[A new approach for explaining viral organotropism: fusion of HBV transfected cells with hepatocytes].
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Biomedical subjects
Publications and source records attributed to M Lambert.
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Somatostatin can be helpful after liver transplantation in some well-defined indications. In uncontrolled digestive haemorrhage, a short course of somatostatin therapy can be of great help in controlling the acute bleeding and to avoid emergency laparotomy. Somatostatin could also be helpful in bilio-pancreato-intestinal fistula, but in this case its advantage over elective surgical treatment remains to be confirmed.
We report a case of primary bronchogenic adenocarcinoma, complicated by pleural effusion, in which very high pleural amylase activity was found, whilst serum amylase was normal. Isoamylase determination showed a salivary-type amylase. Concerning the origin of this enzyme, ultrastructural study of the malignant cells obtained from the pleural fluid suggested a local amylase synthesis. The pathophysiological significance of electron-dense granules found in these cells is also discussed.
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Patients on chronic hemodialysis may have a spuriously low TBG level, tentatively ascribed to uremia-induced changes in TBG immunoreactivity. In order to test this hypothesis, the effect of restoration of a normal renal function on TBG immunoreactivity was evaluated. TBG concentration was measured in 20 patients both by radioimmunoassay and by a T4-binding capacity assay, before, 4 and 10 months after a successful renal transplantation. Mean pretransplant TBG value measured by RIA was in the low normal range (1.60 +/- 0.14 mg/dl; normal limits 1.6-2.4 mg/dl). Twelve patients (60%) had TBG levels below 1.6 mg/dl (group I), while T4-binding capacity of TBG (TBC) measured in 7 of them was normal, so that the TBG/TBC ratio was characteristically reduced. The 8 remaining patients (group II) had TBG levels within or slightly above the normal range (mean value 2.26 +/- 0.17 mg/dl) and in the 5 tested patients, TBC and TBG/TBC ratio were normal. Four months after transplantation, mean TBG increased significantly in group I from 1.15 +/- 0.03 mg/dl before transplantation to 1.54 +/- 0.12 mg/dl (p less than 0.01). TBC increased also from 269 +/- 37.5 to 335 +/- 24 nmol/l (p less than 0.01) but to a significantly lesser extent than TBG (24% vs 48%, p less than 0.05). As a result, the TBG/TBC ratio returned to normal values, rising from 0.79 +/- 0.07 to 0.95 +/- 0.07 (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
Two Tay-Sachs disease (TSD) patients of French-Canadian origin were shown by Myerowitz and Hogikyan to be homozygous for a 7.6-kb deletion mutation at the 5' end of the hexosaminidase A alpha-subunit gene. In order to determine whether all French-Canadian TSD patients were homozygotes for the deletion allele and to assess the geographic origins of TSD in this population, we ascertained 12 TSD families of French-Canadian origin and screened for occurrence of mutations associated with infantile TSD. DNA samples were obtained from 12 French-Canadian TSD families. Samples were analyzed using polymerase-chain-reaction (PCR) amplification followed by hybridization to allele-specific oligonucleotides (ASO) or by restriction analysis of PCR products. In some cases Southern analysis of genomic DNA was performed. Eighteen of the 22 independently segregating mutant chromosomes in this sample carried the 7.6-kb deletion mutation at the 5' end of the gene. One chromosome carried the 4-nucleotide insertion in exon 11 (a "Jewish" mutation). In this population no individuals were detected who had the substitution at the splice junction of exon 12 previously identified in Ashkenazi Jews. One chromosome carried an undescribed B1 mutation; this allele came from a parent of non-French-Canadian origin. Patients in three families carried TSD alleles different from any of the above mutations. The 5' deletion mutation clusters in persons originating in southeastern Quebec (Gaspé) and adjacent counties of northern New Brunswick.
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Homozygous familial hypercholesterolemia (HFH) is characterized by a very shortened lifespan, mainly due to cardiac events, and by resistance to conventional lipid lowering therapies. Two patients are described for whom a combination of portacaval shunt and mammary coronary bypass graft were done with good long term success. A review of the actual forms of treatment of HFH is made. To the authors' knowledge, there is no report in the literature of this double surgical approach.
A variety of techniques has been used to relieve the obstructive symptoms of pyloric stenosis. Endoscopic dilatation using hydrostatic balloon dilators, multiple-diameter bougies, and electrocautery with a sphincterotome have been described. The neodymium yttrium aluminum garnet laser also has been used, with both noncontact and contact probes. We describe a new technique using a guidewire-directed contact probe for laser recanalization of pyloric stenosis in a patient with radiation-induced gastric outlet obstruction.
Alteration of posterior pituitary function in the empty sella syndrome is rare. A case of central diabetes insipidus and clear-cut deficiency of gonadotropins associated with an empty sella is described. Although computed tomographic scan revealed a defect of the diaphragma sellae, other pathogenic mechanisms are considered. Previously documented cases of empty sella syndrome associated with diabetes insipidus are reviewed.
In the course of a systematic survey of DMD and BMD patients with intronic probes and with cDNA probes covering three-fourths of the coding sequence, 45 molecular deletions within the DMD gene were investigated. Forty-two percent of the breakpoints were located in the intronic sequence containing probe P20, whereas the other deletions were widespread around the more proximal part of the gene. Most of the BMD deletions were in the P20 region. Pulsed field gel electrophoresis was used to determine the size of some deletions and allowed us to estimate the physical distance between the intronic probes JBir and P20. The reading frame was checked in 11 cases with proximal deletions and found to be disrupted in 6 of 7 DMD patients, in 1 intermediate case, and, unexpectedly, in 3 BMD patients.
