Whole body MR imaging in ankylosing spondylitis: a descriptive pilot study in patients with suspected early and active confirmed ankylosing spondylitis

Background  

Ankylosing spondylitis is a chronic inflammatory rheumatic disorder which usually begins in early adulthood. The diagnosis is often delayed by many years. MR imaging has become the preferred imaging method for detection of early inflammation of the axial skeleton in ankylosing spondylitis.     

Stimulation of β-adrenoceptors inhibits store-operated channel currents via a cAMP-dependent protein kinase mechanism in rabbit portal vein myocytes

Previously we have described the properties of store-operated channel currents (SOCs) in freshly dispersed rabbit portal vein smooth muscle cells. In addition to Ca²⁺ store depletion these SOCs could also be activated by α-adrenoceptor stimulation and diacylglycerol (DAG) via a protein kinase C (PKC)-dependent mechanism. In the present study we have investigated the effect of β-adrenoceptor stimulation on SOCs in rabbit portal vein myocytes. With whole-cell recording the selective β-adrenoceptor agonist isoprenaline reduced the current evoked by cyclopiazonic acid (CPA, sarcoplasmic/endoplasmic reticulum ATPase inhibitor) by over 85%. With cell-attached patch recording, bath application of isoprenaline produced a pronounced inhibition of SOC activity evoked by either CPA or the acetoxymethyl ester form of BAPTA (BAPTA-AM). SOC activity evoked by CPA, the DAG analogue, 1-oleoyl-acetyl- sn -glycerol (OAG) or the phorbol ester, phorbol-12,13-dibutyrate (PDBu) was also markedly inhibited by the adenylate cyclase activator, forskolin, and the cell-permeable non-hydrolysable analogue of cyclic adenosine monophosphate (cAMP), 8-Br-cAMP. With inside-out patches, bath application of PDBu evoked channel currents with similar properties to SOCs which were inhibited by over 90% by a catalytic subunit of protein kinase A (PKA) and by 8-Br-cAMP. Moreover bath application of PKA inhibitors, H-89, KT5720 and an inhibitory peptide to quiescent cell-attached or inside-out patches, activated channel currents with similar properties to SOCs. These data suggest that in rabbit portal vein myocytes, stimulation of β-adrenoceptors inhibits SOC activity via a cAMP-dependent protein kinase signal transduction cascade. In addition it is concluded that constitutive PKA activity has a profound inhibitory effect on SOC activity in this vascular preparation.     

Risk Factors and Effect of Acute Kidney Injury on Outcomes Following Total Hip and Knee Arthroplasty

BackgroundDevelopment of acute kidney injury (AKI) following primary total joint arthroplasty (TJA) is a potentially avoidable complication associated with negative outcomes including discharge to facilities and mortality. Few studies have identified modifiable risk factors or strategies that the surgeon may use to reduce this risk.MethodsWe identified all patients undergoing primary TJA at a single hospital from 2005 to 2017, and collected patient demographics, comorbidities, short-term outcomes, as well as perioperative laboratory results. We defined AKI as an increase in creatinine levels by 50% or 0.3 points. We compared demographics, comorbidities, and outcomes between patients who developed AKI and those who did not. Multivariate regressions identified the independent effect of AKI on outcomes. A stochastic gradient boosting model was constructed to predict AKI.ResultsIn total, 814 (3.9%) of 20,800 patients developed AKI. AKI independently increased length of stay by 0.26 days (95% confidence interval [CI] 0.14-0.38, P < .001), in-hospital complication risk (odds ratio = 1.73, 95% CI 1.45-2.07, P < .001), and discharge to facility risk (odds ratio = 1.26, 95% CI 1.05-1.53, P = .012). Forty-one predictive variables were included in the predictive model, with important potentially modifiable variables including body mass index, perioperative hemoglobin levels, surgery duration, and operative fluids administered. The final predictive model demonstrated excellent performance with a c-statistic of 0.967.ConclusionOur results confirm that AKI has adverse effects on outcome metrics including length of stay, discharge, and complications. Although many risk factors are nonmodifiable, maintaining adequate renal perfusion through optimizing preoperative hemoglobin, sufficient fluid resuscitation, and reducing blood loss, such as through the use of tranexamic acid, may aid in mitigating this risk.     

凌晨3:00皮下注射短效胰岛素治疗2型糖尿病黎明现象

目的:观察应用凌晨3:00皮下注射短效胰岛素治疗2型糖尿病黎明现象的疗效。方法:对40例有黎明现象的2型糖尿病患者,使用短效胰岛素凌晨3:00注射4~6U。抽取肘静脉血测定空腹血糖(FPG)及早餐后2h血糖(2hPG),免疫比浊法测定糖化血红蛋白(HbA1c),比较治疗前后上述指标变化。结果:本组患者FPG从治疗前(9.5±1.6)mmol/L下降至(6.0±0.4)mmol/L,治疗2个月后仍保持为(5.6±0.4)mmol/L;2hPG从治疗前(13.8±0.8)mmol/L下降至(7.4±0.4)mmol/L,在治疗2个月后保持为(7.9±0.3)mmol/L;FPG和2hPG与治疗前比较,均具有显著性差异(P<0.01)。治疗2个月后,HbA1c从治疗前(8.3±0.6)%下降至(6.5±0.3)%,与治疗前比较,有显著性差异(P<0.01)。结论:短效胰岛素强化治疗黎明现象具有快速稳定的降血糖和降糖化血红蛋白作用。