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)

Both amplification of normal visceral phenomena and the personality trait of alexithymia are factors in the process of somatization, whereby somatic symptoms become metaphors for emotional distress. The relationship between these two variables was investigated in 101 psychiatric out-patients. Each subject was administered the Somatosensory Amplification Scale (SSA); the Toronto Alexithymia Scale (TAS); the NEO-FFI, which measures five personality factors; and the health locus of control (HLC). In addition, anxiety and depression were quantitatively measured. SSA and TAS significantly correlated only in the female subjects. A regression model found neuroticism to contribute the most variance in predicting SSA while TAS did not fit into the model. Amplification is a perceptual element in potentiating somatization, whereas alexithymia contributes to the cognitive aspects of the process. The role of neuroticism is discussed as a mediating factor.
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PMID:The relationship between somatosensory amplification, alexithymia, and neuroticism. 799 59

Ethanol, a risk factor for myocardial dysfunction, depresses myocardial contraction. This study was to determine whether ethanol-induced myocardial depression is affected by hypertension. Mechanical properties of ventricular myocytes isolated from both normotensive Wistar-Kyoto (WKY) and spontaneously hypertensive (SHR) rats were evaluated using a video edge-detection system. Myocytes were electrically stimulated to contract at 0.5 Hz. Contractile properties analyzed include peak twitch amplitude (PTA), time-to-PTA (TPS), time-to-90% relengthening (TR(90)), and maximal velocities of shortening/relengthening (+/-dL/dt). Intracellular Ca(2+) transients were measured as fura-2 fluorescence intensity (DeltaFFI) changes. Acute ethanol exposure (80-640 mg/dl) caused a concentration-dependent inhibition of PTA and DeltaFFI in both WKY and SHR myocytes. The extent of maximal inhibition of PTA and FFI was significantly greater in SHRs (53.7 and 38.9%) compared to the WKY group (21.0 and 25.4%). Ethanol did not affect TPS but shortened TR(90) and slowed +/-dL/dt at high concentration ranges. Interestingly, the augmented ethanol-induced inhibition of cell shortening in hypertension was greatly attenuated by Ca(2+) channel opener BayK 8644 (1 microM). These results suggest that ethanol-induced myocardial depression may be augmented in hypertension, possibly due to mechanism(s) involving sarcolemmal Ca(2+) channels.
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PMID:Hypertension augments ethanol-induced depression of cell shortening and intracellular Ca(2+) transients in adult rat ventricular myocytes. 1040 46

The current mainstay of treatment in glycogen storage disease type I (GSD I) is dietary management that includes providing a frequent source of glucose to prevent hypoglycaemia. To ensure compliance, routine follow-up by a health care team, including a dietitian, experienced in the treatment of GSD is necessary. We describe an adolescent patient with GSD Ib in good metabolic control who was admitted with a 3-month history of weakness, depression, vomiting, decreased appetite and a 11.4-kg weight loss. He had a recent onset of unsteady gait, inability to write, and sore mouth. After an extensive work-up, the patient was found to have vitamin B12, folate, iron and other nutritional deficiencies, which explained his symptoms. The patient improved within 72 h of initiation of total parenteral nutrition and therapeutic doses of deficient micronutrients, with a complete recovery in 2 months. Dietary restrictions, dependence on non-food products (e.g. cornstarch in GSD I), and social and developmental issues place individuals with metabolic disorders at a high risk for developing an array of nutritional deficiencies. This case highlights the importance of both close follow-up of the metabolic control and close monitoring of growth and nutritional intake in individuals with inborn errors of metabolism. This case also illustrates the importance of daily supplementation with appropriate multivitamins, calcium and other minerals needed to meet the Recommended Dietary Allowances (RDAs) in these patients.
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PMID:Nutritional deficiencies in a patient with glycogen storage disease type Ib. 1051 79

