Thyroxine transport in choroid plexus

The role of the choroid plexus in thyroid hormone transport between body and brain, suggested by strong synthesis and secretion of transthyretin in this tissue, was investigated in in vitro and in vivo systems. Rat choroid plexus pieces incubated in vitro were found to accumulate thyroid hormones from surrounding medium in a non-saturable process. At equilibrium, the ratio of thyroid hormone concentration in choroid plexus pieces to that in medium decreased upon increasing the concentration of transthyretin in the medium. Fluorescence quenching of fluorophores located at different depths in liposome membranes showed maximal hormone accumulation in the middle of the phospholipid bilayer. Partition coefficients of thyroxine and triiodothyronine between lipid and aqueous phase were about 20,000. After intravenous injection of 125I-labeled thyroid hormones, choroid plexus and parts of the brain steadily accumulated 125I-thyroxine, but not [125I]triiodothyronine, for many hours. The accumulation of 125I-thyroxine in choroid plexus preceded that in brain. The amount of 125I-thyroxine in non-brain tissues and the [125I]triiodothyronine content of all tissues decreased steadily beginning immediately after injection. A model is proposed for thyroxine transport from the bloodstream into cerebrospinal fluid based on partitioning of thyroxine between choroid plexus and surrounding fluids and binding of thyroxine to transthyretin newly synthesized and secreted by choroid plexus.     

Thyroxine effects on parameters of glucose turnover in BHE rats fed menhaden oil

The effect of hyperthyroidism on glucose turnover in BHE rats fed menhaden oil was studied. Thyroxine-treated rats had a greater glucose mass, a greater absolute glucose synthesis rate, less hepatic and muscle glycogen levels, and greater hepatic and peripheral fat cell lipogenic rates than nontreated rats. No differences in body weight gain were observed, nor were there differences in blood glucose levels, glucose space, or fractional reversible or irreversible glucose use. These observations suggest that thyroxine and menhaden oil were additive in their effects on glucose metabolism in BHE rats, which are genetically programmed to develop non-insulin-dependent diabetes mellitus.     

Glycosylation in viral hepatitis

BackgroundThe interaction between hepatitis viruses and host cells is regulated by glycans exposed on the surfaces of human and viruses cells. As the biosynthesis and degradation of human glycoproteins take place at the highest level in the liver, the changes in glycosylation of serum proteins may potentially be useful in the diagnosis of liver pathology. On the other hand, specific alterations in viruses envelope glycans could cause large changes in the entry process of hepatitis viruses into a host cells.Scope of reviewUnique alterations in glycosylation of specific proteins can be detected in HBV and HCV infected patients especially with confirmed fibrosis/cirrhosis. On the other hand, viral envelope proteins that bind to host cells are glycosylated. These glycosylated proteins play a key role in recognition, binding and penetration of the host cells. In this review we summarized the knowledge about significance of glycosylation for viral and host factors.Major conclusionsGlycosylation changes in single serum glycoproteins are noticed in the sera of patients with viral hepatitis. However, a more specific biomarker for the diagnosis of chronic hepatitis than that of a single glycosylated molecule is systemic investigation of complete set of glycan structures (N-glycome). Glycans play important roles in the viral biology cycle especially as a connecting element with host receptors.General significanceThe interaction between virus glycoproteins and cellular receptors, which are also glycoproteins, determines the possibility of virus penetration into host cells. Therefore these glycans can be the targets for the developing of novel treatment strategies of viral hepatitis.     

Trace elements in viral hepatitis

In this study, serum trace elements, including selenium (Se), zinc (Zn), copper (Cu), were determined by using Atomic Absorption Spectrophotometer (SpectrAA 250 Plus Zeeman, Varian, Australia) in sera of patients with viral hepatitis (A, B, C, D, E) cases (n = 102), and statistically compared with the controls (n = 52). In viral hepatitis, Cu levels were found as 3.23 ± 1.02 mg/L, and this value was significantly higher than the control group (1.13 ± 0.21) (p < 0.01). Both, Se and Zn levels found to be significantly low in viral hepatitis cases (p < 0.01). While Se level was 81.4 ± 26.01 μg/L in viral hepatitis (n = 101), it was found to be 166.15 ± 4.58 μg/L in healthy individuals. Meanwhile, Zn levels were 0.230 ± 0.081 mg/L and 0.748 ± 0.392 mg/L in hepatitis cases (n = 101) and the control group, respectively. There was no difference amongst viral hepatitis groups classified in regard with agents and clinical manifestation, such as A, acute hepatitis B, chronic hepatitis B, C, D and E. Previously, it was indicated that absorption disorders in gastrointestinal system, especially in chronic cases, were not main causes of decrease of trace elements by iron and several other parameters in sera of the cases. Therefore, we suggest that decrease in Zn and Se levels and elevation in Cu levels are probably resulted from defence strategies of organism and induced by the hormone-like substances.     

The epidemiological differential diagnostic signs of viral hepatitis A and viral hepatitis E]

A retrospective epidemiologic analysis of cases diagnosed as hepatitis A (HA) has been made in territories characterized by high intensity (4 towns in Central Asia) and low intensity (Novomoskovsk, Tula Province) of the epidemic process development. Morbidity structures for different age and social groups of the population, as well as the morbidity time course, both annual and over many years, were analyzed over 1973-1986. Specific features in the development of the epidemic process in HA and hepatitis E (HE), formerly called hepatitis non-A, non-B with the fecal/oral mechanism of the infection transmission, were studied. Twelve epidemiological differential diagnostic signs of these two infections were formulated, classified, and validated. Contribution of centralized water supply and sewage systems to the development of HE epidemic process and the regulating role of infectious immunological mechanisms in the development of HA epidemic process were demonstrated.     

New movements in neurofilament transport, turnover and disease

Revealing the mechanisms by which neurofilament transport and turnover are regulated has proven difficult over the years but recent studies have given new insight into these processes. Mature neurofilament fibers may incorporate a fourth functional subunit, alpha-internexin, as new evidence suggests. Recent findings have made the role of phosphorylation in regulating neurofilament transport velocity controversial. Kinesin and dynein may transport neurofilaments in slow axonal transport as they have been found to associate with neurofilaments. Neurofilament transport and turnover rates may be reduced depending on the existing stationary neurofilament network. Finally, mutations in neurofilament light that have been linked to Charcot-Marie-Tooth disease as well as other neurofilament abnormalities in human disease are discussed.