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Biomedical subjects

V A Levin

Publications and source records attributed to V A Levin.

At least 217 records · Page 12Linked to original sources
PubMed1976

Computed tomography in the evaluation of malignant glioma before and after therapy.

Sixty-three patients with malignant glioma undergoing chemotherapy and radiotherapy were evaluated with electroencephalography, 99mTc-DTPA imaging, and computed tomography (CT). Tumor size, central lucency, contrast enhancement, surrounding edema, and ventricular size were assessed. CT findings were found to be reliable and often predicted the clinical course. Tumor size, central lucency, and contrast enhancement increased in patients with clinical deterioration and decreased in those with improvement. The CT scan also provided additional information of value in adjunctive therapy, such as the presence of cysts or ventricular obstruction. In general, CT gave a more complete profile of tumor characteristics than other diagnostic modalities.

Antineoplastic Agents↗
PubMed1976

The relationship of polyamines in cerebrospinal fluid to the presence of central nervous system tumors.

Cerebrospinal fluid (CSF) polyamine concentrations were assayed in patients with and without central nervous system tumors, using a high-pressure liquid chromatographic technique. Definite elevations were found in the CFS polyamine concentrations of patients with untreated malignant central nervous system tumors when compared with those concentrations observed in the CSF of patients without neoplasia. Patients undergoing successful tumor therapy for malignant central nervous system tumors showed CSF polyamine concentrations that closely approximated the concentrations found in the CSF of patients without tumor.

Adenoma↗
PubMed1976

BCNU (NSC-409962) and procarbazine (NSC-77213) treatment for malignant brain tumors.

Sixty-five patients with malignant brain tumors were treated with a combination of BCNU (100 mg/m2 qd X 1) and procarbazine (100 mg/m2 qd X 14); the cycle was repeated in 1 month and then on a 6-week schedule with procarbazine being given for 21 days. Forty-five patients had malignant gliomas (glioblastoma multiforme, anaplastic astrocytoma, malignant glioma, or gemistocytic astrocytoma) and were evaluated as a group. All patients had either shown evidence of tumor regrowth after previous surgery and/or radiotherapy, or had deep unbiopsied tumors presumed to be malignant gliomas. Of these 45 patients, 13 of 45 (30%) were judged to be unequivocal responders and an additional eight of 45 (17%) were designated as probable responders. The median duration of clinical response was 34 weeks for responders and 20 weeks for probable responders. The combination of BCNU and procarbazine, therefore, was somewhat inferior to a previous combination of procarbazine, CCNU, and vincristine.

Astrocytoma↗
PubMed1976

Pharmacological principles of brain tumor chemotherapy.

In conclusion, I would like to reiterate the belief that curative therapy will require both CCNS cytocidal drugs and appropriately timed CCS agents. Lipophilic drugs will remain our most valuable drugs unless new agents appear that have very high therapeutic indices and can be given by prolonged or intermittent infusion. The lipophilic drugs have the advantages of greater penetrability of tumor cells and preferential partitioning in lipid membranes and cellular structures. Potentially, combinations of differently acting CCNS agents should maximize DNA damage and prevent DNA repair. Infusions of CCS drugs for 3 to 4 days, following an interval of 6 to 14 days after the administration of CCNS agents, should result in maximum damage to proliferating tumor cells, preventing cell division for 1 week and contributing another 1 log cell kill to the therapy.

Animals↗
PubMed1976

Intracarotid BCNU (NSC-409962): a toxicity study in six rhesus monkeys.

Intracarotid artery (ica) BCNU was given at doses of 1-20 mg/kg/week for 4 weeks in six rhesus monkeys. Vascular, neurologic, and ophthalmic toxic effects were minor. The monkey receiving a dose of 15 mg/kg had transient left hemiparesis and slowing in her electroencephalogram which cleared 1 week after the third ica infusion of BCNU. At autopsy no vascular, neural, or ophthalmic lesions were found. At doses of 20 mg/kg for two injections, one monkey developed fatty metamorphosis of the liver and Alzheimer II glia in the brain, yet did not develop arteriolitis, corneal damage, or neurologic deficit. It is concluded that reasonable doses of BCNU (less than the systemic maximum tolerated dose) should be well tolerated by ica administration in man.

Animals↗
PubMed1975

Permeability characteristics of brain adjacent to tumors in rats.

The brain immediately surrounding 9L sarcoma and Walker 256 carcinosarcoma was evaluated, using radioactive water, albumin, red blood cells, urea, and sodium to quantitate isotopic exchange and permeability in the brain adjacent to tumor (BAT), normal brain, and, to a lesser extent, tumor. Exchange between blood and BAT for 14C-urea and 22Na averaged 53% of that for comparable regions of normal brain. This reduction in exchange is not explainable by differences in capillary surface area for transcapillary exchange in the BAT. This reduction in capillary permeability in the BAT could be detrimental to the delivery of watersoluble and rapidly binding drugs.

Animals↗
PubMed1975

Factors influencing the survival of rat brain tumor cells after in vitro treatment with 1,3-bis(2-chloroethyl)-1-nitrosourea.

The shape of dose-response curves obtained for asynchronous, exponentially growing 9L rat brain tumor cells treated in vitro with 1,3-bis(2-chloroethyl)-1-nitrosourea changed as a function of the drug exposure time. For short treatment times (less than 1 hr), the dose-response curves had shoulders, indicating that the cells may accumulate sublethal damage; however, after longer treatments (greater than 1 hr), little if any shoulder was apparent. The slope of the exponential portion of the dose-response curve increased progressively with treatment periods from 15 min to 2 hr. Longer exposure times (up to 24 hr) produced no further changes in the cell-kill kinetics. Cell survival was directly related to the BCNU exposure dose [o integral t Co(t)dt] and to the amount of bound BCNU per cell. Extrapolation of the curves for these two variables indicated that some BCNU damage accumulates before death occurs. The amount of serum and cell products available in the medium to bind BCNU affected the level of survival; however, there was no evidence that extracellular spontaneous breakdown products or chemical transformation products were involved in the cell-killing mechanism.

Animals↗
PubMed1971

Cerebrospinal fluid production by the choroid plexus and brain.

The production of cerebrospinal fluid and the transport of (24)Na from the blood to the cerebrospinal fluid were studied simultaneously in normal and choroid plexectomized rhesus monkeys. Choroid plexectomy reduced the production of cerebrospinal fluid by an average of 33 to 40 percent and the rate of appearance of (24)Na in the cerebrospinal fluid and its final concentration were proportionately reduced. In both normal and plexectomized animals, (24)Na levels were found to be markedly greater in the gray matter surrounding the ventricles and in the gray matter bordering the subarachnoid space. That sodium exchanges in these two general areas of the brain may be linked to the formation of the cerebrospinal fluid is discussed here.

Animals↗