Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0040586 (tracheobronchitis)
 449 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The case report of a fatal result in an abortion requested because X-ray diagnostic studies of the gallbladder and intestine had been made during an undiagnosed early pregnancy is presented. A uterine vacuum aspirator had not been purchased by the hospital. A portable laboratory vacuum pump with an appropriate suction trap was used. The apparatus had been used previously in several abortion cases. After dilatation of the cervix and insertion of the aspirating cannula, the pump was turned on. A sudden massive effusion of bloody froth issued from around the cannula. The cannula was removed immediately. It was found that the tubing had been incorrectly connected. The aspirator tube was connected with the pressure outlet of the pump. The tubing was then correctly placed and the uterus emptied. The patient was given succinyl choline, intubated, placed in the Trendelenburg position, and monitored cardiographically. About 30 seconds after the uterine insufflation blood pressure became unobtainable. The pulse slowed to 50 beats/minute and respiration diminished. Cardiac ausculation revealed no sounds. Respiration was maintained using oxygen through an endoctracheal tube. The pulse was still palpable and the EKG showed abnormal QRS complexes. Cyanosis then became evident. Closed chest cardiac massage was used for 1 minute but the patient became pulseless and QRS complexes were bizarre. Then the chest was opened and each ventricle was needled. From each ventricle of the distended heart air hissed under pressure through the needle vent site. The ascending aorta was needled and air escaped under pressure. Cardiac color and action improved when aided by massage. Iv isoproterenol and intracardiac epinephrine were given. An electric defibrillator converted the cardiac rhythm to a sinus rhythm. Norepinephirne brought about hypertension. Blood and albumin were given iv. The patient never regained consciousness. Tracheostomy and a feeding gastrostomy were required. Urinary and respiratory infections followed and the patient died after 2 1/2 months. Autopsy revealed tracheobronchitis, bronchopneumonia, and pulmonary edema. The brain showed extensive cerebral cortical necrosis. The heart was normal. This maternal death was preventable.
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PMID:Air embolism and maternal death from therapeutic abortion. 502 50

Hepatocyte growth factor (HGF) promotes lung epithelial repair after injury. Because prior studies established that human neutrophil proteases inactivate HGF in vitro, we predicted that HGF levels decrease in lungs infiltrated with neutrophils and that injury is less severe in lungs lacking HGF-inactivating proteases. After establishing that mouse neutrophil elastase cleaves mouse HGF in vitro, we tested our predictions in vivo by examining lung pathology and HGF in mice infected with Mycoplasma pulmonis, which causes neutrophilic tracheobronchitis and pneumonia. Unexpectedly, pneumonia severity was similar in wild type and dipeptidylpeptidase I-deficient (Dppi-/-) mice lacking neutrophil serine protease activity. To assess how this finding related to our prediction that Dppi-activated proteases regulate HGF levels, we measured HGF in serum, bronchoalveolar lavage fluid, and lung tissue from Dppi(+/+) and Dppi(-/-) mice. Contrary to prediction, HGF levels were higher in lavage fluid from infected mice. However, serum and tissue concentrations were not different in infected and uninfected mice, and HGF lung transcript levels did not change. Increased HGF correlated with increased albumin in lavage fluid from infected mice, and immunostaining failed to detect increased lung tissue expression of HGF in infected mice. These findings are consistent with trans-alveolar flux rather than local production as the source of increased HGF in lavage fluid. However, levels of intact HGF from infected mice, normalized for albumin concentration, were two-fold higher in Dppi(-/-) versus Dppi(+/+) lavage fluid, suggesting regulation by Dppi-activated proteases. Consistent with the presence of active HGF, increased expression of activated receptor c-Met was observed in infected tissues. These data suggest that HGF entering alveoli from the bloodstream during pneumonia compensates for destruction by Dppi-activated inflammatory proteases to allow HGF to contribute to epithelial repair.
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PMID:Regulation of hepatocyte growth factor in mice with pneumonia by peptidases and trans-alveolar flux. 2593 94