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)

Depression is often associated with insulin resistance, owing to cortisol overproduction; conversely, many studies suggest that diabetics are at increased risk for depression. Recent evidence indicates that insulin is transported through the blood-brain barrier and influences brain function via widely distributed insulin receptors on neurons. These receptors are particularly dense on catecholaminergic synaptic terminals, and, while effects are variable dependent on brain region, several studies indicate that insulin promotes central catecholaminergic activity, perhaps by inhibiting synaptic re-uptake of norepinephrine. Additionally, it is well known that insulin enhances serotonergic activity in increasing blood-brain barrier transport of tryptophan. Since impaired monoaminergic activity in key brain pathways is believed to play an etiological role in depression, techniques which promote effective insulin activity, both centrally and peripherally, may be therapeutically beneficial in this disorder. This may rationalize anecdotal reports of improved mood in clinical depressives and diabetics receiving the insulin-sensitizing nutrient chromium picolinate. This nutrient, perhaps in conjunction with other insulin-sensitizing measures such as low-fat diet and aerobic exercise training (already shown to be beneficial in depression), should be tested as an adjuvant for the treatment and secondary prevention of depression.
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PMID:Enhancing central and peripheral insulin activity as a strategy for the treatment of endogenous depression--an adjuvant role for chromium picolinate? 783 10

The immune system of patients with head and neck cancer is frequently depressed. Serum inhibitory factors and immune cell dysfunction are known contributors to this depression, but their relative roles are unclear. We have examined these factors to determine whether a common pathway is involved. Is the defect an unresponding "switched-off cell" or is it a remedial defect responsive to the removal of serum inhibitory factors and/or to lymphokine restoration? Immune tests were performed in 66 patients with high-stage head and neck cancer. Serum inhibitory factors were measured by incubation of heat-inactivated serum (10%) with phytohemagglutinin (PHA)-stimulated lymphocytes or natural killer (NK) cells using the K562 assay. Lymphokine-activated killer (LAK) cell cytotoxicity was measured (in the presence/absence of serum) using chromium 51-labeled Raji tumor cells cultured 5 days with interleukin-2 (IL-2) (100 or 1,000 U/mL) and/or interferon-alpha (INF-alpha) (100 U/mL). IL-2 receptors, CD25 or p55 (low affinity) and p75 (high affinity), were measured by flow cytometry through fluorescence-activated cell sorter analysis. Serum inhibitory factors were detected in more than 50% of the patients. Head and neck cancer sera significantly inhibiting the normal lymphocyte response to PHA (11 of 22 patients), as well as significantly inhibiting the NK response of normal lymphocytes and the functional expression of the IL-2 receptor. LAK cell function at low-dose IL-2 was depressed in 45% of the patients (9 of 20) and was restored by increased IL-2 (1,000 U/mL) or a combination of IL-2 and INF-alpha. Twenty-five percent of the patients were unresponsive to maximum lymphokine stimulation. Half of the patients had depressed expression of the low-affinity IL-2 receptor (CD25). The cause of immune depression in patients with head and neck cancer is multifactorial and is related to serum inhibitory factors, as well as to inherent cellular defects. Based on these data, we would suggest a therapeutic approach in selected patients that includes the removal of serum inhibitory factors by plasmapheresis and restoration of cellular defects by combined IL-2 with or without INF-alpha.
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PMID:Contribution of serum inhibitory factors and immune cellular defects to the depressed cell-mediated immunity in patients with head and neck cancer. 821 99

Investigations on the precaecal and postileal apparent digestibility (net absorption) of trace elements (copper, zinc, iron, manganese) were performed in ileumfistulated and intact dogs (4 each). The animals were fed 3 different protein sources (greaves, soy protein, corn gluten), either isolatedly (except corn gluten) only with mineral and vitamin supplement or as a part of a complete diet (55% of the respective protein source plus rice, cellulose, soy oil and vitaminated mineral supplement). Precaecal and total apparent digestibility of trace elements were evaluated by the marker method (chromium oxide). 1. Copper was mainly net absorbed in the small intestine, with the other elements absorption and secretion in the small and large intestine was seen. 2. The variation of the protein supply in the own experiments did not influence the net absorption of trace elements. 3. Own results and data from the literature show a depression of Zn- and Fe-absorption with diets containing low digestible carbohydrates or crude fibre, in part there may be considerable net losses of trace elements under these conditions. With regard to the feeding practice a suboptimal trace element status of the animal may result not only from low intake but also from an impaired net absorption in the intestinal tract, especially concerning zinc from diets containing low digestible carbohydrates.
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PMID:[Observations on the apparent digestibility of copper, iron, zinc and magnesium in dogs]. 859 61

