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Biomedical subjects

T S Herman

Publications and source records attributed to T S Herman.

At least 109 records · Page 6Linked to original sources
PubMed1985

Late relapse among patients treated for Hodgkin's disease.

Of 1360 consecutive patients with Hodgkin's disease treated at Stanford University, 1312 patients (96%) had complete remission, but 424 patients had a relapse. Fifty-five patients had relapses 36 months or more after completion of therapy. The actuarial risk of relapse in patients disease-free 3 years after therapy was 12.9%. The occurrence of late relapse was significantly related to stage I disease and nodular sclerosis histologic subtype. Late relapse was detected in 88% of patients by history, physical findings, or chest radiographs. Most patients with stage III and IV disease had late relapses in previously irradiated nodes or extranodally, but patients with stage I and II disease had late relapses primarily in unirradiated nodes. Disease-free survival after salvage therapy for late relapse was similar to that seen after treatment of earlier relapse. Prolonged surveillance of patients for late relapse is necessary after treatment of patients with Hodgkin's disease.

Adolescent↗
PubMed1985

Antiemetic efficacy of levonantradol compared to delta-9-tetrahydrocannabinol for chemotherapy-induced nausea and vomiting.

The antiemetic efficacy of im levonantradol, a synthetic cannabinoid, given at a dose of 1 mg every 4 hours, was compared to oral delta-9-tetrahydrocannabinol (THC) given at a dose of 15 mg every 4 hours in a double-blind crossover study. Twenty-six patients receiving emetogenic cancer chemotherapy were evaluated. For each drug, 28% of treated patients had no nausea. The median number of emetic episodes with levonantradol was 2.0 versus 3.0 for THC (P = 0.06). Side effects occurred in 91.7% and 97.3% of levonantradol and THC patients, respectively, with drowsiness and dizziness most commonly seen. Side effects were generally well-tolerated, with only 13.9% of levonantradol and 21.6% of THC patients discontinuing treatment because of side effects. Levonantradol appears to be at least as effective an antiemetic as THC and is the only cannabinoid available for parenteral use.

Adult↗
PubMed1984

Effect of step-down heating on the cytotoxicity of adriamycin, bleomycin, and cis-diamminedichloroplatinum.

The cytotoxicity of a number of anticancer drugs can be potentiated by mild hyperthermia. Since the cytotoxicity of low-hyperthermic temperatures in the range of 39-43 degrees can be potentiated by using a step-down heating (SDH) sequence (short times at greater than or equal to 45 degrees followed by longer times at lower temperatures), we investigated the combined effects of SDH (specifically 45 degrees, 10 min, followed by time at 41.5 degrees) and three chemotherapeutic drugs known to be more toxic at elevated temperatures. In agreement with previous observations with Chinese hamster cells, we found that cultured RIF tumor cells showed an increased rate of cell killing at 41.5 degrees when the low-temperature heat treatment was preceded by an acute heat shock of 10 min, 45 degrees. Similarly, RIF cells showed enhanced cytotoxicity of Adriamycin, bleomycin, and cisplatin at 41.5 degrees over that at 37 degrees, as reported previously for hamster cells. When SDH and drug exposures were combined, the rate of cell killing was greater than that observed with the drugs at a constant 41.5 degrees. SDH alone reduced the Do on the 41.5 degrees survival curve from approximately 500 min to 100 min after 10 min at 45 degrees. Adriamycin cytotoxicity (0.3 microgram/ml) at 41.5 degrees was characterized by a Do of approximately 160 min for treatment times of 1 to 4 hr; with SDH, this was reduced to 52 min. Similarly, bleomycin (5 micrograms/ml) and cisplatin (0.5 microgram/ml) showed a decrease in Do by factors of 1.4 (68 to 48 min) and 2 (25.2 to 13.5 min), respectively, with the SDH sequence when compared with drug toxicity at 41.5 degrees alone. However, the sensitization to cisplatin was the same when 10 min at 45 degrees was followed by drug exposure at 37 degrees, or at 41.5 degrees. The results indicate that Adriamycin and bleomycin, but not cisplatin, cytotoxicity was increased by SDH over that achievable with 41.5 degrees alone. Possible clinical implications are discussed briefly.

Animals↗
PubMed1984

Cellular ATP content of heated Chinese hamster ovary cells.

Hyperthermia at either 41.5 or 45 degrees C with variable heating times to reduce cell survival up to three orders of magnitude did not decrease significantly cellular ATP content when measured either immediately or up to 7 hr after a heat treatment. Similarly, cellular ATP content was not significantly reduced with step-down heating, precooling prior to hyperthermia, or thermotolerance induction. The data suggest that heat-induced depletion of intracellular ATP content is not a critical factor in the thermal death of cells heated under normal culture conditions.

