患者男,17岁.因“间断发热伴咳嗽、咳痰7年,再发加重2月余”于2018年1月25日入住华中科技大学同济医学院附属同济医院.2010年10月因发热伴咳嗽、咳痰就诊于当地医院,并入住ICU治疗,当时体温最高39℃,诊断重症肺炎,Ⅰ型呼吸衰竭,给予抗感染治疗(具体不详)及呼吸支持后好转出院.近7年来,患者反复出现发热、咳嗽及咳痰症状,多次在外院住院治疗并行胸部CT检查(未见胶片),诊断为“支气管扩张合并感染”,给予抗感染治疗后好转.

目的 比较不同临床分型的新型冠状病毒肺炎患者实验室检查结果与病情严重程度的相关性.方法 以2020年2月1日至2020年2月21日在华中科技大学同济医学院附属同济医院发热病房住院的50例确诊新型冠状病毒肺炎患者为研究对象,根据国家卫生健康委员会的诊断标准,该50例患者被分为危重型(8例)、重型(32例)、普通型(10例),比较不同型别患者的血常规、血生化、凝血常规结果和炎症因子的表达水平,分析上述指标的变化规律及其与临床分型的关系.结果 危重型患者白细胞和中性粒细胞计数明显高于重型和普通型患者(P<0.05);危重型和重型患者淋巴细胞计数下降较普通型患者更明显(P<0.05);危重型患者较重型和普通型患者乳酸脱氢酶水平升高,肾功能损害、凝血功能异常更明显(均P<0.05);危重型患者的降钙素原、超敏C反应蛋白、IL-6和TNF-α水平升高较重型和普通型患者更明显(均P<0.05);超敏C反应蛋白水平在重型和普通型患者之间的差异也具有统计学意义(P<0.05).结论 危重型新型冠状病毒肺炎患者更易合并细菌感染和多器官功能损害;超敏C反应蛋白、IL-6、TNF-α表达水平可灵敏反映患者全身炎症反应程度,有助于疾病临床分型.

随着对2019新型冠状病毒肺炎科研的投入及临床认识的加深,其诊疗方案也不断更新.该文主要通过对《新型冠状病毒肺炎诊疗方案(试行第七版)》进行解读,并与第六版进行比较,重点介绍新版的更新要点,以便更好服务于临床实践.

目的 探讨非小细胞肺癌组织中Jun二聚化蛋白2(Jdp2)、Phf手指蛋白2(Phf2)的表达变化及意义.方法 选取非小细胞肺癌患者86例,采用免疫组化法检测癌组织及正常肺组织(距肿瘤边缘>5 cm)中Jdp2、Phf2的表达,分析二者表达与非小细胞肺癌患者临床病理特征的关系,Spearman相关分析二者表达的相关性;对患者进行随访,分析Jdp2、Phf2表达与患者预后的关系.结果 非小细胞肺癌组织中Jdp2、Phf2阳性表达率低于正常肺组织(P均<0.05).非小细胞肺癌组织中Jdp2与Phf2表达呈正相关(r=0.672,P<0.05).非小细胞肺癌组织中Jdp2、Phf2阳性表达与肿瘤TNM分期、分化程度有关(P均<0.05).Jdp2、Phf2阳性表达患者5年生存率低于Jdp2、Phf2阴性表达患者(P<0.05).结论 非小细胞肺癌组织中Jdp2、Phf2均呈低表达,二者表达变化与肿瘤分期、分化程度及患者预后有关.

骨髓增生异常综合征(MDS)是一组造血干细胞异常克隆导致的恶性疾病,具有无效造血、血细胞减少、血细胞及其前体细胞发育异常、克隆性染色体异常以及高风险向急性白血病进展等特征.多发于50岁以上的老年人,男性发病率约为女性的1.5倍,近年来发病率有逐年上升的趋势,多数年轻患者的发病大多由于治疗或药物继发.MDS不论在疾病特征、临床表现还是实验室检查等方面均存在较大异质性,给疾病的诊断和治疗选择带来一定的难度.

