[Technical note on transnasal canthopexy].
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Biomedical subjects
Publications and source records attributed to G Peri.
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Macrophages were isolated from 22 human ascitic ovarian epithelial tumors and their growth-inhibitory capacity was tested using as targets the following in vitro tumor cell lines: murine TLX9 lymphoma and FS6 sarcoma; human myeloid K562 leukemia and human E cell line derived from an ovarian carcinoma. Macrophage preparations were heterogeneous in their interaction with tumor target cells, and assay conditions, such as the type of target cell, incubation time, and attacker to target cell (A:T) ratio critically affected the evaluation of the cytotoxic potential of tumor-associated macrophages. At an A:T ratio of 7:1 no cytostatic activity on TLX9 and K562 cells was ever observed, but in the presence of specific antibody 8 out of 12 macrophage preparations tested showed significant antibody-dependent cytotoxicity on TLX9 lymphoma cells. Macrophage preparations from two patients significantly inhibited growth of the FS6 sarcoma and a cytostatic activity on E cells was observed in five additional patients. Significant stimulation of the proliferative capacity of at least one of the target cell lines was observed in 11 subjects at an A:T ratio of 7:1. In 12 patients, macrophage cytostatic activity on E cells was also tested at an A:T ratio of 35:1; eight out of 12 preparations showed significant cytotoxicity under these conditions. When the same subject was repeatedly tested at short intervals the same pattern of inhibition or stimulation of tumor growth was observed.
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A case of symptomatic esophageal achalasia due to a slowly growing neoplastic infiltration of the esophageal wall by a mammary indifferentiated carcinoma operated ten years before is presented. At admission, the clinical history and the endoscopic appearance of the esophageal lumen and mucosa led to the diagnosis of idiopathic achalasia, while the esophageal manometry showed a rather long high pressure zone (6--8 cm), which did not relax with deglutition. Barium study confirmed the length of the achalasic tract. Only thoracotomy permitted a correct diagnosis. On the basis of this case achalasia is thus considered as a syndrome which can be either idiopathic or secondary to Trypanosoma cruzi, high troncular vagotomy, benign or malignant tumor infiltrating the esophageal wall. The difficult diagnosis of some cases from the clinical point of view is underlined. Stress is laid on the necessity that all findings (history, radiology, endoscopy, manometry) be carefully evaluated to reach a preoperative diagnosis.
The storage and release of acetylcholine and choline were studied in the isolated superior cervical ganglion of the rat by a radioenzymic method. The acetylcholine and choline contents were 202.2 +/- 5.1 and 624.7 +/- 20.2 pmole/ganglion, respectively. The transmitter tissue store was unaffected during 1 h of superfusion in choline--Krebs solution, while a 20% decrease was exhibited after 2 h and then remained approximately stable. Conversely, choline content declined to 50% within 1 h and further to 37% of the original level by 4 h. About 24% of the choline assayed in the intact preparation is located in the connective sheath. Preganglionic nerve stimulation at 10--20/sec or potassium stimulation (40 mM KCl) invariably decreased the transmitter tissue stores by 25--45%; such a depletion is independent of the presence or absence of external choline. By contrast, the presence of choline proved to be a prerequisite for the efficient release of acetylcholine from eserinized ganglia during continuous 10/sex stimulation. A drastic depression in the acetylcholine release is described which is related to the time of preincubation of the ganglia with eserine prior to stimulation. Indeed, a 30 min exposure to eserine, compared with a 5 min period, resulted in a 4-fold decrease in the steady output rate. Under optimal conditions, the initial volley output at 10/sec was 1.3 X 10(-4) of the releasable transmitter pool and 1.9 X 10(-4) during the steady-state output. These results are discussed in the light of the electrophysiological knowledge of the quantal release process at the ganglionic synapse.
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Spleen natural killer (NK) activity was investigated in cells from C57BL/6J mice treated with various chemotherapeutic agents; 51Cr-labeled YAC-1 lymphoma cells were used as targets. Treatment with azathioprine (a single injection of 100-400 mg/kg ip or 5 daily doses of 80 mg/kg lp) and cyclophosphamide (a single injection of 50--200 mg/kg ip or 5 daily doses of 25 mg/kg ip) resulted in a marked dose-dependent inhibition of NK activity 2 days later. NK cells recovered rapidly from drug-induced suppression; by 7 days after drug treatment, no difference from control values was observed. Dimethyltriazenoimidazole carboxamide (20--200 mg/kg ip) and adriamycin (10--15 mg/kg iv) did not impair natural cytotoxicity per unit number of lymphoid cells, daunomycin (10 mg/kg iv) caused borderline impairment of NK acitivity, and N-trifluoroacetyl-adriamycin-14-valerate (80 mg/kg iv) markedly suppressed natural cytotoxicity. These results are discussed in light of the known effects of these agents on T-cells, B-cells, and K-cells and on hematopoietic histocompatibility-type reactions.
The authors studied salivary pH at different sites in 172 patients receiving psychotropic therapy in hospital. For statistical purposes, the study was limited to individuals receiving a "moderate" dose of: --a benzodiazepine derivative --a neuroleptic and benzodiazepine --antidepressant, neuroleptic and benzodiazepine. Regardless of the type of psychotropic therapy and of the site of measurement, acidification of salivary pH which was statistically significant in comparison with values found in healthy subjects was noted. This acidification was particularly marked with regard to "lingual" pH. In addition, regardless of the site of measurement, a higher degree of acidification of salivary pH was seen in individuals receiving a combination of psychotropic agents. This acidification was particularly striking with regard to salivary pH in patients given a combination of antidepressant, neuroleptic and a benzodiazepine derivative. The cause of this acidification is not definitely known. A number of hypotheses may be put forward: decrease in salivary volume (Laudenbach, 6, and Vermeil, 7), excretion of acid metabolites by the salivary glands, effect of psychotropic agents upon the action itself of the salivary glands.
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The authors describe an electrochemical technique for the measurement of salivary pH by contact. They present a critical study fo 167 cases. The values obtained are characteristic in terms of age and the site of determination (dorsal surface of the tongue, orifice of Wharton's or Stenon's ducts).