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Large Accumulation (large + accumulation)
Selected AbstractsOral health of Adelaide nursing home residents: longitudinal studyAUSTRALASIAN JOURNAL ON AGEING, Issue 2 2004JM Chalmers Objective: The Adelaide Dental Study of Nursing Homes aimed to quantify oral disease experience, incidence and increments in Adelaide nursing home residents. Methods: Questionnaires and dental inspections were completed at baseline and at 1-year for residents from randomly selected Adelaide nursing homes. Results: The residents were very functionally dependent, cognitively impaired and behaviourally difficult older adults with complex oral problems and dental treatment needs. The prevalence of edentulism (total tooth loss) (63%) decreased and more residents were retaining natural teeth. Existing residents had a mean of 10.8 teeth present and new residents had a mean of 12.7 teeth present. Residents' previous experiences of caries (decay) were high , existing residents had a mean of 1.2 decayed teeth and new residents had a mean of 0.8 decayed teeth. Residents' caries increments (new decay) over the 1-year period were high (coronal = 2.5 surfaces; root = 1.0 surfaces), especially in those who had lost weight and who could eat fewer food types. These levels of caries were many times greater than had been reported for community-dwelling older adults. Large accumulations of plaque, calculus and debris (food) were evident on residents' natural teeth and dentures, especially those with dementia. Up to 25% of residents owned dentures that were not worn. Residents with dementia gave their carers complex and challenging oral hygiene care problems. Existing and new residents had similar general health and oral health characteristics, with the exceptions that new residents had significantly more filled tooth surfaces, and fewer decayed retained roots. Conclusion: New residents were being admitted to the nursing homes with a compromised oral health status or developed severe oral diseases and conditions within several months of their admittance. Residents' oral diseases, especially coronal and root caries, rapidly progressed during their stay in residential care. [source] Spontaneous "Cardiomegaly" Following PericardiectomyJOURNAL OF CARDIAC SURGERY, Issue 6 2009Jeffrey B. Geske M.D. Chest x-ray revealed development of interval "cardiomegaly." Bedside echocardiography revealed a large accumulation of pericardial fluid despite absence of pericardium. Diagnostic and therapeutic mediastinocentesis was performed and confirmed the diagnosis of mediastinal hemorrhage. Subsequent to pericardiectomy, mediastinal hemorrhage can masquerade as cardiomegaly and may require urgent intervention. [source] N-terminal residues regulate proteasomal degradation of AANATJOURNAL OF PINEAL RESEARCH, Issue 3 2010Zheping Huang Abstract:, Serotonin N -acetyltransferase (AANAT) catalyzes the conversion of serotonin to N -acetylserotonin, which is the immediate precursor for formation of melatonin. Although it is known that AANAT is degraded via the proteasomal proteolysis, detailed mechanisms are not defined. In this paper, we tested the in vivo role of proteasome inhibition on AANAT activity and melatonin release and examined the amino acid residues in AANAT that contribute to the proteasome degradation. We have shown that inhibition of proteasome activities in vivo in the intact pineal gland fails to prevent the light-induced suppression of melatonin secretion. Furthermore, in cell lines stably expressing AANAT, inhibition of proteasomal proteolysis, which resulted in a large accumulation of AANAT protein, similarly failed to increase AANAT enzyme activity proportional to the amount of proteins accumulated. Site-directed mutagenesis analysis of AANAT revealed that the AANAT degradation is independent of lysine and the two surface cysteine residues. Deletion analysis of N-terminus identified the second amino acid leucine (L2) as the key residue that contributes to the proteasomal proteolysis of AANAT protein. These results suggest that rat AANAT protein is degraded via the N-end rule pathway of proteasomal proteolysis and the leucine at the N-terminus appears to be the key residue recognized by N-end rule pathway. [source] Heteropterys aphrodisiaca Infusion Reduces the Collateral Effects of Cyclosporine A on the TestisTHE ANATOMICAL RECORD : ADVANCES IN INTEGRATIVE ANATOMY AND EVOLUTIONARY BIOLOGY, Issue 7 2008Juliana C. Monteiro Abstract Cyclosporine A (CsA) is known to have testicular toxicity, leading to male infertility. Stimulant and aphrodisiac properties have been attributed to the plant, Heteropterys aphrodisiaca. Thus, the present work was undertaken to evaluate the association of the drug and the medicinal herb in Wistar rats, applying testicular morphometry and ultrastructure. Twenty-four rats were used, divided into four groups: I, control; II, CsA; III, simultaneous use of CsA and H. aphrodisiaca; IV, H. aphrodisiaca. Daily administration by gavage was carried out, during 56 days, of water (sham), CsA in a dose of 15 mg/kg per day and/or H. aphrodisiaca in a dose of 0.5 ml of the infusion prepared with 25 g of roots/100 ml of boiling water. Increased body weight was observed for all groups, but the animals that received only CsA showed the smallest body weight gain. Morphometry showed increased connective tissue volumetric proportion and decreased Leydig cell volumetric proportion in CsA-treated rats. Using transmission electron microscopy, it was possible to ascertain that CsA caused seminiferous epithelium degeneration, resulting in Sertoli cell vacuolization, abnormal round and elongated spermatids and large accumulation of residual cytoplasm at the epithelium border next to the lumen. Expanded intercellular spaces between germ cells were still observed in H. aphrodisiaca -treated rat testes. The administration of H. aphrodisiaca infusion to CsA-treated rats diminished nearly all the CsA-induced damage to the testis ultrastructure, suggesting that H. aphrodisiaca infusion may be used combined with CsA to reduce CsA-induced injuries in the testis. Anat Rec, 291:809-817, 2008. © 2008 Wiley-Liss, Inc. [source] | |||||||||||||