Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Phenothiazine-induced bone marrow depression (BMD) was evaluated in three separate but complementary data bases: (1) Among 1,048 patients admitted to psychiatric hospitals, there was no evidence of subclinical depression of the white blood cell (WBC) count attributable to phenothiazines used before admission. (2) Among 18,587 medical inpatients, there were 34 patients admitted for BMD in the absence of neoplasia or prior cytotoxic drug therapy; one of the latter reported using chlorpromazine hydrochloride, but it is doubtful whether this drug was the cause of the BMD. (3) Among 24,795 medical, surgical, and gynecological patients surveyed over a ten-month period in 1972, there were four who were admitted for BMD; one of the latter had a reversible leukopenia attributed to trifluoperazine hydrochloride.
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PMID:Outpatient phenothiazine use and bone marrow depression. A report from the drug epidemiology unit and the Boston collaborative drug surveillance program. 0 Sep 78

The mechanisms controlling secretion of glucagon and other pancreatic hormones were studied in a patient affected with multihormone-secreting islet-cell tumor. Fasting glucagon levels (3,000 pg./ml.) rose to 10 ng./ml. following arginine stimulation. While oral glucose load and intravenous glucose infusion did not suppress glucagon secretion, insulin administration induced a prompt depression in glucagon levels. Glucagon, insulin, and gastrin levels were suppressed by somatostatin while calcium infusion caused a paradoxical increase. It is suggested that only some of the stimulation-inhibition mechanisms were conserved in this case of glucagon-secreting pancreatic tumor.
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PMID:Suppression and stimulation mechanisms controlling glucagon secretion in a case of islet-cell tumor producing glucagon, insulin, and gastrin. 0 26

Cytotoxic T-lymphocytes (CTL's) harvested from mixed splenic lymphocyte cultures (DBA/2 + C57BL) were tested for their ability to lyse allogeneic P815 mastocytoma cells under various tumor-like assay conditions, with or without previous exposure to ionizing radiation or hyperthermia (43 degrees). There was little or no decrease of immune cytolysis when CTL's were assayed by 51Cr release under tumor-like conditions (plateau-phase target cells, low pH, or anoxia) or after irradiation, but cytolytic activity was greatly reduced when CTL's were exposed to heat; 45 min of hyperthermic treatment decreased activity by greater than or equal to 99% while reducing the apparent cell viability (as indicated by trypan blue exclusion) by only 30%. When the P815 target cells rather than the CTL's were exposed to heat their susceptibility to immune lysis was not affected even after treatment times that were lethal to the tumor cells. Despite the dissimilar heat sensitivities of CTL and P815 cells, the dose-response curves for inhibition of protein synthesis by heat, as indicated by [3H]leucine incorporation, were similar for both cell types: neither the depression of protein synthesis in heated CTL's nor the decreased cytolytic ability of these cells was reversed within 3 hr. When irradiated or heated P815 cells were incubated with CTL's, the resulting survival curves were always additive, indicating that neither irradiation nor heat treatment affected the susceptibility of the tumor cells to immune attack. The extreme heat sensitivity of cytotoxic T-lymphocytes raises important questions about the possible effects of hyperthermic treatment on the immune competence of cancer patients.
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PMID:Effects of Tumor-like assay conditions, lonizing radiation, and hyperthermia on immune lysis of tumor cells by cytotoxic T-lymphocytes. 0 45

Several experiments conducted by our group over a period of 6 years have shown that nutritional stress, especially protein and/or calorie deprivation, leads to many, often dramatic, changes in the immune responses of mice, rats, and guinea pigs. Chronic protein deprivation (CPD) has been shown to create an enhancing effect on the cell-mediated immune responses of these animals. Humoral responses under CPD conditions were most often found to be depressed, but sometimes were unaffected, depending on the nature of the antigen employed. Chronic protein deprivation, consistent with the pattern just mentioned, improved tumor immunity by depressing production of B-cell blocking factors, and, in at least one instance, resistance to development of mammary adenocarcinoma in C3H mice was associated with evidence of increased numbers of T suppressor cells. Profound nutritional deficits (less than 5% protein per total daily food intake) depressed both cellular and humoral immunity. Early, though temporary, protein deprivation caused a long-term depression of both cellular and humoral immunity also, with the humoral component being the first to recover. Manipulation of protein and calories was found to have a profound effect on certain autoimmune conditions. Diets high in fat and low in protein favored reproduction but shortened the life of NZB mice, whereas diets high in protein and low in fat inhibited development of autoimmunity and prolonged life. Chronic moderate protein restriction permitted NZB mice to maintain their normally waning immunologic functions much longer than mice fed a normal protein intake. Further, the low-protein diet was associated with a delay in development of manifestations of autoimmunity. Decreasing dietary calories by a reduction of fats, carbohydrates, and proteins more than doubled the average life span of (NZB X NZW)F1 mice, a strain prone to early death from autoimmune disease. Histopathologic studies using immunofluorescent microscopy revealed that the development of the renal lesions caused by the deposition of antigen-antibody complexes, which is so characteristic of these mice, was markedly delayed.
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PMID:Nutritional deficiency, immunologic function, and disease. 0 88

