Variation of red blood cell parameters in Behcet’s disease: association with disease severity and vascular involvement

Clinical Rheumatology - Behcet’s disease (BD) is a systemic and chronic inflammatory vasculitis with unknown etiology. Diagnosis is determined by evaluating several clinical criteria, but the...     

Assessment of diagnostic utility,clinical phenotypic associations,and prognostic significance of anti-NXP2 autoantibody in patients with idiopathic inflammatory myopathies: a systematic review and meta-analysis

Clinical Rheumatology - The objectives of this study are to analyze the association between anti-nuclear matrix protein 2 (NXP2) autoantibody and idiopathic inflammatory myopathies (IIMs) and to...     

阑尾腔内息肉内镜下治疗的初步观察

2016年1月—2020年12月间,在首都医科大学附属北京友谊医院消化内科行内镜下治疗的阑尾腔内息肉病例共6例,息肉直径0.3~1.3 cm。6例阑尾腔内息肉均顺利完成内镜下治疗,其中3例行内镜黏膜切除术整块切除、1例行内镜黏膜切除术分片切除、1例行内镜黏膜下剥离术切除、1例予活检钳冷钳除。6例术后均未出现出血、穿孔、感染和急性阑尾炎等并发症。3例术后复查创面愈合良好、无复发,其余3例暂未复查结肠镜。以上结果初步证实,阑尾腔内息肉行内镜下治疗安全和有效。     

Effect of Information-Motivation-Behavioral Model Based on Protection Motivation Theory on the Psychological Resilience and Quality of Life of Patients with Type 2 DM

Psychiatric Quarterly - Diabetes mellitus (DM) is one of the remarkable disease challenges in the twenty-first century and poses threat to patients’ physical health. Given the difficulty of...     

Molecular and clinicopathological analysis of dermatofibrosarcoma protuberans

Dermatofibrosarcoma protuberans (DFSP) is a dermal and subcutaneous tumor of intermediate malignancy. The most remarkable cytogenetic feature of DFSP is the chromosomal translocation t(17;22)(q22;q13), causing a fusion of the platelet-derived growth factor beta chain (PDGFB) gene at 22q13, and the collagen type 1 alpha 1 (COL1A1) at 17q22. The aim of the study was to analyze the molecular characteristic of DFSP in conjunction with histopathological and clinical features.     

Treatment with an Angiopoietin-1 mimetic peptide promotes neurological recovery after stroke in diabetic rats

AimVasculotide (VT), an angiopoietin‐1 mimetic peptide, exerts neuroprotective effects in type one diabetic (T1DM) rats subjected to ischemic stroke. In this study, we investigated whether delayed VT treatment improves long‐term neurological outcome after stroke in T1DM rats.MethodsMale Wistar rats were induced with T1DM, subjected to middle cerebral artery occlusion (MCAo) model of stroke, and treated with PBS (control), 2 µg/kg VT, 3 µg/kg VT, or 5.5 µg/kg VT. VT treatment was initiated at 24 h after stroke and administered daily (i.p) for 14 days. We evaluated neurological function, lesion volume, vascular and white matter remodeling, and inflammation in the ischemic brain. In vitro, we evaluated the effects of VT on endothelial cell capillary tube formation and inflammatory responses of primary cortical neurons (PCN) and macrophages.ResultsTreatment of T1DM‐stroke with 3 µg/kg VT but not 2 µg/kg or 5.5 µg/kg significantly improves neurological function and decreases infarct volume and cell death compared to control T1DM‐stroke rats. Thus, 3 µg/kg VT dose was employed in all subsequent in vivo analysis. VT treatment significantly increases axon and myelin density, decreases demyelination, decreases white matter injury, increases number of oligodendrocytes, and increases vascular density in the ischemic border zone of T1DM stroke rats. VT treatment significantly decreases MMP9 expression and decreases the number of M1 macrophages in the ischemic brain of T1DM‐stroke rats. In vitro, VT treatment significantly decreases endothelial cell death and decreases MCP‐1, endothelin‐1, and VEGF expression under high glucose (HG) and ischemic conditions and significantly increases capillary tube formation under HG conditions when compared to non‐treated control group. VT treatment significantly decreases inflammatory factor expression such as MMP9 and MCP‐1 in macrophages subjected to LPS activation and significantly decreases IL‐1β and MMP9 expression in PCN subjected to ischemia under HG conditions.ConclusionDelayed VT treatment (24 h after stroke) significantly improves neurological function, promotes vascular and white matter remodeling, and decreases inflammation in the ischemic brain after stroke in T1DM rats.     

