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)

The endocardium of Oniscus asellus L. and Asellus aquaticus L. consists of lipid cells. The epicardium consists of a layer of cells with a vesiculated cytoplasm covered by a thick extracellular fibrous sheet. The myocardium is a single layer of cells, the sarcolemma invaginates at Z disc level forming transverse tubules, and longitudinal tubules branch off from these. At the A-I level longitudinal tubules from transverse systems, which form couplings with the sarcoplasmic reticulum. The sarcoplasmic reticulum appears as perforated sheets enveloping the myofibrils. Two types of nerve terminal are found: one is embedded in a myocardial cell process, the other lies in a myocardial cell depression. They contain clear and dense-cored synaptic vesicles.
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PMID:The ultrastructure of the heart of Oniscus asellus L. and Asellus aquaticus L (Crustacea, Isopoda). 747 Nov 75

Mutational inactivation of p53, a potential tumor-suppressor gene, has been found in many tumors of humans as well as rodents. The p53 status in normal and transformed mouse liver cell lines has, however, not been investigated. We examined possible point mutations and compared mRNA and protein expression of the p53 gene in normal vs. transformed mouse liver cells. The transformed cells studied included lines spontaneously transformed by sub-culture, virally transformed by simian virus 40 (SV40), and chemically transformed by N-methyl-N-nitro-N-nitrosoguanidine (MNNG) or methylcholanthrene epoxide (MC). A heterozygous G-->A point mutation at codon 241, position 1, of p53 was detected in MNNG-transformed cells after screening of 5 evolutionarily conserved regions where mutation hot-spots are clustered. The mutation causes a gly-->arg substitution. No mutations were found in normal or other transformed cells. The steady-state levels of p53 mRNA were decreased in chemically transformed (both MNNG- and MC-transformed) cells. Elevated levels of p53 protein were found in spontaneously transformed and SV40-transformed cells, an observation that may reflect a longer half-life of the protein, as has been shown in other transformed lines. The low level of the p53 protein in MC-transformed cells may result from transcriptional depression of the p53 gene. We conclude from these data that abnormal p53 status, such as point mutation or altered expression, may play a role during the malignant transformation of mouse liver cells.
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PMID:Alterations of the p53 tumor-suppressor gene in transformed mouse liver cells. 750 57

We followed weekly the evolution of serum lipid concentrations in two bodybuilders undergoing a cycle of treatment with anabolic steroids. These drugs caused maximum depression of high-density lipoprotein cholesterol concentrations by 69.1% in the fifth week after the beginning of the cycle for subject 1, and by 72.4% in the fourth week for subject 2. Maximum increases in low-density lipoprotein cholesterol concentrations were 144% and 156%, respectively. Total cholesterol and apolipoprotein (apo) B were highly increased with anabolic steroid use. We also saw depression of apo A-I by 84% and 91%, and lipoprotein(a) decreased to undetectable amounts in both cases. These effects were reversed 10 weeks after the end of the steroid cycle in subject 1, but subject 2 still presented abnormal concentrations of serum lipids 13 weeks after drug cessation. The periods until reversibility of anabolic steroid effects on lipids were longer than those reported in previous studies.
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PMID:Evolution of serum lipids in two male bodybuilders using anabolic steroids. 866 91

Paraoxonase is a high-density lipoprotein (HDL)-associated enzyme capable of hydrolysing lipid peroxides. We measured the activity of serum paraoxonase together with serum concentrations of a variety of lipid constituents--total cholesterol, high-density lipoprotein (HDL) and low-density lipoprotein (LDL), cholesterol, triglycerides, apolipoproteins A-I and B--in 60 hemodialyzed (HD) patients. We found that the paraoxonase activity was significantly reduced in HD patients compared with 64 healthy controls (mean median and interquartile values: 93, 63, 87 IU/l in HD patients and 151, 120 and 135 IU/l in controls). In patients, the trimodal frequency of distribution of paraoxonase activity showed a shift toward lower levels. The effect of NaCl on enzyme activation was more pronounced in the patient group, as compared with controls, suggesting a higher frequency of the B allozyme (more responsive to NaCl) in this population. We suggest that altered HDL subfraction, present in HD patients, may be the main cause of the widespread depression of paraoxonase. Furthermore, the higher frequency of allozyme B among HD patients might increase the risk of coronary artery disease. In conclusion, paraoxonase activity may be an adjunctive index of altered lipoprotein metabolism with important repercussions on atherosclerosis.
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PMID:Serum paraoxonase activity is decreased in uremic patients. 892 Feb 28

