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Biomedical subjects

D Michaeli

Publications and source records attributed to D Michaeli.

At least 19 recordsLinked to original sources
PubMed1979

Development of a storable Leishmania tropica vaccine: field testing with frozen promastigotes.

The development of a frozen vaccine against cutaneous leishmaniasis offers the possibility of controlling the quality, efficiency and sterility of the promastigotes used for inoculation. Thirty-nine soldiers in a settlement in a hyperendemic area were inoculated with a fresh isolate of Leishmania tropica that was stored at the temperature of liquid nitrogen. Thirty of the soldiers were injected by conventional syringe while the rest were inoculated by an intradermal jet injector. The infective material was transported either in ice or at liquid nitrogen temperature. All the subjects developed lesions at the site of inoculation, without unwarranted reactions. One month after inoculation 31 subjects were examined by a physician. All the reactions were positive--12 ulcers and 19 nodules. After four months, all 39 soldiers were examined: 25 (64%) had ulcers; eight (21%) had nodules; and six (15%) were without visible reaction. The different methods of transporting the vaccine, as well as the different responses of men and women, are discussed.

Adolescent↗
PubMed1977

Murine typhus and spotted fever in Israel in the seventies.

One hundred and eleven cases of rickettsial disease-100 cases of murine typhus and 11 cases spotted fever--seen over a four year period at the Chaim Sheba Medical Center are reviewed. The clinical picture of murine typhus (caused by Rickettsia mooseri and transmitted by Xenopsylla cheopis) could not be distinguished from that of spotted fever (caused by a Rickettsia similar to Rickettsia conori and transmitted by Rhipicephalus). Some quite severe cases of murine typhus and some relatively mild cases of spotted fever were seen.

Adolescent↗
PubMed1977

Protracted arthritis in familial Mediterranean fever.

A review of the files of familial Mediterranean fever (FMF) confirmed the rarity of patients suffering protracted arthritic attacks and the propensity of the joints, in general, to recover. While 70% of those afflicted suffered bouts of synovitis, only 57 patients (5% of the FMF-population) experienced protracted attacks involving a total of 84 joints, 36 of them knees and 25 hips. Functional and, usually, anatomical integrity was regained in all but 27 joints. Of the 27 joints producing residual incapacity, 21 were hips. Seven hips showed roentgenologically typical aseptic necrosis of the femoral head and 14 only sclerosis and narrowing of the joint space. Eight hips eventually required total prosthetic replacement. We suggest that the poor prognosis of the hip, in contrast to other joints affected by protracted FMF-arthritis, is related not directly to the metabolic aberrration underlying the disease but to attenuation of the arterial blood supply of the femoral head by synovial exudation. Early aspiration of exudate could alter the prognosis by preventing the complication of aseptic necrosis.

Adolescent↗
PubMed1977

Inhibition of fibrin-platelet interactions by fibrinogen-degradation fragment D.

Homogenized fibrin induced platelet aggregation and the release of serotonin from human platelets. Fragment D, purified from a plasmin digest of human fibrinogen, inhibited these platelet-fibrin interactions. Using a radiolabeled fragment D, it was possible to demonstrate saturable binding of fragment D to fibrin. Nonlabeled fragment D competed with the radiolabeled fragment D for binding to fibrin. Furthermore, the binding of fragment D to fibrin paralleled its ability to inhibit the fibrin-induced release of platelet serotonin. It is postulated that the inhibitory effect of fragment D on fibrin activation of platelets is due to the binding of fragment D to fibrin. The bound fragment D may cover up or block sites on fibrin that are involved in fibrin-platelet interactions. This would then result in inhibition of the fibrin-induced platelet aggregation and release of platelet serotonin.

Blood Platelets↗
PubMed1976

Fibrin-induced release of platelet serotonin.

Human platelets were reacted with polymerized fibrin formed from human fibrinogen. The platelets adhered to the fibrin particles and this adhesion was followed by the release of serotonin from prelabeled platelets. The adhesion of platelets to fibrin was not inhibited by adenosine or prostaglandin E1. However, the subsequent Ca2+-dependent release of platelet serotonin was completely inhibited by these compounds. After the initial platelet-fibrin interaction, ADP and serotonin released from activated platelets may lead to additional platelet aggregation and release. Therefore, in addition to clot stabilization, fibrin serves as an initiator of the platelet release reaction. This in turn initiates the self-amplifying process of platelet aggregation.

Adenosine↗