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

The effects of exposure to natural sunlight on the immune system were studied in 15 normal human subjects. Exposure was for 1 hr each day for 12 days over 2 wk and tests were carried out before, on completion, and 2 wk after completion. In comparison to concurrent studies on 13 age- and sex-matched controls, sun-exposed subjects had a significant increase in their circulation of T cells recognized by OKT8 monoclonal antibodies and a decrease in OKT4 positive T cells. Suppressor T cell activity measured in pokeweed mitogen-stimulated cultures of T and B cells was significantly increased against IgG and IgM production. These changes were still evident in many of the subjects 2 weeks after completion of the sun exposure. A trend for depression of natural killer cell activity against a melanoma target cell was noted in the present study, but this did not appear as marked as that noted previously in subjects exposed to radiation in solariums. The differences between the effect of radiation from solariums and natural sunlight on the immune system may result from the higher dosage of UV-A in radiation from solariums. The results suggest that exposure to sunlight may favor the induction of suppressor pathways in response to antigenic stimuli and that this may limit immune responses against tumor cells such as melanoma. They support the idea from animal studies that systemic changes in the immune system may be an important factor in the association of UV radiation with malignancy.
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PMID:Alteration of T cell subsets and induction of suppressor T cell activity in normal subjects after exposure to sunlight. 622 71

The in vivo and in vitro effects of human alpha-interferon (IFN) on blood natural killer (NK) cell activity were studied in patients with malignant melanoma. The initial response to an i.m. injection of IFN was a depression of blood NK cell activity, being detectable at 4 h and reaching a nadir at 12 h. Blood NK cell activity returned to or exceeded pretreatment levels within 24 h. The frequency of large granular lymphocytes among peripheral blood lymphocytes (PBL), however, remained unchanged during the first 24 h of IFN treatment. In a single cell cytotoxicity assay in agarose the number of lymphocytes forming conjugates with K562 target cells was not affected at 12-h points of IFN treatment, while the frequency of lytic conjugates with dead target cells was decreased by 12 h. Thus, the number of active NK cells was reduced by IFN administration. While in vitro exposure to IFN resulted in an augmentation of NK cell activity of PBL from untreated patients, IFN failed to enhance the activity of PBL obtained 12 h post IFN injection. When PBL obtained 12 h after IFN injection were cultured overnight, they recovered their responsiveness to NK-boosting effects of IFN. Blood monocytes obtained at 12-h points from IFN-treated patients suppressed IFN-induced enhancement of NK cell activity, although these monocytes did not inhibit the base line level of NK cell activity. In contrast, the streptococcal preparation OK432 was able to augment NK cell activity of PBL obtained 12 h post IFN administration and of control PBL even in the presence of suppressor monocytes. PBL obtained 24 h post IFN injection expressing enhanced NK cell activity were also unresponsive to IFN in vitro. However, monocytes obtained 24 h after IFN injection were no longer able to inhibit IFN-induced augmentation of NK cell activity. These results indicate that in vivo administration of IFN-alpha to cancer patients results in rapid and transient generation of suppressor monocytes capable of inhibiting IFN-dependent development of functional NK cell activity, which could be responsible for the initial and transient decline in blood NK cell activity.
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PMID:In vitro modulation of human natural killer cell activity by interferon: generation of adherent suppressor cells. 623 64

The acute in vitro actions of two potent melanocytolytic agents, hydroquinone (HQ) and beta-mercaptoethanolamine (MEA), were determined in the B-16, Cloudman S-91 and Harding-Passey (HP) murine melanomas grown in vivo. Drug treated melanoma dice (5--480 min) were analyzed for tyrosinase activity and cyclic nucleotide levels (cAMP, cGMP). HQ and MEA effects on tyrosinase activity are complex and vary with tumor type, duration of treatment and agent tested. MEA or HQ inhibited B-16 tyrosinase activity. With combined drug therapy, low concentrations of MEA plus HQ stimulate B-16 tyrosinase activity while high concentrations of the drugs have little effect on enzymatic activity. MEA depresses tyrosinase activity while HQ elevates enzymatic activity in the S-19 melanoma. Both high and low concentrations of the combined drugs (MEA plus HQ) elicit the same response, stimulation at 10 min followed by continued depression of tyrosinase activity for the remainder of the 4 h study period. MEA initially stimulates HP tyrosinase activity followed by depression of enzymic activity. In contrast, HQ initially depresses HP tyrosinase activity followed by stimulation of enzyme activity. In combination the drugs inhibit HP tyrosinase activity. The effects of MEA and/or HQ on murine melanoma cyclic nucleotide levels are equally complex. MEA or HQ elevate cAMP and cGMP levels in all three tumors with the exception of S-91 cGMP levels which are not altered. In combination the drugs increase cyclic nucleotide levels in each of the three tumor types but at different times. No correlation is present between cyclic nucleotide levels and tyrosinase activity. Thus, the action of increased cyclic nucleotide levels in melanogenesis can not be separated from the direct actions of MEA and HQ upon melanogenesis. The divergent effects of MEA and/or HQ on tyrosinase activity and cyclic nucleotide levels in these melanomas are not correlated with the known in vivo melanocytolytic activity of these drugs. Thus, these parameters appear to be inadequate indicators of melanoma cell viability in chemotherapeutic screening of drugs effective in destroying malignant melanoma.
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PMID:Acute effects of two melanocytolytic agents, hydroquinone and beta-mercaptoethanolamine, upon tyrosinase activity and cyclic nucleotide levels in murine melanomas. 625 89

