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J Martel

Publications and source records attributed to J Martel.

At least 91 records · Page 5Linked to original sources
PubMedDate not supplied

Effect of cadmium on membrane potential in isolated rat hepatocytes.

The effect of cadmium (Cd) on rat hepatocytes upon short term exposure was studied by focusing on the integrity of mitochondria and on the possible consequences of its disturbance, such as alterations in plasma membrane potential and loss of cell viability. Changes in the potential of mitochondrion and plasma membranes were monitored using [3H]triphenylmethylphosphonium (TPMP+) and [14C]SCN- probes, respectively. Isolated rat hepatocytes were exposed to increasing CdCl2 concentrations for short time periods (30-120 min). Cd measurement by atomic absorption showed that the cells efficiently accumulated Cd, as did mitochondria in situ. In CdCl2-treated cultures, it was observed that the release of TPMP+, which revealed a drop in the mitochondrial membrane potential, was time- and concentration-dependent, and that the first significant efflux was caused by a 30-min exposure to 89 microM CdCl2. No significant change in plasma membrane potential, as judged from the increase in the uptake of SCN-, was detected after 30 min, suggesting the greater precocity of the mitochondrial attack. Finally, the release of lactate dehydrogenase (LDH) occurred only after 2 h of exposure, reflecting ultimate stages of cell injury induced by Cd. These results suggest that Cd induces an alteration in mitochondrial function in hepatocytes which may lead to the loss of plasma membrane potential and cell viability. The study therefore adds further evidence of the role of mitochondria as primary targets in Cd-induced cytotoxicity.

Animals↗
PubMedDate not supplied

Neuroradiologic abnormalities in Marchiafava-Bignami disease of benign evolution.

Marchiafava-Bignami disease has been recognized since 1903, but only recently has it become possible to achieve a probable diagnosis before death occurs. Imaging of the central nervous system with MR and CT have contributed significantly to such a diagnosis. Two cases of the disease are reported in patients, aged 33 and 59 years, with benign evolution of neurologic symptoms the diagnosis was confirmed by neurologic imaging with MR and CT and both were studied with evoked responses. Reversibility of the disease and possible prognostic indicators in these and other patients reported in the literature are discussed. The important role that diagnostic procedures, especially MR imaging, play in the management of this disease is emphasized.

Adult↗
PubMedDate not supplied

Effect of phosphate supplementation on the expression of the mutant phenotype in murine X-linked hypophosphatemic rickets.

The X-linked Hyp mouse, a murine homologue of X-linked hypophosphatemia in humans, is characterized by rachitic bone disease, hypophosphatemia, impaired renal brush-border membrane Na(+)-phosphate cotransport and abnormal regulation of renal vitamin D metabolism. We demonstrated that short-term phosphate supplementation decreases renal 1,25-dihydroxyvitamin D3 (1,25-(OH)2D) catabolism and increases serum 1,25-(OH)2D levels in Hyp mice (Tenenhouse & Jones 1990). In the present study, we compared several other parameters in normal and Hyp mice fed control (1%) and high (1.6%) phosphate diets for 4 days. Phosphate supplementation significantly raised serum phosphate levels and decreased renal brush-border membrane Na(+)-phosphate but not Na(+)-glucose, cotransport in both genotypes (67% of control diet, p < 0.05). However, under both dietary conditions, the phosphate/glucose transport ratio was significantly reduced in Hyp mice (58% of normal littermates, p < 0.05). Renal PTH-stimulated cAMP accumulation, which was significantly blunted in Hyp mice compared to normal mice under control dietary conditions (p < 0.05), was not altered by phosphate supplementation in either genotype. Serum alkaline phosphatase activity was significantly higher than normal in Hyp mice on the control diet and was further increased in mutants but not in normals fed the high phosphate diet (p < 0.05). Measurements of serum bilirubin and electrophoresis of serum alkaline phosphatase suggested that the elevation in serum alkaline phosphatase activity in phosphate-supplemented Hyp mice represents the bone-derived isozyme.(ABSTRACT TRUNCATED AT 250 WORDS)

Alkaline Phosphatase↗
PubMedDate not supplied

The MDR1 (P-glycoprotein) and MRP (P-190) transporters do not play a major role in the intrinsic multiple drug resistance of Jurkat T lymphocytes.

