Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019270 (hernia)
 15,856 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Any thrombotic affection can involve the deep veins as well as the superficial veins of the calf. It is considered that venous thrombosis may be a result of low concentrations of the activator of plasminogen levels in the vein wall, which produces a mediocre fibrinolytic response. The concentrations of the activator of plasminogen in these veins are little knows. Immediately after amputation, for pain in the decubitus position, samples of the soleus vein (N = 9) and long saphenous vein (LSV; N = 9) were removed and frozen in liquid nitrogen. In 6 limbs operated for varicose veins, samples of the vein in the calf (VC; N = 6) were removed and frozen. As a control, we examined samples of normal veins removed from the groin of patients undergoing hernia repairs. The quantitative determination of the activator of plasminogen was achieved thanks to a homogenate technique, and the results were expressed in taps by the minute by a tissue microgram. The median activity and the range of results were: LSV 1675 (777-8119); soleus vein 6795 (2232-21 570); CV 2356 (676-4099); inguinal veins 11 221 (6717-13 410). The low concentration of activator of plasminogen in the calf veins may contribute to a mediocre fibrinolytic response in these veins. This is not likely to be the case in the soleus veins. The results may indicate a different thrombotic mechanism in the two types of veins.
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PMID:[Quantitative determination of tissue-type plasminogen activator in varicose soleus veins]. 312 2

To study blood-brain barrier permeability and proteolytic changes in in patients with severe brain injury and to evaluate their impact on its course and outcome, the concentrations of albumin, plasminogen (plasmin), alpha 2-macroglobulin, alpha 2-antiplasmin, and alpha 1-antitrypsin were examined in 58 victims by enzyme immunoassay. The control group comprised 20 patients examined for lumbar discal hernia. The studies indicate that early severe brain injury showed blood-brain barrier dysfunction whose severity can be detected by the spinal fluid levels of albumin, plasminogen, and alpha 2-macroglobulin. Proteolytic changes in spinal fluid are determined by its albumin, plasminogen (plasmin), alpha 2-macroglobulin, alpha 2-antiplasmin, and alpha 1-antitrypsin concentrations and affect the development of secondary brain lesion and they are of practical value.
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PMID:[The permeability of the hemato-encephalic barrier and the proteolytic potential of the cerebrospinal fluid in severe craniocerebral trauma]. 1069 80

The role of plasminogen in preventing thrombosis requires activation by tissue plasminogen activator (t-PA) encoded by PLAT. While case-control associations have been pursued for common variants in PLAT, no disease-causing mutations have been reported. We describe a consanguineous family with two children who died shortly after birth due to complications related to severe hydranencephaly and diaphragmatic hernia. A combined exome/autozygome analysis was carried out with informed consent. We identified a homozygous null mutation in PLAT that abrogated t-PA level in patient cells. This is the first reported human knockout mutation of PLAT. The apparent association with hydranencephaly, diaphragmatic hernia and postnatal lethality requires further validation.
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PMID:A lethal phenotype associated with tissue plasminogen deficiency in humans. 2741 37