2周胰岛素强化治疗对口服药失效的2型糖尿病患者外周血核因子κB的影响

目的比较胰岛素强化治疗前后口服抗糖尿病药失效2型糖尿病(T2DM)患者外周血单核细胞中核因子κB(NF-κB)表达水平的变化,探讨胰岛素的抗炎作用。方法选择对照组20名(NC组),口服药失效的T2DM患者20例(DM组)给予胰岛素强化治疗2周。检测DM组治疗前后空腹血糖(FBG)、空腹胰岛素(Fins)和c肽以及餐后2hBG、胰岛素和c肽水平的变化及采用流式细胞仪(FCM)、竞争性酶联免疫吸附法(ELISA)检测治疗前后外周血单核细胞NF-κB表达水平的变化。结果与NC组比较,T2DM患者外周血单核细胞NF-κB表达升高(P0.01);与治疗前比较,胰岛素强化治疗2周后,NF-κB表达降低(P0.01);FBG、2hBG和HOMA-IR降低;胰岛素、C肽和HOMA-β升高。结论 T2DM患者2周胰岛素强化治疗后,血糖明显改善的同时,单核细胞中NF-κB表达明显降低。     

胰岛素强化治疗对新诊断2型糖尿病患者外周血单核细胞中核因子kB表达的影响

目的观察胰岛素强化治疗前后初发2型糖尿病（T2DM）患者外周血单核细胞中核因子KB（NF-kB）表达水平的变化,探讨胰岛素的抗炎作用机判。方法健康成人20例为正常对照（NC）组,新诊断T2DM20例为DM组,DM组胰岛素强化治疗2周。治疗前后采用ELISA、FCM法检测NF-KB表达水平,同时测定治疗前后WBC、N％和Fins,计算HOMA—IR。结果与NC组比,DM组NF-kB表达水平显著增高（P〈01．01）;DM组与治疗前比,治疗后NF-kB水平显著降低（P〈0．05）,WBC、N％和HOMA—IR也明显降低（P均＜0．01）。结论2型糖尿病患者体内存在低度炎症,胰岛素强化治疗可降低单核细胞NF-kB表达,减轻炎症反应。     

甘精胰岛素和预混胰岛素用于老年2型糖尿病患者的疗效和不良反应对比分析

目的评价甘精胰岛素和预混胰岛素在老年T2DM治疗中的优越性。方法68例老年T2DM患者随机分为甘精胰岛素组（Gla组）和预混胰岛素组（Pre组）,比较两组治疗前后FBG、2hBG、HbA1c、空腹C肽（FC-P）及75g OGTT后2hC肽（2hC-P）水平、体重变化、低血糖发生率及患者满意度。结果治疗后两组FBG、2hBG、HbA1c水平均较治疗前显著降低（P〈0．01）,Gla组FBG、HbA1c水平较Pre组显著降低（P〈0.05）,Pre组2hC-P水平较治疗前显著增加（P〈0.05）。Gla组体重增加、低血糖发生率显著低于Pre组（P〈0.05或P〈0．01）。结论老年T2DM患者应用甘精胰岛素是有益的治疗方案。     

胰岛素强化治疗对新诊断2型糖尿病患者内皮脂肪酶的影响

目的观察胰岛素强化治疗前后初发2型糖尿病(T2DM)患者血清内皮脂肪酶水平的变化。方法健康成人20例为正常对照组(NC组),新诊断2型糖尿病30例为DM组,DM组胰岛素强化治疗2周,治疗前后采用酶联免疫吸附法检测血清内皮脂肪酶水平,同时测定治疗前后超敏C反应蛋白、空腹血糖、餐后2小时血糖。结果与NC组比,DM组血清内皮脂肪酶水平显著增高(P<0.01);DM组治疗前与治疗后比较血清内皮脂肪酶水平显著降低(P<0.01),超敏C反应蛋白、空腹血糖、餐后2小时血糖明显降低(P均<0.01)。结论 2型糖尿病患者体内存在轻度炎症,胰岛素强化治疗可减轻炎症反应,降低血清内皮脂肪酶的水平。     

