Monk seal mortality: virus or toxin?

During the past few months, more than half of the total population of about 300 highly endangered Mediterranean monk seals (Monachus monachus) on the western Saharan coast of Africa, died in a mysterious disease outbreak. Epizootiological and postmortem findings were reminiscent of similar outbreaks amongst pinniped and cetacean species in recent years, which were caused by an infection with newly discovered morbilliviruses (for review see osterhaus et al.). Virological, as well as toxicological, analysis performed on tissue samples collected from relatively fresh carcasses during the outbreak indicate that infection with a virus closely related to dolphin morbillivirus (DMV), possibly originating from affected dolphins in the same area, was the primary cause of the outbreak. Therefore it is concluded that vaccination with a safe and effective non-replicating vaccine should be considered as a management tool in the conservation of Mediterranean monk seals.     

Posterolateral dislocation of the elbow with concomitant fracture of the lateral humeral condyle: case report

We describe a case of a 6-year-old girl with a posterolateral elbow dislocation and a concomitant fracture of the lateral humeral condyle. After reduction of the dislocation, the fracture was diagnosed and treated by open reduction and fixation, with a good functional result. In doubtful cases, oblique, heterolateral, and varus stress films, or even arthrography may be necessary.     

Clonal relationships among high-level penicillin-resistant Streptococcus pneumoniae in the United States

Emu antibody responses to avian influenza virus (AIV) infection were evaluated by the competitive enzyme-linked immunosorbent assay (C-ELISA), agar gel immunodiffusion (AGID) and hemagglutination inhibition (HI) tests. All birds infected with AIV H5N1, H5N3, or H7N7 developed antinucleoprotein (NP) antibodies as early as 7 days postinfection as detected by the C-ELISA. The responses lasted 49 days for the emus receiving H5N3 and at least 56 days for emus receiving the other two viruses. By evaluating 50 emu field serum samples, the C-ELISA was found more sensitive than the AGID test for the detection of anti-NP antibodies. This study indicates that emus experimentally infected with AIV developed antibody responses that can be detected by C-ELISA, AGID, and HI tests. The results from this and our previous studies demonstrate the use of the C-ELISA as a substitute for the AGID test in a routine serodiagnostic screening for detection of antibodies to AIV infection in multiple avian species.     

Reconstructive and plastic microsurgery in the treatment of combat trauma to the extremities

In the department of microsurgery of A.A. Vishnevsky Central Hospital the transplantation and transposition of the at the gunshot injuries of the extremities have begun to execute since 1990. For this time 94 surgical interventions have been conducted at 88 wounded: 57 transplantations and 37 transpositions of the bloody tissues. The transplantation and transposition of the vascularized complexes of tissues with application of microsurgical technique is the effective method of the treatment of the wounded in the extremities. In the conditions of the local armed conflicts it is necessary to provide deployment of the department of microsurgery at stages of the specialized medical care.     

The effect of phospholipase C on human blood platelets

The effect of phospholipase C (EC 3.1.4.3) on human blood platelets has been studied. Phospholipase C from Bacillus cereus was purified to homogeneity as judged by analytical and sodium dodecyl sulphate disc gel electrophoresis and by immunoelectrophoresis. Human platelets isolated from platelet-rich plasma by gel filtration or by centrifugation and washing were incubated with phospholipase C. A loss of 20-45% of the total platelet phospholipid was observed, whereas 88% was hydrolyzed when platelet homogenates were submitted to identical enzyme treatment. Intact platelets lost 50-75% phosphatidylethanolamine, 20-50% phosphatidylcholine, and 20-25% phosphatidylserine. Sphingomyelin was not a substrate for the enzyme under the conditions used. The platelets contained no detectable endogenous phospholipase C activity. The loss of phospholipid was not accompanied by aggregation of the platelets, nor did the platelets lose their ability to aggregate with ADP or thrombin. Total platelet factor 3 releasable by freezing and thawing was reduced. Measurements of releasable platelet factor 4 and the efflux of serotonin showed that no release reaction was triggered even when up to 45% of the total phospholipid in the platelets was hydrolyzed. When sphingomyelinase was added together with, before, or after phospholipase C, aggregation occurred. Sphingomyelinase alone gave no aggregation. The gel-filtered platelets also aggregated upon addition of purified phospholipase C from Clostridium perfringens. The distribution of phospholipids in the platelet membrane is discussed.     

Parathyroid hormone (PTH) stimulates adrenocorticotropin release in AtT-20 cells stably expressing a common receptor for PTH and PTH-related peptide

Complementary DNA encoding a rat bone PTH/PTHrP receptor was stably expressed in the murine corticotroph cell line, AtT-20. Several clones, expressing variable numbers of PTH/PTHrP receptors, were developed. In contrast to the relatively low binding affinity (apparent Kd = 15 nM) observed in COS-7 cells transiently expressing the PTH/PTHrP receptor, all AtT-20 stable transfectants bound [Nle8,18,Tyr34]bPTH(1-34)NH2 (NlePTH) with an affinity that was indistinguishable from that observed in ROS 17/2.8 cells expressing native PTH/PTHrP receptors. Additionally, NlePTH dramatically increased cAMP accumulation and ACTH release in AtT-20 cells expressing the PTH/PTHrP receptor with an ED50 of 0.6 +/- 0.3 and 0.3 +/- 0.1 nM, respectively. The high binding affinity and the high efficacy of NlePTH in stimulating cAMP accumulation and ACTH release indicate that the PTH/PTHrP receptor is efficiently coupled to the intracellular signalling system responsible for stimulation of ACTH release in AtT-20 cells. No additivity of cAMP accumulation or of ACTH release was observed when these cells were treated with maximally active concentrations of both NlePTH and CRF. This suggests that the receptors for both of these hormones share the same intracellular effectors, and that intracellular signaling in AtT-20 cells is not compartmentalized. Additionally, the ability of NlePTH to stimulate ACTH release in AtT-20 cells, a function that is normally performed by CRF, demonstrates promiscuity between activated receptors and distal biological functions.