补肾活血饮治疗原发性帕金森病的疗效观察

目的观察中药补肾活血饮配合西药治疗帕金森病(PD)的临床疗效。方法采用随机对照试验,纳入PD患者100例,剔除5例、脱落4例,完成研究者共91例。其中治疗组(中药+西药组)47例,对照组(西药组)44例,疗程3个月。采用统一帕金森病评定量表(UPDRS)评分、H-Y分级的变化来评价治疗的有效率、运动功能的改善情况等。结果治疗组有效率44.68%,疗效优于对照组(11.36%,P<0.05)。治疗组治疗后各时间点UPDRS总分较对照组下降明显(P<0.05)。治疗组各时间点UPDRSⅡ评分与治疗前相比明显降低(P<0.01),对照组仅治疗后1个月较治疗前降低(P<0.05);与对照组比较,治疗后2、3个月时治疗组UP-DRSⅡ评分下降更为明显(P<0.05)。治疗组各时点UPDRSⅢ评分与治疗前相比明显降低(P<0.01),对照组在治疗后1、3个月较治疗前降低(P<0.05)。两组间UPDRSⅢ评分、H-Y分级变化差异无统计学意义(P>0.05)。结论补肾活血饮具有增效减毒作用,与西药联合应用在改善PD患者的运动功能和日常生活能力方面优于单用西药。     

磁共振扩散张量成像(DTI)在诊断中枢神经系统疾病中的应用

目的评价磁共振扩散张量成像(DTI)在诊断中枢系统疾病中的用途。方法 86例临床证实的中枢神经系统疾病患者包括超急性及急性期脑梗死40例,脑肿瘤32例,脑白质疏松7例,多发性硬化4例,脑中毒3例以及作为正常对照的健康志愿者9例均经常规磁共振序列和DWI、DTI检查,对患侧和健侧大脑白质纤维束感兴趣区各向异性分数(FA)值进行定量分析,获得方向编码彩色(DEC)图和黑白各向异性(FA)图,扩散张量纤维束成像(DTI)显示脑白质纤维束走形方向、损伤、受压、移位等情况。结果健康组不同部位的脑白质的FA值不同,但大脑半球两侧的FA值差异无统计学意义。超急性(发病后小于6 h)脑梗死区白质FA值与对侧相比轻度增高或降低,急性期(发病后6～72 h)脑梗死区白质FA值显著减低,FA图为低信号,健侧脑白质为高信号,均有明显差别。良恶性脑肿瘤FA值仅在瘤周水肿区的比较中有统计学差异,FA图肿瘤实质为稍低信号,中心坏死及周围水肿表现为低信号。脑白质病变和正常对照组感兴趣区测量FA值,病变区FA值降低,两组差异有统计学意义。结论 DTI可无创且清晰地显示白质纤维束走行方向及分布情况,对诊断中枢神经系统病变有重要用途。     

鹰嘴豆芽提取物对Caco-2细胞凋亡的作用

目的研究鹰嘴豆芽乙醇提取物（CSE）对人结肠腺癌Caco-2细胞增殖及细胞凋亡的影响。方法提取鹰嘴豆芽的活性成分并测定含量;MTT法观察提取物对Caco-2细胞增殖的影响;透射电镜观察细胞超微结构;琼脂糖凝胶电泳法进行细胞凋亡的DNA分析;流式细胞术检测凋亡情况。结果 CSE含23.53%皂苷、14.73%异黄酮;不同浓度的CSE对Caco-2细胞均有一定的增殖抑制作用,且呈量效和时效关系;细胞出现染色质边移和凋亡小体;DNA电泳呈现梯度条带,表明CSE可诱导Caco-2细胞凋亡;3、5、10μg/ml的CSE作用后,细胞凋亡率分别为32.6%、68.8%、73.9%,与对照组（0.9%）比较差异显著（P〈0.05）。结论 CSE可通过诱导细胞凋亡而抑制人结肠腺癌株Caco-2细胞的生长,为鹰嘴豆应用于结肠癌的临床治疗和预防提供了理论依据。     

孤立性肺结节的CT诊断

目的分析孤立性肺结节(SPN)的CT征象,并提高诊断水平。方法回顾性分析经临床和病理证实的40例SPN的CT表现,其中周围型肺癌20例,结核球8例,炎性假瘤8例,错构瘤2例,肺AVM和支气管囊肿各1例,均经胸部CT平扫。30例同时行CT增强,包括周围型肺癌15例,结核球6例,炎性假瘤6例,错构瘤、支气管囊肿及肺AVM各1例。结果长、短毛刺、深分叶及卫星病灶在良、恶性结节组间有显著差异(P<0.05);恶性SPN强化值大于等于30 HU,良性SPN强化值小于30 HU,二者间有统计学差异(P<0.05)。结论 SPN的CT表现多种多样,良恶性结节之间的表现存在许多重叠,特征性的表现很少,需要综合分析这些征象的形态学及强化表现,并密切结合临床及相关实验室检查,才能尽早做出准确诊断。     