Evidence suggests a pathophysiological role of insulin-like growth factor 1 (IGF-1) in hypertension. Cardiac function is altered with advanced age, similar to hypertension. Accordingly, the effects of IGF-1 on cardiac myocyte shortening and intracellular Ca(2+) were evaluated in hypertension at different ages. Ventricular myocytes were isolated from Wistar-Kyoto rats (WKY) and spontaneously hypertensive rats (SHR), aged 12 and 36 weeks. Mechanical and intracellular Ca(2+) properties were examined by edge-detection and fluorescence microscopy. At 12 weeks, IGF-1 (1 to 500 ng/mL) increased peak twitch amplitude (PTA) and FFI changes (DeltaFFI) in a dose-dependent manner in WKY myocytes, with maximal increases of 27.5% and 35.2%, respectively. However, IGF-1 failed to exert any action on PTA and DeltaFFI in the age-matched SHR myocytes. Interestingly, at 36 weeks, IGF-1 failed to exert any response in WKY myocytes but depressed both PTA and DeltaFFI in a dose-dependent manner in SHR myocytes, with maximal inhibitions of 40.5% and 16.1%, respectively. Myocytes from SHR or 36-week WKY were less sensitive to norepinephrine (1 micromol/L) and KCl (30 mmol/L). Pretreatment with nitric oxide synthase inhibitor N(omega)-nitro-L-arginine methyl ester (L-NAME, 100 micromol/L) did not alter the IGF-1-induced response in 12-week WKY myocytes but unmasked a positive action in 12-week SHR and 36-week WKY myocytes. L-NAME also significantly attenuated IGF-1-induced depression in 36-week SHR myocytes. In addition, the Ca(2+) channel opener Bay K8644 (1 micromol/L) abolished IGF-1-induced cardiac depression in 36-week SHR myocytes. Collectively, these results suggest that the IGF-1-induced cardiac contractile response was reduced with advanced age as well as with hypertension. Alterations in nitric oxide and intracellular Ca(2+) modulation may underlie, in part, the resistance to IGF-1 in hypertension and advanced age.
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PMID:Influence of age on contractile response to insulin-like growth factor 1 in ventricular myocytes from spontaneously hypertensive rats. 1060 Nov 21

Serum lipid profiles and apolipoproteins were measured in 148 patients with silent myocardial ischemia (SMI) and 30 healthy control subjects comparable in age. The serum lipid profiles and apolipoproteins were abnormal in all types of SMI which were more significant in type II and III. The extent of ST segment depression in ECG were positively correlated with serum TG, TC, LDL, B100, B100/A1, Lp(a); and negatively correlated with A1, HDL1, HDL2, HDL-C/TC. Multiple-factor stepwise regression analysis revealed that the increased concentration of serum TG, LDL, and B100/A1 ratio and decrease of HDL2-C are independent risk factors in SMI.
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PMID:[Changes of blood lipids and apolipoproteins in patients with silent myocardial ischemia]. 1068 93

The authors compared the internal consistency, 1-year temporal stability, and self-informant agreement of ratings of personality trait (NEO Five-Factor Inventory; NEO-FFI; P. T. Costa & R. R. McCrae, 1992) and personality disorder symptom severity (Structured Clinical Interview for DSM-III-R Personality Disorders Questionnaire; SCID-II-Q; R. L. Spitzer, J. B. W. Williams, M. Gibbon, & M. First, 1990) in 131 substance-dependent inpatients. Internal consistency coefficients were acceptable to very good for most NEO-FFI and SCID-II-Q scales, and temporal stability correlations were significant for all measures. Agreement between patient and informant ratings was more modest. Substance abuse and depression symptom severity moderated the temporal stability and self-informant agreement of several personality trait and disorder ratings. The authors did not find that the five factors were more reliable than the Axis II symptoms. Issues related to the reliability of personality assessment in multiply diagnosed patients are discussed.
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PMID:Reliability of personality disorder symptoms and personality traits in substance-dependent inpatients. 1135 28

Research in unipolar depression suggests that neuroticism is associated with poor long-term outcome and greater chronicity. The objective of this study was to determine whether baseline neuroticism scores predict response to treatment with fluoxetine in depressed outpatients. Seventy-six depressed outpatients participating in a clinical trial of fluoxetine (fixed/flexible dosing) completed the NEO-FFI (five factor inventory short form) at baseline. Clinical response was defined as a 50% or greater decrease in the 17-item Hamilton Depression Rating Scale (HAM-D-17) total score (final visit--baseline). Logistic regression evaluated NEO-FFI factor scores as predictors of treatment outcome within an intent-to-treat model. Scores on the neuroticism scale were not found to significantly predict treatment response as measured by the HAM-D-17. Strengths of this study include a standardized treatment protocol and use of structured interview instruments, while limitations include a modest sample size, lack of continuation data, state/trait effects, and lack of generalizability to other antidepressant treatments.
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PMID:NEO-FFI factor scores as predictors of clinical response to fluoxetine in depressed outpatients. 1185 46

