Search PubMed⌕ Search

Biomedical subjects

J Kabat

Publications and source records attributed to J Kabat.

7 recordsLinked to original sources
PubMed1998

Phosphorylation of tau at both Thr 231 and Ser 262 is required for maximal inhibition of its binding to microtubules.

The paired helical filaments (PHFs) found in Alzheimer's disease (AD) brains are composed primarily of the microtubule-associated protein tau. PHF-tau is in a hyperphosphorylated state and is unable to promote microtubule assembly. We investigated whether the inhibition of tau binding to microtubules is increased when tau is phosphorylated by different kinases in combination with GSK-3. We found that when tau was first phosphorylated by A-kinase, C-kinase, cdk5, or CaM kinase II and then by GSK-3, its binding to microtubules was inhibited by 45, 61, 78, and 79%, respectively. Further, the kinase combinations cdk5/GSK-3 and CaM kinase II/GSK-3 rapidly phosphorylated the sites Thr 231 and Ser 235. When these sites were individually replaced by Ala and the phosphorylation experiments repeated, tau binding to microtubules was inhibited by 54 and 71%, respectively. By comparison, when Ser 262 was replaced by Ala, tau binding to microtubules was inhibited by only 8% after phosphorylation by CaM kinase II. From these observations we estimate that the phosphorylation of Thr 231, Ser 235, and Ser 262 contributes approximately 26, approximately 9, and approximately 33%, respectively, of the overall inhibition of tau binding to microtubules. Together, our results indicate that the binding of tau to microtubules is controlled by the phosphorylation of several sites, among which are Thr 231, Ser 235, and Ser 262.

Amino Acid Sequence↗
PubMed1997

Predicting readmission to the psychiatric hospital in a managed care environment: implications for quality indicators.

OBJECTIVE: This study examined predictors of hospital readmission to determine whether readmissions can serve as a quality indicator for an inpatient psychiatric service. METHOD: A series of 255 patients consecutively admitted to any of seven psychiatric hospitals in a regional managed care program were followed to determine whether they were readmitted within 6 months of discharge. Case managers assessed patients with the use of a reliable outcome management/decision support system designed for acute psychiatric services. RESULTS: Patients with greater impairment in self-care, more severe symptoms, and more persistent illnesses were more likely to be readmitted than other patients. Suicidal patients were less likely to be readmitted. There was no evidence to suggest that poor hospital outcome or premature discharge was associated with readmission either within 30 days or within 6 months. CONCLUSIONS: Although patients at risk for hospital admission can be identified, it does not appear that the success of the hospital intervention per se influences the likelihood of readmission. Use of readmission rates as quality indicators for hospital care providers is not recommended.

Acute Disease↗
PubMed1997

[Comparison of early results for pancreato-jejunal and pancreato-gastric anastomosis after pancreatoduodenectomy].

The aim of the study was to compare two types of anastomosis of the pancreatic stump with the digestive tract after pancreatoduodenectomy. 64 patients have been studied. Eighteen of them underwent pancreatoduodenectomy followed by the anastomosis of the pancreatic stump with the posterior wall of the stomach, in 46 patients pancreato-jejunal anastomosis has been done. Short term results of those two types of anastomosis did not differ significantly. Pancreato-gastric anastomosis seems to be technically easier, can be endoscopically controlled and does not impair recovery of gastric motility.

Adult↗
PubMed1997

[Biostatic endoprosthesis of the esophagus for prevention of leakage and stenosis at the site of anastomosis].

The authors present the results of using endoprosthesis made of bowine fascia which was conserved in special way. The endoprosthesis was used to cure salivary fistula in the place of anastomosis oesophagus with its replacement of the neck. The endoprosthesis was used to prevent leakness or stenosis in difficult operative circumstances and to pass the substitutive oesophagus in non-anatomical way. Prophylactic using of the endoprosthesis in technical difficulties caused by operative circumstances prevents leakness and stenosis in the place of anastomosis.

Anastomosis, Surgical↗
PubMed1993

Molecular characterization of the minimal protease resistant tau unit of the Alzheimer's disease paired helical filament.

The Alzheimer's disease paired helical filament (PHF), after digestion with Pronase, retains its characteristic morphological features. We term this the protease resistant core PHF. A 12 kDa tau fragment can be released from the core as an essentially pure preparation. Sequence analysis of this fragment revealed six distinct N-termini beginning in the repeat region of tau. The precise C-terminus is unknown, but the fragment is approximately 100 residues long. A monoclonal antibody, mAb 423, which recognizes the core PHF and the 12 kDa tau fragment, does not recognize normal full-length tau. We describe cDNA synthesis and expression of candidate 12 kDa tau analogues which permit the mapping of the mAb 423 epitope. mAb 423 recognizes all and only those analogues which terminate at Glu391, which lies beyond the homology repeat region. Addition or removal of a single residue at the C-terminus abolishes immunoreactivity. Therefore, mAb 423, together with knowledge of the N-terminus, can be used to measure the precise extent of 12 kDa PHF core tau fragment which we term the minimal protease resistant tau unit of the core PHF. This unit is 93-95 residues long, which is equivalent to three repeats, but is 14-16 residues out of phase with respect to the maximum homology organization of the repeat region. mAb 423 labels isolated PHFs prior to Pronase digestion and intracellular granular and neurofibrillary degeneration in Alzheimer's disease tissues. The constraints which determine endogenous truncation at Glu391 appear to be characteristic of an assembled configuration of tau, either within the PHF or its precursor.

Alzheimer Disease↗