Chinese clinical guidelines for continuous glucose monitoring (2018 edition)

Blood glucose monitoring is an important part of diabetes management. Continuous glucose monitoring (CGM) technology has become an effective complement to conventional blood glucose monitoring methods and has been widely applied in clinical practice. The indications for its use, the accuracy of the generated data, the interpretation of the CGM results, and the application of the results must be standardized. In December 2009, the Chinese Diabetes Society (CDS) drafted and published the first Chinese Clinical Guideline for Continuous Glucose Monitoring (2009 edition), providing a basis for the standardization of CGM in clinical application. Based on the updates of international guidelines and the increasing evidence of domestic studies, it is necessary to revise the latest CGM guidelines in China so that the recent clinical evidence can be effectively translated into clinical benefit for diabetic patients. To this end, the CDS revised the Chinese Clinical Guideline for Continuous Glucose Monitoring (2012 Edition) based on the most recent evidence from international and domestic studies.     

Gliotoxin ameliorates development of fibrosis and cirrhosis in a thioacetamide rat model

Activation of hepatic stellate cells causes most of the pathological changes in cirrhosis. The fungal metabolite gliotoxin was shown to induce apoptosis of hepatic stellate cells in vitro. We examined whether gliotoxin may prevent or reverse liver fibrosis in a rat model of thioacetamide-inducedcirrhosis, and whether gliotoxin administration in vivo causes apoptosis of activated stellate cells. Gliotoxin treatment resulted in a significant decrease in liver fibrosis in rats, but did not improve liver functions. We observed a significant reduction in the numbers of activated hepatic stellate cells in the gliotoxin-treated rats. Gliotoxin administration also resulted in parenchymal apoptosis of hepatocytes and hepatic stellate cells. In conclusion, gliotoxin reduces hepatic fibrosis, an effect accompanied by reduction of the numbers of activated hepatic stellate cells in the liver.     

心电图在判定急性下壁心肌梗死犯罪血管

目的评定心电图在判定急性下壁心肌梗死罪犯血管的意义。方法对５６例急性下壁心肌梗死患的心电图及冠状动脉造影资料进行分析。结果①罪犯血管是右冠状动脉占８５．７％,回旋支占１４．３％;②窦性心动过缓、房室传导阻滞、室颤是右冠状动脉闭塞指标;③ＳＴＩ．ａＶＬ压低≥１．０ｍｍ是右冠状动脉闭塞敏感指标（Ｐ＜０．０５及Ｐ＜０．０１）,敏感性及特异性分别为６９％、７５％及９２％、７５％,而缺乏ＳＴＩ．ａＶＬ压低     

42例弗氏窦瘤的外科治疗及远期疗效

我院自 1984年 11月至 1998年 5月共收治弗氏窦瘤破裂 4 2例 ,男性 2 7例 ,女性 15例 ,年龄 8～57岁 ,平均 2 8.2岁。其中弗氏窦瘤破入邻近心腔形成心脏瘘者 37例 ,未破裂者 5例。合并畸形 :室间隔缺损 2 5例 (59.5% ) ,右室双腔心 3例 (71% ) ,卵圆孔未闭 1例 (2 .4 % )。同时并发主动脉瓣关闭不全 12例(2 8.6 % ) ,细菌性心内膜炎 2例 (4 .8% ) ,其中三尖瓣赘生物 1例 ,二尖瓣、主动脉瓣均有赘生物 1例 ,二尖瓣关闭不全 1例 (2 .4 % )。对窦瘤及合并畸形进行外科治疗 ,无围术期死亡。随访 6个月到 13年 ,平均 5 4年。6例失访 ,远期死亡 2例 ,再次手术 3例 ,完全性房室传导阻滞 1例 ,无痛性心肌缺血 1例 ,主动脉瓣中度关闭不全 1例 ,余 2 8例临床效果良好。本文就弗氏窦瘤及合并畸形的诊断及外科治疗进行讨论     