早期、短期胰岛素强化治疗对初发2型糖尿病胰岛β细胞功能的影响

选择初发120例T2DM患者,经胰岛素强化治疗4周,比较治疗前、后空腹血糖(FBG)、空腹胰岛素(FINS)、空腹C-P(FC-P)、餐后2小时血糖(PBG)、餐后2小时C肽,糖化血红蛋白(HbA1c)、胰岛素抵抗指数(HOMA-IR)(HO-MA-IR=FBG X FINS/22.5)的变化。结果:经4周胰岛素强化治疗后,与治疗前相比FBG、PBG、HbA1c均显著降低,FINS、FC-P,餐后2小时C肽有明显升高,胰岛素抵抗指数(HOMA-IR)有明显降低,差异有统计学意义(P<0.05)。结论:对初诊断的2型糖尿病患者进行早期、短期胰岛素强化治疗,可使血糖迅速达标,消除高血糖的毒性副作用,可改善胰岛β细胞功能。     

短期胰岛素强化治疗对2型糖尿病患者C肽的影响

对35例T2DM患者进行为期两周的胰岛素强化治疗,分析比较治疗前后FPG、（2hPG）、HbA1c、空腹及餐后1、2,3小时C肽分泌。结果胰岛素强化治疗后,FPG、2hPG、HbA1c均较治疗前明显下降（P〈0．01）;空腹及餐后1、2、3小时C肽均较治疗前明显升高。结论短期胰岛素强化治疗可显著改善T2DM患者C肽的释放。     

短期诺和锐强化治疗对初诊2型糖尿病患者胰岛β细胞功能的影响

目的　探讨短期诺和锐强化治疗对初诊2型糖尿病(T2DM)患者胰岛β细胞功能和血糖控制的影响。　方法　对45例初诊T2DM患者进行为期两周的诺和锐强化治疗,分析比较治疗前后空腹(FPG)及餐后2 h血糖(2 hPG)、糖化血红蛋白(HbA1c)、静脉葡萄糖耐量试验时第一时相胰岛素及C肽分泌和胰岛素及C肽曲线下面积、胰岛素抵抗指数、胰岛素分泌指数、胰岛素敏感指数、空腹胰岛素(FIns)与FPG比值。　结果　诺和锐强化治疗后,FPG、2 hPG、HbA1c均较治疗前明显下降(P<0.01);空腹及第一时相胰岛素和C肽的分泌、胰岛素和C肽曲线下面积、FIns与FPG比值、胰岛素分泌指数、胰岛素敏感指数均较治疗前明显升高(P<0.01)。胰岛素抵抗指数较治疗前明显下降(P<0.01)。　结论　短期诺和锐强化治疗可显著改善初诊T2DM患者胰岛β细胞功能。     

初诊2型糖尿病胰岛素治疗疗效观察

分析短期应用胰岛素治疗的初诊T2DM36例，以同期口服药物治疗的初诊T2DM47例为对照。按初诊时空腹血糖（FBG）浓度分为A组FBG〈13．9mmol／L，B组FBG13．9-15．6mmol／L，C组FBG〉15．6mmol／L。观察2～3月后各组FBG、P2hBG、HbA1c变化情况。结果：B组和C组胰岛素明显优于对照组（P〈0．05）。结论：FBG≥13．9mmol／L有短期使用胰岛素治疗的指征。     

初诊2型糖尿病胰岛素治疗疗效观察

分析短期应用胰岛素治疗的初诊T2DM36例，以同期口服药物治疗的初诊T2DM47例为对照。按初诊时空腹血糖（FBG）浓度分为A组FBG〈13．9mmol／L，B组FBG13．9-15．6mmol／L，C组FBG〉15．6mmol／L。观察2～3月后各组FBG、P2hBG、HbA1c变化情况。结果：B组和C组胰岛素明显优于对照组（P〈0．05）。结论：FBG≥13．9mmol／L有短期使用胰岛素治疗的指征。     

