We conclude that phPTX with NPS R-568 is responsible for a decrease of MAP in SHR.

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Background: The human leucocyte antigen (HLA) system plays an important role in the modulation of the immune response. An association between HLA and pulmonary tuberculosis (TB) has been examined in several populations but the results have been inconsistent. The aim of this study was to evaluate the correlation of DQB1 alleles with TB patients and healthy controls in the same ethnic group in Poland. Method: The DQB1 alleles of 38 patients with TB and 58 healthy university staff volunteers were determined by a PCR-SSP low resolution method. Results: The DQB1*05 allele occurred more frequently (p adjusted for multiple comparison = 0.002, OR = 2.84, 95% CI 1.57 to 5.15) and the DQB1*02 allele occurred less frequently (p = 0.01, OR = 0.39, 95% CI 0.21 to 0.71) in patients with TB than in controls. The occurrence of DQB1*03,*04,*06 alleles was similar in the two populations. Conclusions: The occurrence of specific DQB1 alleles may be linked to susceptibility/resistance to tuberculosis.

We explored the biochemical mechanism by which thyroid hormone (T3) and low-phosphate diet (LPD) cause an adaptive increase in Na+-Pi cotransport across renal brush-border membrane (BBM). The rate of Na+-Pi cotransport was determined by 32Pi uptake by BBM vesicles (BBMV), and the number of Na+-Pi symporters was assessed by binding of [14C]phosphonoformic acid (PFA) on BBMV. In BBMV of both T3-treated rats and LPD-fed rats, the Na+ gradient-dependent 32Pi uptake increased (Vmax increased; Km Pi was not changed). The Na+-dependent [14C]PFA binding on BBMV increased (higher Vmax, no change in Km PFA) in response to T3, but it remained unchanged in rats fed LPD. Both the increase of Na+-Pi cotransport and of Na+-dependent [14C]PFA binding in response to T3 were blocked by actinomycin D or cycloheximide. Addition of benzyl alcohol to BBMV in vitro increased Na+-Pi cotransport, but [14C]PFA binding did not change; the [3H]phlorizin binding and cotransports of other solutes decreased or did not change. The exposure of BBMV to cholesterol decreased Na+-Pi cotransport without changing [14C]PFA binding. We suggest that the adaptive increase of Na+-Pi cotransport elicited by T3 is due to an increase in number of Na+-Pi cotransporters in BBM. In contrast, in response to LPD the number of Na+-Pi cotransporters is unchanged, and the increased Na+-Pi cotransport is due to faster translocation of Na+ with Pi due to enhanced fluidity of BBM.

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