated involution diminishes thymic reserve and HIV is clearly thymotoxic, clinical trials have nonetheless shown that large proportions of patients who sustain adequate control of viral replication with highly active antiretroviral therapy (HAART) will demonstrate some evidence for thymic-dependent immune reconstitution, which is associated with improved immune competence. Furthermore, patients with insufficient or absent immune reconstitution following HAART generally lack evidence for thymopoiesis. Current studies are focused on improving our understanding of the causes for thymic failure in HIV infection. Recent work has demonstrated that some HIV strains, especially those that are CXCR4 trophic, are more thymotoxic and may contribute to irreversible thymic damage in this population.     

Ornithine decarboxylase activity as a biochemical marker in individuals predisposed to lung cancer

Ornithine decarboxylase (ODC) is the first enzyme in the pathway of mammalian polyamine biosynthesis. "Tumor promoters" appear to induce ODC. In addition, increased ODC activity has been observed in normal appearing colonic mucosa of patients with familial polyposis, an autosomal dominant disorder associated with a high incidence of colon cancer. Ornithine decarboxylase activity was measured in bronchoscopic mucosal biopsy specimens from the noninvolved lung in patients with unilateral lung masses. No correlation could be determined in ODC levels from "normal" mucosa between patients with lung cancer compared to those with benign disease, despite elevated ODC activity in the tumors themselves.     

Thymic function in HIV infection

Current models hold that CD4+ depletion occurs as a result of direct and indirect effects of HIV, which both kill peripheral CD4+ cells and prevent adequate regeneration. Although age-associated involution diminishes thymic reserve and HIV is clearly thymotoxic, clinical trials have nonetheless shown that large proportions of patients who sustain adequate control of viral replication with highly active antiretroviral therapy (HAART) will demonstrate some evidence for thymic-dependent immune reconstitution, which is associated with improved immune competence. Furthermore, patients with insufficient or absent immune reconstitution following HAART generally lack evidence for thymopoiesis. Current studies are focused on improving our understanding of the causes for thymic failure in HIV infection. Recent work has demonstrated that some HIV strains, especially those that are CXCR4 trophic, are more thymotoxic and may contribute to irreversible thymic damage in this population.     

The direct excitatory effects of cimetidine on the smooth muscle of guinea pig ileum

1. Cimetidine produced dose-dependent contractions in isolated guinea pig ileum and these responses were not blocked by mepyramine the H₁-receptor antogonist.
2. Atropine competitively inhibited the cimetidine-induced contractions in the guinea pig ileum.
3. Cimetidine-induced reponses were potentiated in the presence of eserine.

Magnesium ions non-competitively inhibited the contractions due to cimetidine. Our findings suggest that cimetidine excites the guinea pig ileum through muscarinic receptors by releasing acetylcholine.     

Characterization of a complex translocation [t(4;9;22)(p16;q34;q11)] in chronic myelogenous leukemia by fluorescence in situ hybridization technique

A patient was referred with a high leukocyte count and diagnosed with chronic myelogenous leukemia (CML). Although practically asymptomatic since the time of diagnosis, he had a variable and inconsistent response to treatment. All of his bone marrow cells had a complex, three-way translocation, involving chromosomes 4, 9 and 22. Translocation of chromosome 4 to chromosome 9 was undetectable by routine cytogenetic techniques; however, by the fluorescence in situ hybridization technique, a three-way translocation was identified, 46,XYt(4;9;22)(p16;q34;q11). Although, other chromosomes are frequently involved in complex or variant translocations with chromosome 9 and 22, participation of chromosome 4 is a very rare event. So far, two previous cases have been described in the literature with translocations involving chromosome 4p16. We present a third case of CML having similar break points whose clinical presentation is unusual.