寻常型银屑病患者BMD、ALP、Ca、P、TRACP-5b的检测及其意义

目的检测寻常型银屑病患者骨代谢生化指标及骨密度的情况,以了解寻常型银屑病患者的骨代谢异常状况。方法采用双能X线吸收法对48例寻常型银屑病患者(实验组)和40例健康对照者(对照组)行腰椎、股骨颈、左前臂骨密度检测;在相同条件下用贝克曼自动生化分析仪检测两组血液中ALP、Ca、P的浓度;ELSIA法检测两组血清中抗酒石酸酸性磷酸酶-5b(TRACP-5b)的浓度。结果寻常型银屑病患者血清TRACP-5b、ALP的浓度明显高于对照组(P<0.05),差异具有统计学意义;血清Ca浓度较正常对照组低,差异有统计学意义(P<0.05);血清P的浓度和正常对照组比较差异无统计学意义(P>0.05),腰椎、股骨颈、左前臂的骨密度及T值与对照组比较,具有统计学意义(P<0.05)。结论寻常型银屑病患者骨形成和骨吸收相关酶较正常人的血清水平升高,骨密度较正常人降低,说明寻常型银屑病患者骨代谢异常并已致骨量减少。血钙异常可能是寻常型银屑病骨代谢异常的原因之一,而血P在寻常型银屑病骨代谢异常中无影响。     

Apelin-13 inhibits apoptosis and excessive autophagy in cerebral ischemia/reperfusion injury

Apelin-13 is a novel endogenous ligand for an angiotensin-like orphan G-protein coupled receptor, and it may be neuroprotective against cerebral ischemia injury. However, the precise mechanisms of the effects of apelin-13 remain to be elucidated. To investigate the effects of apelin-13 on apoptosis and autophagy in models of cerebral ischemia/reperfusion injury, a rat model was established by middle cerebral artery occlusion. Apelin-13(50 μg/kg) was injected into the right ventricle as a treatment. In addition, an SH-SY5 Y cell model was established by oxygen-glucose deprivation/reperfusion, with cells first cultured in sugar-free medium with 95% N2 and 5% CO2 for 4 hours and then cultured in a normal environment with sugar-containing medium for 5 hours. This SH-SY5 Y cell model was treated with 10–7 M apelin-13 for 5 hours. Results showed that apelin-13 protected against cerebral ischemia/reperfusion injury. Apelin-13 treatment alleviated neuronal apoptosis by increasing the ratio of Bcl-2/Bax and significantly decreasing cleaved caspase-3 expression. In addition, apelin-13 significantly inhibited excessive autophagy by regulating the expression of LC3 B, p62, and Beclin1. Furthermore, the expression of Bcl-2 and the phosphatidylinositol-3-kinase(PI3 K)/Akt/mammalian target of rapamycin(mTOR) pathway was markedly increased. Both LY294002(20 μM) and rapamycin(500 nM), which are inhibitors of the PI3 K/Akt/mTOR pathway, significantly attenuated the inhibition of autophagy and apoptosis caused by apelin-13. In conclusion, the findings of the present study suggest that Bcl-2 upregulation and mTOR signaling pathway activation lead to the inhibition of apoptosis and excessive autophagy. These effects are involved in apelin-13-induced neuroprotection against cerebral ischemia/reperfusion injury, both in vivo and in vitro. The study was approved by the Animal Ethical and Welfare Committee of Jining Medical University, China(approval No. 2018-JS-001) in February 2018.     

Prolactin and glucocorticoid receptors in the prefrontal cortex are associated with anxiety-like behavior in prenatally stressed adolescent offspring rats

Prenatal stress (PS) causes anxiety in mothers and their offspring and chewing is a commonly observed behavior during maternal stress. Prolactin (PRL) is an anti-anxiety factor that suppresses the hypothalamic–pituitary–adrenal axis. Here, we studied the roles of PRL, corticosterone (CORT), and their receptors in PS-induced anxiety-like behavior in dams and their offspring. We further investigated whether chewing during maternal stress could prevent PS-induced harmful consequences. Pregnant rats were randomly divided into PS, PS + chewing, and control groups. Anxiety-like behaviors of dams and their adolescent offspring were assessed using the open field test and elevated plus maze. Serum levels of PRL and CORT were measured by ELISA. Expression of mRNA and protein of PRLR and glucocorticoid receptor (GR) in the prefrontal cortex (PFC) were evaluated by qRT-PCR and western blotting, respectively. Compared to the control rats, dams and their female offspring, but not male offspring, in the PS group showed increased anxiety-like behaviors. The PS-affected rats had a lower serum PRL level and increased PRLR expression in the PFC. In contrast, these rats had a higher serum CORT level and decreased GR expression in the PFC. Chewing ameliorated anxiety-like behaviors and counteracted stress-induced changes in serum PRL and CORT, as well as the expression of their receptors in the PFC. Conclusion: PS-induced anxiety-like behavior is associated with changes in the serum levels of PRL and CORT and expression of their receptors in the PFC. Moreover, chewing blunts the hormonal and receptor changes and may serve as an effective stress-coping method for preventing PS-induced anxiety-like behavior.     