Arginine metabolism plays an important role in many aspects of inflammation and wound healing. In this study, we tested the hypothesis that steroids and vitamin A have differential effects on arginine metabolism and thereby may provide a mechanism by which steroids impair wound healing, and vitamin A improves this impairment. Rats were treated with subcutaneous corticosterone pellets 2 days prior to wounding. Intraperitoneal injections of all-trans retinoic acid in peanut oil were administered at the same time and repeated 2 and 4 days later. Polyvinyl alcohol sponges were implanted subcutaneously through a dorsal incision. On Postwounding Days 1, 5, 10, and 15, wound fluid was recovered from the sponges and assayed for nitrite/nitrate (NOx), citrulline, arginine, and ornithine concentrations as well as arginase activity. Steroid treatment decreased the metabolism of arginine to nitric oxide in the early phase of wound healing, and retinoic acid did not change this relationship. Corticosterone also decreased metabolism of arginine to ornithine in the later wound. This depression was inhibited by concomitant administration of retinoic acid. Considering the importance of nitric oxide in host defense and ornithine as a precursor for polyamine and proline synthesis, these data provide a mechanism by which vitamin A improves wound strength, but does not improve wound infection rates in steroid-treated animals.
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PMID:Altered wound arginine metabolism by corticosterone and retinoic acid. 922 33

Circulating phagocytic cells (hemocytes) of the snail Biomphalaria glabrata, intermediate host of the human blood fluke Schistosoma mansoni, were treated with the tetrapeptide, arg-gly-asp-ser (RGDS), an integrin-specific adhesion inhibitor, and assessed for their ability to adhere and spread on uncoated and snail plasma protein-coated glass slides. Although cells were capable of adherence, RGDS significantly inhibited the spreading ability of hemocytes in both a time and RGDS concentration-dependent fashion regardless of plasma protein coating. The inhibition of hemocyte spreading by RGDS was a specific response, since treatment of cells with a glutamic acid-substituted control peptide (RGES) did not exert the same inhibitory effect. A comparison of RGDS-responses between hemocytes of two strains of B. glabrata, one resistant (R; 13-16-R1 strain) and the other susceptible (S; NMRI strain) to infection by S. mansoni, revealed several snail strain-specific differences. At concentrations of 0.5 mM RGDS, R snail hemocyte spreading was unaffected, whereas a significant depression of spreading was seen in cells of the S snail. Moreover, we observed that R strain hemocytes spread more rapidly on homologous plasma-coated surfaces than the S snail strain following peptide pretreatment and removal. These data suggest that hemocytes from S and R snails may differ either in the number of RGDS-binding receptors or in their affinity for the RGDS peptide. In order to identify the type(s) of integrin-like RGD-binding receptors that may be present on the surface of snail immunocytes, washed hemocytes were placed on various mammalian extracellular matrix proteins and evaluated for their spreading function in the presence of specific or non-specific peptides. Hemocyte aggregation or clumping was observed on all test protein substrates, and this aggregation behavior was specifically inhibited by RGDS. Thus, RGD-binding receptors appear to play a critical role in cellular motility on matrix-coated surfaces and/or cell-cell binding. Our data provide functional evidence for an integrin-like receptor on circulating phagocytes of snails, and for an RGD-binding mechanism involved in cell-substrate interactions.
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PMID:Integrin-like RGD-dependent binding mechanism involved in the spreading response of circulating molluscan phagocytes. 961 82

Mice harboring random gene-trap insertions of a lacZ (beta-galactosidase)-neomycin resistance fusion cassette (beta-geo) were analyzed for expression in the hippocampus. In 4 of 15 lines reporter gene activity was observed in the hippocampal formation. In the obn line, enzyme activity was detected in the CA1-3 hippocampal subfields, in hpk expression was restricted to CA1, but in both lines reporter activity was also present in other brain regions. In the third line, kin, reporter activity was robustly expressed throughout the stratum pyrimidale of CA1-3, with only low-level expression elsewhere. The final line (glnC) displayed ubiquitous expression of the reporter and was not analyzed further. Fusion transcripts for the first three lines were characterized; all encode polypeptides with features of membrane-associated signalling proteins. The obn fusion identified a human cDNA (B2-1) encoding a pleckstrin homology (PH) domain, while hpk sequences matched the Epstein-Barr Virus (EBV) inducible G-protein coupled receptor, EBI-1. kin identified an alternative form of the abl-related nonreceptor tyrosine kinase c-arg. Electrophysiological studies on mice homozygous for the insertions revealed normal synaptic transmission, paired pulse facilitation and paired-pulse depression at Schaffer collateral-commissural CA1 synapses, and normal long-term potentiation (LTP) in obn and kin. hpk mice displayed an increase in hippocampal CA1 long-term potentiation (LTP), suggesting a role for this receptor in synaptic plasticity.
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PMID:Gene-trapping to identify and analyze genes expressed in the mouse hippocampus. 982 57

