食管异物合并严重并发症的临床治疗分析

目的 探讨食管异物合并严重并发症的治疗方法。方法 回顾性分析解放军总医院第一医学中心耳鼻咽喉头颈外科2014年7月-2018年7月收治的23例合并食管穿孔、颈胸部感染等严重并发症的食管异物患者的临床资料,其中男11例、女12例,年龄2~87岁,病程2～11 d。术前CT扫描评估异物位置、食管损伤及周围炎症情况,其中异物位于第一狭窄16例、第二狭窄4例、第三狭窄1例及第四狭窄2例,合并食管穿孔23例、食管周围炎17例、食管周围脓肿3例、颈部脓肿2例、纵隔脓肿1例。23例中,行经硬性食管镜异物取出术17例、颈侧切开探查异物取出术5例、开胸探查异物取出术1例,围手术期配合胃肠减压、抗感染、营养支持等综合措施治疗。术后根据Stooler分级标准评价食管损伤后食管狭窄程度。结果 本组23例均顺利完成手术;经手术及围手术期综合治疗,均顺利拔除鼻饲管,行颈侧切开和开胸探查的患者均顺利拔除伤口引流管,均痊愈出院。1例患者于术后1个月并发颈段食管狭窄Ⅱ级,行食管扩张治疗后恢复正常。患者出院后随访3～5个月,23例均正常进食普通饮食,标准食管狭窄程度Stooler分级均为0级。结论 伴有严重并发症的食管异物应依据异物嵌顿部位及患者临床表现采取不同的手术方法取出异物,同时给予围手术期胃肠减压、抗感染、营养支持等综合治疗措施,多学科联合施救是挽救患者生命的重要举措。     

Assessment of naturally occurring covalent and total dimer levels in human IgG1 and IgG2

Antibody dimers, two self-associated monomers, have been detected on both recombinantly expressed and endogenous human IgG proteins. Nearly 10 years ago, Yoo et al. (2003) described low levels of IgG2 covalent dimer, in human serum, but did not quantify the levels. Here we quantify the total and covalent dimer levels of IgG2 and IgG1 in human blood, and study the origin of covalent dimer formation. Low levels (<1%) of total IgG1 and IgG2 dimers were measured in freshly prepared human plasma. Both IgG1 and IgG2 covalent dimers were also found in plasma. Whereas IgG1 covalent dimer levels were significantly reduced by steps intended to eliminate artifacts during sample preparation, IgG2 covalent dimer levels remain stable in such conditions. About 0.4% of IgG2 in plasma was in a covalent dimer form, yet very little (<0.03%) of IgG1 covalent dimer could be considered naturally occurring. IgG2 dimer also formed in vitro under conditions designed to mimic those in blood, suggesting that formation occurs in vivo during circulation. Thus, small amounts of covalent IgG2 dimer do appear to form naturally.     

Assessment of ZnT3 and PSD95 protein levels in Lewy body dementias and Alzheimer's disease: association with cognitive impairment

The loss of zinc transporter 3 (ZnT3) has been implicated in age-related cognitive decline in mice, and the protein has been associated with plaques. We investigated the levels of ZnT3 and postsynaptic density protein 95 (PSD95), a marker of the postsynaptic terminal, in people with Parkinson's disease dementia (PDD, n = 31), dementia with Lewy bodies (DLB, n = 44), Alzheimer's disease (AD, n = 16), and controls (n = 24), using semiquantitative western blotting and immunohistochemistry in 3 cortical regions. Standardized cognitive assessments during life and semiquantitative scoring of amyloid β (Aβ), tau, and α-synuclein at postmortem were used to investigate the relationship between ZnT3 and PSD95, cognition and pathology. Associations were observed between ZnT3 and PSD95 levels in prefrontal cortex and cognitive impairment (p = 0.001 and p = 0.002, respectively) and between ZnT3 levels in the parietal cortex and cognitive impairment (p = 0.036). Associations were also seen between ZnT3 levels in cingulate cortex and severity of Aβ (p = 0.003) and tau (p = 0.011) pathologies. DLB and PDD were characterized by significant reductions of PSD95 (p < 0.05) and ZnT3 (p < 0.001) in prefrontal cortex compared with controls and AD. PSD95 levels in the parietal cortex were found to be decreased in AD cases compared with controls (p = 0.02) and PDD (p = 0.005). This study has identified Zn²⁺ modulation as a possible novel target for the treatment of cognitive impairment in DLB and PDD and the potential for synaptic proteins to be used as a biomarker for the differentiation of DLB and PDD from AD.     

Neuroimaging in dementia

Over the last few years, advances in neuroimaging have generated biomarkers, which increase diagnostic certainty, provide valuable information about prognosis, and suggest a particular pathology underlying the clinical dementia syndrome. We aim to review the evidence for use of already established imaging modalities, along with selected techniques that have a great potential to guide clinical decisions in the future. We discuss structural, functional and molecular imaging, focusing on the most common dementias: Alzheimer's disease, fronto-temporal dementia, dementia with Lewy bodies and vascular dementia. Finally, we stress the importance of conducting research using representative cohorts and in a naturalistic set up, in order to build a strong evidence base for translating imaging methods for a National Health Service. If we assess a broad range of patients referred to memory clinic with a variety of imaging modalities, we will make a step towards accumulating robust evidence and ultimately closing the gap between the dramatic advances in neurosciences and meaningful clinical applications for the maximum benefit of our patients.     

