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Biomedical subjects

G L Floersheim

Publications and source records attributed to G L Floersheim.

At least 37 records · Page 2Linked to original sources
PubMed1984

Influence of zinc, D-penicillamine and oxygen on poisoning with Amanita phalloides. Zinc accelerates liver regeneration and prevents the depletion of brain noradrenaline caused by the mushroom.

Pretreatment with zinc aspartate increased the survival rate of mice poisoned with a lyophilisate from the mushroom Amanita phalloides (APL). In the livers of the zinc-treated animals, confluent necrosis was cleared earlier. Zinc also prevented the reduction of brain noradrenaline caused by the mushroom as well as the rise of brain dopamine and brain weight. D-Penicillamine also protected against the lethal effects of APL. The survival afforded by zinc pretreatment was marginally ameliorated by additional oxygenation.

Amanita↗
PubMed1984

Protection by bone marrow grafts against lethal doses of 5-fluorouracil.

C3H (H-2k) mice were treated with lethal doses of the antimetabolite 5-fluorouracil (5-FU). After 16 hr the mice received an intravenous injection of 25 X 10(6) syngeneic or allogeneic bone marrow cells. With syngeneic cells, survival after a single dose of 350 mg/kg 5-FU was increased from 27 to 83% and after 450 mg/kg 5-FU from 14 to 84%. Allogeneic CBA (H-2k) donor cells allowed 81% of the mice to survive after 350 mg/kg 5-FU and 42% after 450 mg/kg 5-FU. Allogeneic marrow from A (H-2a) donors was ineffective after both doses of 5-FU. The results show that the lethality of 5-FU is largely prevented by a hemopoietic graft. Experimentally, 5-FU belongs to the agents which may be applied in cancer chemotherapy at lethal and thus potentially tumor-eradicative doses in combination with autologous or syngeneic bone marrow. In humans it remains to be seen whether the use of this protocol is precluded by prevailing gut toxicity.

Animals↗
PubMed1982

[Clinical death-cap (Amanita phalloides) poisoning: prognostic factors and therapeutic measures. Analysis of 205 cases].

205 cases of clinical poisoning with the mushroom Amanita phalloides (death cap) in the period 1971 to 1980 have been studied retrospectively. The lethality was 22.4%. Age and latency between the ingestion of the mushrooms and the first clinical symptoms were of prognostic significance. The death rate was 51.3% in children below 10 years of age but only 16.5% in patients older than 10 years. The average latency period was 10.3 hours for the fatal cases and 12.6 hours for the surviving patients. Country, year, sex and time of hospitalization did not influence lethality. Prognostic relevance could also be attributed to the thromboplastin time (Quick). 84% of the patients with values below 10% died, while all patients with minimal values of more than 40% survived. The correlation with the outcome was weaker for the serum transaminases and nil for creatinine. The patients underwent on the average 8 therapeutic measures, but up to 20 therapies could be administered to the same patient. Eight of the 30 recorded treatments involved general support, 7 toxin elimination and the remaining 14 could be classified as pharmacotherapy. With the aid of multiple regression analysis taking into account age, latency period and the effects of all the other measures, penicillin and hyperbaric oxygenation were found to contribute independently to a higher survival rate. As compared to penicillin, the combination of penicillin with silybin was associated with still further increased survival. On the other hand, several measures, including exchange transfusion, thiocytic acid, sulfamethoxazole, plasma expanders, haemodialysis, treatment of the hemorrhagic diathesis and THAM/sodium bicarbonate were administered more often to patients who did not survive. For the remaining 20 therapeutic measures our analysis revealed neither a positive nor a negative correlation with the clinical outcome.

Adolescent↗
PubMed1982

Decreased tolerance to dimethyl-myleran, cyclophosphamide and radiation in lymphoma-bearing mice.

A lethal dose of the cytotoxic agent dimethyl-myleran (DMM) is survived by 75-100% of mice reinfused with autologous bone marrow. In mice inoculated beforehand with a syngeneic Moloney lymphoma and then treated with lethal DMM, hemopoietic restoration and survival are compromised. With subcutaneous tumour challenge, in the face of substantial early toxicity, a therapeutic effect of DMM prevails. With intravenous or intraperitoneal tumour challenge the restorative potency of the autograft and thus the therapeutic drug effect are lost since practically all animals die from DMM. The reduced tolerance of mice carrying the Moloney lymphoma applies more generally to cytotoxic measures. The toxicity from sublethal doses of DMM, cyclophosphamide (CY) and total-body irradiation (TBI) is increased in mice inoculated subcutaneously shortly before with the lymphoma cells. The LD50 of the three agents is reduced by up to 70% according to the number of injected tumour cells or the time allowed for their multiplication. The effect is also provided by a cell-free tumour filtrate. Since the filtrate reduces bone marrow cellularity, the decreased tolerance could be due to the impairment of hemopoiesis by a tumour factor. Two human cancers growing as xenografts in immunosuppressed mice did not increase the sensitivity to DMM.

