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Biomedical subjects

G A Curt

Publications and source records attributed to G A Curt.

43 records · Page 3Linked to original sources
PubMed1983

Phase II and pharmacokinetic study of aziridinylbenzoquinone [2,5-diaziridinyl-3,6-bis(carboethoxyamino)-1,4-benzoquinone, diaziquone, NSC 182986] in high-grade gliomas.

2,5-Diaziridinyl-3,6-bis(carboethoxyamino)-1,4-benzoquinone (AZQ; Diaziquone, NSC 182986) is a rationally designed antitumor drug possessing sufficient lipid solubility to allow penetration into the central nervous system. Thirty-one patients with high-grade glioma and progressive disease following radiation, with or without previous chemotherapy, have been treated with 144 cycles of drug, consisting of 20 mg/sq m given as an i.v. infusion on Days 1 and 8 of a 28-day cycle. Responses were measured by serial computer tomography scanning. Of the 28 evaluable patients, 6 (21%) had limited improvement (10 to 40% reduction in tumor size) on computer tomography scan, 10 (36%) had disease stabilization, and 12 (43%) had progressive disease. The drug was well tolerated clinically, with little acute toxicity. The major toxicity was myelosuppression, which appeared cumulative, using this dose regimen. AZQ was measurable in both tumor tissue and tumor cyst fluid in patients on therapy. Plasma samples taken during the period of infusion confirm that 50% or more of the total AZQ exposure occurs during the infusion period. AZQ behaves as intended by design and demonstrates activity in this poor-prognosis group of patients.

Adult↗
PubMed1982

Liposomally trapped AraCTP to overcome AraC resistance in a murine lymphoma in vitro.

Two cell lines, one sensitive and one resistant to the cytotoxic effects of cytosine arabinoside (AraC) were studied in vitro as a drug-resistance model. The sensitivity of these cell lines, to the effects of free and liposomally trapped AraC and AraCTP as well as empty liposomes alone and mixed with free drug, was studied. This was done by following the inhibition of [3H]-dT incorporation into cellular DNA during exposure to the various drugs and liposomes. Some of the liposomal-lipid compositions inhibited [3H]-dT incorporation at very low concentrations, which made them unsuitable for further study. Liposomes composed of a 7:2:1 molar ratio of phosphatidylcholine:cholesterol:phosphatidic acid were selected as a suitable non-inhibitory carrier. Sensitivity of the two cell lines to free AraC differed by 3 logs, when compared in the [3H]-dT-incorporation assay. The resistant cell line was studied further, and was found to be up to 2 logs more sensitive to AraCTP when given in liposomes than to either the free drug alone or mixed with empty liposomes. It appears from these studies that liposomes are able to help overcome drug resistance in this cell line in vitro.

Animals↗
PubMedDate not supplied

Immunoaugmentative therapy. A primer on the perils of unproved treatments.

Immunoaugmentative therapy is an unproved cancer treatment that until recently was offered to patients by zoologist Lawrence Burton, PhD, at a facility in Freeport, Bahamas. The therapy consists of serum measurements of certain "immune deficiencies" and purportedly restores immune function by injection of products variously derived from tumor tissue and blood from individuals with cancer and healthy volunteers. Immunoaugmentative therapy represents a potentially serious public health risk, since it is capable of transmitting hepatitis B and the presumed etiologic agent for the acquired immunodeficiency syndrome. Physicians and health officials who learn of patients receiving this therapy are advised that its efficacy remains unproved and that the risk of receiving contaminated blood products is considerable.

Abscess↗
PubMedDate not supplied

Reversible acute pulmonary edema due to uncontrolled hyperglycemia in diabetic individuals with renal failure.

On eight separate occasions, four functionally anephric diabetic patients (on maintenance hemodialysis) experienced episodes of severe hyperglycemia with acute interstitial and alveolar pulmonary edema demonstrated clinically and by chest x-ray without electrocardiographic or enzymatic evidence of an acute myocardial lesion. Three patients had normal stress 201T1 scanning. The fourth patient, who experienced three such episodes, had normal coronary angiograms and only a mild elevation of the left-ventricular end-diastolic pressure. Clinical and chest x-ray improvement were immediate following insulin therapy and control of hyperglycemia, without phlebotomy or dialysis. Since these episodes were observed during a 1-yr period, this syndrome may be more common than suspected. It is concluded that in functionally anephric diabetic individuals: (1) pulmonary edema can be precipitated by uncontrolled diabetes; (2) endogenous fluid shifts may contribute to the cause of acute pulmonary edema; (3) clinical and radiologic improvement can be achieved with adequate insulin therapy; and (4) blood glucose levels should be monitored and controlled in diabetic patients with renal failure.

Acute Disease↗