METHODS: We analysed frozen samples from 105 OSCC as well as 105 oral specimens derived from healthy individuals. PCR assays targeting two regions of the virus were used. PCR amplification for the analysis of p53 codon 72 arginine/proline alleles was carried out in a separate reaction.
RESULTS: HPV DNA was detected in 51.4% OSCC samples, while 24.8% controls were found to be HPV positive. HPV was found to be significantly associated with OSCC (P
OBJECTIVES: The GBD (Global Burden of Disease) 2015 study integrated data on disease incidence, prevalence, and mortality to produce consistent, up-to-date estimates for cardiovascular burden.
METHODS: CVD mortality was estimated from vital registration and verbal autopsy data. CVD prevalence was estimated using modeling software and data from health surveys, prospective cohorts, health system administrative data, and registries. Years lived with disability (YLD) were estimated by multiplying prevalence by disability weights. Years of life lost (YLL) were estimated by multiplying age-specific CVD deaths by a reference life expectancy. A sociodemographic index (SDI) was created for each location based on income per capita, educational attainment, and fertility.
RESULTS: In 2015, there were an estimated 422.7 million cases of CVD (95% uncertainty interval: 415.53 to 427.87 million cases) and 17.92 million CVD deaths (95% uncertainty interval: 17.59 to 18.28 million CVD deaths). Declines in the age-standardized CVD death rate occurred between 1990 and 2015 in all high-income and some middle-income countries. Ischemic heart disease was the leading cause of CVD health lost globally, as well as in each world region, followed by stroke. As SDI increased beyond 0.25, the highest CVD mortality shifted from women to men. CVD mortality decreased sharply for both sexes in countries with an SDI >0.75.
CONCLUSIONS: CVDs remain a major cause of health loss for all regions of the world. Sociodemographic change over the past 25 years has been associated with dramatic declines in CVD in regions with very high SDI, but only a gradual decrease or no change in most regions. Future updates of the GBD study can be used to guide policymakers who are focused on reducing the overall burden of noncommunicable disease and achieving specific global health targets for CVD.
METHODS: A total 98 in-hospital first ever acute stroke patients were recruited, and their Barthel Index scores were measured at the time of discharge, at 1 month and 3 months post-discharge. The Barthel Index was scored through telephone interviews. We employed the random intercept model from linear mixed effect regression to model the change of Barthel Index scores during the three months intervals. The prognostic factors included in the model were acute stroke subtypes, age, sex and time of measurement (at discharge, at 1 month and at 3 month post-discharge).
RESULTS: The crude mean Barthel Index scores showed an increased trend. The crude mean Barthel Index at the time of discharge, at 1-month post-discharge and 3 months post-discharge were 35.1 (SD = 39.4), 64.4 (SD = 39.5) and 68.8 (SD = 38.9) respectively. Over the same period, the adjusted mean Barthel Index scores estimated from the linear mixed effect model increased from 39.6 to 66.9 to 73.2. The adjusted mean Barthel Index scores decreased as the age increased, and haemorrhagic stroke patients had lower adjusted mean Barthel Index scores compared to the ischaemic stroke patients.
CONCLUSION: Overall, the crude and adjusted mean Barthel Index scores increase from the time of discharge up to 3-month post-discharge among acute stroke patients. Time after discharge, age and stroke subtypes are the significant prognostic factors for Barthel Index score changes over the period of 3 months.
METHODS: A cross-sectional study of 252 AEA identified by computed tomography (CT) of the paranasal sinuses. The multiplanar CT images were acquired from SOMATOM® Definition AS+ and reconstructed to axial, coronal and sagittal view at 1 mm slice thickness.
RESULTS: 42.5% of AEA was within skull base (grade I), 20.2% at skull base (grade II) and 37.3% coursed freely below skull base (grade III). The prevalence of supraorbital ethmoid cell (SOEC) and suprabullar cell (SBC) was 29.8% and 48.0%. The position of AEA at skull base has significant association with SOEC (p