NMDA Receptor Modulates Spinal Iron Accumulation Via Activating DMT1(-)IRE in Remifentanil-Induced Hyperalgesia

N-methyl-D-aspartate (NMDA) receptor activation is known to be critical in remifentanil-induced hyperalgesia. Evidence indicates that iron accumulation participates in NMDA neurotoxicity. This study aims to investigate the role of iron accumulation in remifentanil-induced hyperalgesia. Remifentanil was delivered intravenously in rats to induce hyperalgesia. The NMDA receptor antagonist MK-801 was intrathecally administrated. The levels of divalent metal transporter 1 without iron-responsive element [DMT1(-)IRE] and iron were detected. Behavior testing was performed in DMT1(-)IRE knockdown rats and rats treated with iron chelator DFO. Meanwhile, the spinal dorsal horn neurons were cultured and transfected with DMT1(-)IRE siRNA, and then respectively incubated with remifentanil and MK-801. The levels of intracellular Ca²⁺ and iron were assessed by fluorescence imaging. Our data revealed that spinal DMT1(-)IRE and iron content significantly increased in remifentanil-treated rats, and MK-801 inhibited the enhancements. DMT1(-)IRE knockdown and DFO prevented against remifentanil-induced hyperalgesia. Notably, the levels of Ca²⁺ and iron increased in remifentanil-incubated neurons, and these growths can be blocked by MK-801. DMT1(-)IRE knockdown attenuated iron accumulation but did not influence Ca²⁺ influx. This study suggests that DMT1(-)IRE-mediated iron accumulation is likely to be the downstream event following NMDA receptor activation and Ca²⁺ influx, contributing to remifentanil-induced hyperalgesia.PerspectiveRemifentanil-induced hyperalgesia is common even when used within clinical accepted doses. This study presents that aberrant iron accumulation is involved in the development of remifentanil-induced hyperalgesia in vivo and in vitro. Iron chelation may be a potential therapeutic strategy for the prevention of hyperalgesia in populations at high risk.     

精神分裂症断裂基因 1基因多态性与帕利哌酮治疗精神分裂症疗效及微小 RNA?134?5p关联性分析

目的观察精神分裂症断裂基因 1(dierupted in schizophrenia 1,DISC1)基因多态性与帕利哌酮治疗精神分裂症疗效及微小 RNA?134?5p(miR?134?5p)的关联性分析。方法选取 2018年 3月至 2019年 3月绵阳市第三人民医院精神分裂症病人 109例为疾病组,采用帕利哌酮单药治疗,选取同期健康体检者 109例为健康组,检测并比较两组 DISC1基因单核苷酸多态性(SNPs)位点间差异。比较疾病组不同基因型病人帕利哌酮治疗前与治疗 6个月后阳性和阴性症状量表(PANSS)、精神分裂症认知功能成套测验共识版(MCCB)评分以及血清 miR?134?5p水平。结果 DISC1 SNPs位点比较中,疾病组 rs821616位点与健康组差异有统计学意义(P＜0.05)。疾病组不同基因型病人帕利哌酮治疗后 PANSS评分均较治疗前降低, MCCB评分较治疗前升高(P＜0.05)。 rs821616基因型病人中 TT型病人 PANSS评分(46.3±7.1)分低于 AA型病人(59.4±5.8)分, TT型病人 MCCB评分(154.7±32.3)分高于 AA型病人(131.3±32.1)分, AT型(0.32±0.07)和 TT型(0.41±0.09)病人 miR?134?5p水平高于 AA型病人(0.30±0.11)。 rs11122319基因型病人中 GG型、 AG型病人 PANSS评分低于 AA型病人, GG型病人 MCCB评分和 miR?134?5p水平高于 AA型和 AG型病人(P＜0.05)。 rs1417584基因型病人中 GG型、 AG型病人 PANSS评分低于 AA型病人, GG型病人 MCCB评分高于 AA型和 AG型, GG型病人 miR?134?5p水平高于 AA型病人(P＜0.05)。结论帕利哌酮可以改善精神分裂症病人症状,改善病人认知功能,提高 miR?134?5p水平,不同 DISC1基因型病人间治疗效果存在差异。     