Manganese intake can vary greatly with food choices, water composition, and supplement use. Thus, individuals consuming Western diets consume from < 1 to > 10 mg Mn/d. The levels of manganese intake associated with adverse effects (both deficient and toxic) are debatable. Moreover, many of the symptoms of manganese deficiency (growth retardation, changes in circulating HDL cholesterol and glucose levels, reproductive failure) and manganese toxicity (growth depression, anemia) are non-specific. The bone deformities observed in manganese-deficient animals and neurological symptoms of individuals who have inhaled excess manganese are permanent and illustrate the need to identify sensitive biomarkers of manganese status that appear before these symptoms. Manganese balance and excretion data are not useful biomarkers of manganese exposure but demonstrate that the body is protected against manganese toxicity primarily by low absorption and/or rapid presystemic elimination of manganese by the liver. Serum manganese concentrations in combination with lymphocyte manganese-dependent superoxide dismutase (MnSOD) activity and perhaps blood arginase activity, appear to be the best ways to monitor ingestion of insufficient manganese. Serum manganese concentrations in combination with brain MRI (magnetic resonance imaging) scans, and perhaps a battery of neurofunctional tests, appear to be the best ways to monitor excessive exposure to manganese.
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PMID:Nutrition versus toxicology of manganese in humans: evaluation of potential biomarkers. 1038 84

1. Arginase, an important part of the arginine-regulating system modulates nitric oxide generation; a neuroregulatory agent, which has been implicated in various neuropathological conditions. 2. In this regard, the authors investigated the arginine-nitric oxide pathway by measuring serum arginase activity in drug free major (n=18) and minor depressed outpatients (n=12) and healthy control subjects (n=30) in order to make a contribution to the understanding of disease mechanism. 3. Major depressed patients were found to have significantly higher serum arginase activity compared to controls (p<0.001) and minor depressives (p=0.001). Moreover, there was significant positive correlation between arginase activity and severity of depression in patients (p<0.001). 4. Results suggest that the arginine-nitric oxide pathway is involved in depression. Enhanced arginase activity in major depressed patients possibly leading to a decrease in nitric oxide synthesis may contribute to the symptomatology of depression.
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PMID:Increased serum arginase activity in depressed patients. 1080 Jul 45

Post fertilization growth of tobacco ovary tissues treated with inhibitors of polyamine (PA) biosynthesis was examined in relation to endogenous PA titers and the activities of arginine decarboxylase (ADC, EC 4.1.1.19) and ornithine decarboxylase (ODC, EC 4.1.1.17). DL-alpha-Difluoromethylornithine (DFMO) and DL-alpha-difluoromethylarginine (DFMA), specific, irreversible ("suicide") inhibitors of ODC and ADC in vitro, were used to modulate PA biosynthesis in excised flowers. ODC represented >99% of the total decarboxylase activity in tobacco ovaries. In vivo inhibition of ODC with DFMO resulted in a significant decrease in PA titers, ovary fresh weight and protein content. Simultaneous inhibition of both decarboxylases by DFMO and DFMA produced only a marginally greater depression in growth and PA titers, indicating that ODC activity is rate-limiting for PA biosynthesis in these tissues. Paradoxically, DFMA alone inhibited PA biosynthesis, not as a result of a specific inhibition of ADC, but primarily through the inactivation of ODC. In vivo inhibition of ODC by DFMA appears to result from arginase-mediated hydrolysis of this inhibitor to urea and DFMO, the suicide substrate for ODC. Putrescine conjugates in tobacco appear to function as a storage form of this amine which, upon hydrolysis, may contribute to Put homeostasis during growth.
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PMID:In vivo inhibition of polyamine biosynthesis and growth in tobacco ovary tissues. 1153 96


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