Studies of fibrinolytic activity of uremic and longterm hemodialytic patients with special reference to fibrinolytic inhibitor.

Fibrinolytic activities on cases with chronic renal failure, 13 cases at pre and post introduction of hemodialysis and 40 cases at pre and post hemodialysis of maintenance hemodialysis with 38 normal controls were investigated. The plasminogen activator of untreated chronic renal failure was lower than controls, yet increased with the introduction of hemodialysis. On the other hand the antiplasmin was lowered with the introduction. In cases with maintenance hemodialysis, the plasminogen activator was lower than controls, but was elevated with hemodialysis. The level of antiactivator was higher in uremia of either pre or post hemodialysis than controls. The levels of alpha 2-macroglobulin and alpha 1-antitrypsin were reduced at prehemodialysis state comparing to controls, and yet, increased with hemodialysis, respectively. The low molecular weight antiplasmin and antiactivator, molecular weight below 30,000 were separated with Sephadex G-50 gel filtration of plasma. The low molecular weight fibrinolysis inhibitors of plasma with untreated uremia were elevated comparing to controls, but decreased with the hemodialysis. The removable fibrinolytic inhibitors were indicated, however, the ratio of the low molecular weight fibrinolytic inhibitors to the total fibrinolytic inhibitors were little.     

Statistical Mechanical Theory of DNA Denaturation

Thermodynamic quantities of a coupled sine-lattice chain, which is a simplified model of DNA (rotator model) are calculated for both in low and high temperature regions. In the high temperature region those quantities are expressed as a series expansion in terms of modified Bessel functions of an integer order. The results of numerical calculations are presented in connection with DNA denaturation (melting).     

Cell death of motoneurons in the chick embryo spinal cord. X. Synapse formation on motoneurons following the reduction of cell death by neuromuscular blockade

Chronic treatment of chick embryos with neuromuscular blocking agents, such as curare, rescues motoneurons from naturally occurring cell death. In the present study, embryos treated with curare from E6 to E9 had 35% more motoneurons than controls on E10 and 42% more than controls on E16. Previous studies have shown that several aspects of motoneuron differentiation occur normally in curare-treated embryos. We report here that dendrite growth and arborization is also unaltered on E10 and E16 following curare treatment. A quantitative analysis of afferent synapses on motoneurons shows that the packing density of both axosomatic and axodendritic synapses is also normal on E10 in curare-treated embryos, despite the greater number of motoneurons present. This indicates that the interneurons that provide presynaptic input to motoneurons are able to compensate for the increased number of synaptic sites made available by curare treatment. However, by E16 the packing density of synapses is reduced by about half. Because motoneurons and their dendrites continue to grow between E10 and E16, the further increase in synaptic sites made available in curare-treated embryos apparently exceeds the compensatory capacity of presynaptic interneurons on E16. One can conclude from these results that the increased survival of motoneurons in curare-treated embryos is not owing to an increase in afferent synapses. Motoneurons in these embryos continue to survive in the face of either no change (E10) or a reduction (E16) in the number of axodendritic and axosomatic synapses. Therefore, increased motoneuron survival in this situation is very likely regulated primarily by motoneuron-target interactions.     

Frequent Detection of Hepatitis C Virus Subtype 3a (HCV-3a) Isolates in Thailand by PCR Using Subtype-Specific Primers

By means of a polymerase chain reaction (PCR) method using subtype-specific primers for hepatitis C virus (HCV) subtypes 1a, 1b, 2a, 2b and 3a, the prevalence of each subtype among HCV isolates in Chiang Mai, Thailand, was determined. HCV-3a appeared to be the most common subtype in blood donors, and was also frequently found in patients with liver disease. HCV-1b, but not HCV-2a or ?2b, was also commonly found in this area, while a considerable percentage of the total HCV isolates still remained unclassifiable by the above methods. Serotype analysis of the HCV isolates using C14-1 and C14-2 recombinant peptides revealed that HCV-3a was likely to carry an antigenic determinant(s) different from those of the major types 1 (HCV-1a and ?1b) and 2 (HCV-2a and ?2b).     

Causes of the urinary concentrating defect in mice with nephrogenic diabetes insipidus

In a strain of mice called DI +/+ Severe, nephrogenic (or vasopressin-resistant) diabetes insipidus is caused by an inability of the antidiuretic hormone (ADH, or vasopressin) to increase the water permeability of the renal collecting system. That inability, in turn, arises from abnormally high activity of the enzyme cAMP-phosphodiesterase, specifically of the isozyme type III (PDE-III), which hydrolyzes cAMP and prevents the intracellular buildup of this second messenger. Two rather specific inhibitors of PDE-III, rolipram and cilostamide, used either in vitro or in vivo, reverse the deficiencies in DI +/+ Severe mice by increasing intracellular cAMP and water permeability toward or to their normal values. These results have implications for the treatment of nephrogenic diabetes insipidus in human patients.