Summer distribution of the purplegray sculpin <Emphasis Type="Italic">Gymnocanthus detrisus</Emphasis> (Cottidae) in Waters of Primorsky Krai,Sea of Japan

Results of trawl catches show that in the summer period, in the waters of Primorsky Krai, Russia, Sea of Japan, the purplegray sculpin Gymnocanthus detrisus occurs at depths of 20 to 411 m, preferring the range 80–250 m. The temperature of the species’ habitat varies from 0.8 to 8.6 ° C, and the optimal one is 1.2–2.2 °C. G. detrisus occurs at the preferred depths more frequently in the southern area—the Peter the Great Bay, which is more favorable for foraging; in the area of North Primorsky Krai it was found both at greater and lesser depths. The latter is probably determined by the more limited spreading of waters with unsuitable temperatures for the species there. The body size of the purplegray sculpin grows with depth. Juveniles avoid depths over 200 m, where inflow of low-temperature waters is recorded. G. detrisus, which inhabits waters of Primorsky Krai, is represented mainly by females; the proportion of males exceeds that of females only in the 21–27 cm size group. This may be related to the lower growth rate in males after maturation as compared to females.     

Alpha 2-antiplasmin in bovine plasma

Bovine and human blood plasma contains alpha 2-antiplasmin which possesses affinity to lysin-binding sites in plasmin and inhibits the human plasmin. Its isolation was conducted for two stages: separation of plasminogen on lysin-cellulose, fractionation by ammonium sulphate, desalination on molselector G-25, chromatography on DEAE-Sephadex A-50 and affinity chromatography on plasmin-sepharose with the blocked active site.     

Changes of the dermal-fascial autograft after transplantation on the vascular-nervous connections using a microsurgical technique

In 56 dogs 86 microsurgical operations on transplantation of free dermal-facial autografts from the internal knee surface have been performed on the hidden vascular-nervous bundle. The animals have been observed for 1 day up to 1 year. The implanted grafts (63) have been studied, using a complex of anatomical, histological and roentgenological methods. During early time (up to 7 days) after the operation in the flap signs of edema, dystrophy and inflammatory infiltration of tissues predominate. The graft gets blood at the expense of the restored main artery and has no vascular connections with the surrounding tissues. Its nervous conductors are fragmented. During 2 weeks--1 month epidermis completely regenerates along the line of the dermal suture. In the flap bed mature granulations result in vascular connections with its surrounding tissues. These connections become stable by the end of the first month, this means that the graft has implanted. Its nervous fibers are also restored. Long-term observations demonstrate that the adaptive changes of the flap and its vascular bed are near to completion. By the end of the 1st year restoration of the main innervational connections of the graft takes place. According to the data obtained, the nervous conductors grow into it along the sewed hidden nerve and along the course of paravasal nerve plexuses. Across the scar from the surrounding tissues the dermal-fascial autograft does not reinnervate.     

Apparent activation of rabbit lung membrane adenylate cyclase by cytosolic proteins possessing adenylate kinase activity.

Lung cytosolic fraction (23500 x g supernatant) activates cAMP synthesis by lung membrane adenylate cyclase (AC). 23 kDa and 29 kDa proteins were isolated from rabbit lung cytosolic fraction in a homogeneous state, as 'activators' of lung membrane AC. Both of these proteins possess high adenylate kinase (AK) activity and are able to mimic the 'activating' effect of lung cytosol on the lung membrane AC in the standard incubation mixture devoid of adenylate kinase. The activating effect is abolished in the presence of adenylate kinase inhibitor DAPP and after heat- or trypsin-treatment of the cytosolic fraction. Commercial adenylate kinase or nonionic detergent Lubrol PX activate cAMP synthesis by lung membrane AC in a similar manner to that of cytosolic fraction. In the presence of commercial adenylate kinase or Lubrol PX no activating effect of the cytosolic fraction on lung membrane AC is revealed. The ability of cytosolic fraction, commercial adenylate kinase, Lubrol PX or purified 23 kDa and 29 kDa proteins to activate cAMP synthesis by lung membrane AC correlates with their ability to support the constant ATP (AC substrate) concentration in the AC assay mixture. Our data indicate that 'activation' of lung membrane AC in the presence of cytosolic fraction may be produced by cytosolic adenylate kinase activity which regenerates ATP from AMP in the presence of creatine kinase and creatine phosphate providing the substrate for cAMP synthesis by AC.     

