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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To establish a baseline for conservation of a threatened clonal tree, Magnolia tomentosa, we investigated size distribution and genetic structure within a population, using six microsatellite markers. Within the study site, 1044 living ramets (stems) were distinguished into 175 genets (individuals). The mean number of ramets per genet was 5.97, and 76% of all genets had multiple ramets. Genets, which apparently produced new ramets through sprouting and layering, were generally composed of several large ramets and many small ramets. Spatial autocorrelation analysis of microsatellite alleles revealed positive autocorrelation over short distances for both ramets and genets. The Moran's I-value of ramets in the shortest distance class was 3.8 times larger than that of genets, reflecting the effect of clonal growth. To analyse the size-class differences in genetic structure, the 175 genets were separated into two size classes, small and large. The correlogram for the small genets exhibited positive spatial autocorrelation in the shortest distance class, but this was not the case for the correlogram for the large genets, indicating that genetic structure is weakened or lost through self-thinning as the genets grow. The FIS value over all loci for the small genets was positive and deviated significantly from zero, while the corresponding value for the large genets was close to zero. The excess homozygotes in the small genets may be the result of genetic substructuring and/or inbreeding, and the reduction in homozygote frequency from the small to large genets may be because of loss of genetic structure and/or inbreeding depression.
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PMID:Size distribution and genetic structure in relation to clonal growth within a population of Magnolia tomentosa Thunb. (Magnoliaceae). 1531 77

Atrophic dermatofibroma, a newly proposed entity in recent times, is thought to be a specific variant of dermatofibroma. We report a typical case of atrophic dermatofibroma on the thigh of a 69-year-old female. The lesion consisted clinically of a light brown, intracutaneous nodule with a central crateriform depression, and histologically of fibrohistiocytic components in the thinning dermis. On elastica van Gieson stain, loss of elastic fibres and dense accumulation of elastic fibres around medium-sized vessels were observed in the lesion.
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PMID:Atrophic dermatofibroma. 1532 99

We present a case in which mfERG and OCT helped to make a diagnosis of an old BRAO in the setting of compound heterozygous MTHFR genotype. A 44-year-old woman presented for evaluation of a 10 month history of persistently cloudy vision OS. She had been worked up previously for MS versus BRAO, and she was on coumadin, folate, and multivitamin at the time of presentation. The patient has a fraternal twin sister who was diagnosed with MS. Dilated fundus examination OS showed subtle inferior optic atrophy with slight narrowing of the inferotemporal retinal artery, and HVF test revealed a superonasal depression OS. mfERG also showed superonasal depression OS. Retinal origin of the chief complaint was further confirmed by OCT, which showed thinning of the NFL in the corresponding region of the retina OS. Coagulopathy evaluation revealed C677T/A1298C compound heterozygous genotype for MTHFR, and plasma homocysteine level after 6 months of folate and multivitamin supplementation was 10 microM (reference range 4-10 microM). The patient was diagnosed with BRAO and maintained on coumadin therapy.
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PMID:Branch retinal artery occlusion associated with compound heterozygous genotype for methylenetetrahydrofolate reductase. 1735 7

There is some evidence of corpus callosum abnormalities in elderly depression, but it is not known whether these deficits are region-specific or differ based on age at onset of depression. Twenty-four patients with early-onset depression (mean age = 68.00, SD+/-5.83), 22 patients with late-onset depression (mean age = 74.50, SD+/-8.09) and 34 elderly control subjects (mean age = 72.38; SD+/-6.93) were studied. Using 3D MRI data, novel mesh-based geometrical modeling methods were applied to compare the midsagittal thickness of the corpus callosum at high spatial resolution between groups. Neuropsychological correlates of midsagittal callosal area differences were additionally investigated in a subsample of subjects. Depressed patients exhibited significant callosal thinning in the genu and splenium compared to controls. Significant callosal thinning was restricted to the genu in early-onset patients, but patients with late-onset depression exhibited significant callosal thinning in both the genu and splenium relative to controls. The splenium of the corpus callosum was also significantly thinner in subjects with late- vs early-onset depression. Genu and splenium midsagittal areas significantly correlated with memory and attention functioning among late-onset depressed patients, but not early-onset depressed patients or controls. Circumscribed structural alterations in callosal morphology may distinguish late- from early-onset depression in the elderly. These findings suggest distinct abnormalities of cortical connectivity in late- and early-onset elderly depression with possible influence on the course of illness. Patients with a late onset of depression may be at higher risk of illness progression and eventually dementia conversion than early-onset depression, with potentially important implications for research and therapy.
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PMID:Mapping callosal morphology in early- and late-onset elderly depression: an index of distinct changes in cortical connectivity. 1771 48