Adenosine Triphosphate↗
PubMed1984

Exposure to pretreatment hypothermia as a determinant of heat killing.

When Chinese hamster ovary (CHO) cells were exposed to 22 degrees C for 2 hr prior to 42.4 degrees C hyperthermia, neither the shoulder region of the survival curve nor the characteristic development of thermotolerance after 3-4 hr of heating were observed. Absolute cell survival after 4 hr at 42.4 degrees C was decreased by a factor of between 10 and 100 (depending on the rate of heating of nonprecooled controls). Conditioning at 30 degrees C for 2 hr, 26 degrees C for 2 hr, or 22 degrees C for 20 min followed by heating to 42.4 degrees C over 30 min did not result in sensitization. Prolonged (16 hr) conditioning at 30 degrees C, however, increased the cytotoxicity of immediate exposure to 41.4 or 45 degrees C with maximum sensitization to 45 degrees C occurring after 6 hr at 30 degrees C. Both 3- and 18-hr pretreatments at 30 degrees C similarly increased the cytotoxicity of 45-41.5 degrees C step-down heating (D0 = 28 min in precooled versus 40 min in nonprecooled cells).

Animals↗
PubMed1983

Effects of urine pretreatment on calcium oxalate crystallization inhibition potentials.

Activated carbon and calcium oxalate solids have been used as adsorbents to remove crystallization inhibiting species from centrifuged and dialyzed normal urines. The urine supernatants, following adsorption treatments, have been examined for their calcium oxalate monohydrate crystallization inhibitory potentials by means of a constant composition potentiostatic seeded growth method. The supersaturation of the reactant solution was maintained constant during the crystallization process by the potentiometrically monitored addition of solutions containing crystal lattice ions controlled by a specific calcium ion selective electrode. The experimental results indicate that normal urine contains a number of inhibiting species of variable molecular weight and adsorbability. In addition, preliminary results indicate that substances present in normal urine interfere substantially with the adsorption of crystallization inhibiting species by calcium oxalate monohydrate crystal surfaces. Both charcoal and CaOx adsorbents have been successfully used to completely remove a synthetic, model urinary crystallization inhibitor, ethylene-diamine-tetramethylene-phosphonic acid, ENTMP, from relatively concentrated solutions in 0.15 M NaCl.

Adsorption↗
PubMed1983

Temperature dependence of adriamycin, cis-diamminedichloroplatinum, bleomycin, and 1,3-bis(2-chloroethyl)-1-nitrosourea cytotoxicity in vitro.

We have examined the effect of mildly hypothermic temperatures (22-32 degrees) on the cytotoxicity of Adriamycin, cis-diamminedichloroplatinum, bleomycin, and 1,3-bis(2-chloroethyl)-1-nitrosourea in Chinese hamster ovary cells in vitro. Over a dose range of Adriamycin, cell killing at 30 degrees was reduced by 1 to 3 orders of magnitude as compared to that at 37 degrees. cis-Diamminedichloroplatinum was also less cytotoxic at 30 degrees (0.4 to 1.2 orders of magnitude) than at 37 degrees. For bleomycin and 1,3-bis(2-chloroethyl)-1-nitrosourea, the reduction in cytotoxicity at 30 degrees in comparison to 37 degrees was less marked. All drugs were more toxic at 42.4-43 degrees than at 37 degrees. Precooling of cells for 2 hr at 30 degrees did not alter the cell killing caused by these drugs at elevated temperatures. These results suggest that a more selective anticancer effect might result if some chemotherapeutic drugs were administered during whole-body hypothermia and regional-local hyperthermia of tumor masses.

Animals↗
PubMed1983

The personal microcomputer: its operation and application in the laboratory.

Several laboratory vendors have begun marketing quality control programs for use on personal microcomputers. To appreciate fully its utility, the first-time microcomputer user must have a basic understanding of its operation, application and limitations. This article presents an introduction to microcomputer operation for the computer novice. Laboratory applications and criteria for selecting additional application programs are discussed.

Computers↗
PubMed1983

Effect of temperature on the cytotoxicity of vindesine, amsacrine, and mitoxantrone.

