Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0030567 (Parkinson's disease)
 63,064 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Necrotizing enterocolitis (NEC) is the most common gastrointestinal emergency in newborn premature infants. Clinical studies show increased incidence of NEC in premature infants with enteral formula feeding; however, pathogenesis remains unclear. To identify the NEC-related proteins for molecular mechanisms, we applied proteomics analysis to characterize changes in the protein expression profile of newborn premature piglet intestines with NEC developed after enteral formula feeding for 24 h. Changes in protein expression were identified using 2-dimensional gel electrophoresis and peptide mass fingerprinting with MS as well as western blotting analysis. Nineteen differentially expressed proteins were identified and these have roles in oxidative stress, chaperone, signal transduction, protein folding and degradation, oxygen transport, signal transduction, and energy metabolism. Proteins with increased levels include manganese-containing superoxide dismutase and hemoglobin subunit and proteins with decreased expression include sorbitol dehydrogenase, mitochondrial aldehyde dehydrogenase 2, glucose-regulated protein 75, CRY protein, snail homolog 3, thyroid hormone-binding protein precursor, and DJ1 (Parkinson's disease 7) etc. The data provided novel mechanistic insights into the pathogenesis of NEC and the insults of a formulated diet to the premature gut.
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PMID:The small intestine proteome is changed in preterm pigs developing necrotizing enterocolitis in response to formula feeding. 1880 98

The objective of this study was to evaluate the pathology time course of the LRRK2 knockout rat model of Parkinson's disease at 1-, 2-, 4-, 8-, 12-, and 16-months of age. The evaluation consisted of histopathology and ultrastructure examination of selected organs, including the kidneys, lungs, spleen, heart, and liver, as well as hematology, serum, and urine analysis. The LRRK2 knockout rat, starting at 2-months of age, displayed abnormal kidney staining patterns and/or morphologic changes that were associated with higher serum phosphorous, creatinine, cholesterol, and sorbitol dehydrogenase, and lower serum sodium and chloride compared to the LRRK2 wild-type rat. Urinalysis indicated pronounced changes in LRRK2 knockout rats in urine specific gravity, total volume, urine potassium, creatinine, sodium, and chloride that started as early as 1- to 2-months of age. Electron microscopy of 16-month old LRRK2 knockout rats displayed an abnormal kidney, lung, and liver phenotype. In contrast, there were equivocal or no differences in the heart and spleen of LRRK2 wild-type and knockout rats. These findings partially replicate data from a recent study in 4-month old LRRK2 knockout rats and expand the analysis to demonstrate that the renal and possibly lung and liver abnormalities progress with age. The characterization of LRRK2 knockout rats may prove to be extremely valuable in understanding potential safety liabilities of LRRK2 kinase inhibitor therapeutics for treating Parkinson's disease.
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PMID:Loss of leucine-rich repeat kinase 2 (LRRK2) in rats leads to progressive abnormal phenotypes in peripheral organs. 2424 10