Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.2.1.36 (hyaluronidase)
4,606 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The trophedema Nonne-Milroy-Meige has an exceptional position within the group of the primary lymphatic edemas (l.e.) because of its hereditary. Its frequency less than 1% of primary l.e. The trophedema is caused by a genetic determined defect of the morphogenese of parts of lymphatic system, which is mainly autosomal dominantly transmitted. It is morphologically and lymphografically characterized by a lack and reduction respectively of the number of lymphatic vessels. The trophedema results an emotional (cosmetic) and physical stress. Complicationes will rarely arise. In this paper it is described the case of the development of a cancer upon a trophedema, which seems to be the first case ever published. It will be shown, that an test-section have to be carried out in all cases of damages at a l.e. als soon as possible. The best conservative method at present used is the treatment with cortisone and hyaluronidase including bandage. However a real cure of the primary l.e. including the trophedema can not be attained by therapeutic methods presently used, because the defect of the lymphatic-vessels-system is hereditary. On the other hand therapeutic nihilism cannot be recommended.
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PMID:[The trophedema (Nonne-Milroy-Meige). Carcinogenesis as a rare complication]. 78 57

Earlier studies have shown that hyaluronidase exerts a potent influence upon the lymphatic system of the myocardium and that it reduces the size of myocardial infarcts after coronary occlusion. In this study we compared, in mongrel dogs, the effect of intravenous hyaluronidase or CLS 2210 upon the cardiac lymphatic vessels. We observed that in CLS 2210-treated animals the number of visualized cardiac lymphatic vessels was significantly higher than in the hyaluronidase-treated control group. We have previously demonstrated a cardioprotective effect of hyaluronidase in the treatment of acute myocardial infarction. The present experimental data indicate that intravenous CLS 2210 may have a definite role in the management of acute coronary occlusion. Further studies are needed to confirm these preliminary findings.
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PMID:CLS 2210, hyaluronidase and the cardiac lymphatic system. 383 39

An 8-year-old male Rottweiler was presented for recurrent episodes of dysphagia and vomiting with chronic weight loss. Radiography revealed a mediastinal mass in the heart base region. Necropsy revealed a firm, white mediastinal mass extending along the distal esophagus, through the diaphragm, to the gastric cardia, leftward to the convex visceral aspect of the fundus, and rightward along the lesser curvature of the stomach to the pyloric antrum. The gastric lymph node was enlarged and the omentum contained several nodules. Histologically, deep fundic mucosa contained pleomorphic, vacuolated cells with intracytoplasmic mucin, which was hyaluronidase resistant. Neoplastic cells were cytokeratin positive and vimentin negative. Transmural invasion was evidenced by the presence of cytokeratin-positive cells between smooth muscle bundles of the gastric wall. The mediastinal mass was composed of clusters of neoplastic cells in a stroma of dense and loose connective tissue. Neoplastic cells were also within blood and lymphatic vessels, tracheobronchial and gastric lymph nodes, and around peripheral nerves. This carcinoma most likely arose from the gastric fundus and extended to the cardia, from where it advanced proximally to the mediastinum as well as further rightward along the lesser curvature, demonstrating an anatomic continuity suggestive of a direct invasion. Metastasis, evidenced by the presence of lymphatic, blood, and perineural tumor emboli, also occurred.
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PMID:Scirrhous gastric carcinoma with mediastinal invasion in a dog. 1268 Jun 48

A functional renin-angiotensin system (RAS) is required for normal kidney development. Neonatal inhibition of the RAS in rats results in long-term pathological renal phenotype and causes hyaluronan (HA), which is involved in morphogenesis and inflammation, to accumulate. To elucidate the mechanisms, intrarenal HA content was followed during neonatal completion of nephrogenesis with or without angiotensin converting enzyme inhibition (ACEI) together with mRNA expression of hyaluronan synthases (HAS), hyaluronidases (Hyal), urinary hyaluronidase activity and cortical lymphatic vessels, which facilitate the drainage of HA from the tissue. In 6-8days old control rats cortical HA content was high and reduced by 93% on days 10-21, reaching adult low levels. Medullary HA content was high on days 6-8 and then reduced by 85% to 12-fold above cortical levels at day 21. In neonatally ACEI-treated rats the reduction in HA was abolished. Temporal expression of HAS2 corresponded with the reduction in HA content in the normal kidney. In ACEI-treated animals cortical HAS2 remained twice the expression of controls. Medullary Hyal1 increased in controls but decreased in ACEI-treated animals. Urine hyaluronidase activity decreased with time in control animals while in ACEI-treated animals it was initially 50% lower and did not change over time. Cells expressing the lymphatic endothelial mucoprotein podoplanin in ACEI-treated animals were increased 18-fold compared to controls suggesting compensation. In conclusion, the high renal HA content is rapidly reduced due to reduced HAS2 and increased Hyal1 mRNA expressions. Normal angiotensin II function is crucial for inducing these changes. Due to the extreme water-attracting and pro-inflammatory properties of HA, accumulation in the neonatally ACEI-treated kidneys may partly explain the pathological renal phenotype of the adult kidney, which include reduced urinary concentration ability and tubulointerstitial inflammation.
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PMID:Angiotensin converting enzyme inhibition blocks interstitial hyaluronan dissipation in the neonatal rat kidney via hyaluronan synthase 2 and hyaluronidase 1. 2093 85