The response of T cells in relation to the cell cycle has not been extensively studied. We have attempted to address this question using Jurkat T cells treated with cytostatic drugs known to arrest cells at various transition points of their cycle. We tested several concentrations of drugs that act at G1/S (hydroxyurea, lovastatin, thymidine), early S (aphidicolin, cyclosporin A, rapamycin) or G2+M (colchicine, nocodazole) in 24 h cultures. Cytofluorimetric analyses showed that cycling Jurkat cells were equally distributed between the G1 (44.9 +/- 6.5%) and S (42.3 +/- 8.0%) phases. Cell distribution in G2+M was 12.7 +/- 2.8%. Hydroxyurea but not lovastatin increased the percentage of cells in S phase to approximately 60-70% and both drugs decreased it to approximately 30% in G1. Thymidine had no effects. Aphidicolin increased the distribution in S phase to approximately 70% with a decrease in G1 to approximately 30%. Cyclosporin A and rapamycin increased the percentage of the cells in G1 to approximately 70% and decreased it to approximately 25% in S phase. Nocodazole increased cell distribution in G2+M to approximately 60% and induced a decrease in G1 to approximately 10%. The effects of the drugs were not related to their toxicity and their limited efficiency raised the possibility that Jurkat cells possessed an intrinsic resistance to these xenobiotics. Time-course analysis showed (scanning electron microscopy) that the early morphological changes induced by colchicine were reversible. Drug efflux experiments (vinblastine) suggested that an ATP-dependent process could be involved. However, Northern blot analyses showed a weak signal for MDR1 (P-glycoprotein). In contrast, a probe for MRP (P-190) showed a strong signal in Jurkat and peripheral lymphocytes. The presence of drugs (cyclosporin A, nocodazole, thymidine) (24 h) did not upregulate its message and cell treatment with DL-butathione (S,R)-sulfoximine only moderately affected the efficiency of the glutathione S-conjugate MRP transporter. Our data suggest that the intrinsic multidrug resistance of leukemic Jurkat T cells does not appear to involve the MDR1 and MRP members of the ABC family of reverse drug transporters and these observations raise the possibility of the involvement of multifaceted mechanisms.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMedDate not supplied

Complete resolution of CMV-associated acute hydramnios by single large volume reduction amniocentesis and maternal indomethacin. A case report.

Acute hydramnios is a rare complication of pregnancy, usually of idiopathic etiology and associated with a very poor perinatal prognosis. In this single case report, acute hydramnios at 21 weeks' gestation, associated with fetal CMV infection, was treated by a single large volume reduction amniocentesis combined with maternal indomethacin therapy and result in delivery of a near term survivor.

Adult↗
PubMedDate not supplied

[Breast metastases of an ovarian adenocarcinoma].

INTRODUCTION: Breast metastases are rare. Primary tumors are cutaneous, pulmonary, digestive and prostatic. A malignant tumor of the ovary is rarely responsible. OBSERVATION: A 69-year-old women presented a voluminous unilateral mastitis in a poly-metastatic context 3 years after the discovery of an ovarian adenocarcinoma. The anatomo-pathological examination confirmed the ovarian origin of the breast nodules observed. Progression was poor and the patient died 8 months after the first clinical signs in the breast. COMMENTS: The difficulty in differentiating a primary from a secondary carcinomatous mastitis is enhanced when the primary cancer is unknown. In our patient, the immunohistochemical study did not discriminate between the breast and ovarian origin. The diagnosis was finally made on the basis of standard histology and the anatomoclinical correlation. Since immunohistochemical examinations may not be specific enough, such as was the case in our patient, the anatomoclinical confrontation is essential.

Aged↗