Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:Q9UIJ5 (Rec)
 58,342 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An opiate-based anaesthetic technique has been developed for use in dogs with end-stage heart failure due to dilated cardiomyopathy. It has been used in dogs undergoing translocation of the left latissimus dorsi around the descending thoracic aorta to create an autologous counterpulsation system. Anaesthesia was induced with barbiturate (10 mg/kg thiopentone) and fentanyl (500 micrograms) and maintained by an infusion of fentanyl (0.5 micrograms/kg/minute) [corrected] in addition to halothane (0.1 to 0.5 per cent) and nitrous oxide (20 to 60 per cent). This technique provided safe anaesthesia for major intrathoracic surgery.
Vet Rec 1991 Nov 02
PMID:Development of an opiate-based anaesthetic technique for use in dogs with cardiomyopathy. 154 87

Dilated cardiomyopathy is a primary disease of the heart muscle that has been reported in Holstein-Friesian cattle worldwide in the past 20 years. Nine cases of the condition were compared in terms of their clinical and pathological characteristics with nine unaffected animals matched for age, sex and breed. Their clinical signs included right-sided heart failure with severe subcutaneous oedema, ascites and/or hydrothorax and distended jugular veins. There were no characteristic biochemical or haematological changes. Postmortem, the affected hearts were enlarged with all the chambers dilated and walls of variable thickness. In most cases the kidneys were pale with a pitted surface. Histologically there was marked perimysial and endomysial fibrosis, extensive loss of cardiomyocytes by coagulative or colliquative necrosis, increased variation in the cross-sectional area of the myocardial fibres, and multifocal disarray and vacuolation of myocytes. Scanning electron microscopy showed that in all cases there was a mild myocardial inflammatory infiltrate, either diffuse or multifocal, which was identified by immunohistochemical labelling as T cells.
Vet Rec 2004 Sep 18
PMID:Clinical and pathological features of dilated cardiomyopathy in Holstein-Friesian cattle. 1549 3

Gap junction expression has been studied in the atrioventricular junction (AVJ) of many species, however, their distribution in the human AVJ is unknown. The AVJ expression of the gap junction protein connexin 43 (Cx43) is species dependent; therefore we investigated its distribution in the human AVJ. Using Masson trichrome histology, we reconstructed the AVJ of three normal human hearts and one with dilated cardiomyopathy in three dimensions. Cx43 was immunolabeled with vimentin and alpha-actinin to determine the cellular origin of Cx43 and was quantified in the following structures: interatrial septum (IAS), His bundle, compact node (CN), lower nodal bundle (LNB), leftward and rightward nodal extensions (LE and RE), and inferior, endocardial, and left-sided transitional cells. Histology revealed two nodal extensions in three of four hearts. Cx43 was found in the myocytes, but not fibroblasts, of the AVJ. LE and CN Cx43 was lower than the IAS (P < 0.05) and the RE, LNB, and His all expressed Cx43 similarly, with approximately half of IAS expression (RE: 44 +/- 36%; LNB: 50 +/- 26%; His: 48 +/- 12%, P = NS compared with IAS). Cx43 levels in transitional cells were similar to the IAS (P = not significant). Cx43 was found in myocytes of the human AVJ, and its expression pattern delineates two separate continuous structures: one consists of the LE and CN with little Cx43, and the other consists of the His, LNB, and RE expressing approximately half the Cx43 of the IAS. The differential Cx43 expression may provide each structure with unique conduction properties, contributing to arrhythmias arising from the AVJ.
Anat Rec (Hoboken) 2008 Feb
PMID:Connexin 43 expression delineates two discrete pathways in the human atrioventricular junction. 1808 35

Members of the formin family are known to be involved in the regulation of the actin cytoskeleton. We have recently identified a muscle specific splice variant of the formin FHOD3 and demonstrated its role in the maintenance of the contractile filaments of cardiomyocytes. Here, we characterize the expression and subcellular localization of FHOD3's closest relative, FHOD1, in the heart. Confocal microscopy shows that FHOD1 is mainly located at the intercalated disc, the special type of cell-cell contact between cardiomyocytes, but also partially associated with the myofibrils. Subcellular targeting of FHOD1 is probably mediated by its N-terminal domain, since expression constructs lacking this domain show aberrant localization in primary cultures of neonatal rat cardiomyocytes. Finally, we show that in contrast to FHOD3, FHOD1 shows increased expression levels in dilated cardiomyopathy, suggesting that the two formins play distinct roles and are differentially regulated in cardiomyocytes.
Anat Rec (Hoboken) 2014 Sep
PMID:The formin FHOD1 in cardiomyocytes. 2512 70

Myosin VI (MVI) is a unique unconventional myosin translocating, unlike other myosins, towards the minus end of actin filaments. It is involved in numerous cellular processes such as endocytosis, intracellular trafficking, cell migration, and transcription. In mammalian skeletal muscles it localizes mainly to sarcoplasmic reticulum and is also present within the muscle nuclei and at the neuromuscular junction (Karolczak et al. Histochem Cell Biol 2013; 23:219-228). We have also shown that in denervated rat hindlimb muscle the MVI expression level is significantly increased and its localization is changed, indicating an important role of MVI in striated muscle pathology. Here, we addressed this problem by examining the distribution and expression levels of myosin VI in biopsies of skeletal muscles from patients with different myopathies. We found that, particularly in myopathies associated with fiber atrophy, the amount of MVI was enhanced and its localization in affected fibers was changed. Also, since a mutation within the human MVI gene was shown to be associated with cardiomyopathy, we assessed MVI localization and expression level in cardiac muscle using wild type and MLP(-/-) mice, a dilated cardiomyopathy model. No significant difference in MVI expression level was observed for both types of animals. MVI was found at intercalated discs and also at the sarcoplasmic reticulum. In the knockout mice, it was also present in ring-like structures surrounding the nuclei. The data indicate that in striated muscle MVI could be engaged in sarcoplasmic reticulum maintenance and/or functioning, vesicular transport, signal transmission and possibly in gene transcription.
Anat Rec (Hoboken) 2014 Sep
PMID:Myosin VI localization and expression in striated muscle pathology. 2512 83