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S Vogl

Publications and source records attributed to S Vogl.

34 records · Page 2Linked to original sources
PubMed1989

Suppression of experimental autoimmune encephalomyelitis by dual cyclo-oxygenase and 5-lipoxygenase inhibition.

The release of leukotriene C4 (LTC4), an important 5-lipoxygenase product of the arachidonic acid metabolism from polymorphonuclear leucocytes (PMNLs) of guinea pigs with experimental allergic encephalomyelitis (EAE), the animal model of MS, has been found to be significantly increased compared with healthy animals. Subsequently, the dual cyclo-oxygenase and 5-lipoxygenase inhibitor BW755C was applied to 15 guinea pigs with EAE. Two control groups (15 each) were treated with the cyclo-oxygenase inhibitor indomethacin or physiological saline, respectively. In the BW755C treated group, no animal developed symptoms of the disease in contrast to, respectively, 5 and 3 animals in the 2 other groups. Histological examination of the CNS revealed a highly significantly lower inflammation score in the BW755C treated animals, and the release of LTC4 from PMNLs was highly significantly decreased in this group compared with each of the others. The findings suggest that the vascular permeability enhancing LTC4 plays a pathogenetic role in EAE and indicate that inhibition of this sulfidopeptide leukotriene suppresses the disease. Therefore, the application of leukotriene inhibitors could contribute to the future treatment of MS.

4,5-Dihydro-1-(3-(trifluoromethyl)phenyl)-1H-pyraz↗
PubMed1987

Biological efficacy of partial hepatectomy and hepatopoietin in long-term selenium-deficient mice.

After partial hepatectomy the normal low proliferation rate of hepatocytes increases dramatically. This is based on a feed-back system whose central link is a liver cell proliferation hormone, the so-called hepatopoietin. This glycoprotein is organ-specific but not species-specific, i.e. an extract from rats is also active in mice. In order to examine the influence of selenium on liver cell proliferation, male albino NMRI mice were fed a selenium-deficient diet containing less than 10 ppb Se for at least 2 months (Se-). In the plasma protein profile and in the basic DNA synthesis rate of Se(-)-animals, no significant changes were observed compared to controls. However, liver cell proliferation induced by hepatopoietin or by partial hepatectomy was increased about 3-fold in Se-deficient mice. We assume a compensated metabolic Se-deficiency state in mice under these nutritional conditions, which leads to expression of enhanced metabolic capacity when induced by stress.

Animals↗
PubMed1986

Increased proliferative activity in selenium-deficient mouse liver.

Male albino NMRI mice were fed a selenium-deficient (Se-), torula yeast-based diet containing less than 10 ppb Se for at least 2 months (Se-) while a control group received the same diet supplemented (Se+) with 330 ppb Se as Na2SeO3. The Se-(-)animals showed multiple enzyme modulations of liver enzyme activities indicating that they were in a severely Se- state. No significant difference in the basic DNA synthesis rate of Se-(-)animals compared to Se+ controls was measured. However, when liver cell proliferation was induced by either hepatopoietin pretreatment or by partial hepatectomy, an about 3-fold increase in DNA replication rates was found in Se- compared to controls. We conclude that the enhanced proliferative activity in Se- mouse liver is expressed in an emergency situation.

Animals↗
PubMed1986

Phase II trial of misonidazole (MISO) and cyclophosphamide (CYC) in metastatic renal cell carcinoma.