Expression of lysyl oxidase from cDNA constructs in mammalian cells: The propeptide region is not essential to the folding and secretion of the functional enzyme

Rat aortic lysyl oxidase cDNA was expressed under a metallothionein promoter in Chinese hamster ovary cells using a dihydrofolate reductase selection marker. One methotrexate-resistant cell line, LOD-06, generated by transfecting with full-length cDNA, yielded lysyl oxidase proteins consistent with the 50 kDa proenzyme and a 29 kDa mature catalyst. A second cell line, LOD32–2, was generated by transfection with a truncated cDNA lacking sequences which code for the bulk of the propeptide region. Both cell lines secreted apparently identical, 29 kDa forms of mature lysyl oxidase each of which catalyzed the deamination of human recombinant tropoelastin and alkylamines, consistent with the known specificity of lysyl oxidase. The secreted enzyme forms were inhibited by chemical inhibitors of lysyl oxidase activity, including β-aminopropionitrile, phenylhydrazine, ethylenediamine, α,α′-dipyridyl, and diethyl-dithiocarbamate. Sensitivity to these agents is consistent with the presence of copper and carbonyl cofactors in the expressed enzymes, characteristic of lysyl oxidase purified from connective tissues. These results indicate the lack of essentiality of the deleted proprotein sequence for the proper folding, generation of catalytic function, and secretion of lysyl oxidase. © 1995 Wiley-Liss, Inc.     

Expression of BDNF and TrkB Phosphorylation in the Rat Frontal Cortex During Morphine Withdrawal are NO Dependent

Nitric oxide (NO) mediates pharmacological effects of opiates including dependence and abstinence. Modulation of NO synthesis during the induction phase of morphine dependence affects manifestations of morphine withdrawal syndrome, though little is known about mechanisms underlying this phenomenon. Neurotrophic and growth factors are involved in neuronal adaptation during opiate dependence. NO-dependent modulation of morphine dependence may be mediated by changes in expression and activity of neurotrophic and/or growth factors in the brain. Here, we studied the effects of NO synthesis inhibition during the induction phase of morphine dependence on the expression of brain-derived neurotrophic factor (BDNF), glial-derived neurotrophic factor (GDNF), nerve growth factor (NGF), and insulin-like growth factor 1 (IGF1) as well as their receptors in rat brain regions after spontaneous morphine withdrawal in dependent animals. Morphine dependence in rats was induced within 6 days by 12 injections of morphine in increasing doses (10–100 mg/kg), and NO synthase inhibitor L-N^G-nitroarginine methyl ester (L-NAME) (10 mg/kg) was given 1 h before each morphine injection. The expression of the BDNF, GDNF, NGF, IGF1, and their receptors in the frontal cortex, striatum, hippocampus, and midbrain was assessed 40 h after morphine withdrawal. L-NAME treatment during morphine intoxication resulted in an aggravation of the spontaneous morphine withdrawal severity. Morphine withdrawal was accompanied by upregulation of BDNF, IGF1, and their receptors TrkB and IGF1R, respectively, on the mRNA level in the frontal cortex, and only BDNF in hippocampus and midbrain. L-NAME administration during morphine intoxication decreased abstinence-induced upregulation of these mRNAs in the frontal cortex, hippocampus and midbrain. L-NAME prevented from abstinence-induced elevation of mature but not pro-form of BDNF polypeptide in the frontal cortex. While morphine abstinence did not affect TrkB protein levels as well as its phosphorylation status, inhibition of NO synthesis decreased levels of phosphorylated TrkB after withdrawal. Thus, NO signaling during induction of dependence may be involved in the mechanisms of BDNF expression and processing at abstinence, thereby affecting signaling through TrkB in the frontal cortex.