The main-sequence rotation-colour relation in the Coma Berenices open cluster

We present the results of a photometric survey of rotation rates in the Coma Berenices (Melotte 111) open cluster, using data obtained as part of the SuperWASP exoplanetary transit-search programme. The goal of the Coma survey was to measure precise rotation periods for main-sequence F, G and K dwarfs in this intermediate-age (~600 Myr) cluster, and to determine the extent to which magnetic braking has caused the stellar spin periods to converge. We find a tight, almost linear relationship between rotation period and J - K colour with an rms scatter of only 2 per cent. The relation is similar to that seen among F, G and K stars in the Hyades. Such strong convergence can only be explained if angular momentum is not at present being transferred from a reservoir in the deep stellar interiors to the surface layers. We conclude that the coupling time-scale for angular momentum transport from a rapidly spinning radiative core to the outer convective zone must be substantially shorter than the cluster age, and that from the age of Coma onwards stars rotate effectively as solid bodies. The existence of a tight relationship between stellar mass and rotation period at a given age supports the use of stellar rotation period as an age indicator in F, G and K stars of Hyades age and older. We demonstrate that individual stellar ages can be determined within the Coma population with an internal precision of the order of 9 per cent (rms), using a standard magnetic braking law in which rotation period increases with the square root of stellar age. We find that a slight modification to the magnetic-braking power law, P ~ t0.56, yields rotational and asteroseismological ages in good agreement for the Sun and other stars of solar age for which p-mode studies and photometric rotation periods have been published.

Evaluation of hepatic changes and local and systemic immune responses in goats immunized with recombinant Peroxiredoxin (Prx) and challenged with Fasciola hepatica

Protection against Fasciola hepatica in goats immunized with Peroxiredoxin (Prx) was assessed. The experimental trial consisted of three groups of seven animals: group 1 were unimmunized and uninfected, group 2 were immunized with adjuvant only and group 3 were immunized with recombinant Prx in adjuvant (immunized and infected). Immunization with Prx in Quil A adjuvant, group 3, induced a reduction in fluke burden of 33.04% when compared to adjuvant control, group 2, although this difference was not significant. The hepatic gross and microscopical morphometric study revealed lower damage in the Prx-immunized compared to group 2 (p

Immunovirological Correlates in Human Rabies Treated With Therapeutic Coma

A 37-year-old woman was admitted to hospital and over the next 5 days developed a progressive encephalitis. Nuchal skin biopsy, analyzed using a Rabies TaqMan(C) PCR, demonstrated rabies virus RNA. She had a history in keeping with exposure to rabies whilst in South Africa, but had not received pre- or post-exposure prophylaxis. She was treated with a therapeutic coma according to the

Vitamin B-6 deficiency in rats reduces hepatic serine hydroxymethyltransferase and cystathionine beta-synthase activities and rates of in vivo protein turnover, homocysteine remethylation and transsulfuration

Vitamin B-6 deficiency causes mild elevation in plasma homocysteine, but the mechanism has not been clearly established. Serine is a substrate in one-carbon metabolism and in the transsulfuration pathway of homocysteine catabolism, and pyridoxal phosphate (PLP) plays a key role as coenzyme for serine hydroxymethyltransferase (SHMT) and enzymes of transsulfuration. In this study we used [H-2(3)]serine as a primary tracer to examine the remethylation pathway in adequately nourished and vitamin B-6-deficient rats pi and 0.1 mg pyridoxine (PN)/kg diet]. [H-2(3)]Leucine and [1-C-13]methionine were also used to examine turnover of protein and methionine pools, respectively, All tracers were injected intraperitoneally as a bolus dose, and then rats were killed (n = 4/time point) after 30, 60 and 120 min. Rats fed the low-PN diet had significantly lower growth and plasma and liver PLP concentrations, reduced liver SHMT activity, greater plasma and liver total homocysteine concentration, and reduced liver S-adenosylmethionine concentration. Hepatic and whole body protein turnover were reduced in vitamin B-6-deficient rats as evidenced by greater isotopic enrichment of [H-2(3)]leucine. Hepatic [H-2(2)]methionine production from [H-2(3)]serine via cytosolic SHMT and the remethylation pathway was reduced by 80.6% in vitamin B-6 deficiency. The deficiency did not significantly reduce hepatic cystathionine-beta-synthase activity, and in vivo hepatic transsulfuration flux shown by production of [H-2(3)]cysteine from the [H-2(3)]serine increased over twofold. In contrast, plasma appearance of [H-2(3)]cysteine was decreased by 89% in vitamin B-6 deficiency. The rate of hepatic homocysteine production shown by the ratio of [1-C-13]homocysteine/[1-C-13]methionine areas under enrichment vs. time curves was not affected by vitamin B-6 deficiency. Overall, these results indicate that vitamin B-6 deficiency substantially affects one-carbon metabolism by impairing both methyl group production for homocysteine remethylation and flux through whole-body transsulfuration.

