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)

A severe, progressive myopathy developed in an 11-year-old, phosphofructokinase (PFK)-deficient, male, English Springer Spaniel dog. Results from a routine neurological examination were normal. Examination of histologic sections of skeletal muscle revealed large accumulations of material in some myofibers. These deposits were pale, basophilic, somewhat flocculent, and slightly granular with hematoxylin and eosin stain. Most fascicles examined in sections of limb and trunk muscles were affected to some degree, with up to 10% of muscle fibers being involved. Deposits stained strongly with periodic acid-Schiff and were resistant to digestion by alpha amylase but were removed by incubation with gamma amylase. Deposits were faintly positive with Gomori's methenamine silver technique and alcian blue (pH 2.5) and were brown-gray with Lugol's iodine solution but were negative with other stains. Based on staining characteristics, the deposits seemed to consist primarily of an amylopectin-like polysaccharide(s). Alcian blue staining (pH 2.5) was removed by treatment with neuraminidase but not with hyaluronidase, indicating that some sialic acid residues were also present. Electron microscopically, the deposits were composed of short granular filaments, small granules and amorphous material. They were not membrane bound. The morphologic appearance and staining characteristics of the deposits were remarkably similar to deposits previously described in human PFK-deficient myopathy. As expected, total PFK activities were markedly reduced when assayed in skeletal muscles of this dog. In contrast with other PFK-deficient dogs, muscle glycogen in this animal was not increased above that of normal dogs.
 ...
PMID:Polysaccharide storage myopathy in canine phosphofructokinase deficiency (type VII glycogen storage disease). 213 52

The myotoxic effect of the subcutaneous administration of N,N1-dimethyl-p-phenylenediamine (DPPD) in rats was enhanced by the simultaneous administration of hyaluronidase. The resulting myopathy was associated with an early and dramatic increase in activity of glucose-6-phosphate dehydrogenase and 6-phosphogluconate dehydrogenase. Administration of actinomycin D or cycloheximide prior to the combined DPPD and hyaluronidase treatment prevented the increase in activity of both pentose phosphate pathway enzymes, indicating that the increase in activity requires RNA synthesis and protein synthesis. The possibility that the increase in activity of both NADPH-regenerating enzymes results from the modification by effectors of existing less active forms of these enzymes leading to more highly active forms was refuted.
 ...
PMID:The inhibitory effect of actinomycin D and cycloheximide on the increase in activity of glucose-6-phosphate dehydrogenase and 6-phosphogluconate dehydrogenase in experimentally induced diseased skeletal muscles. 648 Apr

White rhinoceroses (Ceratotherium simum) anesthetized with etorphine combinations develop severe pathophysiologic changes, including hypoventilation, hypoxemia and metabolic acidosis. The aim of this study was to evaluate the addition of butorphanol to the immobilizing mixture on the cardiopulmonary effects in free-ranging white rhinoceroses darted from the helicopter. In the control group (n=15), the rhinoceroses were anesthetized with etorphine, azaperone, detomidine, and hyaluronidase administered intramuscularly. In the treatment group (n=16), 10-20 mg of butorphanol was added to the combination. Within 10 min of becoming immobile, vital parameters (heart rate, respiratory rate, and temperature) and blood gas analyses were taken, and measurements were repeated after 10 (treatment group) and 20 min (control group). Both groups showed respiratory and metabolic acidosis, hypoxemia, and hypercapnia. In the control group, the arterial partial pressure of oxygen was significantly higher and the alveolar-to-arterial oxygen pressure gradients were significantly lower in all body positions compared with the butorphanol group. Oxygen hemoglobin saturation in the control group was higher than in the butorphanol group only in the lateral position. Improvements in arterial oxygen levels were observed in all animals when placed in sternal recumbency. There were no significant differences in the mean induction times between groups, but the distance the butorphanol group ran was significantly less after darting than in the control group. By adding butorphanol to the immobilizing mixture, no benefits in ventilation were seen; although, size differences make comparisons difficult. Running for a shorter distance during induction could be beneficial in the prevention of severe acid-base imbalances and capture myopathy.
 ...
PMID:The cardiopulmonary effects of etorphine, azaperone, detomidine, and butorphanol in field-anesthetized white rhinoceroses (Ceratotherium simum). 1793 46