80例大鼠异位心脏移植的体会

为研究心脏移植后急性排异反应及心脏缺血再灌注损伤 ,我们建立了大鼠异位心脏移植模型。Wistar大鼠心脏的升主动脉及主肺动脉分别与SD大鼠的腹主动脉和后腔静脉做端侧吻合 ,将Wistar大鼠心脏移植于SD大鼠腹腔内。 80例大鼠异位心脏移植模型成功建立 ,手术成功率 90 0 %。我们从以下方面作了总结 :1 麻醉 ;2 供心的摘取及保存 ;3 受体的准备 ;4 心脏移植 ;5 术后处理     

Collateral formation and clinical variables in obstructive coronary artery disease: the influence of hypercholesterolemia and diabetes mellitus

BACKGROUND: Collateral circulation is severely compromised in patients who have a limited degree of spontaneous myocardial angiogenesis and arteriogenesis. METHOD: To determine the clinical characteristics associated with angiographic apparent collaterals (AAC) and myocardial blush score (MBS), this study compared the clinical variables in various AAC and MBS grades (0 = no, 1 = minimal, 2 = moderate and 3 = maximal collaterals defined by the two variables) among a consecutive group of 112 patients (aged 62 +/- 12 years, 76% men) with a native artery chronic total coronary occlusion studied by selective coronary angiograms. RESULTS: By univariate analysis, including variables such as age, sex, diabetes, hypertension, hypercholesterolemia, smoking and ejection fraction, the only variable that was found more frequently in patients with greater AAC grade was hypercholesterolemia (59%, 63%, 71% and 78% in patients with AAC grade 0, 1, 2 and 3, P = 0.003). Ejection fraction tended to be more preserved in patients with greater AAC score (46%, 48%, 51% and 54% in patients with AAC grade 0, 1, 2 and 3, respectively, P = 0.052). Diabetes mellitus was the only factor that was negatively associated with MBS (23%, 22%, 18% and 16% in patients with MBS grade 0, 1, 2 and 3, P = 0.01). Using a multivariate logistic regression analysis to predict maximal AAC grade, the only independent predictor found was hypercholesterolemia (odds ratio = 1.3, confidence limits = 1.05-1.9, P = 0.048). Diabetes mellitus was the only predictor found to be negatively associated with MBS (odds ratio = 0.72, confidence limits = 0.46-0.98, P = 0.04). It is concluded that collateral grade is associated with hypercholesterolemia and myocardial blush is negatively associated with diabetes mellitus. These findings may reflect a conflicting impact of hypercolesterolemia and diabetes mellitus upon collateral formation, leading to enhanced or depressed angiogenesis in response to obstructive coronary artery disease.     

gax基因转染对血管平滑肌细胞中基质金属蛋白酶2和骨桥蛋白转录的影响

目的:探讨腺病毒介导gax基因转染血管平滑肌细胞(VSMC)后,VSMC中基质金属蛋白酶2(MMP2)和骨桥蛋白基因转录的变化。方法:以携带大鼠gax基因表达序列的复制缺陷型5型腺病毒载体(AdCMV-gax)转染VSMC后,应用免疫细胞化学染色检NGax蛋白表达的变化,以RT-PCR技术检测VSMC中MMP2 mRNA和骨桥蛋白mRNA的变化。结果:AdCMV-gax转染后:(1)VSMC中Gax蛋白的表达比转染前显著增高(P<0.01); (2)VSMC中MMP2 mRNA和骨桥蛋白mRNA 比未转染组均显著降低(P<0.05)。结论:增强gax基因表达可抑制MMP2和骨桥蛋白的转录。     

Other iatrogenic immunodeficiency-associated lymphoproliferative disorders in a patient with anti-melanoma differentiation-associated gene 5-positive dermatomyositis: A case report and systematic literature review

A 58-year-old man with anti-melanoma differentiation-associated gene 5-positive dermatomyositis (MDA5-DM) developed Epstein–Barr virus (EBV)-associated malignant lymphoma as other iatrogenic immunodeficiency-associated lymphoproliferative disorders (OIIA-LPD) during the combined immunosuppressive therapy of high-dose prednisolone, tacrolimus, and intravenous cyclophosphamide for MDA5-DM. Serum EBV DNA was detected, and EBV-encoded small RNA was positive in the tissue sample of LPD, indicating that EBV reactivation contributed to the pathogenesis of LPD in our case. The patient underwent chemotherapy, including rituximab, promptly after discontinuation of tacrolimus and cyclophosphamide, resulting in complete remission of the malignant lymphoma, and MDA5-DM has not recurred with 3.5 mg/d of prednisolone monotherapy. We reviewed 19 cases of OIIA-LPD in patients with idiopathic inflammatory myopathies and herein report the first case of MDA5-DM complicated with OIIA-LPD. Among the 19 patients, 7 showed regression of LPD only following withdrawal of immunosuppressants, 9 took chemotherapy for LPD, and 5 died. It should be noted that patients with MDA5-DM-associated rapidly progressive interstitial lung disease could develop OIIA-LPD because they receive aggressive immunosuppressive therapy.     

