CCSVI is uncommon and is a secondary epiphenomenon in MS and related to more neurological disability and the presence of varicose veins at the legs.

Rat lens α‐crystallin contains, besides the usual αA and αB subunits, an additional minor chain. This subunit was purified by ion‐exchange chromatography and its primary structure studied. It appeared to be an elongated αA‐like chain, having an insertion of 22 residues between position 63 and 64 of an otherwise normal αA2 chain. Therefore this subunit was called αAIns, i.e. an αA chain with an inserted sequence. This inserted region, which contains three methionyl, five basic and no acidic residues, apparently results in an adequately functioning αAIns chain. The αAIns chain may be the product of a gene which has originated, after duplication of the αA gene, by insertion in one of the copies of a stretch of 66 nucleotides of unknown origin, or alternatively be the result of unusual transcription or processing of precursor mRNA (pre‐mRNA), leaving an extra 66 nucleotides internally in the mRNA to be translated.

The diagnosis chylothorax is based on a chemical analysis of the pleural effusion. According to the literature, this analysis can be rather straightforward, comprising measurements of triglycerides, chylomicrons, and cholesterol. In this report we present an autopsy case that alerted us to interpret these results critically. Although the laboratory tests of the pleural effusion in this patient with parenteral nutrition suggested chylothorax, additional tests (potassium (11.3 mmol.L(-1)) and glucose (128 mmol.L(-1)) proved otherwise. Comparison of the pleural effusion analysis and the content of the parenteral nutrition led to the final conclusion that the effusion was due to a leakage of parenteral nutrition instead of chylothorax. We therefore suggest adding glucose and potassium measurements to the biochemical work-up of a patient under suspicion of chylothorax.

Summary:One hundred and sixteen insulin treated diabetic patients were evaluated for the relationship between the presence of microalbuminuria and several lipid, glyco-metabolic, coagulation and fibrinolysis factors. A significant correlation existed only between microalbuminuria and HbA lc (r = 0.23, p = 0.008) and D-dimer (r = 0.28, p = 0.002). After the subdivision of the patients in a group without (n = 85) and a group with microalbuminuria (n = 31) significant differences were found between these two groups for the HDL-cholesterol content (p < 0.05), the HbAi c level (p < 0.01) and for the D-dimer concentration (p < 0.01).Comparison of the patient groups without and with microalbuminuria separately with a healthy volunteers group without albuminuria resulted in significant differences for HDL-cholesterol, triacylglycerols, HbA lc , fructosamine, fibrin monömer and D-dimer, whereas fibrinogen also was significantly different between the diabetic group without microalbuminuria and the healthy volunteers group. Several factors predisposing for atherosclerosis (decrease of HDL-cholesterol, increase of triacylglycerols, coagulation activation with relatively msufficient fibrinolysis) were nöticed in both diabetic groups without or with microalbuminuria, but more pronounced in the latter group. The appliance of a Receiver Operating Characteristic (ROC) curve for HbA JC against microalbuminuria (cuf-off level 20 g/min) reconfirmed the value of adequate glycaemic control in diabetics for the prevention of microalbuminuria. In conclusion the results of this study show a significantly pporer glycaemic control in insulin treated diabetics with microalbuminuria than in those without microalbuminuria. The presence of lower HDL-cholesterol, higher triacylglycerols and the elevation of fibrin monomers and D-dimers is more pronoüiiced in the microalbuminuria group. No direct correlation could however be found between the coagulation.and fibrinolysis factors and the extent of microalbuminuria in the diabetic patient groups.

Serum NGAL is an independent inflammatory marker for somatic depressive symptoms in HF and may function as an immunopathogen linking somatic symptoms of depression to HF.