In animal models pre-treatment with misonidazole, a hypoxic cell radiosensitizer, enhances the antineoplastic effects of alkylating agent chemotherapy. Laboratory data suggest that hypoxic tumor cells may be more resistant to chemotherapy because of suboptimal drug delivery, reduced rates of cell division, or because hypoxia confers relative drug resistance. The therapeutic potential depends on the tumor type, doses of radiosensitizer and alkylating agent, the time interval between drug administration, and the ratio of sensitization of normal and malignant tissues. A Phase II trial of misonidazole and cyclophosphamide was initiated by the Eastern Cooperative Oncology Group to determine the response rate and toxicity in patients with metastatic renal cell cancer. Patients received 5 gm/m2 of misonidazole intravenously two hr before 1200 mg/m2 of cyclophosphamide every 3 wk. Patients with prior chemotherapy or radiotherapy received 1000 mg/m2 of cyclophosphamide. Misonidazole was discontinued after a total dose of 15 gm/m2. The median total misonidazole dose was 23.5 gm (range 4.5-34.5 gm). The median number of cyclophosphamide cycles was 2 (range 1-12). Of the 30 patients evaluable for response, only one patient had an objective partial response. Twenty-nine patients had stable or progressive disease. One patient remains on cyclophosphamide after 9 mo. Estimated median survival is 4.8 mo. There have been no lethal toxicities; however, 9 patients (25%) experienced life-threatening leukopenia and an additional 42% experienced severe hematologic toxicity. Eight patients had WBC less than 1000 on days 7-14 of cycle 1. Thrombocytopenia and grade 3 anemia occurred in 1 and 2 patients, respectively. Moderate or severe nausea and vomiting occurred in 47% and 19% of patients, respectively. Only 3 patients experienced severe neurotoxicity. Four additional patients had moderate neurotoxicity. In summary, misonidazole in this dosing schedule does not enhance the antitumor activity of cyclophosphamide in renal cell carcinoma.

Carcinoma, Renal Cell↗
PubMed1986

A randomized trial of the four most active regimens for metastatic non-small-cell lung cancer.

Between October 1981 and June 1983, the Eastern Cooperative Oncology Group (ECOG) conducted a prospectively randomized trial (EST 1581) of the four most active chemotherapy regimens for metastatic non-small-cell lung cancer (NSCLC). Four hundred eighty-six good performance status patients (PS 0 or 1; 81%) were randomized to receive cyclophosphamide, doxorubicin, methotrexate, and procarbazine (CAMP); mitomycin, vinblastine, and cisplatin (MVP); etoposide and cisplatin (VP-P); or vindesine and cisplatin (VDA-P). All regimens were administered in the doses and schedules originally reported. Complete response (CR) plus partial response (PR) rates for the four regimens were CAMP, 17%; MVP, 31%; VP-P, 20%; and VDA-P, 25%. The response rate for MVP was significantly higher in patients with squamous and adenocarcinoma histologies, but there was no impact on median survival (overall, 24.5 weeks). The duration of response did not differ by treatment as previously suggested for VDA-P. There were 15 CRs (CAMP, one; MVP, six; VP-P, two; VDA-P, six), and 12 patients have survived more than 2 years. Toxicity was significant with 20 treatment-related deaths. CAMP was significantly less toxic than the other regimens (P less than .001). VDA-P demonstrated significantly more life-threatening (seven) and lethal (three) episodes of nephrotoxicity (P less than .001) despite an aggressive hydration program that in itself caused significant morbidity. Analysis of the toxicity data showed, however, that most of the severe toxicity occurred in the 19% of patients who were initially PS 2, suggesting that they are not appropriate candidates for trials of new agents or combinations. None of these regimens can be recommended as a standard therapy for metastatic NSCLC.

Aged↗
PubMed1985

Recurrent ovarian carcinoma: retreatment utilizing combination chemotherapy including cis-diamminedichloroplatinum in patients previously responding to this agent.

Eleven women with advanced ovarian cancer treated postoperatively with combination chemotherapy (cytoxan, hexamethylmelamine, Adriamycin, and cis-platinum) had disease-free intervals of 5 to 46 months (mean: 22 months) and subsequently developed recurrent carcinoma. Each patient was then retreated with combination chemotherapy which included cis-platinum. There was a 72% response rate to retreatment (36% complete, 36% partial). These overall and complete remission rates are comparable to those of platinum-based combination chemotherapy in patients without prior treatment. Those patients who responded to retreatment had a significantly longer mean survival rate than those who did not.

Adult↗
PubMed1984

Regulation of hepatocyte proliferation. The feed-back system of hepatopoietin.

After partial hepatectomy the low proliferation rate of hepatocytes increases dramatically. This is based on a feed-back system whose central link is a liver cell proliferation hormon, the so-called hepatopoietin. The hormon originates from the Peyer's patches: after their resection, the liver cell proliferation after partial hepatectomy decreases by about 80%. Hepatopoietin effects organ specific but species nonspecific.

Animals↗
PubMed1983

Is there cumulative or delayed toxicity from cis-platinum?

