Indoor radon concentration in the rural dwellings of Chhattisgarh state (India).

Inhalation of radon and its daughter products is the major contributor to the total exposure of the population to natural radiation. An indoor radon survey has been carried out in the state of Chhattisgarh (80.26 degrees N to 84.41 degrees N and 17.8 degrees E to 24.1 degrees E), India under the national coordinated radon project of the Department of Atomic Energy. In the frame of this project indoor radon concentration has been measured in 105 dwellings situated in different villages of Chhattisgarh state. Houses were selected for measurements to cover the most common type of houses generally existing in the rural areas. Measurements have been done on quarterly integrating cycle for one full year in each dwelling using radon cup dosemeter employing LR-115, type-II (pelliculable), solid-state nuclear track detectors. The gamma radiation level was also checked in each dwelling using a gamma survey meter. It was found that the annual average indoor radon concentration in these dwellings varies from 9.91 to 87.84 Bq m(-3) with overall mean value of 26.48 Bq m(-3). Gamma level in these rural dwellings varies from 14.84 to 26.56 microR h(-1) with mean value of 18.68 microR h(-1). We observed that the radon concentration is relatively higher in the houses where the floor is bare but relatively lower in those houses where the floor is tiled or cemented.

T cell proliferation and cytokine secretion to T cell epitopes of Asp f 2 in ABPA patients.

The pathogenesis of allergic bronchopulmonary aspergillosis (ABPA) involves specific cytokines secreted by lymphocytes in response to Aspergillus fumigatus (Af) allergens. To gain information about the lymphoproliferative response and cytokine production against a major Af allergen, Asp f 2, we studied Asp-f-2-specific T cell clones (TCCs) from ABPA patients. TCCs were stimulated with rAsp f 2, its deletion mutants, and synthetic peptides to identify the T cell epitope(s) and to understand cytokine production. PBMCs from four of five ABPA patients showed proliferation in response to Asp f 2. Three TCCs from one patient showed higher IL-5 secretion compared to IL-4 and IFN-gamma. Two TCCs from the second patient showed a mixed Th1/Th2 response, as evidenced by production of IL-4, IL-5, and IFN-gamma. An epitope from the N-terminal region of Asp f 2 induced only IL-5 secretion. High IL-5 secretion might explain the marked eosinophilia observed in ABPA patients.

High cytosolic pool of p75 TNF receptors and delayed surface downmodulation by mononuclear cells from non-hodgkin's lymphoma patients.

Analysis of the expression of TNF-Rs on fresh peripheral blood mononuclear cells (PBMNC) by Scatchard analysis showed that Gr I (stages I and II) but not Gr II (stages III and IV) NHL patients have a significantly higher expression of surface TNF-Rs than normal controls. A rapid decrease in the binding of radiolabelled anti-p75 TNF-R Mab which gradually increased after 16 h was seen in normal controls, while NHL patients showed a rapid increase in the binding of the Mab after activation of cells and a decrease in binding was observed only after 24 h. Western blot analysis for normal controls showed a weak presence of the 42 kDa fragment only, while the cytosolic extracts from fresh PBMNCs of NHL patients showed presence of both intact p75 TNF-R, as well as a 42 kDa fragment corresponding to a soluble form of p75 TNF-R. Our results suggest that increased cytosolic pools of TNF-R in NHL patients might contribute to a rapid increase in its surface expression following activation of cells.

Altered release of tumor necrosis factor and its soluble receptor in non-Hodgkin's lymphoma patients.

Increased expression and elevated serum levels of tumor necrosis factor-alpha (TNF-alpha) have been shown to be associated with the presence of constitutional B symptoms and poor prognosis in non-Hodgkin's lymphoma (NHL) patients. Soluble TNF receptors (sTNF-R) are suggested to act as biological buffers in inflammatory conditions by binding and inactivating increased circulating TNF. Whereas studies have shown elevated TNF to be correlated with B symptoms, similar studies showing the status of soluble receptor release in these patients have not been conducted. Here, we show that there is increased soluble p75 TNF receptor release from peripheral blood mononuclear cells (PBMNC) in NHL patients in the early stages of the disease but it is severely depressed in patients with advanced disease. Decreased release is associated with presence of B symptoms in these patients. All NHL patients also show increased TNF secretion and a decreased rate of receptor release with time compared with healthy controls. These findings imply that decreased sTNF-R receptor release, in addition to increased TNF secretion, is also important in predisposing the patients to B symptoms. This opens up the possibility of the use of sTNF-Rs as a therapeutic tool to counter increased TNF and alleviate systemic symptoms in these patients and also as a marker for the progression of the disease.

Expression of adhesion molecules in B-cell chronic lymphocytic leukaemia: an analysis in lymphoid compartments--peripheral blood, bone marrow and lymph node.

The trafficking or homing of different lymphoid subsets to particular microenvironment is mediated by specific cell adhesion molecules (CAMs) expressed on lymphocytes and endothelial cells. B-cell chronic lymphocytic leukaemia (B-CLL) or Non-Hodgkin's lymphoma of small lymphocytic, B-cell type are monoclonal expansions of mature lymphocytes. The relative distribution of the tumor lymphocytes among various lymphoid compartments vary from patient to patient. Very few studies underlying this issue are available. To this effect, we have analysed the expression of LFA-1; VLA-4, ICAM-1; CD44H and CD44v6 (haematopoietic and variant form respectively) on freshly isolated lymphocytes obtained from bone marrow (BM), peripheral blood (PB) and lymph node (LN) by flow cytometry. Overall, we find strong expression of CD44H, low to moderate expression of LFA-1, negative to low expression of VLA-4 and lack of expression of CD44v6. ICAM-1 expression was observed only in patients with prominent lymphadenopathy. Higher expression of CD44H in PB lymphoid cells relative to that of BM lymphoid cells correlated with higher PB lymphocytosis (p < 0.001). Proliferating cell nuclear antigen expression in LN sections correlated inversely with VLA-4 expression on BM and PB lymphoid cells (p < 0.05). There was no significant correlation between expression of CAMs and bcl-2 protein.