This study was performed to elucidate the relation between in vivo measurements of two-dimensional principal strains and the progression of left ventricle (LV) wall thinning during development of dilated cardiomyopathy in the protein kinase C-epsilon (PKC-epsilon) transgenic (TG) overexpressing mouse heart. Principal two-dimensional strains, E1 and E2, were determined in the LV wall of the anesthetized mouse using cardiac MRI tagging at 14.1 T. PKC-epsilon TG provided a model of pure dilated cardiomyopathy without evidence of hypertrophy (PKC-epsilon TG, n = 6). Ejection fraction, wall thickness, and principal strains were determined at 1-mo intervals in hearts of PKC-epsilon TG vs. age-matched, nontransgenic mice (NTG, n = 5) from age 6 to 13 mo. Through the study, PKC-epsilon TG displayed lower ejection fraction than NTG. At 7 mo, average principal strain E1 in PKC-epsilon TG hearts was lower compared with NTG (PKC-epsilon TG = 0.14 +/- 0.03, NTG = 0.19 +/- 0.03, P < 0.05). The greatest reductions in regional E1 occurred in the lateral segments. The principal strain E2 did not change significantly in either group. At 9 mo, LV wall thinning occurred in PKC-epsilon TG mice (P < 0.01 vs. 8 mo) to 21% below values in NTG (P < 0.001). Average E1 strain diverged between PKC-epsilon TG and NTG hearts by 25-43%. These E1 changes preceded LV wall thinning and predated the eventual transition from a compensated circumstance to the dilated phenotype. The findings indicate a near step function in E1 depression that precedes the onset of LV wall thinning and suggest E1 as a prognostic indicator of dilated cardiomyopathy.
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PMID:Principal strain changes precede ventricular wall thinning during transition to heart failure in a mouse model of dilated cardiomyopathy. 1796 77

The activity of the pituitary-adrenal axis can profoundly impact on body composition. This is dramatically seen in Cushing's syndrome (CS) but changes in body composition are also implicated in depression and alcoholic pseudocushing's. The pathophysiological mechanisms underlying these changes remain poorly understood. Changes to body composition in CS include increased fat mass, decreased bone mass, thinning of the skin and reduced lean mass. Why these tissues are affected so dramatically is unclear. Additionally, the change in body composition between individuals varies considerably for reasons which are only now becoming evident. This paper reviews the phenotypic changes with altered pituitary-adrenal axis activity and discusses the mechanisms involved. The primary focus is on adipose, bone, muscle and skin since the most dramatic changes are seen in these tissues.
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PMID:The pituitary-adrenal axis and body composition. 1832 75

Disrupted-in-Schizophrenia-1 (DISC1), identified by positional cloning of a balanced translocation (1;11) with the breakpoint in intron 8 of a large Scottish pedigree, is associated with a range of neuropsychiatric disorders including schizophrenia. To model this mutation in mice, we have generated Disc1(tr) transgenic mice expressing 2 copies of truncated Disc1 encoding the first 8 exons using a bacterial artificial chromosome (BAC). With this partial simulation of the human situation, we have discovered a range of phenotypes including a series of novel features not previously reported. Disc1(tr) transgenic mice display enlarged lateral ventricles, reduced cerebral cortex, partial agenesis of the corpus callosum, and thinning of layers II/III with reduced neural proliferation at midneurogenesis. Parvalbumin GABAergic neurons are reduced in the hippocampus and medial prefrontal cortex, and displaced in the dorsolateral frontal cortex. In culture, transgenic neurons grow fewer and shorter neurites. Behaviorally, transgenic mice exhibit increased immobility and reduced vocalization in depression-related tests, and impairment in conditioning of latent inhibition. These abnormalities in Disc1(tr) transgenic mice are consistent with findings in severe schizophrenia.
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PMID:Schizophrenia-related neural and behavioral phenotypes in transgenic mice expressing truncated Disc1. 1894 97