For the analysis of the mechanism of cancer metastasis, effects of anticancer agents on the NK activity of spleen cells and on the artificial metastasis of B-16 melanoma cells were comparatively studied. The inhibitory effect of these anticancer agents on the growth of B-16 melanoma inoculated to foot pad of C57/BL6 mice was also examined. The growth of B-16 melanoma was inhibited by intravenous administration of 6 mg/kg of MMC, 18 mg/kg of KW-2083 and 5 mg/kg of CDDP, but not of 6 mg/kg of KW-2083. The NK activities in spleen cells of C57/BL6 mice administered with 6 mg/kg of MMC and 18 mg/kg of KW-2083 were decreased, but they were not decreased in mice administered with 6 mg/kg of KW 2083 and 5 mg/kg of CDDP. Significant increases in the number of artificial pulmonary and liver metastasis were observed in mice administered with 6 mg/kg of MMC and 18 mg/kg of KW-2083. It is suggested that the depression of NK activity induced by anticancer agents results in the promotion of metastatic disease.
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PMID:[Analysis of the mechanism of cancer metastasis by using anticancer agents]. 642 Dec 47

Previous reports of an association between cigarette smoking and the depression of immune function were investigated by studies of 35 subjects before, and three months after, they had ceased to smoke cigarettes. The studies included tests of natural killer cell (NK) activity against several target cells and the measurement of immunoglobulin levels in sera and saliva. Similar tests were conducted on 29 control subjects who continued to smoke. The results indicated a significant decrease in lymphocyte counts and a significant increase in NK activity against cultured melanoma cells in subjects who ceased smoking. Serum IgG and IgM levels rose significantly in those who ceased smoking cigarettes, but there was no change in IgA levels. Similar increases in immunoglobulin levels (IgA and IgG) in mucosal secretions (saliva) were noted after cessation of smoking. The NK activity and immunoglobulin levels of smokers who continued to smoke did not show significant changes. These results were consistent with the reversal of changes in immune function associated with smoking. We suggest that these findings may provide further insight into the association of smoking with an increased incidence of certain malignant diseases and respiratory infections.
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PMID:Effects of cigarette smoking on the immune system. Follow-up studies in normal subjects after cessation of smoking. 663 6

The mechanism of artificial and spontaneous metastases of tumor was analyzed in B16 melanoma cells and C57BL/6 mice by using anti-asialo GM1 antibody and anticancer agents. Single administrations of 500 micrograms anti-asialo GM1 antibody resulted in significantly decreased NK activity in spleen cells of C57BL/6 mice, lasting 10 days from the day following administration. Treatment with anti-asialo GM1 antibody never decreased the function of T lymphocytes measured by blastogenesis with phytohemagglutinin or T cell growth factor. The tumoricidal functions of activated macrophages but not of resident macrophages were decreased by in vivo treatment with anti-asialo GM1 antibody. The anti-asialo GM1 antibody was evaluated in terms of the enhancing effect on pulmonary metastases with regard to the timing of administration. Treatment with anti-asialo GM1 antibody 1 day before or on the day of tumor inoculation resulted in a substantial increase in the number of artificial pulmonary metastases. In the experimental system of spontaneous metastases, anti-asialo GM1 antibody most effectively increased the number of pulmonary metastases when administered 1-2 weeks before the removal of primary tumor, when the tumor cells are thought to be released into blood circulation from the primary site. In addition, accelerated growth of transplanted tumors at the primary site was observed in mice treated with anti-asialo GM1 antibody. These results strongly suggest that anti-asialo GM1 antibody enhances the incidence of in vivo tumor metastases and the growth of transplanted tumor mainly by suppressing the function of NK cells. The maximum effective dose (MED) of mitomycin C or its derivative (M-83) suppressed NK activity significantly, and pretreatment with these anticancer agents enhanced the growth of the artificial pulmonary and liver metastases. In contrast, the MED of cDDP showed no effect on the NK activity or the numbers of pulmonary and liver metastases. These results indicate that the depression of NK activity induced by chemotherapy results in the promotion of metastatic disease. From these studies it can be concluded that NK cells have a key role in the control of metastases of malignant disease, and that support of NK activity is very important for the prevention of metastases.
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PMID:Analysis of metastatic spread and growth of tumor cells in mice with depressed natural killer activity by anti-asialo GM1 antibody or anticancer agents. 673 2