颌下腺内鱼刺1例报告

<正>临床工作中颌下腺内异物相对少见,目前文献报道有笤帚梢杆经口底黏膜进入颌下腺内1例,采取手术治疗[1];吞咽麦芒1月后颌下不适,超声检查发现麦芒异物1例,手术取出异物[2];也有报道颌下腺内铅笔芯1例,但因病史较长文献未能提供异物移行颌下腺内的可能途径。本文报道咽部鱼刺异物移行颌下腺1例。1临床资料患者,男,42岁,因"右侧颌下区反复肿痛1月"入院。查体:右侧颌下区肿胀,肿胀区压痛明显,皮     

大肠杆菌表达的人血管内皮细胞生长因子的复性与纯化研究

以包涵体的形式在大肠杆菌中表达人血管内皮细胞生长因子（VEGF121）,采用发酵罐进行工程菌的高密度发酵,得到菌干重46g／L,VEGF121包涵体4．5g／L。包涵体经洗涤、溶解、超滤法复性,得率为81％。复性后的目标蛋白经离子交换色谱及SepharcryS-100凝胶过滤色谱纯化,目标蛋白的纯度达到95％,目标蛋白的总得率31％。采用该工艺制备的VEGF121能刺激人脐静脉血管内皮细胞增殖,具有天然VEGF生物学活性。     

少腹逐瘀汤联合孕三稀酮治疗子宫内膜异位症前瞻性研究

目的:探讨少腹逐瘀汤联合西药保守治疗子宫内膜异位症的临床价值。方法:我院诊治的80例子宫内膜异位症患者为研究对象,按随机双盲分组原则分为观察组和对照组,各40例。两组均给予孕三稀酮进行治疗,观察组在此基础上加用少腹逐瘀汤。对比两组临床疗效,记录两组治疗前后中医症状评分、血液流变学(血浆黏度、全血高切黏度、全血低切黏度、红细胞沉降速率、红细胞聚集指数、纤维蛋白原)及外周血糖类抗原125(CA125)含量,并观察两组在治疗期间不良反应发生情况。结果:观察组临床总有效率90.00%显著高于对照组72.50%,差异有统计学意义(P<0.05)。两组治疗后痛经、腰骶肛门坠胀、月经周期、经期、形寒肢冷症状评分较治疗前显著降低(P<0.05); 观察组治疗后痛经、腰骶肛门坠胀、月经周期、经期、形寒肢冷症状评分显著低于对照组(P<0.05)。观察组治疗后血液流变学指标及外周血CA125含量显著低于对照组(P<0.05)。结论:采用少腹逐瘀汤联合孕三稀酮治疗子宫内膜异位症,能提高临床疗效,减轻患者临床症状,加快病情康复。     

Abnormalities of resting-state EEG in patients with prodromal and overt dementia with Lewy bodies: Relation to clinical symptoms

ObjectiveHere we tested if cortical sources of resting state electroencephalographic (rsEEG) rhythms may differ in sub-groups of patients with prodromal and overt dementia with Lewy bodies (DLB) as a function of relevant clinical symptoms.MethodsWe extracted clinical, demographic and rsEEG datasets in matched DLB patients (N = 60) and control Alzheimer’s disease (AD, N = 60) and healthy elderly (Nold, N = 60) seniors from our international database. The eLORETA freeware was used to estimate cortical rsEEG sources.ResultsAs compared to the Nold group, the DLB and AD groups generally exhibited greater spatially distributed delta source activities (DLB > AD) and lower alpha source activities posteriorly (AD > DLB). As compared to the DLB “controls”, the DLB patients with (1) rapid eye movement (REM) sleep behavior disorders showed lower central alpha source activities (p < 0.005); (2) greater cognitive deficits exhibited higher parietal and central theta source activities as well as higher central, parietal, and occipital alpha source activities (p < 0.01); (3) visual hallucinations pointed to greater parietal delta source activities (p < 0.005).ConclusionsRelevant clinical features were associated with abnormalities in spatial and frequency features of rsEEG source activities in DLB patients.SignificanceThose features may be used as neurophysiological surrogate endpoints of clinical symptoms in DLB patients in future cross-validation prospective studies.     

A novel SNCA E83Q mutation in a case of dementia with Lewy bodies and atypical frontotemporal lobar degeneration

In this case report, we discuss a patient presenting with parkinsonism followed by a non-amnestic dementia with aphasic clinical features, as well as frontal dysexecutive syndrome. There was a family history of dementia with an autopsy diagnosis of “Pick's disease” in the proband's father. Neuroimaging of the patient revealed focal and severe temporal lobe and lesser frontoparietal lobe atrophy. At autopsy, there was severe frontotemporal lobar degeneration. Histologic evaluation revealed an absence of tau or transactivation response DNA-binding protein of 43 kDa (TDP) pathology but rather severe Lewy body deposition in the affected cortices. Genetic phenotyping revealed a novel missense mutation (p.E83Q) in exon 4 of the gene encoding α-synuclein (SNCA). This case study presents a patient with a novel SNCA E83Q mutation associated with widespread Lewy body pathology with prominent severe atrophy of the frontotemporal lobes and corresponding cognitive impairment.