Gene/Protein Disease Symptom Drug Enzyme Compound
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The effects of denervation on the gastrocnemius muscle of the frog were studied by histologic and histochemical methods. Thirteen Rana pipiens underwent unilateral sciatic neurotomy and were sacrificed weekly as long as 46 days. Of the three normal populations of muscle fibers, the small fibers underwent atrophy, the intermediate sized fibers remained unchanged in size, and the large fibers either did not change or underwent hypertrophy between 21 and 46 days. Necrosis of muscle fibers did not occur. Histochemical stains showed persistence of the normal pattern after denervation. The small fibers continued to have a high concentration of both oxidative and glycolytic enzyme activity (NADH-TR, SDH, phosphorylase), and the large fibers continued to have a low concentration of these enzymes. Depletion of glycogen stores was seen with PAS. Hypertrophic muscle fibers had mostly subsarcolemmal nuclei and few internal nuclei, suggesting that they may be physiologically tonic rather than twitch fibers. Achilles tenotomy at the time of denervation prevented the hypertrophy of large fibers. Abnormal inclusions have been demonstrated in mammalian muscle following tenotomy alone, but were not seen in the frog.
Anat Rec 1977 Mar
PMID:Effects of denervation and tenotomy on the gastrocnemius muscle in the frog: a histologic and histochemical study. 13 33

The most commonly encountered nutritional bone disease is nutritional secondary hyperparathyroidism. This is primarily of importance in the dog but is occasionally seen in kittens, particularly of the Siamese breed, and is often associated with the feeding of owner compiled, meat-rich diets. Classic rickets is now a rare clinical entity. Hypertrophic osteodystrophy is regularly seen in the larger breeds of dog and the aetiology remains obscure. Hypervitaminosis A associated with liver-rich diets is often encountered in the cat. Hypovitaminosis A has been described but its true clinical significance is unknown.
Vet Rec 1976 Apr 17
PMID:Nutrition and bone disease in the dog and cat. 77 53

We examined the spatio-temporal pattern of type X collagen mRNA and its protein in the embryonic chick vertebrae undergoing ossification by in situ hybridization and immunohistochemistry. Hypertrophic chondrocytes, producing type X collagen, were developed as islands of cells in a few vertebral body segments of stage 36 embryos. These cells were increased in number at stages 37 and 38 and they expressed high levels of type X collagen mRNA and deposited its protein in the matrix. Blood vessels entered from the perichondrium at stage 37 and invaded deeply into hypertrophic cartilage at stage 38. As the vertebrae grew further at stage 40, the leading front of active hypertrophic chondrocytes with high levels of type X mRNA shifted from the midvertebral perivascular area towards intervertebral borders, while the perivascular area retained a number of inactive hypertrophic chondrocytes with low levels of type X mRNA. Type X collagen was found in large amounts throughout the matrix areas containing both active and inactive hypertrophic chondrocytes. Calcium was detected by von Kossa's technique in hypertrophic cartilage matrix in a small amount at stage 37, in parts of the matrix with type X collagen deposition in succeeding stages, and finally in almost the entire area of type X collagen deposition at stage 45. The vertebral segments of stage 45 embryos also showed a clearly reversed pattern of expression between type X collagen mRNA and types II and IX collagen mRNAs. The results demonstrate that the production of type X collagen by hypertrophic chondrocytes precedes both vascular invasion and mineralization of the matrix, suggesting that hypertrophic chondrocytes have an important role in regulating these events.
Anat Rec 1991 Apr
PMID:Spatiotemporal pattern of type X collagen gene expression and collagen deposition in embryonic chick vertebrae undergoing endochondral ossification. 204 50

Hypertrophic scars and keloids appear to be unique to humans since animals are not known to form these lesions. Therefore, in an effort to develop an experimental model for their study, implants of these human lesions were made in nude (athymic) mice (nu/nu) in suprascapular subcutaneous pockets. The implants were recovered from 2 to 246 days. By histological and fine structural parameters all implants remained viable and their morphological character was maintained. Selected mice were injected with barium to confirm by microangiography vascular flow between mouse and implant. Hoechst stain for DNA, used to distinguish mouse cells from human cells, confirmed vascular anastamosis between host and implant: barium-filled vessels in the interior of the implant demonstrated human endothelial cells. Peripheral vascularization of the implant with minimal ingrowth of mouse vessels occurs during the first 8 days. Anastamosis probably occurs sometime before 16 days postimplantation, or earlier, depending upon the availability of patent microvessels in the implanted tissue. The presence of the implant does not appear to prompt a continuing vascular growth into or throughout the implant. The time frame of 16 days postimplantation should be taken into account when developing schemata of experimental or therapeutic modalities.
Anat Rec 1989 Nov
PMID:Use of nude (athymic) mice for the study of hypertrophic scars and keloids: vascular continuity between mouse and implants. 281 36

The cardiac sarcomere is the functional unit for myocyte contraction. Ordered arrays of sarcomeric proteins, held in stoichiometric balance with each other, respond to calcium to coordinate contraction and relaxation of the heart. Altered sarcomeric structure-function underlies the primary basis of disease in multiple acquired and inherited heart disease states. Hypertrophic and restrictive cardiomyopathies are caused by inherited mutations in sarcomeric genes and result in altered contractility. Ischemia-mediated acidosis directly alters sarcomere function resulting in decreased contractility. In this review, we highlight the use of acute genetic engineering of adult cardiac myocytes through stoichiometric replacement of sarcomeric proteins in these disease states with particular focus on cardiac troponin I. Stoichiometric replacement of disease causing mutations has been instrumental in defining the molecular mechanisms of hypertrophic and restrictive cardiomyopathy in a cellular context. In addition, taking advantage of stoichiometric replacement through gene therapy is discussed, highlighting the ischemia-resistant histidine-button, A164H cTnI. Stoichiometric replacement of sarcomeric proteins offers a potential gene therapy avenue to replace mutant proteins, alter sarcomeric responses to pathophysiologic insults, or neutralize altered sarcomeric function in disease.
Anat Rec (Hoboken) 2014 Sep
PMID:Cell biology of sarcomeric protein engineering: disease modeling and therapeutic potential. 2512 79