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411.
Summary Prospective studies have shown a relationship between hyperinsulinaemia, an indirect index of insulin resistance, and IHD in men with normal glucose tolerance. In NIDDM this association is less clear possibly due to the poor significance of insulin and C-peptide concentrations as an index of insulin resistance. Therefore, only a direct measurement of insulin sensitivity could clarify the possible relationship between insulin resistance and IHD in NIDDM. We have evaluated insulin sensitivity, by means of an ITT, and some risk factors for IHD in 72 men with NIDDM, 36 with and 36 without IHD, attending our out-patient Diabetic Clinic. The two groups were of similar age, duration of diabetes, glycaemic control and body composition. Subjects with IHD were more insulin resistant (KITT index 2.45±0.18 vs 3.12±0.13% per min, in patients with and without IHD, respectively, p<0.004), had higher total (p=0.011) and LDL serum cholesterol levels (p=0.010) and greater prevalence of hypertension (p=0.001) compared to subjects without IHD. Using step-wise logistic regression analysis, insulin resistance (odds ratio 2.57, 95% CI 1.87–3.28, p=0.008), hypertension (odds ratio 8.17, 95% CI 6.86–9.48, p=0.002), total serum cholesterol levels (odds ratio 1.02, 95% CI 1.005–1.035, p=0.015) and BMI (0.79, 95% CI 0.67–0.97, p=0.049) were independently associated with IHD. After adjustment for age and duration of diabetes, only insulin sensitivity was directly related to the age of onset of IHD, independently from other clinical and metabolic parameters (p<0.015). In conclusion: in NIDDM, patients with IHD are more insulin resistant compared to subjects without IHD. Insulin resistance is associated with IHD, independently from other cardiovascular risk factors. A higher insulin resistance seems to be related to an earlier clinical onset of IHD.Abbreviations NIDDM non-insulin-dependent diabetes mellitus - IHD ischaemic heart disease - ITT insulin tolerance test - CI confidence interval - ACE angiotensin-converting-enzyme  相似文献   
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Background

Gastric motility and accommodation have a critical role in maintaining normal gastrointestinal homeostasis. Different modalities can be adopted to quantify those processes, that is, scintigraphy to measure emptying time and intragastric Barostat for accommodation assessment. However, magnetic resonance imaging (MRI) can assess the same parameters noninvasively without ionizing radiation. Our study aimed to develop a detailed three-dimensional (3D) MRI model of the stomach to describe gastric volumes, surface areas, wall tension distribution, and interobserver agreement.

Methods

Twelve healthy volunteers underwent an MRI protocol of six axial T2-weighted acquisitions. Each dataset was used to construct a 3D model of the stomach: First, the volumes of the whole stomach, gastric liquid, and air were segmented. After landmark placing, a raw 3D model was generated from segmentation data. Subsequently, irregularities were removed, and the model was divided into compartments. Finally, surface area and 3D geometry parameters (inverse curvatures) were extracted. The inverse curvatures were used as a proxy for wall tension distribution without measuring the intragastric pressure.

Key Results

The model was able to describe changes in volume and surface geometry for each compartment with a distinct pattern in response to filling and emptying. The surface tension was distributed nonhomogeneously between compartments and showed dynamical changes at various time points.

Conclusion & Inferences

The presented model offers a detailed tool for evaluating gastric volumes, surface geometry, and wall tension in response to filling and emptying and will provide insights into gastric emptying and accommodation in diseases such as diabetic gastroparesis.  相似文献   
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Objective

To examine the clinical differences and the type and extent of organ damage in late‐ versus early‐onset systemic lupus erythematosus (SLE).

Methods

A nested case–control study was performed in the context of LUMINA (LUpus in MInorities, NAture versus nurture), a large, longitudinal, multiethnic cohort. Patients who developed SLE at or after the age of 50 years were considered cases. Two controls (patients who developed SLE at age ≤49 years) per case, matched for sex and disease duration, were randomly chosen. Selected baseline socioeconomic/demographic, behavioral, and psychological features, self‐reported quality of life, and cumulative clinical data (clinical manifestations, laboratory data, disease activity, damage, and mortality) were compared between cases and controls. Multivariable analyses with late‐onset lupus, damage accrual, and mortality as dependent variables were then performed.

Results

Two hundred seventeen patients were studied. Of them, 73 were cases. Cases were more likely to have neurologic involvement, arterial thrombotic events, osteoporosis, and hypertriglyceridemia, while renal involvement and anti‐Sm antibodies were less frequent. Disease activity at baseline was lower among cases. Cases also exhibited more cardiovascular and ocular damage. Late‐onset lupus was an independent predictor of damage accrual (t‐test = 2.23, P = 0.028), any damage at last visit (odds ratio [OR] 23.32, 95% confidence interval [95% CI] 3.98–141.56) (P < 0.001), and mortality (OR 10.74, 95% CI 3.07–37.56) (P < 0.001).

Conclusion

Patients with late‐onset lupus exhibit distinct clinical features. Although disease activity tends to be lower in these patients, they tend to accrue more damage and experience higher mortality than patients with early‐onset lupus. These findings probably reflect the contribution exerted by other comorbid conditions in the overall impact of lupus in these patients.
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