Biomedical subjects
Publications and source records attributed to L Kong.
The amino acid sequence deduced from the nucleotide sequence of an open reading frame adjacent to the frdA gene of Escherichia coli shows 30.5% identity with the C terminus of Escherichia coli lysyl-tRNA synthetases. The three motifs characteristic of aminoacyl-tRNA synthetases of class 2 are recognizable within this sequence.
Proteins resistant to proteinase K are rare because of the potency, wide pH optimum, and low peptide bond specificity of this enzyme. Previously, only the prion proteins associated with transmissible spongiform encephalopathies, possibly related proteins in the mollicute Spiroplasma mirum, and proteinase K itself have been reported. We identified a new proteinase K-resistant protein, p40-pr, in two strains of Mycoplasma hyorhinis and in extracts of these organisms. p40-pr's are similar to prion proteins in their resistance to high doses of proteinase K and in the reversal of this resistance by strong denaturing conditions. However, p40-pr's were distinct immunologically, in relative molecular mass, and in their method of extraction. Two immunologically related forms of p40-pr were identified on sodium dodecyl sulfate (SDS) gels and Western immunoblots, a 40-kDa species in boiled samples and a 120-kDa species dissociable by boiling in SDS. Reduction with 2-mercaptoethanol did not affect the mass of p40-pr's or the 120-kDa forms. The development of proteinase K resistance of p40-pr correlated to age-dependent increases in organism protein-lipid ratios. p40-pr-like proteinase K-resistant proteins of 46 to 50 kDa were identified in four of eight additional species of the class Mollicutes but not in S. mirum. However, these mycoplasmal proteins did not react with antibody to the denatured 40-kDa form of M. hyorhinis p40-pr purified by electroelution. The chromatographically purified 46-kDa proteinase K-resistant protein of Mycoplasma orale was an arginine deiminase.
The authors examined potential associations between air-pollution exposures and respiratory symptoms and illnesses of 4,108 adults who resided in 4 districts of 3 large, distinct Chinese cities. Data on respiratory health outcomes and relevant risk factors for parents and children were obtained via standardized questionnaires in the winter of 1988. (The effects in children were described previously.) The yearly averages of ambient levels of total suspended particles in the 4 districts for the years 1985-1988 differed greatly. The authors constructed logistic-regression models to assess the respiratory health parameters of parents of the children. The results revealed significant and strong effects, by district, on prevalence rates of cough, phlegm, persistent cough and phlegm, and wheeze for both the mothers and the fathers. In addition, the odds ratios increased as ambient total suspended particle concentration increased across the 3 urban districts. Other local within-city risk factors, however, may have confounded the total suspended particles-effects association, especially for asthma prevalence. Findings for adults were similar to those found for their children. A strong adverse effect of active tobacco smoking on the fathers' respiratory health was observed. The children appeared to be more strongly affected by passive smoking exposure received in their homes than their mothers.
The purpose of this study was to investigate cross-sectional and longitudinal associations between hearing acuity and tooth loss in 1156 US veterans taking part in the Veterans Affairs' Normative Aging (NAS) and Dental Longitudinal (DLS) Studies in the Boston, MA, area. The mean age was 48 years (SD = 8.9), 5.3% were edentulous, and 15.4% had < 17 teeth at baseline. Hearing acuity was determined by puretone, air- and bone-conduction audiometry, and speech discrimination tests at triennial examinations over a 20-year follow-up period. Hearing decline was defined as a change from baseline in the average puretone air-conduction thresholds of > or = 20 dB at 0.25, 0.5, 1, 2, 3, 4, 6, and 8 kHz. The explanatory variables of interest were change since baseline in dentate status (cut points at < 1, < 17, and < 20 teeth), and in the number of teeth lost (linear). Linear and logistic regression models--which controlled for baseline audiological status, age, air-bone gap, and otoscopic examination at current visit--showed that subjects who went from having > or = 17 to < 17 teeth had 1.64 times (95% CI, 1.24-2.17) as high odds of having hearing decline as those with no change in their dentate status. For every tooth lost since baseline, there was a 1.04 times as high odds (95% CI, 1.02-1.06) for hearing decline, when additional baseline and time-varying covariates were taken into account in the model.
In recent years, considerable research efforts have been directed at elucidating the mechanisms underlying the pathophysiologic alterations associated with reperfusion (reoxygenation) of ischemic (hypoxic) skeletal muscle. This intensive effort has led to the accumulation of a large body of evidence supporting the concept that reactive oxygen metabolites, generated at the onset of reperfusion, initiate the formation and release of proinflammatory agents, which subsequently attract and activate granulocytes. The activated neutrophils adhere to the microvascular endothelium, extravasate, and release cytotoxic oxidants and hydrolytic enzymes. As a consequence of these pathologic events, vascular permeability and transcapillary fluid filtration are increased and the no-reflow phenomenon (ie, some capillaries fail to reperfuse upon reinstitution of blood flow) becomes apparent. These microvascular alterations may be of considerable functional importance since the marked accumulation of fluid in the interstitial spaces, coupled with the incomplete and maldistributed blood flow, increases the functional diffusion path length for nutrients. Thus cellular nutrition is limited during reperfusion, which in turn impairs the functional recovery of postischemic muscles. Moreover, the infiltrating neutrophils are able to direct a focussed attack on myocytes, thereby exacerbating contractile dysfunction and tissue injury during reperfusion. These observations indicate that alterations in the microcirculation play a critical role in the genesis of ischemia/reperfusion injury in skeletal muscle. This review summarizes the evidence we have accumulated in support of the view that reactive oxygen metabolites and neutrophils contribute to production of postischemic microvascular dysfunction and describes the experimental models we have used to examine the mechanisms involved in the pathogenesis of ischemia and reperfusion.
OBJECTIVE: The lesion is Sjögren's syndrome consists of lymphocytic infiltration and has a pathology characteristic of the potential apoptotic death of salivary gland secretory epithelial cells. To examine the role of the glandular epithelial cells in the pathogenesis of autoimmune exocrinopathy, we studied Fas and Fas ligand (FasL) expression and quantitated the levels of apoptosis in salivary and lacrimal glands from NOD and NOD-scid mice, an animal model that develops a Sjögren's syndrome-like pathology. METHODS: The parotid, submandibular and lacrimal tissues of NOD, NOD-scid, and BALB/c mice were evaluated by immunohistochemical analysis for the expression of Fas and FasL. Nuclear fragmentation of DNA from the epithelial cells of exocrine tissues was evaluated by the terminal UTP nucleotide end labeling method (TUNEL). Messenger RNA was isolated from 8 and 18 week old mice and was analyzed by the reverse transcription-polymerase chain reaction (RT-PCR) for the expression of Fas and FasL. RESULTS: We found suggestive evidence that apoptosis of the secretory epithelial cells occurs in both NOD and NOD-scid mice despite the lack of T- and B-lymphocytes in the latter. FasL mRNA and cell surface protein were expressed in salivary and lacrimal gland epithelial cells from 8 and 18 week old NOD, NOD-scid, and BALB/c mice. Fas protein and mRNA were expressed only in the exocrine glands from 18 week old NOD and NOD-scid mice. Glandular secretory epithelial cell apoptosis was elevated in both NOD and NOD-scid mice, however; there was little evidence of apoptosis in the control strain of BALB/c mice. CONCLUSION: These results suggest a potential apoptotic process dependent on Fas:FasL interactions occurring in NOD-scid glandular secretory epithelial cells in the absence of lymphocytic infiltration.