A 2 x 4 factorial arrangement of treatments was used in a randomized complete block designed study to determine the effects of chromium level and source on growth and immune response of stressed and non-stressed 3-wk-old crossbred weanling pigs (BW was 6.35 kg). Factors included 1) immune stress or control and 2) no supplemental Cr or .2 ppm of supplemental Cr from either CrCl3, Cr-picolinate, or Cr-nicotinic acid complex. The basal diet was a corn-soybean meal-whey diet containing 1.2% lysine. Escherichia coli lipopolysaccharide (LPS) was the stress-inducing agent and was injected on d 7, 10, and 13 of the experiment. Immune challenge with LPS resulted in reduced gain (P < .05) and feed intake (P < .10). Supplementation with Cr was not effective in alleviating the depression in growth due to LPS. However, supplementation of control pigs with Cr tended to improve (P < .10) gain and feed intake. In vitro cellular immune response as measured by a lymphocyte blastogenesis assay was increased (P < .10) in pigs fed supplemental Cr from CrCl3, or Cr-picolinate. Antibody response to sheep red blood cells tended to be increased (P < .10) in pigs supplemented with Cr-nicotinic acid, but antibody response to ovalbumin was decreased (P < .05) in pigs supplemented with organic forms of Cr. At the end of the study, effects of Cr supplementation on lymphocyte proliferative response were investigated before and after ACTH administration. Injections of ACTH resulted in increased (P < .001) serum cortisol levels and increased lymphocyte proliferation. Supplementation of Cr did not affect lymphocyte blastogenic response before or after ACTH injection (P > .10). These data suggest that Cr supplementation was not beneficial during immune stress in pigs.
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PMID:Immune response and growth of stressed weanling pigs fed diets supplemented with organic or inorganic forms of chromium. 905 63

Incubation of primary cultures of rat hepatocytes with K2CR2O7 and deferoxamine (DFO), an iron chelator, resulted in a marked decrease in cellular levels of DNA single-strand breaks caused by K2Cr2O7. Cellular treatment with DFO also suppressed both dichromate-induced cytotoxicity--evaluated by the leakage of lactate dehydrogenase, and lipid peroxidation--as monitored by malondialdehyde formation. In addition, treatment with DFO attenuated the suppression of the levels of vitamin E and C as well as the inhibition of alkaline phosphatase and glutathione peroxidase activity attributed to K2Cr2O7. However, DFO had no influence on the cellular level of glutathione or the activity of glutathione reductase and superoxide dismutase suppressed by dichromate. Under the same experimental conditions, cellular uptake and distribution of chromium were not affected by DFO. These results indicate that DFO protects cells from chromium (VI)-induced DNA strand breaks, cytotoxicity, lipid peroxidation, vitamin E and C depression, and glutathione peroxidase inhibition The role of antioxidants in chromium (VI)-induced cytotoxicity, DNA breaks, and lipid peroxidation is discussed.
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PMID:Protective effect of deferoxamine on chromium (VI)-induced DNA single-strand breaks, cytotoxicity, and lipid peroxidation in primary cultures of rat hepatocytes. 919 15

Depressed mood has been associated with reduced natural killer cell activity (NKCA). Further, amelioration of depressive symptoms by pharmacotherapy has resulted in augmented NKCA. Serotonin, an indoleamine implicated in the pathophysiology of affective disorders, enhances NKCA in vitro and lymphocytes possess serotonin transporters and receptors. The present study evaluated NKCA in depressed outpatients before and during treatment with the selective serotonin reuptake inhibitor (SSRI) fluoxetine (Prozac(R)). Further, the SSRIs, fluoxetine and paroxetine (Paxil(R)), were also incubated in vitro with lymphoid cells to evaluate possible direct effects of SSRIs on NKCA. Depressed outpatients were administered fluoxetine (20 mg/day) for 4 weeks. NKCA and severity of depression were evaluated at weeks 0, 1, 2, and 4. Serum concentrations of fluoxetine and norfluoxetine were obtained as well. Mononuclear cells obtained from nonpatient volunteers were incubated with pharmacologic concentrations of fluoxetine or paroxetine and NKCA measured with a standard chromium release assay. Fluoxetine treatment resulted in decreased symptoms of depression and increased serum concentrations of fluoxetine and norfluoxetine. Further, fluoxetine treatment was associated with augmented NKCA in a subgroup of depressed outpatients exhibiting low NKCA at baseline. Fluoxetine had no effect on NKCA in depressed individuals exhibiting high NKCA at baseline. Incubation of mononuclear cells with fluoxetine and paroxetine augmented NKCA in vitro. The enhancing effects of antidepressants on NKCA in vivo and in vitro indicate a possible direct drug interaction with lymphoid cells during pharmacotherapy, suggesting that pharmacologic treatment of depression may result in enhanced immune competence as indexed by enhanced NKCA and that NKCA could be pharmacologically augmented with antidepressants in individuals with compromised immune function.
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PMID:Antidepressants augment natural killer cell activity: in vivo and in vitro. 989 55