Administration of tissue plasminogen activator without coagulation results in a Chinese population

Routine coagulation test before intravenous tissue plasminogen activator (tPA) use increases the door to needle time (DNT). We sought to evaluate the safety of tPA use without coagulation results and its impact on prognosis. In our stroke registry, tPA was delivered with coagulation results from December 2015 to April 2016 and without coagulation results from May 2016 to December 2016. Differences of demographics, clinical characteristic, and prognosis between these two groups were analyzed. In addition, logistic regression analysis was conducted to identify predictors for DNT of over 60 min. A total of 201 stroke patients were included in the final analysis. Of these, 81 patients received tPA with coagulation results and 120 patients without coagulation results. Only one (0.8%) patient with abnormal coagulation results met the exclusion criteria of tPA use in patients without coagulation results. The difference of DNT between groups with (mean, 61.7 min) and without (mean, 41.9 min) coagulation results was significant (P?=?0.00). The group without coagulation results had a higher rate of favorable 90-day outcome (74.2 vs 70.4%) and lower rates of symptomatic intracranial hemorrhage/nonintracranial hemorrhage (4.9 and 22.2% vs 1.7 and 19.2%) than the group with coagulation results did; these differences were not statistically significant. In multivariate analysis, only tPA use with coagulation results was the predictor for DNT of over 60 min (P?=?0.0030, OR?=?2.44, 95% CI 1.28–4.65). The present study suggests that tPA could be delivered safely without coagulation results in patients without suspected coagulopathy, and avoiding coagulation tests reduces significantly the DNT interval.     

p38MAPK在体外培养星形胶质细胞缺氧/复氧损伤中的表达

目的 建立SD大鼠星形胶质细胞缺氧复氧损伤模型,探讨p38MAPK活性变化与星形胶质细胞损伤的关系.方法 体外培养新生SD大鼠星形胶质细胞,实验设正常对照组（N）、SB203580组（SB组,10 μmol/L）、缺氧/复氧组（H/R组）和缺氧/复氧组＋SB203580阻断p38MAPK组（H/R＋SB组）.应用MTT法、WB法、ELISA法检测缺氧4 h、8 h、复氧6 h、12 h、24 h、48 h时细胞存活率,p38MAPK、p-p38（磷酸化p38MAPK）及TNF-α的变化.结果 培养星形胶质细胞GFAP阳性表达率大于97%.缺氧/复氧使星形胶质细胞活力降低,SB203580阻断p38MAPK细胞活力高于H/R组,各组星形胶质细胞总p38MAPK水平无显著变化,缺氧复氧干预后p-p38表达上调,TNF-α水平显著增高.用SB203580阻断p38MAPK通路后,SB＋H/R组较H/R组p-p38、TNF-α水平降低.SB组总p38MAPK、p-p38、TNF-α水平与N组比较无显著变化.结论 p38MAPK信号通路参与了星形胶质细胞缺氧复氧损伤过程.     

High expression of cyclooxygenase-2 in uterine fibroids and its correlation with cell proliferation

Objective

To investigate the expression of cyclooxygenase-2 (COX-2) in uterine fibroids and healthy uterine smooth muscle as well as its role in the pathogenesis of uterine fibroids.

Methods

We collected uterine fibroid tissues and their paired adjacent healthy uterine smooth muscle tissues from 30 cases of uterine fibroids. We used immunohistochemistry and quantitative real-time PCR, as well as western blot to detect COX-2 expression. Using the COX-2 inhibitors NS-398 and celecoxib, we observed the response to the inhibitors in the healthy and fibroid smooth muscle cell pairs.

Results

COX-2 was detected by immunohistochemistry in both uterine fibroids and uterine smooth muscle, with higher immunoreactivity in uterine fibroids; the positive index of the smooth muscle cells was 11.90 and the positive index of uterine fibroids cells was 46.50 (P < 0.05). The expression of COX-2 mRNA in uterine fibroids was higher (0.122 ± 0.062) than in normal smooth muscle tissue (0.025 ± 0.009; P < 0.05). Also, the western blot results showed that COX-2 expression was significantly higher in uterine fibroid cases, as compared to the expression in uterine smooth muscle. Immunofluorescence showed that the occurrence of COX-2 was obviously higher in smooth muscle cells of uterine fibroids than in the healthy smooth muscle cells. NS-398 or celecoxib significantly inhibited the proliferation of smooth muscle cells of uterine fibroids, but did not inhibit the proliferation of healthy smooth muscle cells. Accordingly, NS-398 or celecoxib significantly reduced the expression of the downstream metabolite of COX-2, PGE2, in the smooth muscle cells of uterine fibroids, but not in healthy smooth muscle cells.

Conclusion

COX-2 expression in uterine fibroids was significantly higher than in healthy uterine smooth muscles. The inhibition of COX-2 activity significantly reduced the proliferation of smooth muscle cells of the uterine fibroids, suggesting that COX-2 plays an important role in the pathogenesis of uterine fibroids.