We examined the ability of uridine to increase the therapeutic index of 5-fluorouracil (FUra) against C57BL/6 X DBA/2 F1 mice bearing a Day 1 B16 melanoma or L1210 leukemia. FUra (400, 600, or 800 mg/kg, i.p.) followed in 24 hr by a 5-day s.c. infusion with uridine (5 g/kg/day, s.c.) was compared with the maximum tolerated dose of FUra (200 mg/kg, i.p.) plus a 5-day infusion with 0.9% NaCl solution. High-dose FUra plus delayed infusion with uridine was more effective than FUra (200 mg/kg) in inhibiting the growth of the B16 melanoma. High-dose FUra plus uridine rescue was, however, no more effective than FUra (200 mg/kg) in increasing the survival times of mice bearing the L1210 leukemia. To see if uridine rescue from FUra toxicity correlated with effects against a sensitive normal tissue, bone marrow nucleated cellularity of normal, non-tumor-bearing mice was monitored after drug treatment. In mice treated with FUra (200 mg/kg) followed in 24 hr by a 5-day infusion with either uridine (5 g/kg/day) or 0.9% NaCl solution, there was not as great a decrease in cellularity at the nadir with uridine, and, in addition, uridine accelerated recovery as compared to 0.9% NaCl solution. Furthermore, uridine (5 g/kg/day), but not thymidine (dThd) (5 g/kg/day) or 2'-deoxyuridine (dUrd) (5 g/kg/day), had a sparing effect on the depression in bone marrow nucleated cellularity seen at the nadir on Day 4 after Fura (200 mg/kg). The specificity of uridine to rescue mice from the lethal toxicity of the related fluorinated pyrimidines, 5-fluorouridine and 5-fluoro-2'-deoxyuridine, was also examined. Mice were treated with 5-fluorouridine (250 mg/kg, i.p.) followed in 24 hr by a 5-day infusion with uridine (1, 5, or 10 g/kg/day), dThd (1, 5, or 10 g/kg/day), or dUrd (1 or 5 g/kg/day). Uridine (1, 5, or 10 g/kg/day) rescued mice from the lethal toxicity of 5-fluorouridine, whereas dThd or dUrd was ineffective. Similarly, a 5-day infusion with uridine, but not dThd or dUrd, rescued mice from the lethal toxicity of 5-fluoro-2'-deoxyuridine (1800 mg/kg, i.p.).
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PMID:Use of uridine rescue to enhance the antitumor selectivity of 5-fluorouracil. 685 Jun 28

Twelve patients who were referred to the Oncology Service of Wills Eye Hospital, Philadelphia, with a pigmented epibulbar lesion that clinically resembled malignant melanoma of the choroid with extraocular extension were found to have other ophthalmic entities. The most common conditions that simulated extraocular extension of uveal melanoma were conjunctival malignant melanomas, which accounted for four of the 12 pseudomelanomas. Three of the 12 patients had staphylomas or scleral ectasis. Two of the 12 had subconjunctival hematomas. Senile scleral plaques, a presumed cellular blue nevus, and ocular melanocytosis accounted for the other three conditions. A thorough history, indirect ophthalmoscopy with scleral depression, ultrasonography, gonioscopy, and transillumination were helpful in distinguishing uveal malignant melanoma with extrascleral extension from other, often less serious, ophthalmic disorders.
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PMID:Epibulbar lesions simulating extraocular extension of uveal melanomas. 716 29

The E-rosette forming capacity of lymphocytes was measured in 39 melanoma patients, performing the test at 4 degrees C and at 20 degrees C, prior to treatment, following surgery, and in 11 patients was carried out at three points: before and after surgery as well as after immunochemotherapy with DTIC and BCG. The results have shown a marked depression in E-rosettes at 4 degrees C and at 20 degrees C, whereas more expressed inhibition was registered at 4 degrees C. Following surgical removal there were no significant changes in the E-rosettes. After immunochemotherapy an increase of the E-rosettes was observed.
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PMID:Changes in the rosette forming capacity of lymphocytes after surgery or surgery and immunochemotherapy of malignant melanoma in man. 716 2

Sequential evaluation of lymphocyte blastogenic response (LBR) to PHA was performed in 10 melanoma patients and in 10 gastric cancer patients undergoing radical operations. Preoperative determinations showed a significant depression of LBR in both patient groups as compared to healthy controls. In patients operated for melanoma the average duration of anesthesia was 101 minutes and in patients who underwent gastric resection it was 192 minutes. In both patient groups a further significant depression of LBR was observed in the early postoperative period; however the LBR returned to preoperative levels more promptly in patients who underwent melanoma excision than in those who underwent gastric resection.
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PMID:[Sequential evaluation of lymphocytic blastogenesis in cancer patients after surgical treatment]. 731 75


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