Surveillance of trend and distribution of stroke mortality by subtype, age, gender, and geographic areas in Tianjin, China, 1999–2006

The purpose of this study was to analyze the epidemiological trend and distribution of stroke mortality in the city of Tianjin, China, in order to provide evidence for the prevention and control of stroke. Methods The study was based on 102 718 cases of stroke mortality in Tianjin between 1999 and 2006. The cause of death was coded according to the International Classification of Diseases into stroke subtypes. Standardized mortality rates were calculated for stroke and its subtypes, adjusted for age and gender using the year 2000 world standard population. The age, gender, and geographic distribution of stroke and subtype mortality were analyzed. Χ 2 -tests were used to determine the statistical significance of differences in mortality trends. Results The stroke mortality rate in Tianjin declined from 133·52/100 000/year in 1999 to 102·52/100 000/year in 2006. The stroke mortality rate for males was higher than that for females. Stroke mortality rates increased with increasing age. The subtypes of stroke have changed considerably in Tianjin. Hemorrhagic was major in 1999–2001, while cerebral infarction attained the first rank and accounted for more than 50% of stroke mortality in 2002–2006. The most pronounced finding was that the proportion of ischemic stroke was 66·65% in the urban population and over 20% higher than that in the rural area. Stroke in the suburban area was mainly hemorrhagic stroke, up to 62·67%. Conclusions There are significant differences in the distribution of stroke mortality by subtype, age, gender, and geographic areas in Tianjin, China. Various subtypes of stroke are associated with different risk factors and therefore require different public health prevention and control measures. This study provides pertinent information for formulation of measures for the prevention and control of stroke.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/72496/1/j.1747-4949.2009.00272.x.pd

Long-Term Results of External Upper Esophageal Sphincter Myotomy for Oropharyngeal Dysphagia

The aim of this work was to assess the efficacy of external myotomy of the upper esophageal sphincter (UES) for oropharyngeal dysphagia. In the period 1991–2006, 28 patients with longstanding dysphagia and/or aspiration problems of different etiologies underwent UES myotomy as a single surgical treatment. The main symptoms were difficulties in swallowing of a solid-food bolus, aspiration, and recurrent incidents of solid-food blockages. Pre- and postoperative manometry and videofluoroscopy were used to assess deglutition and aspiration. Outcome was defined as success in the case of complete relief or marked improvement of dysphagia and aspiration and as failure in the case of partial improvement or no improvement. Initial results showed success in 21 and failure in 7 patients. The best outcomes were observed in patients with dysphagia of unknown origin, noncancer-related iatrogenic etiology, and neuromuscular disease. No correlation was found between preoperative constrictor pharyngeal muscle activity and success rate. After follow-up of more than 1 year, 20 patients were marked as success and 3 as failure. All successful patients had full oral intake with a normal bolus consistency without clinically significant aspiration. We conclude that in select cases of oropharyngeal dysphagia success may be achieved by UES myotomy with restoration of oral intake of normal bolus consistency

Periodontal Ehlers-Danlos Syndrome Is Caused by Mutations in C1R and C1S, which Encode Subcomponents C1r and C1s of Complement

Periodontal Ehlers-Danlos syndrome (pEDS) is an autosomal-dominant disorder characterized by early-onset periodontitis leading to premature loss of teeth, joint hypermobility, and mild skin findings. A locus was mapped to an approximately 5.8 Mb region at 12p13.1 but no candidate gene was identified. In an international consortium we recruited 19 independent families comprising 107 individuals with pEDS to identify the locus, characterize the clinical details in those with defined genetic causes, and try to understand the physiological basis of the condition. In 17 of these families, we identified heterozygous missense or in-frame insertion/deletion mutations in C1R (15 families) or C1S (2 families), contiguous genes in the mapped locus that encode subunits C1r and C1s of the first component of the classical complement pathway. These two proteins form a heterotetramer that then combines with six C1q subunits. Pathogenic variants involve the subunit interfaces or inter-domain hinges of C1r and C1s and are associated with intracellular retention and mild endoplasmic reticulum enlargement. Clinical features of affected individuals in these families include rapidly progressing periodontitis with onset in the teens or childhood, a previously unrecognized lack of attached gingiva, pretibial hyperpigmentation, skin and vascular fragility, easy bruising, and variable musculoskeletal symptoms. Our findings open a connection between the inflammatory classical complement pathway and connective tissue homeostasis