The effect of elevated temperature on the cytotoxicity of three new anticancer drugs (vindesine, mitoxantrone, and amsacrine [AMSA]) was tested in Chinese hamster ovary cells in vitro. Three distinct patterns of interaction with hyperthermia were observed. Vindesine, tested at 37 degrees C, produced a 50% cell kill when concentrations of greater than or equal to 1.0 micrograms/ml (up to 3.0 micrograms/ml) for 1 hour were used. At 42.4 degrees C, concentrations greater than 1.0 micrograms/ml for 1 hour caused a 60% cell kill (an additive cytotoxic effect). Mitoxantrone produced concentration-dependent lethality at 37 degrees C (89% cell kill after 0.25 micrograms/ml for 1 hour; 99% cell kill after 1.0 micrograms/ml for 1 hour). Exposure to mitoxantrone at 42.4 degrees C resulted in synergistic cytotoxicity (97% cell kill after 0.25 micrograms/ml for 1 hour; 99.98% cell kill after 1.0 micrograms/ml for 1 hour). In contrast, treatment with AMSA at 42.4 degrees C inhibited cytotoxicity (99.98% cell kill after 5 micrograms/ml for 1 hour at 37 degrees C; 91% cell kill after 5 micrograms/ml for 1 hour at 42.4 degrees C). AMSA was not inactivated after being heated at 42.4 degrees C for 1 hour prior to treatment of cells at 37 degrees C.

Aminoacridines↗
PubMed1983

Polyamines and polyamine biosynthesis in cells exposed to hyperthermia.

The issue of how polyamines act to sensitize cultured cells to the lethal effects of hyperthermia was investigated using Chinese hamster cells which were induced to express thermotolerance. Intracellular levels of these naturally occurring polycations were manipulated in certain situations by treating whole cells with methylglyoxal bis-(guanylhydrazone), an inhibitor of the S-adenosyl-L-methionine decarboxylases. Exogenous spermine as low as 100 microM in the culture media dramatically sensitized cells expressing thermotolerance to the lethal effects of subsequent 42 degrees C exposures. When thermotolerance was differentially induced in cultures exposed to 42.4 degrees C by varying the rate of heating from 37 to 42.4 degrees C, the most resistant cells had the highest levels of intracellular spermidine and spermine. This finding was explainable in part by the observation that the putrescine-dependent S-adenosyl-L-methionine decarboxylase activity was minimally affected in cells expressing the greatest degree of thermotolerance. When this enzyme activity was inhibited by drug, lowered intracellular polyamine levels did not correspond with subsequent survival responses to heat. Interestingly, cultures treated with methylglyoxal bis-(guanylhydrazone) 24 hr previous to heat exposure showed a reduced capacity to express rate of heating-induced thermotolerance. Together, these results demonstrate that the polyamines, especially spermidine and spermine, enhance hyperthermia-induced cell killing by some mechanism involving the plasma membrane. Further, our data suggest that methylglyoxal bis-(guanylhydrazone) can act to affect thermal responses by a mechanism(s) other than modification of intracellular polyamine levels.

Adenosylmethionine Decarboxylase↗
PubMed1982

Treatment of patients with refractory myelogenous leukemia with BCOMM[1,3-bis-chloro(2-chloroethyl)-1-nitrosourea (BCNU), oncovin (vincristine), cyclophosphamide, high-dose methotrexate and methyl-glyoxal bis-guanylhydrazone (MGBG)].

Ten patients with AML refractory to anthracyclines and cytosine arabinoside were treated with vincristine 1.4 mg/m2 and methotrexate (MTX) 2.5 gm/m2 by intravenous (IV) bolus on day 1 [citrovorum factor (CF) rescue began 24 h later], BCNU 80 mg/m2, and cyclophosphamide 900 mg/m2 IV 36 h after MTX and MGBG 300 mg/m2 IV over 1-2 h on days 3, 4, and 5. Bone marrow aplasia was achieved in all patients by day 12. Five patients (50%) achieved complete remission (CR). Two patients died of sepsis during induction. The median duration of remission was 24 weeks (range 8-38). Maintenance therapy was employed in three patients (high-dose MTX-CF in 2 and MGBG plus BCNU in 1), but did not appear to significantly increase the duration of remission. Nausea and vomiting occurred in eight patients. Five patients developed moderate stomatitis and one developed a moderately severe cutaneous reaction. This pilot experience demonstrates that patients with refractory AML can achieve CR after aggressive treatment with so-called second-line drugs. and may indicate that collateral sensitivity to MTX exists in cells which have become resistant to anthracyclines, a situation we previously described in an experimental cell line.

Adolescent↗
PubMed1982

Hypertension in the elderly.

Successful control of blood pressure through drug therapy can reduce morbidity and mortality in the elderly population. However, age-related factors also make this group prone to adverse side effects. A cautious approach is therefore recommended in the effort to achieve ideal control of blood pressure.

