[Aseptic meningitis in bacterial endocarditis].
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Biomedical subjects
Publications and source records attributed to A Pinto.
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Fischer rat thyroid epithelial cella (FRT) growing continuously in culture were infected with the Kirsten murine sarcoma virus KiMSV(KiMuLV) and found to produce this virus constitutively. Although the morphology of the FRT cells did not change appreciably, the cells became malignant after infection with KiMSV(KiMuLV) as shown by the growth of infected cels in semi-solid media (uninfected FRT cells did not grow) and by the tumorigenicity of infected when injected into syngeneic animals (uninfected FRT cells or FRT cells infected with non-transforming retro-viruses were not tumorigenic). The induced tumors morphologically resembled moderately differentiated carcinomas. Two markers of thyroid epithelial differentiation were absent in the original FRT clone and remained unexpressed after transformation. Fully differentiated rat thyroid epithelial cells (FRT-L cells) infected with another strain of the Kirsten murine sarcoma virus, the KiMSV(MolMuLV), were also transformed as demonstrated by the ability also of these cells to grow as carcinomas (after in vitro transformation) in syngeneic animals. Our results clearly demonstrate that the Kirsten murine sarcoma virus can transform in vitro cells of epithelial as well as of fibroblastic origin.
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Hydrocortisone inhibits prostaglandin generation by rat peritoneal leucocytes by releasing the polypeptide phospholipase inhibitor, macrocortin. The susceptibility of these cells to hydrocortisone is directly correlated with their intracellular macrocortin content. Cells depleted of the peptide by prior incubation with steroid cannot respond to the steroid, until a fresh intracellular store has been synthesized. In vitro, this process requires 4-5 h. Cells remain sensitive to the inhibitory action of the peptide at all times.
Platelets are thought to be involved in the initiation and propagation of arterial and venous thrombi. A new formation of platelet thrombus in a coronary artery has been implicated in the genesis and extension of myocardial infarction. Experimental evidence suggests that platelet aggregates may be responsible for occlusion of small coronary arteries and subsequent ischemia. Whether the thrombotic component of myocardial infarction is primary or secondary in a given patient, platelet function alterations can influence many mechanisms - operating at the microenvironment level from which depends if the thrombotic lesion grows or sends platelet emboli to the smaller myocardial vessels. Although myocardial infarction is usually associated with arteriographic evidence of atherosclerotic coronary obstruction, examples of infarction in the absence of coronary artery disease have been reported. ARterial thrombosis, small vessel coronary disease and arterial spasm are several possibilities that have been described. Recently in some cases of myocardial infarction, coronary artery spasm has been demonstrated angiographically; thromboxanes, vasoconstrictive and platelet aggregating substances, are released by platelets; thromboxanes, vasoconstrictive and platelet aggregating substances, are released by platelets during myocardial ischemia as an increase of prostaglandin synthesis, like prostacyclin, is stimulated by ischemia and hypoxia. The local release of these substance may modify the myocardial cell viability and regional blood flow. The aim of the present study was to investigate some changes in platelet function in relation to the time stimulated with thrombin. The tests showed, in the first three days, an augmented release of BTG levels with a platelet "exhaustion", demonstrated by a reduced formation of MDA by platelets changing to a state of hyperactivity, with a maximal production of MDA in 10th-15th day.
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Eight women had a bullous skin disease that occurred during pregnancy. One patient had clinical, histopathologic, and immunopathologic features of pemphigus. The other seven patients showed the features of herpes gestationis. Oral contraceptives reproduced the disease in the pemphigus patient and in one of the others. When the pemphigus patient was free of active disease, local intraepidermal acantholytic blister formation with deposition of IgG and C3 in the intercellular substance of the epidermis was induced by intradermal injection of progesterone.
We report the first case of L.P. in our country with typical lesions of skin, pharyngeal and laryngeal mucous membranes. Our observation did not indicate any history of consanguinity nor family incidence, nor visceral engagement. The hepatic biopsy was normal. Connected with the main illness we found a radiopaque area in the right frontal bone which engaged the interior and exterior walls, and a calcification nodule in the base of the right maxillary sinus.
A serological investigation on antitoxoplasma antibodies of women in labour and their newborn babies was carried out on a population sample representative of a defined geographical area. The relevant findings revealed: a) high titer antibodies in 21.2% of parturient-newborn pairs; b) slight or non-apparent toxoplasma infection, limited to 2.4% of newborns with high titer antibodies; c) quick drop of antibody titer in two thirds of seropositive women in labour observed 90 days from childbirth; d) a steady proportion of seronegative pregnant women - 40% ca. - detected in all age groups from 20 and 40 years and over. These findings are discussed, and assumptions on their meaning are put forward.
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