Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0162871 (abdominal aortic aneurysm)
 8,664 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The diagnostic value of a strikingly elevated serum lactate dehydrogenase (LDH) level in association with only small or no increases in SGOT and alkaline phosphatase levels was noted in five patients with proved renal infarction. Four had renal artery embolism and infarction in association with atrial arrhythmias; one had an acute extension of an abdominal aortic aneurysm occluding the renal artery. Other causes of a considerable isolated increase in the serum LDH level such as hemolysis and myocardial infarction can usually be easily excluded.
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PMID:Elevation of serum lactate dehydrogenase levels in renal infarction. 44 17

Eight patients after operation for ruptured abdominal aortic aneurysm developed severe jaundice. The jaundice became clinically apparent by the sixth postoperative day, and the average peak total bilirubin level reached 28.4 mg/100 ml, alkaline phosphatase level 8.6 BL units/l, and SGOT 95 Karmen units/ml. In addition to the hepatic dysfunction, all patients developed acute renal failure, seven of eight patients experienced hypovolemic shock, and six of eight patients had respiratory insufficiency requiring ventilatory support. The overall mortality was 83 per cent. The most probable causes for the severe jaundice were increased bile pigment load and hepatocellular dysfunction due to ischemic hypoxic injury of hepatocytes secondary to shock. Morphologically, a picture of cholestasis existed with severe bile-staining of hepatocytes and intracanalicular and intraductal bile thrombi. No evidence of recent or resolving hepatic necrosis was observed.
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PMID:Severe jaundice after rupture of abdominal aortic aneurysm. 59 39

Four patients with disseminated histoplasmosis, two of whom had late relapses after previous therapy with amphotericin B, were treated with ketoconazole 200 to 400 mg daily for 1 year. All patients improved markedly during therapy, with resolution of symptoms decreasing liver and spleen size, and weight gain; resolution of oral ulcers occurred in the two patients in whom they were present. Decrease in serum alkaline phosphatase levels correlated well with clinical improvement. One patient who was much improved while receiving ketoconazole continued to harbor Histoplasma capsulatum in an abdominal aortic aneurysm, which became symptomatic 4 months after cessation of the drug. He underwent aneurysmectomy, and H. capsulatum isolated from the resected aneurysm was susceptible in vitro to ketoconazole. No significant adverse reactions to the drug were noted despite prolonged therapy. Our results indicate that ketoconazole may have a role in the therapy of disseminated histoplasmosis in adults.
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PMID:Progressive disseminated histoplasmosis; favorable response to ketoconazole. 626 75

A randomized, prospective, double-blind test was carried out to compare the effects of heated oyster shell-seaweed calcium (AAA Ca), calcium carbonate, and placebo in 58 elderly, hospitalized women with the mean age of 80 divided into three groups. Group A received 900 mg/day Ca as AAA Ca, Group B 900 mg/day Ca as CaCO3, and Group C placebo besides regular hospital diet containing approximately 600 mg Ca/day for 24 months. From the 25th to the 30th month, all groups were given AAA Ca. Lumbar spine and radial bone mineral density (BMD) were measured at 3-month intervals. Urinary Ca/Cr and serum alkaline phosphatase, intact and midportion serum parathyroid hormone (PTH), and calcitonin were also measured at intervals. From the 6th to the 24th month of the study, the ratio of lumbar spine BMD (L2-L4 by DPX, Lunar) to the basal pretest value was consistently and significantly higher in Group A than Group C but not higher in Group B than in Group C. PTH, measured 12 months after the beginning of the study, was lower in Group A than in Group C, but no significant difference was found between Groups B and C. At 3 months after the placebo was switched to AAA Ca in Group C, serum PTH was significantly decreased from the level during placebo supplement. Morning urine Ca/Cr decreased in Groups A after 18 months and in B after 12 months, but not in C. Serum alkaline phosphatase decreased in Group A significantly compared with Group C, but not in Group B. AAA Ca appears to be effective for increasing BMD in elderly subjects.
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PMID:Heated oyster shell-seaweed calcium (AAA Ca) on osteoporosis. 866 52

In the yeast Saccharomyces cerevisiae, autophagy, a bulk protein degradation in the vacuole, is induced in response to nutrient starvation. In a screen for mutations that result in induction of autophagy even in the presence of nutrients, we have isolated four mutants representing two csc complementation groups. These mutants induce autophagy of which activity is represented by activation of truncated alkaline phosphatase that is designed to be expressed in the cytosol. CSC1 was cloned by complementation of loss of viability phenotype of csc1-1 mutant and shown to be identical to END13/VPS4/GRD13. Though csc1-1 mutation is recessive, cells of delta csc1 do not induce autophagy in rich media, suggesting that csc1-1 allele is not a complete loss-of-function. Csc1p is a member of novel ATPase family named AAA protein including Sec18p/NSF, Cdc48p/p97, and Pas8p. Mutation site in csc1-1 is found in the SRH region that is highly conserved among AAA proteins. Cells of csc1-1 show sorting defect of CPY and the appearance of the class E compartment. These mutant phenotypes suggest the role of the protein that is involved in the traffic among the Golgi, endosome, and the vacuole in autophagy.
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PMID:Mutational analysis of Csc1/Vps4p: involvement of endosome in regulation of autophagy in yeast. 943 54

