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An intrafamilial outbreak in West Bengal, India, involving 5 deaths and person-to-person transmission was attributed to Nipah virus. Full-genome sequence of Nipah virus (18,252 nt) amplified from lung tissue showed 99.2% nt and 99.8% aa identity with the Bangladesh-2004 isolate, suggesting a common source of the virus.  相似文献   
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OBJECTIVE: To evaluate the relationship between chondrocalcinosis and the progression of knee osteoarthritis (OA) using longitudinal magnetic resonance imaging (MRI) assessments. METHODS: Longitudinal knee MRIs were obtained in the Boston OA Knee Study (BOKS) and in the Health, Aging and Body Composition (Health ABC) Study. Chondrocalcinosis was determined as present or absent on baseline knee radiographs. Cartilage morphology was graded on paired longitudinal MRIs using the Whole-Organ Magnetic Resonance Imaging Score in 5 cartilage subregions of each of the medial and lateral tibiofemoral joints. Cartilage loss in a subregion was defined as an increase in the cartilage score of > or = 1 (0-4 scale). The risk for change in the number of subregions with cartilage loss was assessed using Poisson regression, with generalized estimating equations to account for correlations. Analyses were adjusted for age, sex, body mass index, baseline cartilage score, and presence of damaged menisci. RESULTS: In BOKS, 23 of the 265 included knees (9%) had chondrocalcinosis. In Health ABC, 373 knees were included, of which 69 knees (18.5%) had chondrocalcinosis. In BOKS, knees with chondrocalcinosis had a lower risk of cartilage loss compared with knees without chondrocalcinosis (adjusted risk ratio [RR] 0.4, 95% confidence interval [95% CI] 0.2-0.7) (P = 0.002), and there was no difference in risk in Health ABC (adjusted RR 0.9, 95% CI 0.6-1.5) (P = 0.7). Stratification by intact versus damaged menisci produced similar results within each cohort. CONCLUSION: In knees with OA, the presence of chondrocalcinosis was not associated with increased cartilage loss. These findings do not support the hypothesis that chondrocalcinosis worsens OA progression.  相似文献   
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Background

Alcohol consumption has long been considered a trigger for recurrent gout attacks; however, this hypothesis has not been formally tested.

Methods

We conducted an Internet-based case-crossover study to assess several putative risk factors, including alcohol consumption, thought to trigger recurrent gout attacks. Subjects who had an attack within the past year were recruited online and asked to provide access to medical records pertaining to their gout. Data were obtained on the amount and type of alcoholic beverage consumed on each day over the 2-day period before a gout attack and on each day over a 2-day period during the intercritical period. We examined the amount and type of alcohol consumption and the risk of recurrent gout attacks using a conditional logistic regression adjusting for diuretic use and purine intake.

Results

A total of 197 subjects were recruited online over a 10-month period. Of those, 179 (91%) fulfilled the American College of Rheumatology Criteria for gout. Compared with no alcohol consumption, odds ratios for recurrent gout attacks were 1.1, 0.9, 2.0, and 2.5 for 1 to 2, 3 to 4, 5 to 6, and 7 or more drinks consumed over the 2-day period, respectively (P<.005). A dose-response relationship of risk of gout attacks was more evident for alcohol consumed over the last 24 hours. An increased risk of recurrent gout attacks was found for each type of beverage consumed.

Conclusion

Alcohol consumption triggers recurrent gout attacks. This effect was likely to occur within 24 hours after its consumption.  相似文献   
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