Adrenergic beta-Antagonists↗
PubMed1982

Effect of heating on lethality due to hyperthermia and selected chemotherapeutic drugs.

Because the rate of heating alters various cellular events associated with exposure to hyperthermia (including the rate of cell death), effect of this parameter on the cytotoxic interaction between selected anticancer drugs and hyperthermia was studied. The drugs cisplatin, 1,3-bis(2-chloroethyl)-1-nitrosourea, and adriamycin at 42.4 degrees C and bleomycin and methotrexate at 43 degrees C were tested in Chinese hamster ovary (CHO) cells in vitro. Heating times ranged from less than 3 minutes (immediate exposure) to 3 hours. For all drugs tested, synergistic cytotoxicity was not significantly altered by heating to peak temperature over 30 minutes as compared with immediate exposure. When heating to peak temperatures was prolonged to 3 hours, however, cell killing was markedly reduced, although significant sensitization to the drug remained. This was true despite the fact that, in CHO cells, heating to 42.4 degrees C over 3 hours produced no cell killing for up to 6 hours at that temperature. These results suggested that the mechanism(s) responsible for induced thermotolerance are probably different from those that cause cellular resistance to the cytotoxic effects of the drugs tested. These results may also partially explain the relative lack of clinical success with whole-body hyperthermia and chemotherapeutic drugs an anticancer treatment, because heating to therapeutic temperatures often requires 2-3 hours.

Animals↗
PubMed1982

Review of the current status of whole-body hyperthermia administered by water circulation techniques.

Since the mid 1970's, whole-body hyperthermia (WBH) has been actively investigated for the treatment of patients with cancer in the United States. Two basic techniques are currently used; one involves transcutaneous transfer of heat by circulation of heated water, and, in the other, extracorporeally circulated blood is heated. Studies which have used the water circulation method are compared as to protocol design, toxicities encountered, and responses observed with and without concomitant chemotherapy. In vitro data indicating that faster rates of heating are associated with greater cytotoxicity due to hyperthermia alone or with several anticancer drugs are discussed in relationship to the design of future techniques for administration of WBH.

Animals↗
PubMed1981

Adriamycin/cis-platinum/cyclophosphamide combination chemotherapy for advanced carcinoma of the parotid gland.

Five patients were treated with a combination of Adriamycin/cis-platinum/cyclophosphamide for far-advanced and/or recurrent cancer of the salivary gland. Adriamycin, 40 mg/m2, and cis-platinum, 50 mg/m2, were given on day 1; cyclophosphamide, 200 mg/m2 daily for four days, was given by mouth on the third to sixty day of each monthly therapy course. Two patients achieved a complete remission, each lasting five months, and the three others had partial remissions from one to seven months (median six months) in duration. Therapy was well tolerated. Severe nausea and vomiting occurred on the first day of therapy but was self-limited. There was only mild to moderate leukopenia, no significant thrombocytopenia or elevations of serum creatinine, and no evidence of dose-limiting peripheral neuropathy. Adriamycin/cis-platinum/cyclophosphamide chemotherapy appears to be effective in the treatment of advanced parotid gland cancers.

Adult↗
PubMed1981

Rate of heating as a determinant of hyperthermic cytotoxicity.

In Chinese hamster ovary cells and in normal and transformed rat embryonic fibroblasts, survival as a function of time at 42.4 degrees was dependent upon the rate of heating from 37 degrees to 42.4 degrees. Unexpectedly, the untransformed rat fibroblasts were more heat sensitive than were the transformed cells, and the protective effect of slow rates of heating upon survival at 42.4 degrees was also more pronounced in the normal cells than in the transformed cells. In Chinese hamster ovary cells, total cellular cholesterol content and cell volume were found to change significantly with time at 42.4 degrees when cells were heated immediately (37 to 42.4 degrees within 3 min) but did not vary significantly during 6 hr at 42.4 degrees in cells heated from 37 to 42.4 degrees over 3 hr. Chinese hamster ovary cells heated immediately to 42.4 degrees also showed a significant drop in the protein content of the particulate fraction with time at 42.4 degrees. In contrast, cells heated over 3 hr showed a significant increase in the protein content of the particulate fraction with time at 42.4 degrees. These data suggest that, if cells are heated to hyperthermic temperatures over sufficiently long intervals, mechanisms have time to develop which protect the cell membrane against changes associated with cell death in rapidly heated cells. The protective effect of slow rates of heating may partially explain the relative lack of success thus far observed with the use of whole-body hyperthermia in which heating from 37 degrees to 42 degrees often requires 2 to 3 hr.

Animals↗