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Biomedical subjects

M Haut

Publications and source records attributed to M Haut.

5 recordsLinked to original sources

Amnesia due to fornix infarction.

Background and Purpose-The fornix connects various structures involved in memory. We report a patient with anterograde amnesia after an acute ischemic infarct in the anterior fornix. Case Description-A 71-year-old female with acute-onset amnesia had neuroimaging studies showing ischemic infarction of both columns and the body of the fornix and the genu of the corpus callosum. Neuropsychological evaluation revealed anterograde amnesia without evidence of callosal disconnection. The patient showed marked improvement in her memory function on the follow-up visit. Conclusions-Amnesia in this case is likely due to infarction of the anterior fornix structures.

Aged↗

Heparin therapy for congenital antithrombin III deficiency in pregnancy.

A patient with congenital antithrombin III deficiency and a history of thromboembolic events prior to pregnancy was successfully treated with subcutaneous heparin alone throughout two pregnancies. Although adjuvant antithrombin III infusions may have a role in the treatment of this disorder, especially in the peripartum period, there is no evidence that this approach is superior to heparin therapy alone. We present this case as further evidence that heparin therapy alone appears to be a safe and effective treatment for pregnant patients with this rare but serious disorder.

Adult↗

Induction of nm23 gene expression in human colonic neoplasms and equal expression in colon tumors of high and low metastatic potential.

Levels of expression of the murine nm23 gene inversely correlate with metastatic potential in several rodent tumor model systems. Expression of the human nm23 homologue also is lower in human breast cancers of high metastatic potential than in breast cancers of low metastatic potential. In the present study, we examined changes in nm23 expression during colon carcinogenesis as found in 18 matched pairs of normal and neoplastic human colon tissues. We found that a 0.8-kilo-base nm23 transcript was expressed in all samples of morphologically normal colon mucosa. In 16 of 18 colon neoplasms, nm23 expression was further increased in the neoplastic, compared with the morphologically normal, colon mucosa from the same individual. Expression of nm23 was elevated over normal mucosa in 3 of 3 polyps, in 2 of 3 nonmetastatic cancers, and in 11 of the 12 cancers that were metastatic at the initial presentation. The levels of nm23 expressed were similar in the 12 metastatic colon neoplasms and in the 6 colon neoplasms of lower clinical stage. In addition, nm23 expression was maintained in culture in each of 12 cell lines initiated from human colon neoplasms and did not differ between lines established from neoplasms of high or low metastatic capability. We concluded that nm23 was expressed in normal colon mucosa. Expression of nm23 increased during early stages of colon carcinogenesis and remained increased in metastatic colon cancer. Therefore, in the colon, tissue-specific events dissociate nm23 expression from loss of tumor metastatic competence.

Adenocarcinoma↗

Expression of the ErbA-beta class of thyroid hormone receptors is selectively lost in human colon carcinoma.

Members of the erbA gene family are involved both in control of differentiation and in neoplasia. V-erbA, a retroviral oncogene, blocks avian erythroid differentiation. V-erbA-related transcripts are physiologically expressed in multiple normal tissues. They encode a family of transcriptional regulatory factors, some of which are thyroid hormone receptors. In man, two genes, erbA-alpha and erbA-beta, are transcriptionally active. We examined expression of erbA-related transcripts in normal and neoplastic colon. In normal colon mucosa, as well as in a colon polyp and in a colon polyp cell line, three characteristic erbA-related transcripts were consistently found. One transcript of 6 kb was erbA-beta related. Two transcripts of 2.7 and 5.2 kb were erbA-alpha related. In eight patients' colon carcinomas expression of the 6-kb erbA-beta transcript was absent or markedly diminished when compared with the same patients' noninvolved mucosa. In contrast, expression of the two erbA-alpha transcripts was the same in both colon carcinoma and noninvolved mucosa. No evidence was found of erbA-beta gene deletion in any of the tumors lacking erbA-beta expression. These data suggest that selective loss of normally present erbA-beta gene expression accompanies malignant transformation of the colonic epithelial cell.

Cell Line↗