The immunnologic rejection induced by differently treated allografts of bone was compared. Methods Fresh bone (FB), autolyzed antigen-free bone (AAA), bone matrix gelatin (BMG), demineralized bone matrix (DBM) were implanted into the muscle pouch of mice, then, the immunological tests and alkaline phosphatase assay were conducted. Results Allogeneic FB induced the highest level of serum antibody in the host and stimulated lymphocytes proliferation remarkably in vitro; in contrast, AAA, BMG and DBM caused low titer of antibody and inhibited lymphocytes reproduction in vitro. Conclusions. Immunological rejection restrained osteogenesis of the bone implant, whereas the osteoinductive substance of bone suppressed immunological reaction.
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PMID:[Immunological comparison of differently treated allografts of bone]. 959 89

The ftsH gene encodes an ATP- and Zn(2+)-dependent metalloprotease with a molecular mass of about 70 kDa. It was first identified in Escherichia coli where it is also designated hflB, tolZ or mrsC, and seems to be present in most if not all bacteria. The FtsH protein is anchored to the cytoplasmic membrane via two transmembrane regions in such a way that the very short amino- and the long carboxy-termini are exposed into the cytoplasm. FtsH is member of the AAA family (ATPases associated with a variety of cellular activities) which are characterized by a module of about 200 amino acid residues in length containing an ATP-binding site. In Escherichia coli, FtsH forms a complex with a pair of periplasmically exposed membrane proteins, HflK and HflC. The E. coli enzyme is required for proteolytic degradation of some unstable proteins that include both soluble regulatory proteins such as sigma 32 (heat-shock sigma factor) and phage lambda CII (transcriptional activator), and membrane proteins including uncomplexed forms of SecY (forms the translocon together with SecE and SecG) and the a subunit of the F0 complex of the H(+)-ATPase. Its activity can be modulated by the HflKC proteins, by another membrane protein designated YccA which can transiently associate with both the FtsH and the HflKC proteins, or by small peptides such as CIII encoded by phage lambda (involved in lysogenization) or SpoVM (needed for sporulation) encoded by Bacillus subtilis. Besides being a protease, there is circumstantial evidence that FtsH also acts as a molecular chaperone. It influences protein assembly in and through the cytoplasmic membrane and associates with denatured alkaline phosphatase without degrading it. Therefore, FtsH may serve to maintain quality control of some cytoplasmic and membrane proteins. Such ATP-dependent proteases with intrinsic chaperone activity have been designated charonins.
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PMID:FtsH--a single-chain charonin? 1007 51

The optimal surgical procedure for severe renal secondary hyperparathyroidism (sHPT) is still a point of controversy. Total parathyroidectomy (PTX) without auto-transplantation was abandoned for fear of an adynamic bone condition; however, in the case of autotransplantation recurrent sHPT is frequent and promotes atherosclerosis. We studied 11 hemodialysis patients (age 59+/-12 years) on dialysis for 18 (12-30) years in whom total PTX was performed due to severe sHPT (group I; intact PTH: 1,240+/-230 pg/ml), and 5 patients (age 55+/-10 years) without renal insufficiency who inadvertently received total PTX during thyroid surgery (group II). After total PTX (group I, 26+/-18 [9-59] months; group II, 252+/-188 [22 480] months) both groups showed no measurable intact PTH levels. Calcium homeostasis was maintained by oral substitution with calcium (group I, calcium dialysate of 2.0 mmol/l), vitamin D and calcitriol (serum parameters in groups I and II: calcium 2.4 and 2.2 mmol/l; phosphate 1.8 and 1.1 mmol/l; 25(OH)-vitamin D(3) 21 and 34 ng/ml; 1,25(OH)(2)-vitamin D(3) 32 and 41 pg/ml, respectively). In group I, after total PTX there was a rapid and sustained improvement in bone pain with markedly enhanced physical activity and endurance. High turnover osteopathy markedly improved as indicated by declining levels of native osteocalcin (90+/-17 vs. 26+/-18 ng/ml), bone alkaline phosphatase (74+/-12 vs. 12+/-6 ng/ml), and carboxyterminal cross-linked telopeptide of type-I collagen (65+/-16 vs. 40+/-21 ng/ml) but increasing levels of carboxyterminal propeptide of type-I procollagen (120+/-36 vs. 148+/-41 ng/ml). Recalcification of bone was excellent as demonstrated by X-ray and confirmed by bone histology. Itching extravascular calcific deposits and calcifications of blood vessel and cardiac valves immediately stopped after total PTX. Moreover, 6 sHPT patients suffered from severe atherosclerotic lesions such as thoracic aortic aneurysm (n = 3) or abdominal aortic aneurysm (n = 3) which showed size progression before but not after total PTX when annually controlled by ultrasonography. In group II, even long after total PTX, there was no clinical, radiological, histological or biochemical evidence for low turnover osteopathy. In conclusion, our data indicate that substitution with vitamin D(3) metabolites and calcium can prevent deleterious bone effects of hypoparathyroidism in hemodialysis patients and in patients with normal kidney function and may compensate for the missing PTH action. Over this, a better survival rate is expected as a consequence of the beneficial effect of total PTX on the progression of atherosclerotic lesions. We suggest reconsideration of total PTX without autotransplantation in dialysis patients with severe sHPT who are not eligible for renal transplantation.
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PMID:Long-term results of total parathyroidectomy without autotransplantation in patients with and without renal failure. 1043 1