Evidence of increasing risk of nephrotoxicity was sought in the records of 95 patients who had received 300-826 mg/m2 cumulative doses of cis-platinum in single doses of 50-75 mg/m2 every 3-4 weeks, with hydration and diuresis using mannitol and furosemide. The incidence of serum creatinine elevation to greater than 1.5 mg/dl was 4.2% per patient and 0.75% per dose, no higher than the incidence observed at lower cumulative doses. Among 54 of these patients observed for at least 3 months after cessation of cis-platinum chemotherapy, only one had later deterioration of renal function to a serum creatinine of 1.9; both kidneys had been irradiated to 1900 rad in this patient. It was concluded that cumulative, delayed or severe nephrotoxicity are not significant problems related to prolonged cis-platinum administration at moderate doses when hydration and diuretics are routinely used.

Adult↗
PubMed1976

Combination chemotherapy with adriamycin and cis-diamminedichloroplatinum in patients with neoplastic diseases.

Forty-eight patients with a variety of advanced solid tumors were treated with a combination of adriamycin 50 mg/m2, and cis-diamminedichloroplatinum 50 mg/m2, every 2 to 4 weeks. Fifteen patients responded with a greater than 50% regression of measurable tumor; six with lung cancer; one, carcinoma of the breast; one, ovary; one, cervix; one, prostate; one, testis; one, maxillary sinus; and one, salivary gland, plus one patient with chemodectoma and one with adenocarcinoma of unknown primary. Responses lasted 1 to 18 months, with a median of 6 months. An additional six patients, including two with adenocarcinoma of the lung three with carcinoma of the cervix, and one with embryonal cell testicular carcinoma improved (25-50% regression of the tumor). Toxicity encountered included myelosuppression, azotemia, alopecia, nausea, vomitting, and stomatitis. Severe hematologic toxicity occurred only in those with compromised marrow function or with concurrent active hepatitis. Major potentiation of toxicity by the combination does not appear to have occurred.

Adolescent↗
PubMedDate not supplied

Fatal cryptosporidiosis complicating Kaposi's sarcoma in an immunocompromised man.

Fatal cryptosporidiosis in a bisexual immunosuppressed man with disseminated Kaposi's sarcoma and intractable diarrhea is described. Cryptosporidium sp. was isolated from the stool antemortem by Sheather's floation technique. This parasite should be considered in immunosuppressed hosts with chronic diarrhea when routine methods fail to demonstrate etiologic agent. Since this organism is already infectious when passed, stool precautions should be maintained.

Acquired Immunodeficiency Syndrome↗
PubMedDate not supplied

Chemotherapy for inoperable, non-small cell bronchogenic carcinoma: EST 2575, generation II.

Between 1976 and 1978 the Eastern Cooperative Oncology Group tested ten regimens in 415 patients with histologically documented, inoperable non-small cell bronchogenic carcinoma. Most patients were ambulatory (69%) and had extensive disease (69%). Patients were stratified by cell type: squamous cell carcinoma (SQ), large cell anaplastic carcinoma (LC), or adenocarcinoma (AD). Ineffective single agents (including cell types tested and percent complete and partial responses) were dactinomycin (SQ, 6%), dianhydrogalactitol (SQ, 0), ftorafur (AD and LC, 3%), and piperazinedione (AD and LC, 7%), Ineffective combination regimens included the contemporary standard regimen cyclophosphamide (CYT) plus CCNU (SQ, AD, and LC, 9%), methotrexate plus doxorubicin (ADR) plus CYT plus CCNU (MAC) (SQ and AD, 12%), and mitolactol plus ADR (AD and LC, 8%). When compared to CYT plus CCNU the following regimens demonstrated significant activity: CYT plus bleomycin plus cisplatin (SQ, 23%; P = 0.02) and ADR plus 5-FU plus cisplatin (AD and LC, 24%; P = 0.006). Mitomycin demonstrated marginal activity in squamous cell cancer (19%, P = 0.06). Neither "active" regimen improved survival although responders to any regimen had a significant prolongation of median survival (31.6 vs 15.7 weeks, P = 0.002). The MACC regimen, piperazinedione, and mitomycin were substantially more toxic than the two effective regimens, which were adequately tolerated. Ambulatory performance status, limited disease, and prior surgery were significant positive prognostic variables whereas prior radiation and pretreatment weight loss adversely affected response or survival.

Adenocarcinoma↗