<正>患者,女,46岁。1992年3月因"四肢关节疼痛半月"就诊于外院,当时查ANA(+),ENA(-),dsD-NA(-),RF(+),AKA(-),颈椎正侧位片+骨盆正位片+双侧手肘正位片提示:双侧尺侧腕骨间关节稍毛糙模糊,双侧近节指间关节及远节关节略显窄,周围孔组织肿胀,符合类风湿性关节炎(rheumatoid arthritis,RA)改变。考虑诊断RA,给予静脉激素、护胃等治疗(第3～14天激素具体用量不详),病情控制后出院,院外口服激素(泼尼松:10mg,1次/d)和

<正>睡眠呼吸暂停综合症被定义为7 h睡眠中呼吸暂停及低通气反复发作在30次以上,或呼吸紊乱指数(AHI)≥5次/h。由其引起的睡眠时反复发生的低氧血症和高碳酸血症,不仅可导致呼吸系统的病理生理变化,同时可引起循环系统、血液系统、内分

Objective To study the changes of nitric oxide (NO) content in hippocampus of rat by Pentylenetetrazol ( PTZ)-induced seizures models and its effect of toxicity and apoptosis.Methods SD male rats were random divided into three groups,each group has 14 rats.Group A is the saline control group,group B is the pentylenetetrazol induced epileptic group and group C is aminoguanidine ( NOS inhibitor) pretreatment plus pentylenetetrazol induced epileptic group.NO content in rat hippocampus was detected by ultraviolet spectrophotometry,glutamate ( Glu ) immunoreactivity in rat hippocampus was detected by immunohistochemistry (SABC) and caspase-3 mRNA levels in rat hippocampus were detected by reverse transcription-polymerase chain reaction (RT-PCR) respectively at 2,48 h after modeling.Results Group A had no seizure,group B had epilepsia gravior over Ⅴ grade,rats in group C had seizure over Ⅱ Ⅲ grade.The NO content on group B (75.67 ± 2.04) μ mol/L was significantly higher than group A (11.90±0.64) μmol/L and group C (36.19 ±4.48) μmol/L (P＜0.05) ; Glu immunoreactivity and caspase-3 mRNA leves of group A and group C were lower than group B ( P ＜ 0.05 ).Conclusion PTZinduced seizures may lead to excessive production of NO in hippocampus,which had excited toxicity to hippocampal neurons.The intervention of NOS synthetic inhibitor had neuroprotective effects.

Objective:To investigate the molecular cytogenetic abnormalities in multiple myeloma(MM) by fluorescence in situ hybridization(FISH).Method:Twenty-one patients of MM were enrolled in this study.Panel probes of 1q21/RB1、D13S319/p53 and IgH were used to detect the 13q14 deletion,trisomy 1,p53 deletion and IgH gene rearrangements in these patients as well as conventional chromosome karyotype.Result:19 of 21 patients(90.48%) were detected to have at least one kind of molecular cytogenetic abnormalities by FISH.15 patients(71.43%) were detected to have at least more than two kinds of molecular cytogenetic abnormalities.The incidence of molecular cytogenetic abnormalities from high to low was as followed:trisomy 1(66.67%),IgH gene rearrangements(57.14%),13q14 deletion(47.62%) and p53 deletion(23.81%).3 patients(14.29%) were detected to have conventional chromosome abnormalities.The incidence of conventional chromosome abnormalities was significantly lower than that in FISH(P0.01).Conclusion:The incidence of trisomy 1,IgH gene rearrangements and 13q14 deletion was higher in MM.FISH can increase the detection sensitivity of molecular cytogenetic abnormalities in MM.

目的 研究戊四氮致痫模型中,大鼠海马过量产生的H 2O 2对海马神经元兴奋毒性的影响.方法 SD雄性大鼠随机分为3组,每组14只.A组为生理盐水对照组,B组为戊四氮致痫组,C组为H 2O 2酶处理+戊四氮致痫组.动物造模后,观察各组大鼠癫痫发作情况;然后分别采用分光光度法测定大鼠海马H 2O 2含量,免疫组织化学法(SABC法)检测大鼠海马谷氨酸(Glu)免疫反应性,RT-PCR法检测大鼠海马Caspase-3 mRNA水平.结果 A组大鼠无明显癫痫发作,B组大鼠有癫痫大发作达Ⅴ级,C组大鼠癫痫发作为Ⅱ～Ⅲ级.B组大鼠海马H 2O 2含量、Glu免疫反应性、Caspase-3 mRNA表达水平均显著高于A组(均 P ＜0.05),C组海马H 2O 2、Glu免疫反应性、Caspase-3 mRNA表达水平均明显低于B组(均 P ＜0.05).结论 戊四氮诱发癫痫发作后,导致H 2O 2过量产生,其对海马神经元具有兴奋毒性作用.