Animals↗
PubMed1982

Comparative growth of human tumors in pharmacologically immunosuppressed, immune-deprived, cyclosporin A-treated and nude mice.

The growth of three human tumor xenografts, namely an Ewing sarcoma, a colon carcinoma and an osteosarcoma, was compared in nude and conditioned mice. Conditioning protocols included (1) immune deprivation (thymectomy, lethal irradiation and cytosine arabinoside pretreatment); (2) immunosuppression with procarbazine, cyclophosphamide and antithymocyte serum; and (3) continuous administration of cyclosporin A. Similar tumor growth was seen in nude mice, immune-deprived mice and mice treated with the medium and high-dose immunosuppressive protocol. Cyclosporin A allowed only very modest tumor growth. In the main comparative experiment with the Ewing sarcoma and the colon carcinoma, overall survival was lowest with nude mice (17%), higher with immune-deprived mice (61%) and best with immunosuppressed mice (81 and 87%). For the screening of anticancer agents the immunosuppressive protocol consisting of synergistic procarbazine, cyclophosphamide and antithymocyte serum may be added to the already available models. It allows adequate tumor growth with good animal survival and does not require operative procedures and irradiation.

Animals↗
PubMed1981

[Tolerance of large doses of oral zinc sulfate].

The toxicity of oral zinc was investigated in patients hospitalized for chronic leg ulcers. Untoward effects were monitored by reference to clinical tolerance, hematological, hepatic and renal parameters, and serum concentrations of copper and iron. The investigation was conducted by comparing two groups of patients who initially did not differ significantly with regard to ulcer area, hemoglobin, leukocytes, copper, iron and zinc. Both groups had serum zinc concentrations in the lower normal range. One group was treated with 3 daily doses of 220 mg oral zinc sulfate and the other with placebo, and hence, untoward effects of zinc should have become manifest in the zinc-treated group. This was not the case. Therefore, oral zinc appears to be well tolerated clinically and does not cause hematological, renal or hepatic toxicity. In view of the increasing interest in and range of indications for zinc, particularly in conditions associated with cellular immunological hyporeactivity, this finding is a prerequisite for the institution of clinical zinc therapy.

Acrodermatitis↗
PubMed1981

Control of a human tumour (Ewing sarcoma) in mice by a single lethal dose of dimethyl-myleran and bone marrow.

A Ewing sarcoma grown in immunosuppressed mice was eradicated with a single lethal dose of dimethylmyleran (DMM) followed by autologous or syngeneic bone marrow. Sarcomas treated 2 weeks after grafting in a phase of rapid proliferation disappeared and large sarcomas treated after 6 or 10 weeks were reduced to necrotic tissue. A human osteosarcoma also regressed distinctly after this therapy while a human colon carcinoma responded poorly. Sub-lethal DMM treatment induced complete remissions in only 62% of the mice. Tumours which display sensitivity in this model may be treated clinically with lethal doses of DMM and autologous marrow transplantations.

Animals↗
PubMed1981

Inhibition by lymph node cells and promotion by fetal hepatocytes of murine tumours without or with chemotherapy.

The growth of a syngeneic Moloney lymphoma in CBA mice was inhibited by the injection of lymph node cells from normal CBA donors. This cytotherapeutic effect was also seen after chemotherapy with cyclophosphamide (CY) or dimethylmyleran (DMM). Two other murine tumours, the Meth A sarcoma in Balb/c mice and the L1210 leukemia in BDF1 mice, did not respond to treatment with normal syngeneic cells. In the L1210 system, tumour-promoting effects of fetal liver cells were demonstrated. The tumour inhibitory effects of normal lymph node cells against the Moloney lymphoma may be a virus-dependent phenomenon mediated through interferon and natural killer' cells. The experiments also showed the sensitivity of the Moloney lymphoma and the Meth A sarcoma to CY and DMM and the responsiveness of the L1210 leukemia to AAFC.