The incidence of acute cholecystitis complicating standard abdominal aortic aneurysm (AAA) repair has been reported between 0.3 and 18 per cent. This has prompted considerable debate regarding the management of cholelithiasis discovered incidentally during open aortic reconstruction. This study seeks to determine the incidence of cholelithiasis and acute cholecystitis after endovascular AAA repair and evaluate options for management. Between February 1996 and October 2001 492 patients underwent endovascular AAA repair. All the procedures were performed in the operating room under fluoroscopic guidance. Epidural (98.9%), local (0.5%), or general (1.7%) anesthesia was used during these cases. The incidence of cholelithiasis and acute cholecystitis was evaluated by CT scan and abdominal ultrasound. Serum measurements of alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, total and direct bilirubin, and amylase were performed and clinical assessment was conducted at 1, 6, and 12 months postoperatively and annually thereafter. The mean age of these patients was 76.6 years; 84% were male. Comorbid medical conditions were present in all patients (average 3.5 conditions/patient). Follow-up ranged from 2 to 35 months (mean 12.8 months). Endovascular stent graft deployment was successful in 486 of the 492 patients (98.8%). Six patients were converted to standard open repair because of inability to achieve successful endovascular aneurysm repair. The perioperative major morbidity rate was 14.9 per cent. Minor morbidity rate was 8.5 per cent. The perioperative mortality rate was 1.9 per cent. No deaths were related to biliary disease. Cholelithiasis was identified in 64 (13%) patients preoperatively. One of 64 patients with a prior Billroth II reconstruction for peptic ulcer disease developed jaundice 8 days after AAA repair as a result of choledocholithiasis that required surgical repair. One patient without gallstones developed acute acalculous cholecystitis on postoperative day 16 as determined on pathologic analysis of the gallbladder. A third patient who had gallstones identified on preoperative CT scan developed calculous cholecystitis 16 months after endovascular AAA repair. These two patients underwent uncomplicated laparoscopic cholecystectomy and recovered uneventfully. The incidence of postoperative symptomatic cholelithiasis is 1.6 per cent (one of 64). The incidence of postoperative acute cholecystitis was 0.2 per cent (one of 486) and was unrelated to the presence of gallstones. The incidence of delayed symptomatic cholelithiasis was 1.6 per cent (one of 64). Endovascular repair of AAA does not appear to predispose the patient to the development of symptomatic cholelithiasis during the perioperative period. Therefore a preoperative or intraoperative diagnosis of cholelithiasis does not necessitate cholecystectomy in the setting of planned endovascular AAA repair. Patients who develop cholecystitis after endovascular AAA repair may be effectively treated by standard laparoscopic techniques.
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PMID:Abdominal aortic aneurysmorrhaphy and cholelithiasis in the era of endovascular surgery. 1241 7

We previously demonstrated that the ATP/PKA-dependent activation of the human intermediate conductance, Ca2+-activated K+ channel, hIK1, is dependent upon a C-terminal motif. The NH2-terminus of hIK1 contains a multi-basic 13RRRKR17 motif, known to be important in the trafficking and function of ion channels. While individual mutations within this domain have no effect on channel function, the triple mutation (15RKR17/AAA), as well as additional double mutations, result in a near complete loss of functional channels, as assessed by whole-cell patch-clamp. However, cell-surface immunoprecipitation studies confirmed expression of these mutated channels at the plasma membrane. To elucidate the functional consequences of the (15)RKR(17)/AAA mutation we performed inside-out patch clamp recordings where we observed no difference in Ca2+ affinity between the wild-type and mutated channels. However, in contrast to wild-type hIK1, channels expressing the 15RKR17/AAA mutation exhibited rundown, which could not be reversed by the addition of ATP. Wild-type hIK1 channel activity was reduced by alkaline phosphatase both in the presence and absence of ATP, indicative of a phosphorylation event, whereas the 15RKR17/AAA mutation eliminated this effect of alkaline phosphatase. Further, single channel analysis demonstrated that the 15RKR17/AAA mutation resulted in a four-fold lower channel open probability (P(o)), in the presence of saturating Ca2+ and ATP, compared to wild-type hIK1. In conclusion, these results represent the first demonstration for a role of the NH2-terminus in the second messenger-dependent regulation of hIK1 and, in combination with our previous findings, suggest that this regulation is dependent upon a close NH2/C-terminal association.
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PMID:An NH2-terminal multi-basic RKR motif is required for the ATP-dependent regulation of hIK1. 1869 18


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