The brain disturbances that place a person at risk for developing depression are unknown. We imaged the brains of 131 individuals, ages 6 to 54 years, who were biological descendants (children or grandchildren) of individuals identified as having either moderate to severe, recurrent, and functionally debilitating depression or as having no lifetime history of depression. We compared cortical thickness across high- and low-risk groups, detecting large expanses of cortical thinning across the lateral surface of the right cerebral hemisphere in persons at high risk. Thinning correlated with measures of current symptom severity, inattention, and visual memory for social and emotional stimuli. Mediator analyses indicated that cortical thickness mediated the associations of familial risk with inattention, visual memory, and clinical symptoms. These findings suggest that cortical thinning in the right hemisphere produces disturbances in arousal, attention, and memory for social stimuli, which in turn may increase the risk of developing depressive illness.
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PMID:Cortical thinning in persons at increased familial risk for major depression. 1958 94

Few studies comprehensively assessed psychological and behavioral functioning in adolescent kidney transplant patients. The purpose of this cross-sectional study was to evaluate depression, QOL, treatment adherence and presence of side effects from the perspective of the patient and his parents, and to compare scores with norm data. All patients (age 10-18 yr) and their parents completed the following instruments: KIDSCREEN-27 (QOL), a treatment adherence interview, the MTSOSD-59R (side effects) and the Beck Depression Inventory (depression). Twenty-three of 26 patients and 22 parents agreed to participate (70% male; median age 15 yr). Adolescents rated their QOL as satisfactory, but parents reported significant problems on several QOL dimensions. Depressive symptoms occurred in 17.4%, and 75% were non-adherent with their immunosuppressive drugs (confirmed by their parents) and show other problematic health behavior, including smoking, illicit drug use, dietary non-adherence, and suboptimal exercise levels. The most frequently occurring side effects were increased appetite, fatigue and headache; the most distressing ones were hair loss or thinning of hair, warts on hands or feet, and sores in the mouth or on the lips. Our results underscore the need for regular screening and adequate treatment of the above-mentioned aspects.
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PMID:Health-related quality of life, treatment adherence, symptom experience and depression in adolescent renal transplant patients. 1949 17

Cardiotoxicity associated with doxorubicin (DOX) treatment limits the therapeutic efficiency of this drug against cancer. 2-Chloro-N(6)-(3-iodobenzyl)adenosine-5'-N-methyluronamide (Cl-IB-MECA), a selective agonist of A(3) adenosine receptor (A(3)R), reduces DOX toxicity in newborn rat cultured cardiomyocytes. The study's aim was to determine whether the protection demonstrated by Cl-IB-MECA attenuates cardiac depression in vivo. In addition, we wished to examine whether this protective pathway affects the sarcoplasmic reticulum (SR) calcium uptake and release, as well as intramitochondrial Ca(2+) accumulation induced by DOX. Rats were injected every alternate day (6 times) with (1) saline, (2) 2.5mg/kg i.p. DOX, (3) 33 microg/kg i.v. Cl-IB-MECA, (4) DOX+Cl-IB-MECA. Left ventricular functions were assessed by invasive (pressure) and non-invasive (echocardiography) techniques at the end of the injection period and 4 weeks later. Cytosolic and intramitochondrial calcium levels were measured with indo-1 and rhod-2 probes. SR Ca(2+) content was determined by exposing cultured rat cardiomyocytes to caffeine. Echocardiography data demonstrate left ventricular wall thinning (23%), an increase in the end systolic dimension (170%) and decreased fractional shortening (35+/-5% vs. 54+/-5%, p<0.01) in DOX-treated animals, compared to the control group. DOX increased Ca(2+) levels in the cytosol and in mitochondria by diminishing the SR Ca(2+) uptake. Pretreatment with Cl-IB-MECA attenuated left ventricular dysfunction, improved SR calcium storage capacity and prevented mitochondrial Ca(2+) overload. We conclude that the adenosine A(3) receptor agonist is effective in vivo against DOX cardiotoxicity via the restoration of Ca(2+) homeostasis and prevention of mitochondrial damage that occurs as a result of Ca(2+) overload.
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PMID:Adenosine A3 receptor-mediated cardioprotection against doxorubicin-induced mitochondrial damage. 1968 2


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