In these experiments, we tested in various in vivo assays the immune responses of inbred C3H/HeN(MTV-) (C3H-) mice during carcinogenesis by chronic exposure to UV irradiation. Although the UV-treated mice were unable to reject syngeneic UV-induced tumor transplants, they rejected H-2-incompatible tumor allografts and H-2-compatible skin allografts. The primary hemagglutinin response to sheep red blood cells was normal in these mice, as were the induction of a local graft-versus-host reaction with lymphoid cells from UV-irradiated donors and the induction of an inflammatory response to dimethyl sulfoxide in the footpads of UV-treated mice. An early transient depression of two reactions in UV-irradiated mice occurred: delayed hypersensitivity to dinitrochlorobenzene measured by footpad swelling and the graft-versus-host reaction in UV-irradiated recipients measured by the use of the popliteal lymph node weight gain assay. Both of these reactions returned to a normal level before the development of primary tumors. We conclude that the inability of UV-irradiated mice to reject syngeneic and autochthonous UV-induced tumors was not due to a generalized immunosuppressive effect of chronic UV irradiation.
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PMID:In vivo immune responses of mice during carcinogenesis by ultraviolet irradiation. 2 May 14

Single-agent chemotherapy of advanced and recurrent squamous carcinoma of the female genital tract has been largely ineffective. Combination-drug therapy which has augmented the efficacy of chemotherapy in numerous solid and nonsolid human tumors is usually attended by a degree of toxicity that has discouraged its use against malignancies exhibiting a poor response to single agents. A seven-drug regimen consisting of cyclophosphamide, 5-fluorouracil, actinomycin D, vincristine, cytosine arabinoside, methotrexate, and bleomycin administered during a 24 hour period at 4 week intervals was selected for clinical trial against squamous malignancies of the female genitalia because of its proved broad-spectrum activity among solid tumors and its low incidence of serious toxicity. Severe bone marrow depression occurred during only two of 98 drug cycles involving 23 patients. An objective tumor response was observed in nine of 18 evaluable patients. This regimen appears to be useful in the palliative management of squamous carcinoma of the female genital tract.
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PMID:Seven-drug polychemotherapy in the treatment of advanced and recurrent squamous carcinoma of the female genital tract. 5

W/Fu rats inoculated s.c. with less than or equal to 5 x 10(7) syngeneic (C58NT)D (Gross virus-positive) lymphoma tumor cells normally develop a palpable tumor which reaches its maximum size (12 to 14 mm) at 6 to 8 days and is subsequently rejected by 10 to 12 days. However, rats previously sensitized with soluble tumor antigens from (C58NT)D cells prior to (C58NT)D tumor inoculation demonstrate a significant enhancement of tumor growth (the tumor reaches up to 26 mm and is rejected by 16 to 18 days). This enhancement persisted in antigen-treated rats that continued to receive soluble antigen after tumor inoculation. The in vivo enhancement coincided with a significant in vitro depression of cell-mediated cytotoxicity [assessed with 51Cr-labeled (C58NT)D target cells and peripheral blood leukocytes]. The observed tumor enhancement was specific, inasmuch as presensitization to either soluble tumor antigens from WR6 (Gross virus-negative) tumor, syngeneic to W/Fu rats, or to soluble antigen from W/Fu spleen cells had no enhancing effect on (C58NT)D tumor growth. Interestingly, sensitization to soluble tumor antigen alone did not elicit detectable cell-mediated immunity, cytotoxic antibody, or serum-blocking activity to the (C58NT)D tumor. We conclude that sensitization to soluble tumor antigens specifically impairs the immune apparatus normally acting in tumor rejection. This impairment appears to act primarily at the induction phase of the immune response.
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PMID:Specific enhancement of tumor growth and depression of cell-mediated immunity following sensitization to soluble tumor antigens. 5 98

Many studies have suggested that psychotropic drugs may be valuable in the managment of chronic painful conditions and of the pain due to neoplastic disease. An opiate-sparing effect has been postulated. Most of the studies are, unfortunately, uncontrolled. The question arises as to whether psychotropic drugs, in addition to allaying anxiety and depression, alter pain threshold or the appreciation of pain.
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PMID:The use of psychotropic drugs in other painful conditions. 6 74

Thirteen patients with osteogenic sarcoma were treated with multiple drug chemotherapy consisting of bleomycin, cyclophosphamide and dactinomycin. The dosage schedule used was: bleomycin 12 mg/m2/day, cyclophosphamide 600 mg/m2/day, and dactinomycin 450 microgram/m2/day. All drugs were given intravenously for two consecutive days. Treatment was repeated every 2 weeks. Toxicity included severe nausea and vomiting (managed with antiemetics and intravenous hydration) and manifestations of bone marrow depression. Of 13 patients, eight were previously treated with high dose methotrexate with citrovorum factor rescue, cyclophosphamide and Adriamycin. Of these eight, three patients had objective evidence of tumor regression (37.5%). Five of five previously untreated patients had objective evidence of tumor regression. The overall response rate in osteogenic sarcoma patients to BCD was 61.5%. The combination of BCD appears to be more active against osteogenic sarcoma than cyclophosphamide alone or Adriamycin alone. The relative safety with which BCD can be administered makes this combination a valuable adjunct to high dose methotrexate with citrovorum factor rescue and Adriamycin in the treatment of osteogenic sarcoma.
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PMID:Combination chemotherapy with bleomycin, cyclophosphamide and dactinomycin for the treatment of osteogenic sarcoma. 7 9

The research thus far on the relation of the immune system to gliomas has shown that a glioma associated antigen does exist. Small quantities of glioma associated antibodies probably circulate within the patient's serum but there is definite evidence of depression of the cell-mediated vanguard of the immune response. This depression is caused by a blocking factor that may be present as an antigen, antibody, or antigen-antibody complex. Both active and passive immunotherapeutic techniques have been employed in a small number of patients with little success. Considerable understanding of the alteration of the immune system is necessary before a rational approach toward immunotherapy of gliomas may be undertaken. However, it is apparent that reductive therapy consisting of surgery, radiation, and chemotherapy will be necessary before the immune system will be effective against the tumor burden.
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PMID:Tumor immunology: a neurosurgical perspective. II. The immunology of glial neoplasms. 7 64


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