Objective Modulation of K+ channel had been shown to be an integral and important cellular response to O2 deprivation. Method Freshly dissociated neurons from mouse dorsal root ganglion (DRG) were used to test the hypothesis that O2-sensing process was involved in the modulation of K+ channel activity. Whole-cell patch clamp technique was used to record the change in IK of K+ channel. Results Hypoxia caused the change in IK in small size DRG neurons. They responded within 3 min with a change in IK. Majority of cells displayed a reduction in IK during the time course of patch clamp experiment, whereas one out of seven neurons showed an increase in IK. IK inhibition started about 1 min after the onset of hypoxia and maximum inhibition was reached in about 3 min. Hypoxia decreased the IK from test potential of 10 to 70 mV and the utmost decrease was from (304.4±122.9) to (253.9±106.4) pA·pF-1, whereas steady-state activation of IK was not changed significantly. Conclusion The study indicates that hypoxia induced an inhibition of IK in small size DRG neurons and this inhibition of IK might play a protective action in adapting to O2 deprivation in acute and short-term hypoxia.

The present study aimed to investigate whether cannabinoids could modulate the response mediated by ATP receptor (P2X purinoceptor). Whole-cell patch-clamp recording was performed on cultured rat trigeminal ganglionic (TG) neurons. The majority of TG neurons were sensitive to ATP (67/75, 89.33%). Extracellular pretreatment with WIN55212-2, a cannabinoid receptor 1 (CB1 receptor) agonist, reduced ATP-activated current (I(ATP)) significantly. This inhibitory effect was concentration-dependent and was blocked by AM281, a specific CB1 receptor antagonist. Pretreatment with WIN55212-2 at 1×10(-13), 1×10(-12), 1×10(-11), 1×10(-10), 1×10(-9) and 1×10(-8) mol/L reduced I(ATP) (induced by 1×10(-4) mol/L ATP) by (8.14±3.14)%, (20.11±2.72)%, (46.62±3.51)%, (72.16±5.64)%, (80.21±2.80)% and (80.59±3.55)%, respectively. The concentration-response curves for I(ATP) pretreated with and without WIN55212-2 showed that WIN55212-2 shifted the curve downward, and decreased the maximal amplitude of I(ATP) by (58.02±4.21)%. But the threshold value and EC(50) (1.15×10(-4) mol/L vs 1.27×10(-4) mol/L) remained unchanged. The inhibition of I(ATP) by WIN55212-2 was reversed by AM281, suggesting that the inhibition was mediated via the CB1 receptor. Pretreatment with forskolin [an agonist of adenylyl cyclase (AC)] or 8-Br-cAMP reversed the inhibition of I(ATP) by WIN55212-2. These results suggest that the inhibitory effect of cannabinoids on I(ATP) is mediated via the CB1 receptors, that lead to inhibition of the AC-cAMP-PKA signaling pathway.

Whole-cell patch clamp recording was used to investigate the action of β-amyloid peptide1-40 (Aβ1-40) on high voltageactivated calcium channel current (IHVA) in acutely isolated hippocampal CA1 pyramidal neurons in rats and observe its modulation by ginkgolide B (GB). Drug was applied by extracellular bath or adding in the pipette solution, and its effect was determined by comparing the amplitude of IHVA before and after the drug application. Bath application of aggregated Aβ1-40 at concentrations of 0.01 ～30 μmol/L increased the amplitude of IHVA in a dose-dependent manner by (5.43+3.01)% (n=8, P＞0.05), (10.49+4.13)% (n=11, P＞0.05), (40.69+8.01)% (n=16, P＜0.01), (58.32+4.85)% (n=12, P＜0.01), and (75.45+5.81)% (n=6, P＜0.01), respectively, but had no effect on the I-V curve of IHVA; fresh Aβ1-40 almost had no effect on IHVA (n=5, P＞0.05). L-type calcium channel antagonist nifedipine abolished the increase of IHVA by Aβ1-40. The increase of IHVA by Aβ1-40 (1.0 μmol/L) was enhanced to (66.19+5.74)% (P＜0.05) by 8-Br-cAMP (membrane permeable analogue of cAMP) and to (73.21 +6.90)% (P＜0.05) by forskolin, an adenylyl cyclase (AC) agonist, and reduced to (20.08+2.18)% (P＜0.05) by H-89, cyclic adenosine monophosphate (cAMP)-dependent protein kinase A (PKA) antagonist. GB effectively inhibited the increase of IHVA by Aβ1-40. The results indicate that Aβ1-40 leads to an intracellular calcium overload by increasing IHVA via AC-cAMP-PKA. This may be one of the mechanisms for its neurotoxicity. GB can prevent neurons from neurotoxicity by inhibiting abnormal calcium influx caused by Aβ1-40.