Cortical spreading depression (CSD) may be the underlying mechanism of migraine aura. The role of CSD in initiating a migraine headache remains to be determined, but it might involve specific changes in gene expression in the brain. To examine these changes, four episodes of CSD at 5-minute intervals were induced in the mouse brain by application of 300mM KCl, and gene expression was examined 2 hours later using cDNA array and reverse transcriptase-polymerase chain reaction. Controls consisted of groups that received anesthesia only, attachment of recording electrodes only, and application of 0.9% NaCl. Of the over 1,180 genes examined in our experiments, those consistently regulated by CSD included vasoactive peptides; the vasodilator atrial natriuretic peptide was induced by CSD, while the vasoconstrictor neuropeptide Y was downregulated. Other genes specifically regulated by CSD were involved in oxidative stress responses (major prion protein, glutathione-S-transferase-5, and apolipoprotein E). L-type calcium channel mRNA was upregulated. In summary, CSD regulates genes that are intrinsic to its propagation, that identify accompanying vascular responses as a potential source of pain, and that protect against its potential pathological consequences. We believe these observations have strong relevance to the mechanisms of migraine and its outcomes.
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PMID:Cortical spreading depression and gene regulation: relevance to migraine. 1192 Oct 56

The development of civilization and progress in medicine made the prolongation of the life span and increased share of the advanced old age people in the population. The consequence of this process is growth in frequency of diseases related to age including dementia. However diagnosis of cognitive impairment is still difficult and it makes some problems in an everyday medical practice. The aim of this report is to define main and significant determinants of dementia basing on the MMSE scale. This could make it easier to suspect the cognitive disorders to make indepth diagnosis and to start earlier therapy. The sample consisted of 124 community dwelling persons 75-year old and over. 64 of them were mildly, moderately or severely demented according to Katzman scale administered previously and 60 were intellectually intact. The both groups of persons were tested with MMSE. Geriatric Depression Scale, ADL scale (EASY-Care questionnaire) and short internal and neurological examination. The multiple regression model were used, where dependent variable was the MMSE score and independent variables social-demographic data, ADL and GSD scales and data from interview and medical examination. 72 variables were included to the model and 39 of them were significantly connected with cognitive impairment. The valid factors explained dementia in 78.7% (adjusted R2 = 0.787). The strongest connection was found with (1) an ignorance of own date of birth, (2) low education level, (3) behaviour disorders and (4) an advanced old age. These determinants, including difficulties with handling own money, have explained dementia in 57%. The presence such symptoms could make easier to suspect the cognitive disorders, to make in-depth diagnosis, and to start earlier therapy.
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PMID:[Determinants of dementia in the advanced old age elderly]. 1218 87

Before and after hysterectomy, 60 women completed self-report questionnaires. Measures of personality (NEO-Five Factor Inventory, NEO-FFI), coping (Coping Inventory for Stressful Situations, CISS), and procedure appraisal were completed pre-operatively. Measures of depression and anxiety were completed pre- and post-operatively. Pre-op, 34% of women reported depression at clinical levels, and 29% reported clinical anxiety. The prevalence of depression fell to 8% 3-months post-op although clinical levels of anxiety persisted post-op in 22% of women. Regression analyses revealed that the principal risk factors for post-op negative affect were pre-op levels of depression and concerns about hysterectomy outcome. In assessing proposed models of post-hysterectomy outcome, structural equational modelling revealed the key position of neuroticism and extraversion, which were both directly and indirectly related to pre- and post-operative depression and anxiety. The mediating variables in this model included coping dispositions and procedure appraisal. It is concluded that the variables contained within stress moderation models provide a useful framework for understanding the processes that may lead to elevated levels of negative affect both before and after hysterectomy. Such an approach may prove beneficial for other surgical-outcome studies.
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PMID:Understanding pre- and post-hysterectomy levels of negative affect: a stress moderation model approach. 1285 94


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