Ancitabine↗
PubMed1980

[Increased sebum secretion due to oral administration of zinc sulfate].

In 87 patients hospitalized for chronic leg ulcers the effect of oral zinc on sebum secretion was determined. The patients were divided into three groups according to serum zinc concentrations. Patients with zinc levels in the upper normal range (Zn greater than or equal to 1.0 mg/l) were not treated. Patients with zinc levels in the lower normal range (Zn < 1.0 mg/l) received either three daily doses of 220 mg zinc sulphate or a placebo. The zinc-treated group displayed significantly increased sebum secretion. This effect was more marked in males, and may be due to a zinc-induced rise in plasma testosterone. Indications for oral zinc in dermatological conditions are discussed.

Administration, Oral↗
PubMed1980

[Lack of effect of oral zinc sulfate on wound healing in leg ulcer].

The effect of oral zinc on the healing of chronic venous leg ulcers has been investigated in 91 hospitalized patients aged approximately 70 years. The patients were divided into three groups: group A consisted of patients with serum zinc concentrations in the upper normal range (Zn greater than or equal to 1.0 mg/l) who received no zinc therapy. Groups B and C consisted of patients with serum zinc concentrations in the lower normal range (Zn less than 1.0 mg/l) who received either 3 daily doses of 220 mg zinc sulphate (group B) or placebo (group C). In group B, a marked increase in serum zinc concentration occured within one month (from 0.9 to 1.25 mg/L). In group A, serum zinc levels decreased slightly during the observation period of three months (from 1.1 to 1.0 mg/l) while a slight rise was seen in group C (from 0.9 to 1.0 mg/l). The healing rate of the ulcers in group A was not superior to that in group C. Zinc substitution in the low zinc group B did not improve healing as compared to placebo-treated low zinc group C. A favourable effect of oral zinc on wound healing in patients with initially low serum zinc concentrations could not be demonstrated. Initial ulcer areas were significantly smaller in patients with higher serum zinc levels than in patients with lower serum zinc levels. Low serum zinc levels appear to be a consequence of insufficient nutrition, an observation which may indicate a correlation between nutritional deficiency and ulcer area. The healing rate did not depend significantly upon age, sex, weight or cause. It was, however, accelerated in the case of larger ulcers.

Administration, Oral↗
PubMed1980

Growth of human tumors in mice after short-term immunosuppression with procarbazine, cyclophosphamide, and antilymphocyte serum.

A simple combine treatment with immunosuppressive agents permitting the growth of human tumor xenografts in conventional mice is presented. It consists of two simultaneous applications of 90 mg of procarbazine (PCH) per kg and 30 mg of cyclophosphamide (CY) per kg, alternating with two doses of 0.15 ml/10 g of antilymphocyte serum (ALS) for 4 days before grafting. No postgraft treatment is used. With a take rate of 100%, at 60 days after subcutaneous transplantation into male C3H mice, fragments of a human colon adenocarcinoma had grown (on the average) into cherry-sized tumors. Two osteosarcomas, an Ewing sarcoma, and a bronchogenic carcinoma were also studied and grew similarly. Tumors could be established in the three tested mouse strains but grew better in male animals. Synergy of PCH and CY and ALS depends upon the alternating sequence of both drugs and ALS. The histology of the colon carcinoma and the Ewing sarcoma was unchanged as compared to the tumors growing in nude mice. In contrast, the osteosarcoma developed in a more differentiated fashion in the immunosuppressed mice. The presented model may serve as a screening system for anticancer drugs.

Adenocarcinoma↗
PubMed1980

Characterization of the binding of 125I-labelled succinylated porcine relaxin to human and mouse fibroblasts.

A biologically-active succinylated porcine relaxin was iodinated by a modification of the Bolton-Hunter method. Fibroblasts cultured from the mouse pubic symphysis and human skin were used to investigate relaxin binding sites. 125I-labelled relaxin binding to both cell types was time- and temperature-dependent. An accelerated rate of labelled hormone degradation (90%) was observed when both cell types were incubated at 37 degrees C. Specific relaxin binding sites on the mouse and human cells were observed as other peptides, such as insulin, epidermal growth factor, glucagon, hFSH and human prolactin, failed to inhibit relaxin binding. Further results indicate that porcine relaxin is mitogenic to these specific fibroblasts because increasing concentrations (10(-9) to 10(-6) M) of this hormone stimulated cell growth in vitro. These data suggest that the effect of relaxin at the target tissue level is mitotic in nature.

Animals↗