2型糖尿病患者睡眠质量对空腹血糖水平影响的探讨

目的 探讨在2型糖尿病(T2DM)患者睡眠质量对空腹血糖(FBG)水平的影响. 方法 选择在我院糖尿病门诊就诊的合并睡眠障碍的T2DM患者40例,睡眠障碍均经过神经内科专科治疗.同时选择40例不伴睡眠障碍的T2DM患者作为对照组.分别测定患者基线时及合并睡眠障碍的T2DM治疗后的FBG、餐后2小时血糖(2hBG)、HbA1c及空腹胰岛素(FIns)、胰岛素抵抗指数(HOMA-IR). 结果 与不伴睡眠障碍的T2DM患者相比,合并睡眠障碍的T2DM患者的FBG以及HbA1c水平较高,而且存在IR状态,两组间的差异有明显的统计学意义(P<0.05).合并睡眠障碍的T2DM患者的FBG和2hBG以及HOMA-IR较治疗前均减低(P<0.05). 结论 合并睡眠障碍的T2DM患者的FBG以及HbA1c水平较高,且存在IR状态;而针对患者睡眠质量的改善措施对糖尿病患者的血糖水平具有一定影响,尤其FBG更为明显.     

胰岛素瘤的解剖分布特点分析

目的胰岛素瘤是最常见的胰腺神经内分泌肿瘤，因其临床表现多样，导致诊断困难。影像学诊断尤其是超声内镜(EUS)在胰岛素瘤的诊断中起着重要作用，拥有较高的敏感性和特异性。本研究拟通过明确胰岛素瘤的解剖分布特点，以期有助于提高影像学的诊断准确率和降低漏诊率，尤其是在教育和培训实践中对于EUS的学习者更具有指导价值。 方法回顾性分析解放军总医院第一医学中心病案资料数据库1993年1月至2019年11月经外科手术、病理确诊为胰岛素瘤的患者的临床资料，检索方法采取搜索术后病理诊断为"胰岛素瘤"的病例，通过查阅病例的方法，提取出胰岛素瘤的大小和解剖分布等数据，进一步分析其特点。 结果共检索到确诊为胰岛素瘤的患者116例，其中，男45例、女71例，年龄13～76岁，平均年龄(44.4±14.85)岁。胰岛素瘤单发110例(94.8%)、多发6例(5.2%)。位置分布：头颈部46例(39.7%)，单发45例、多发1例；体尾部68例(58.6%)，单发65例、多发3例；全胰腺多发2例(1.7%)。病变大小特点：最大径0.4～3.4 cm，平均大小(1.53±0.58)cm。≤1 cm 29例、>1 cm而≤1.5 cm41例、>1.5 cm而≤2.0 cm28例，≤3 cm 15例，>3 cm 3例。年龄与肿瘤的大小相关，≤44岁患者肿瘤平均大小为(1.36±0.51)cm、>44岁患者肿瘤平均大小为(1.70±0.60)cm，P<0.05。头颈部的肿瘤大于体尾部的肿瘤，头颈部肿瘤平均大小(1.66±0.63)cm，体尾部(1.42±0.52)cm，P<0.05。 结论胰岛素瘤在胰腺体尾部较头颈部更好发；绝大多数单发，但可以全胰腺多发；多数小于1.5 cm，肿瘤的大小与患者年龄和肿瘤的解剖分布相关。     

Pathogenesis of carcinoma of the papilla of Vater

Most adenomas and carcinomas of the small intestine and extrahepatic bile ducts arise in the region of the papilla of Vater. In familial adenomatous polyposis (FAP) it is the main location for carcinomas after proctocolectomy. In many cases symptoms due to stenosis lead to diagnosis at an early tumor stage. In about 80%, curative intended resection is possible. Operability is the most relevant prognostic factor. Most ampullary carcinomas resp. carcinomas of the papilla of Vater develop from adenomatous or flat dysplastic precursor lesions. They can be sited in the ampulloduodenal part of the papilla of Vater, which is lined by intestinal mucosa. They also can develop in deeper parts of the ampulla, which are lined by pancreaticobiliary duct mucosa. Intestinal-type adenocarcinoma and pancreaticobiliary-type adenocarcinoma represent the main histological types of ampullary carcinoma. Furthermore, there exist unusual types and undifferentiated carcinomas. Many carcinomas of intestinal type express the immunohistochemical marker profile of intestinal mucosa (keratin 7?, keratin 20+, MUC2+). Carcinomas of pancreaticobiliary type usually show the immunohistochemical profile of pancreaticobiliary duct mucosa (keratin 7+, keratin 20?, MUC2?). Even poorly differentiated carcinomas, as well as unusual histological types, may conserve the marker profile of the mucosa they developed from. These findings underline the concept of histogenetically different carcinomas of the papilla of Vater which develop either from intestinal- or from pancreaticobiliary-type mucosa of the papilla of Vater. Molecular alterations in ampullary carcinomas are similar to those of colorectal as well as pancreatic carcinomas, although they appear at different frequencies. In future studies, molecular alterations in ampullary carcinomas should be correlated closely with the different histologic tumor types. Consequently, the histologic classification should reflect the histogenesis of ampullary tumors from the two different types of papillary mucosa.     

