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Objective

Low psoas muscle area is shown to be an indicator for worse postoperative outcome in patients undergoing vascular surgical. Additionally, it has been associated with longer durations of hospital stay in patients with cancer who undergo surgery and subsequently greater health care costs in Europe and the United States. We sought to evaluate this effect on hospital expenditure for patients undergoing vascular repair in a health care system with universal access.

Methods

Skeletal muscle mass was assessed on preoperative abdominal computed tomography scans of patients undergoing open aortic aneurysm repair in a retrospective fashion. The skeletal muscle index (SMI) was used to define low muscle mass. Health care costs were obtained for all patients and the relationship between a low SMI and higher costs was explored using linear regression and cross-sectional analysis.

Results

We included 156 patients (81.5% male) with a median age of 72 years undergoing elective surgery for infrarenal abdominal aortic aneurysm in this analysis. The median SMI for patients with low skeletal muscle mass was 53.21 cm2/kg and for patients without, 70.07 cm2/kg. Hospital duration of stay was 2 days longer in patients with low skeletal muscle mass as compared with patients with normal (14 days vs 11 days; P = .001), as was duration of intensive care stay (3 days vs 1 day; P = .01). The median overall hospital costs were €10,460 higher for patients with a low SMI as compared with patients with a normal physical constitution (€53,739 [interquartile range, €45,007-€62,471] vs €43,279 [interquartile range, €39,509-€47,049]; P = .001). After confounder adjustment, a low SMI was associated with a 14.68% cost increase in overall hospital costs, for a cost increase of €6521.

Conclusions

Low skeletal muscle mass is independently associated with higher hospital as well as intensive care costs in patients undergoing elective aortic aneurysm repair. Strategies to reduce this risk factor are warranted for these patients.  相似文献   
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The New Zealand obese mouse (NZO/Hl) is characterised by hereditary obesity and type-2 diabetes, including insulin resistance, hyperinsulinaemia, and glucose intolerance. In other diabetic models, it has been revealed that the proper functioning of the glucose transporter isoform 2 (GLUT2) is essential for adequate secretion of insulin. The aim of this study was to compare the distribution of islet cells and GLUT2, as well as the expression of GLUT2-mRNA, in the pancreas of NZO mice and metabolically unimpaired NMRI (Naval Medical Research Institute) mice. Pancreas tissue was obtained from different stages of development. For molecular determination of the expression level of GLUT2-mRNA, total-RNA was extracted from the pancreas and analysed by quantitative real-time RT-PCR. All investigated NZO mice displayed increased weight, elevated hyperinsulinaemia, and slightly enhanced blood glucose levels compared with the NMRI control mice. By means of immunofluorescence microscopy drastically reduced insulin levels were detected, which might be compensated by the observed islet cell hyperplasia and hypertrophy. Furthermore, the normally peripheral localisation of the alpha-cells within islets was disturbed. By contrast, there were no changes in somatostatin cell distribution. However, considerable differences appeared with regard to GLUT2: whereas the beta-cells of NMRI mice showed dense immunostaining of the GLUT2 transporter on the cell surface, in all age groups of NZO mice, GLUT2 on the plasma membranes was reduced and dispersed in the cytoplasm. These findings agree with the molecular biological results, which displayed decreased mRNA-expression of GLUT2. In summary, the observed alteration of islet morphology and of GLUT2 expression in diabetic mice complements our previous results from a superfusion protocol and further clarifies the mechanisms of diabetogenesis in NZO mice.  相似文献   
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PATIENTS AND METHOD: The aim of the present study was to contribute to a more accurate indication and better integration of developing third molar transplantation into orthodontic space management, using the results gleaned from the authors' own pool of patients. For this purpose, a clinical and radiographic examination of 61 transplanted developing molars in 57 patients was carried out after an average of 3.3 years. RESULTS: The overall success rate was 85%. Failure was due in 10% of cases to impaired periodontal healing (inflammatory root resorption, ankylosis, or increased pocket probing depths) and in 5% of cases to insufficient or arrested postoperative root development accompanied by increased transplant mobility. The incidence of postoperative cessation of further root development was significantly higher (p = 0.011) in transplants at early developmental stages, which also had a negative impact on the final root length, the crown-root ratio and the mobility values of these transplants. CONCLUSIONS: The transplantation of developing third molars should be given stronger consideration in treatment plans for orthodontic space management although it represents a real alternative to orthodontic space closure only in exceptional cases. However, unlike implantological or prosthodontic treatment, it offers an opportunity to replace a missing or non-retainable tooth with a patient's own vital and fully functional tooth, provided the appropriate transplant is selected.  相似文献   
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