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T Lichtor

Publications and source records attributed to T Lichtor.

43 records · Page 3Linked to original sources
PubMed1986

Respiratory patterns in human brain tumors.

It has been recognized for some time that malignant cells have a diminished respiratory rate coupled with an excessive rate of aerobic glycolysis. Subsequent studies indicated, however, that this pattern was neither unique to malignant tumors nor an essential characteristic of all varieties of cancer. In attempting to synthesize the data on oxygen consumption of human brain tumors, it is difficult to relate activity to malignancy, and the integrity of the mitochondrial electron transport chain has not been systematically examined. In this study, oxygen consumption was measured using a whole cell mixture and subsequently with isolated mitochondria prepared by routine differential centrifugation from a variety of human brain tumors. It is clear from these data that low oxidative respiration is not uniquely characteristic of malignant tumors, but that a number of benign tumors such as meningiomas and pituitary adenomas display very low levels of oxygen consumption. Many of these tumors have normal respiration, with isolated mitochondria using substrates that enter at different points in the electron transport pathway. However, several of the tumors in this series showed defects in respiration at various points in the electron transport pathway. These data suggest that both benign and malignant brain tumors have depressed respiratory capacities secondary to either a decrease in mitochondria per cell or defects in electron transport activities.

Adenoma↗
PubMed1985

Severe thrombocytopenia associated with phenytoin and cimetidine therapy.

A 67-year-old man developed a sudden onset of severe isolated thrombocytopenia (platelet count, 1000/mm3) after 10 days of phenytoin administration as a prophylactic measure prior to craniotomy. The patient had also been taking cimetidine for 2 months prior to admission. No other hematological complications were noted, and an extensive hematologic investigation was otherwise unremarkable. Rapid resolution of the thrombocytopenia upon discontinuation of phenytoin and cimetidine strongly suggests a drug-induced adverse reaction.

Aged↗
PubMed1983

Percutaneous microcompression of the trigeminal ganglion for trigeminal neuralgia.

Fifty patients were treated for trigeminal neuralgia by percutaneous microcompression of the trigeminal ganglion. A No. 4 Fogarty balloon catheter was inserted under brief general anesthesia, using biplane fluoroscopy. This procedure is essentially a percutaneous simplication of the older Taarnhøj-Sheldon-Pudenz operation. The follow-up period ranged from 0.5 to 4.5 years. Pain recurred in 12% of cases during that time, and it is anticipated that within 5 years the recurrence rate will reach 20%, which is approximately the same rate as for the alternative established procedures. The advantages of this technique are freedom from discomfort on the part of the patient, a remarkable ease of performance on the part of the operator, absence of associated mortality, and a minimal morbidity rate.

Adolescent↗
PubMed1979

Cytoplasmically inherited respiratory deficiency of a mouse fibroblast line which is resistant to rutamycin.

Mouse fibroblasts resistant to the drug rutamycin were isolated and found also to be respiratory deficient. These cells produce large amounts of lactic acid, and oxygen consumption data indicate that the first complex of the electron transport chain, NADH-coenzyme Q reductase, is defective. Levels of rotenone-sensitive NADH-cytochrome c reductase and pyruvate decarboxylase of the pyruvate dehydrogenase complex are markedly depressed in the mutant cells. Other components of the electron transport chain appear to be fully functional. The mutant cells were enucleated and fused with another cell line, and the resulting cybrid demonstrated a similar pattern of respiratory deficiency as did the original mutant. These results indicate that this defect in respiration is a cytoplasmically inherited characteristic in this cell line.

Animals↗
PubMed1978

Cytoplasmic inheritance of rutamycin resistance in mouse fibroblasts.

Mouse fibroblasts resistant to the drug rutamycin were isolated by selectively introducing BrdUrd into the mitochondrial genome of a line of mouse fibroblasts (clone 1 D) lacking a cytoplasmic thymidine kinase enzyme. The ATPase (ATP phosphohydrolase; EC 3.6.1.3) activity of mitochondria isolated from these cells was resistant to rutamycin. The rutamycin-resistant mutants were enucleated with cytochalasin B and fused with mouse A 9 cells resistant to 8-azaguanine and sensitive to rutamycin. Cytoplasmic hybrids, or cybrids, were selected as cells resistant to rutamycin and 8-azaguanine, and appeared at a high frequency. Other fusions between rutamycin-resistant nucleated cells and A 9 produced colonies at a much lower frequency. Finally, fusions between enucleated clone 1 D cells and A 9 cells produced no rutamycin-resistant colonies. These results indicate that rutamycin resistance is a cytoplasmically inherited characteristic in this cell line.

Adenosine Triphosphatases↗
PubMedDate not supplied

In vivo establishment of T98G human glioblastoma.

Human derived T98G glioblastoma has long been utilized as an in vitro model for epidermal growth factor receptor (EGFR)-mediated growth regulation. Recently, T98G has been employed to develop new types of therapy directed at limiting EGFR expression such as by administration of antisense oligonucleotides directed against EGFR encoding mRNA. A major limitation to extending this model for in vivo application is that T98G implanted s.c. or intracerebrally has been reported not to grow in nude mice. In an effort to extend this model to permit in vivo studies, we evaluated the use of Matrigel and orthotopic (intracranial) implantation techniques. When equal volumes of Matrigel were mixed with T98G cell suspensions, tumors developed at both flank and orthotopic locations. Four groups of nude mice were inoculated into the flanks with either 10(5), 10(6), 4 x 10(6) or 10(7) T98G cells in a 150 microliters total volume with Matrigel. In 1/5, 3/5, 1/5 and 1/3 mice receiving 10(5), 10(6), 4 x 10(6) and 10(7) cells, respectively, tumors developed 11, 15, 15 and 15 weeks, respectively, following inoculation. Out of 4 mice inoculated orthotopically (intracranially into the frontal lobe) with only 4 x 10(4) cells and Matrigel, 2 developed tumors. However, all mice (4/4) inoculated orthotopically with 4 x 10(5) cells in a 10 microliters total volume with Matrigel developed tumors. Two were identified histologically following a scheduled sacrifice at 36 and 60 days and two more at 103 and 118 days after sacrifice following abnormal behavior. The best tumor establishment efficacy combined orthotopic implantation of 4 x 10(5) T98G cells with Matrigel. These techniques permit the use of T98G glioblastoma as an in vivo model for new forms of therapy.

Animals↗