In vitro and in vivo studies of a VEGF121/rGelonin chimeric fusion toxin targeting the neovasculature of solid tumors

Vascular endothelial growth factor (VEGF) plays a key role in the growth and metastasis of solid tumors. We generated a fusion protein containing VEGF(121) linked by a flexible G(4)S tether to the toxin gelonin (rGel) and expressed this as a soluble protein in bacteria. Purified VEGF(121)/rGel migrated as an 84-kDa homodimer under nonreducing conditions. VEGF(121)/rGel bound to purified, immobilized Flk-1, and the binding was competed by VEGF(121). Both VEGF(121)/rGel and VEGF(121) stimulated cellular kinase insert domain receptor (KDR) phosphorylation. The VEGF(121)/rGel fusion construct was highly cytotoxic to endothelial cells overexpressing the KDR/Flk-1 receptor. The IC(50) of the construct on dividing endothelial cells expressing 10(5) or more KDR/Flk-1 receptors per cell was 0.5-1 nM, as compared with 300 nM for rGel itself. Dividing endothelial cells overexpressing KDR were approximately 60-fold more sensitive to VEGF(121)/rGel than were nondividing cells. Endothelial cells overexpressing FLT-1 were not sensitive to the fusion protein. Human melanoma (A-375) or human prostate (PC-3) xenografts treated with the fusion construct demonstrated a reduction in tumor volume to 16% of untreated controls. The fusion construct localized selectively to PC-3 tumor vessels and caused thrombotic damage to tumor vessels with extravasation of red blood cells into the tumor bed. These studies demonstrate the successful use of VEGF(121)/rGel fusion construct for the targeted destruction of tumor vasculature in vivo.     

A mutation in the peroxisome proliferator-activated receptor γ-binding site in the gene for the cytosolic form of phosphoenolpyruvate carboxykinase reduces adipose tissue size and fat content in mice

Regulation of the turnover of triglycerides in adipose tissue requires the continuous provision of 3-glycerophosphate, which may be supplied by the metabolism of glucose or by glyceroneogenesis, the de novo synthesis of 3-glycerophosphate from sources other than hexoses or glycerol. The importance of glyceroneogenesis in adipose tissue was assessed in mice by specifically eliminating the expression of the cytosolic form of phosphoenolpyruvate carboxykinase (PEPCK-C), an enzyme that plays a pivotal role in the pathway. To accomplish this, we mutated the binding site for the peroxisome proliferator-activated receptor gamma (PPAR gamma) called the peroxisome proliferator-activated receptor element (PPARE), in the 5' flanking region of the PEPCK-C gene in the mouse by homologous recombination. The mutation abolished expression of the gene in white adipose tissue and considerably reduced its expression in brown adipose tissue, whereas the level of PEPCK-C mRNA in liver and kidney remained normal. Epididymal white adipose tissue from these mice had a reduced triglyceride deposition, with 25% of the animals displaying lipodystrophy. There was also a greatly reduced level of lipid accumulation in brown adipose tissue. A strong correlation between the hepatic content of triglycerides and the size of the epididymal fat pad in PPARE(-/-) mice suggests that hepatic triglyceride synthesis predominantly utilizes free fatty acids derived from the adipose tissue. Unlike other models, PPARE(-/-) mice with lipodystrophy did not exhibit the lipodystrophy-associated features of diabetes and displayed only moderate hyperglycemia. These studies establish the importance of the PPARE site for PEPCK-C gene expression in adipose tissue and the role of PEPCK-C in the regulation of glyceroneogenesis, a pathway critical for maintaining the deposition of triglycerides in adipose tissue.