Demonstration of the mechanism of action of biguanides

Summary Palmitic acid oxidation in rat diaphragm homogenate is depressed by biguanide concentrations that are still incapable of inhibiting oxidative phosphorylation. Glucose oxidation is not directly effected by the same biguanide concentrations: however, the inhibitory effect of palmitic acid on glucose oxidation is partly removed by biguanides. Inhibition of fatty acid oxidation, which accounts for most of the metabolic effects caused by these drugs, can be regarded as the fundamental mechanism of action of biguanides. There is some evidence suggesting that these drugs might interact with carnitine, thus preventing long-chain fatty acids from being transported across the mitochondrial membrane to the site of oxidation. Traduzione a cura degli AA.     

Lack of correlation of degree of villous atrophy with severity of clinical presentation of coeliac disease

BACKGROUND AND AIM: Both the clinical presentation and the degree of mucosal damage in coeliac disease vary greatly. In view of conflicting information as to whether the mode of presentation correlates with the degree of villous atrophy, we reviewed a large cohort of patients with coeliac disease. PATIENTS AND METHODS: We correlated mode of presentation (classical, diarrhoea predominant or atypical/silent) with histology of duodenal biopsies and examined their trends over time. RESULTS: The cohort consisted of 499 adults, mean age 44.1 years, 68% females. The majority had silent coeliac disease (56%) and total villous atrophy (65%). There was no correlation of mode of presentation with the degree of villous atrophy (p=0.25). Sixty-eight percent of females and 58% of males had a severe villous atrophy (p=0.052). There was a significant trend over time for a greater proportion of patients presenting as atypical/silent coeliac disease and having partial villous atrophy, though the majority still had total villous atrophy. CONCLUSIONS: Among our patients the degree of villous atrophy in duodenal biopsies did not correlate with the mode of presentation, indicating that factors other than the degree of villous atrophy must account for diarrhoea in coeliac disease.     

血吸虫童虫生长发育及其机制的研究进展

血吸虫童虫是宿主免疫系统攻击的重要靶标,包括皮肤型、肺型和肝门型童虫。宿主分子对童虫生长发育具有重要作用。童虫生长发育机制包括免疫调节、信号转导、性别发育及凋亡等。肌动蛋白、组织蛋白酶、烯醇化酶和葡萄糖基转移酶等分子为血吸虫童虫生长发育的重要分子。本文对血吸虫童虫生长发育及其机制的研究进展做一综述。     

124例耐多药结核分枝杆菌基因突变特征分析

目的对临床分离的耐多药结核分枝杆菌相关基因的突变特征进行分析。方法对124例耐多药结核分枝杆菌以及50株敏感株的耐药相关基因(包括异烟肼inh A、kat G、oxyR-ahp C间隔区以及利福平rpo B)进行序列测定,分析其基因突变情况。结果异烟肼耐药inh A基因突变率为14.5%;kat G基因突变率为70.2%(87/124),主要位于315位;oxyR-ahp C间隔区突变率为15.3%;inh A、kat G两种基因同时突变率75.0%,三种基因同时突变率为89.5%。利福平rpo B基因突变的检出率高达95.2%,突变主要发生在531、526、516位点。结论我省耐多药菌异烟肼耐药相关基因最常见突变为kat G 315、inh A C-T(-15)、axyR-ahp C间隔区(-10)C-T,利福平为rpo B531、526、516。结合MDR-TB耐药相关基因的特征分析,可以建立一种快速、准确、特异的适合于我省的检测结核菌耐多药性的新方法。     