纳洛酮对蛛网膜下腔出血大鼠海马区神经细胞自噬的影响

目的探讨纳洛酮对蛛网膜下腔出血(SAH)大鼠海马区神经细胞自噬的影响。方法将 108只健康雄性清洁级 SD大鼠按随机数字表法分为假手术组、 SAH组、纳洛酮组,每组 36只。假手术组只进行造模手术不刺破血管, SAH组利用颈内动脉穿刺法制成大鼠 SAH动物模型,纳洛酮组在造模成功后立即给予纳洛酮(1 mg∕kg体质量)腹腔注射,每 12小时注射 1次,用药至处死的各时相点。假手术组和 SAH组采用同样方法注射同等体积的 0.9%氯化钠溶液。每组又按 6h、24 h、72 h时间点分为 3个亚组(每个亚组 12只 SD大鼠)。穿梭箱实验观察三组大鼠的行为学变化;苏木素 ?伊红(HE)染色观察海马区神经细胞形态变化;免疫组织化学检测自噬特异性标志物 Beclin?1和微管相关蛋白 1轻链 3(LC3?Ⅱ)在大鼠海马区神经细胞的表达。结果与假手术组相比, SAH组 6h、24 h、72 h各时间点逃避反应次数减少［(24.83±3.24)次比(14.41±1.98)次,(25.33±2.64)次比(16.25±2.18)次,(25.16±2.82)次比(18.33±2.57)次］(P＜0.05),逃避反应时间增加［(3.54±0.99)s比(9.09±1.38)s,(3.55±0.84)s比(8.73±1.13)s,(3.54±0.83)s比(8.00±1.04)s］(P＜0.05)海马区正常神经细胞数量减少［(122.67±5.55)个比(84.25±12.63)个,(122.25±5.50)个比(75.58±11.11)个,(121.58±5.68)个7.75±10.55)个］(P＜0.05)表达 Beclin?1和 LC3?Ⅱ蛋白的阳性细胞数量增高［(20.50±3.45)个比(31.41±4.96)个,(20.33±2.77)个比(47.67±7.35)个,(200±3.59)个比(43.17±6.46)个;(17.08±比(6,.5,3.00)个比(27.42±3.40)个,(17.50±2.31)个比(39.83±4.67)个,(17.41±2.57)个比(31.50±4.06)个］(P＜0.05)。与 SAH组比较,纳洛酮组各时间点逃避反应次数增多［(14.41±1.98)次比(16.50±1.93)次,(16.25±2.18)次比(19.25±2.30)次,(18.33±2.57)次比(22.50±2.20)次］(P＜0.05),逃避反应时间减少［(9.09±1.38)s比(8.05±1.24)s,(8.73±1.13)s比(6.56±1.09)s,(8.00±1.04)s比(5.36±0.97)s］(P＜0.05)海马区正常神经细胞数量增多［(84.25±12.63)个比(94.75±11.06)个,(75.58±11.11)个比(84.50±9.21)个,(67.75±10.55)个比.33±9.88)个］(P＜0.05)表达 Beclin?1和 LC3?Ⅱ蛋白的阳性细胞数量增高［(31.41±4.96)个比(77,(36.17±4.06)个,(47.67±7.35)个比(57.58±6.68)43.17±6.46)个比(52.75±7.35)个;(27.42±3.40)个比(30.92±4.19)个,个,(,(39.83±4.67)个比(48.33±5.66)个,(31.50±4.06)个比(38.58±5.40)个］(P＜0.05)。结论纳洛酮的干预可适度激活 SAH大鼠海马区神经细胞自噬的表达,并具有脑保护作用。