A proposed mechanism for chlorpromazine jaundice--defective hepatic sulphoxidation combined with rapid hydroxylation

On the basis of previous experimental studies we postulated that individuals who were phenotypically good hydroxylators but poor sulphoxidisers would be susceptible to chlorpromazine jaundice. Sulphoxidation capacity was assessed in 12 subjects with a history of chlorpromazine jaundice, using S-carboxymethyl-L-cysteine as an in vivo probe. Following an oral dose of 750 mg, unchanged compound and sulphoxide metabolites were measured in urine. All 12 subjects (100%) were shown to be poor sulphoxidisers compared to 22% of normal controls (P less than 0.001) and 23.8% of liver disease controls (P less than 0.001). No subjects with a history of chlorpromazine jaundice had an impaired hydroxylation capacity as assessed by recovery of 4-hydroxydebrisoquine in urine following oral debrisoquine. The results support the hypothesis and demonstrate an inherent metabolic basis of susceptibility to chlorpromazine jaundice.

Tissue plasminogen activator for hepatic vein thrombosis in paroxysmal nocturnal haemoglobinuria

Paroxysmal nocturnal haemoglobinuria (PNH) is an acquired clonal disorder thought to arise in a multipotent haemopoietic stem cell. A distinct clinical feature is a tendency to thrombosis, with a particular predilection for the hepatic veins (Budd-Chiari syndrome). We report here on two patients with PNH who developed hepatic vein thrombosis (HVT) and who were treated with tissue plasminogen activator (t-PA). Both patients had a marked clinical and radiological improvement following the t-PA treatment and remain well over 2 years and 6 years after the treatment. This method of thrombolysis for HVT occurring in PNH has only been reported in two previous patients with limited follow-up. We suggest that this therapy is a useful first-line treatment for PNH patients who develop HVT.

Transcriptional profiling of chronic clinical hepatic schistosomiasis japonica indicates reduced metabolism and immune responses

Schistosomiasis is a significant cause of human morbidity and mortality. We performed a genome-wide transcriptional survey of liver biopsies obtained from Chinese patients with chronic schistosomiasis only, or chronic schistosomiasis with a current or past history of viral hepatitis B. Both disease groups were compared with patients with no prior history or indicators of any liver disease. Analysis showed in the main, downregulation in gene expression, particularly those involved in signal transduction via EIF2 signalling and mTOR signalling, as were genes associated with cellular remodelling. Focusing on immune associated pathways, genes were generally downregulated. However, a set of three genes associated with granulocytes, MMP7, CLDN7, CXCL6 were upregulated. Differential gene profiles unique to schistosomiasis included the gene Granulin which was decreased despite being generally considered a marker for liver disease, and IGBP2 which is associated with increased liver size, and was the most upregulated gene in schistosomiasis only patients, all of which presented with hepatomegaly. The unique features of gene expression, in conjunction with previous reports in the murine model of the cellular composition of granulomas, granuloma formation and recovery, provide an increased understanding of the molecular immunopathology and general physiological processes underlying hepatic schistosomiasis.