氯硝柳胺悬浮剂的毒性评价

目的评价氯硝柳胺悬浮剂的毒性，为现场大规模应用灭螺提供依据。方法按照中华人民共和国国家标准GB 15670-1995《农药登记毒理学试验方法》和鱼类毒性试验方法进行。结果经口、经皮肤的LDso雌、雄性大鼠均>5 000 mg/kg，经呼吸道的LCso雌、雄性大鼠均>5 000mg/m3，该药经口、经皮肤、经呼吸道毒性均属微毒类药物；兔眼用药后，观察期内无不良反应，对眼无刺激性；皮肤用药后对皮肤无刺激性。与氯硝柳胺原药、氯硝柳胺乙醇胺盐原药和氯硝柳胺乙醇胺盐可湿性粉剂相比，氯硝柳胺悬浮剂对鱼急性毒性最低。结论氯硝柳胺悬浮剂属微毒类药物，对鱼的毒性低于其乙醇胺盐可湿性粉剂，适合于现场应用。     

Assessment of quality of life of parents of children with juvenile chronic arthritis

The aim of the study was to assess the quality of life (QOL) and the psychological status of parents of children with juvenile chronic arthritis (JCA). The QOL, anxiety and depression of the parents of 28 children with JCA were evaluated and compared to those of the parents of 28 healthy children. Mothers of JCA children and mothers of healthy children reported similar QOL. The reported anxiety and depression levels were similar for mothers and fathers in both groups. The parents of children with pauciarticular-type JCA reported lower QOL and higher levels of anxiety and depression than the parents of children with other types, namely polyarticular and systemic JCA. These findings may be explained by the fact that the pauciarticular patients had shorter disease duration and were less frequently seen in the outpatient clinic. The QOL of mothers of children with JCA was found to be slightly impaired in the group of children with pauciarticular JCA. Future larger studies are needed to confirm these results, as the number of subjects in the three groups was rather low. Received: 26 September 2001 / Accepted: 8 February 2002     

Numerical Simulation of the Effect of Rate of Change of Glucose on Measurement Error of Continuous Glucose Monitors

Background

A 5-day in-patient study designed to assess the accuracy of the FreeStyle Navigator® Continuous Glucose Monitoring System revealed that the level of accuracy of the continuous sensor measurements was dependent on the rate of glucose change. When the absolute rate of change was less than 1 mg•dl⁻¹•min⁻¹ (75% of the time), the median absolute relative difference (ARD) was 8.5%, with 85% of all points falling within the A zone of the Clarke error grid. When the absolute rate of change was greater than 2 mg•dl⁻¹•min⁻¹ (8% of the time), the median ARD was 17.5%, with 59% of all points falling within the Clarke A zone.

Method

Numerical simulations were performed to investigate effects of the rate of change of glucose on sensor measurement error. This approach enabled physiologically relevant distributions of glucose values to be reordered to explore the effect of different glucose rate-of-change distributions on apparent sensor accuracy.

Results

The physiological lag between blood and interstitial fluid glucose levels is sufficient to account for the observed difference in sensor accuracy between periods of stable glucose and periods of rapidly changing glucose.

Conclusions

The role of physiological lag on the apparent decrease in sensor accuracy at high glucose rates of change has implications for clinical study design, regulatory review of continuous glucose sensors, and development of performance standards for this new technology. This work demonstrates the difficulty in comparing accuracy measures between different clinical studies and highlights the need for studies to include both relevant glucose distributions and relevant glucose rate-of-change distributions.     

Angiographic diagnosis of the degree of serosal invasion of carcinoma of the colon

Angiography using Prostaglandin El^® was performed on 38 patients with carcinoma of the colon in order to diagnose the degree of serosal cancer invasion. The findings at angiography were classified into four groups:1) AG-S3, abnormal change (irregularity and/or encasement) up to marginal vessels; 2) AG-S2, abnormality up to vasa recta; 3) AG-S1, abnormality of penetrating branches of vasa recta within the wall of the colon; and 4) AG-S0, no distinct findings of abovementioned vessels. These angiographic findings were compared with both macroscopic and microscopic serosal cancer invasion. Angiographic diagnosis is in accord with the macroscopic findings in 84.2 percent of cases. Angiographic diagnosis is in accord with the microscopic findings in 32.4 percent of cases. Macroscopic findings confirm the angiographic diagnosis precisely but the conflict with microscopic findings should not be overlooked. This may be the result of inflammatory change, adhesion, and fibrosis around carcinoma of the colon.