Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0851184 (thinning)
 11,252 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The hearts of 16 autopsy cases with a past history of administration of anthracycline antitumor drugs (DNR, ADR and ACM) and a sign of cardiac failure were investigated morphologically. In macroscopic observation, both ventricles were more or less dilated with thinning of the ventricular wall. Mural thrombi were recognized in the left ventricle of 2 cases. Histologically, the myocardial lesions could be roughly classified into two groups, a) myocardial changes in cases with rapidly developed cardiac failure (acute form), and b) myocardial changes in cases with relatively slowly developed cardiac failure. In acute form, myocardial cells showed marked swelling with dilatation of central sarcoplasmic core, marked reduction of myofibrils, vacuolization of cytoplasm and enlargement of nucleus accompanied by distinct large nucleolus. Necrotic myocardial cells were scattered among these degenerative cells. These degenerative and necrotic cells were distributed diffusely in both ventricular walls, but were more frequent in the left ventricular wall than in the right one. Inflammatory cell infiltration was also recognized not only in the myocardium, but also in the endocardium and epicardium. In chronic form, on the other hand, atrophy and attenuation of myocardial cells with a hypereosinophilic change of the cytoplasm and an increase in number of brown pigments, and marked reduction of myocardial cells were most common findings. These changes of chronic form, however, could not be identified as the specific changes of anthracycline cardiotoxicity. Fibrosis was hardly seen in the myocardium of both acute and chronic forms.
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PMID:Anthracycline induced myocardial damage. An analysis of 16 autopsy cases. 346 40

Parkinson's disease (PD) is a progressive neurodegenerative disorder characterized clinically by motor dysfunction (bradykinesia, rigidity, tremor, and postural instability), and pathologically by the loss of dopaminergic neurons in the substantia nigra of the basal ganglia. Growing literature supports that cognitive deficits may also be present in PD, even in non-demented patients. Gray matter (GM) atrophy has been reported in PD and may be related to cognitive decline. This study investigated cortical thickness in non-demented PD subjects and elucidated its relationship to cognitive impairment using high-resolution T1-weighted brain MRI and comprehensive cognitive function scores from 71 non-demented PD and 48 control subjects matched for age, gender, and education. Cortical thickness was compared between groups using a flexible hierarchical multivariate Bayesian model, which accounts for correlations between brain regions. Correlation analyses were performed among brain areas and cognitive domains as well, which showed significant group differences in the PD population. Compared to Controls, PD subjects demonstrated significant age-adjusted cortical thinning predominantly in inferior and superior parietal areas and extended to superior frontal, superior temporal, and precuneus areas (posterior probability >0.9). Cortical thinning was also found in the left precentral and lateral occipital, and right postcentral, middle frontal, and fusiform regions (posterior probability >0.9). PD patients showed significantly reduced cognitive performance in executive function, including set shifting (p = 0.005) and spontaneous flexibility (p = 0.02), which were associated with the above cortical thinning regions (p < 0.05).
IEEE/ACM Trans Comput Biol Bioinform
PMID:Cortical Thinning and Cognitive Impairment in Parkinson's Disease without Dementia. 2961 Jan 5

How to mine the gene regulatory relationship and construct gene regulatory network (GRN) is of utmost interest within the whole biological community, however, which has been consistently a challenging problem since the tremendous complexity in cellular systems. In present work, we construct gene regulatory network using an improved three-phase dependency analysis algorithm (TPDA) Bayesian network learning method, which includes the steps of Drafting, Thickening, and Thinning. In order to solve the problem of learning result is not reliable due to the high order conditional independence test, we use the entropy estimation approach of Gaussian kernel probability density estimator to calculate the (conditional) mutual information between genes. The experiment on the public benchmark data sets show the improved method outperforms the other nine kinds of Bayesian network learning methods when to process the data with large sample size, with small number of discrete values, and the frequency of different discrete values is about same. In addition, the improved TPDA method was further applied on a real large gene expression data set on RNA-seq from a global collection with 368 elite maize inbred lines. Experiment results show it performs better than the original TPDA method and the other nine kinds of Bayesian network learning algorithms significantly.
IEEE/ACM Trans Comput Biol Bioinform
PMID:Gene Regulatory Relationship Mining Using Improved Three-Phase Dependency Analysis Approach. 3028 76