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We report a case of acute haemolytic anaemia complicating infectious mononucleosis in a 19-year old male. There was no evidence for an immune haemolysis and red cell studies revealed a previously undiagnosed congenital spherocytosis. We discuss this rare presentation.
Previous work has shown that exercise training increases the ventricular fibrillation threshold of the isolated perfused rat heart. The aim of our study was to determine whether exercise training that begins after myocardial infarction can similarly increase the ventricular fibrillation threshold. Rats that had suffered an experimental myocardial infarction were subject to a running training program. Thereafter, the ventricular fibrillation threshold was measured before and after the onset of acute reinfarction induced by a second coronary artery ligation. Ventricular fibrillation thresholds were significantly elevated in trained rats during normoxia (13.7 +/- 2.2 vs. 4.7 +/- 0.8 mA, p less than 0.01) and during acute ischemia (6.8 +/- 1.6 vs. 3.0 +/- 0.7 mA, p less than 0.02). The myocardial cyclic AMP level was lower in the nonischemic zone of the trained hearts (0.21 +/- 0.01 vs. 0.28 +/- 0.01 nmol/g, p less than 0.05), which also had lower cyclic AMP levels after epinephrine challenge (0.50 +/- 0.05 vs. 0.73 +/- 0.09 nmol/g, p less than 0.01; 1.41 +/- 0.11 vs. 1.85 +/- 0.09 nmol/g, p less than 0.02 after epinephrine 10(-7) M and 5 x 10(-6) M injection, trained vs. untrained). Both propranolol 10(-6) M and epinephrine 5 x 10(-7) M attenuated the difference in ventricular fibrillation thresholds before and after second coronary artery ligation and eliminated any difference in cyclic AMP content of both the nonischemic and ischemic myocardial tissue.(ABSTRACT TRUNCATED AT 250 WORDS)
Serum TBG concentrations were evaluated in 34 patients on regular hemodialysis. Mean serum TBG level measured by two different radioimmunoassays was markedly decreased (1.24 +/- 0.08 mg/dl - normal limits 1.6-2.4 mg/dl). Twenty-seven (79%) patients had values below 1.6 mg/dl, which contrasted in 21 of them with a lack of reciprocal elevation of T3RU values. By contrast, T4-binding capacity of TBG measured in 14 patients with low TBG concentration was normal, suggesting that the low TBG values were an artefact resulting from an altered immunoreactivity of the protein. In 2 patients with low TBG while on hemodialysis, TBG levels increased significantly after renal transplantation. This suggests that the "low TBG syndrome" (altered immunoreactivity in the face of normal T4-binding capacity) observed in patients on chronic hemodialysis is a consequence of uremia.
Prediction of late clinical events was studied in a series of 145 patients who had control angiographic studies at one year and between two and 14 years after saphenous vein coronary artery bypass graft surgery. During a mean observation interval of 7.4 years, new narrowing or occlusion occurred in grafts of 59% of the patients and progression in non-bypassed arteries was observed in 66%. One or several of the following events were observed in 56% of the patients: recurrent or worse effort angina, unstable angina, myocardial infarction and heart failure. Unstable angina during follow-up was more frequent in young patients and in those who had this clinical presentation before surgery. The incidence of myocardial infarction was likewise greater in patients who had preoperative unstable angina and in those with four to five risk factors for coronary artery disease, as well as those having a lesser number of inserted grafts. Heart failure was predicted independently by either four to five risk factors, a low left ventricular contraction score or fewer grafts placed at surgery. The number of inserted grafts correlated inversely with any one of the late clinical events.
As an approach to identifying specific cellular markers for the cytotoxic action of x rays in mammalian cells, we used the QUEST system of high-resolution, two-dimensional protein gel electrophoresis and a computerized data base on proteins to score quantitative changes in patterns of protein synthesis. We measured the responses elicited after x irradiation of cells from the normal rat cell line REF52 as well as two oncogene-transformed REF52 cell lines with E1a or E1a plus the mutated c-Harvey-ras T24 (HRAS1 T24) allele. The transformed cell lines differed substantially in the patterns of changes in protein synthesis seen immediately after DNA damage. In addition, we identified a specific subset of growth-regulated cellular polypeptides that are correlated with the observed increase in x-ray-induced cell killing in the transformed cell lines. One of these polypeptides was cyclin (proliferating-cell nuclear antigen), a cell-cycle-specific DNA polymerase delta auxiliary factor. Synthesis of this set of coregulated polypeptides was rapidly suppressed by x irradiation in normal REF52 cells only. The inability of x irradiation to induce suppression of protein synthesis in cells from the transformed cell lines correlated with the increased susceptibility to x-ray-induced cell killing. This finding suggests that the cellular processes that underlie regulation of DNA-damage-induced growth arrest at the level of replicative elongation plays a role in determining the survival of x-irradiated cells.
A case of chronic lymphocytic leukemia (CLL) is described during the course of which paraplegia appeared caused by epidural compression of the tissue by leukemic cells. This complication in CLL is rare. The disorders of the nervous system during the course of leukemia are summarized, and, in particular, the circumstances pertaining to the occurrence of paraplegia during chronic lymphocytic leukemia.