Neocytolysis is a recently described physiological process affecting the selective hemolysis of young red blood cells in circumstances of plethora. Erythropoietin (EPO) depression appears to initiate the process, providing the rationale to investigate its contributions to the anemia of renal disease. When EPO therapy was withheld, four of five stable hemodialysis patients showed chromium 51 (51Cr)-red cell survival patterns indicative of neocytolysis; red cell survival was short in the first 9 days, then normalized. Two of these four patients received oral 13C-glycine and 15N-glycine, and there was a suggestion of pathological isotope enrichment of stool porphyrins when EPO therapy was held, again supporting selective hemolysis of newly released red cells that take up the isotope (one patient had chronic hemolysis indicated by isotope studies of blood and stool). Thus, neocytolysis can contribute to the anemia of renal disease and explain some unresolved issues about such anemia. One implication is the prediction that intravenous bolus EPO therapy is metabolically and economically inefficient compared with lower doses administered more frequently subcutaneously.
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PMID:Neocytolysis contributes to the anemia of renal disease. 991 81

The independent use of nutritional supplements has increased dramatically over the past several years. St. John's Wort for the treatment of depression, chromium for improvement of abnormal glucose and insulin regulation, and garlic for hypercholesterolemia, are among the more popular nutritional supplements being used by the population at large for their respective conditions. Depression, diabetes, and hypercholesterolemia are common to the renal patient. However, the efficacy of St. John's Wort, chromium, and garlic for these problems in the patient with impaired renal function is not known. This article reviews the pharmacology, efficacy, safety, and pharmokinetics of these three food supplements in the nonrenal patient. There are encouraging data suggesting successful treatment in the otherwise normal individual. However, clinical studies examining the safety of these three supplements for the treatment of depression, diabetes, and hypercholesterolemia in the patient with renal disease are lacking and preclude recommendation of their use.
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PMID:The effects of nutritional supplements on the treatment of depression, diabetes, and hypercholesterolemia in the renal patient. 1008 60

Authors evaluated the correlation between immune system and metal ions release in blood of 17 subjects with Cr/Co/Ni joint prostheses. For the purpose Chromium (Cr), Cobalt (Co) and Nickel (Ni) serum levels were measured and, at the same time some immunological parameters (Leukocytes, Lymphocytes and Lymphocytes T, B and Natural Killer cells sub-populations) were evaluated. The results showed a significant decrease of Leukocytes, Lymphocytes and of T Lymphocytes sub-populations. At the same time it was demonstrated a significant increase of Chromium, Cobalt and Nickel levels in patients with joint prostheses as compared to control population (23 patients). In conclusion, ions release from metallic surface of the prostheses is correlated with a depression of immune system. This correlation could depend on a toxic action on immune system caused by the products released by the implant. It could also depend on a lymphocytes compartimentalization in periprosthetic tissues as a consequence of a cell-mediated hypersensitivity reaction towards implants corrosion products.
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PMID:The effects of metal corrosion debris on immune system cells. 1036 19

Inhibition of the growth of nerve fibers by mercurials was quantitatively estimated by measuring the length of fibers in the cultured chick dorsal root ganglion. Morphological changes in nonneuronal cells were also evaluated. The growth rates of nerve fibers were constant for 2 to 6 days after the start of incubation. Methylmercury depressed nerve fiber growth dose- and time-dependently by 50% and completely at 3 x 10(-6) M and 7 x 10(-6) M, respectively. About 10-fold higher concentrations of inorganic mercury were required for the same extent of inhibition. The nerve fibers exposed to inorganic mercury shrank at an early stage of exposure and thereafter grew again within 24 hours. Electron microscopic examination revealed that methylmercury decreased microtubule mass extensively in nerve fibers, while inorganic mercury markedly altered surface membrane structure. These results suggested that microtubule disruption is involved in methylmercury-induced depression of nerve fibers but not in that induced by inorganic mercury. Characteristic effects on the growth of nerve fibers and the proliferation of nonneuronal cells were observed on the treatment with other metals such as cadmium, silver and chromium. Thus, dorsal root ganglion culture seems to be useful for the evaluation of toxic effects of metals in vitro.
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PMID:Effects of methylmercury and inorganic mercury on the growth of nerve fibers in cultured chick dorsal root ganglia. 1124 49


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