原发性震颤合并帕金森病与单纯帕金森病或单纯原发性震颤的震颤特征比较

目的 比较分析原发性震颤(ET)合并帕金森病(PD)与ET、PD的震颤特征。方法 选取2019年1月—2021年1月郑州市某医院神经内科收治的100例住院患者为研究对象,根据患者疾病情况分为A组(ET合并PD,34例)、B组(ET,33例)、C组(PD,33例)。采用震颤评分量表(TRS)与肌电图仪收集患者静止、姿势与...     

2种不同弹力纤维染色方法对肿瘤侵犯判读结果的对比研究

目的 比较Victoria blue法(A组)和Verhoeff法(B组)弹力纤维染色在染色过程、染色时间、染色效果方面对肺癌胸膜侵犯和结直肠癌浆膜或静脉侵犯判读的差异。方法 A组、B组均分别纳入肺癌怀疑胸膜侵犯标本50例和结直肠癌怀疑浆膜或静脉侵犯标本20例,进行弹力纤维染色。对比2组染色过程、染色时间、染色效果;根据染色稳定性、清晰度、对比度等综合评价胸膜侵犯和浆膜或静脉侵犯情况,并对染色质量及判读准确性进行评分。结果 A组比B组操作简单,染色质量稳定,肿瘤细胞与脏层胸膜、浆膜或静脉的关系显示更清晰。A组判读评分高于B组,差异有统计学意义(P<0.05)。结论 Victoria blue法染色有助于准确评估肺癌的胸膜侵犯和结直肠癌浆膜或静脉的侵犯,提高判读准确性。     

急性受热及热适应对机体免疫系统的影响

雄性ＳＤ大鼠随机分为５组：２５℃对照组，３７℃每天２ｈ共７天热适应组，４２℃分别受热３０ｍｉｎ、６０ｍｉｎ，９０ｍｉｎ的３个热处理组。检测全血淋巴细胞转化率、α－醋酸萘酯酶活性、腹腔巨噬细胞活性和吞噬功能。结果显示：７天热适应组与受热３０ｍｉｎ组即明显降低，随受热时间延长（超过３０ｍｉｎ），巨噬细胞吞噬功能显著降低，不能形成吞噬峰。７天热适应组与受热３０ｍｉｎ组用ＰＨＡ刺激全血淋巴细胞转化的刺激指数比对照组稍高，但差异不明显（Ｐ＞０．０５），而６０ｍｉｎ和９０ｍｉｎ受热却使该指数显著下降（Ｐ分别为０．００３１和０．００６３）。α－醋酸萘酯酶除热适应组降低外，其余各组无明显变化。结果提示，急性受热时机体免疫系统功能有受抑制倾向。     

医疗设备管理的思考

医疗设备的管理是现代医院发展的硬件保证,根据系统的观念,探讨了医疗设备管理方式及其注意原则,以求发挥医疗设备的最大效能,为新时期医院的改革创造更大的效益。     

抑制聚ADP核糖聚合酶1活性的短发夹RNA载体构建

目的构建抑制人聚ADP核糖聚合酶1(hPARP1)活性的短发夹RNA(shorthairpinRNA,shRNA)表达载体。方法化学合成2对编码短发夹RNA序列的、靶向hPARP1基因的寡核苷酸,各69对碱基,退火,然后利用BamHⅡ及EcoRⅠ与pSIRENRetroQ载体连接。用EcoRⅠ及BglⅡ切取其中U6启动子及下游的shRNA部分,与pEGFPC1载体重组构建pEGFPC1shRNA载体。结果重组构建的pEGFPC1P1、pEGFPC1P2、pEGFPC1N载体经双酶切电泳分析及插入基因片段序列分析,结果表明330个碱基成功插入到预计位点。结论载体的成功构建,为进一步研究聚ADP核糖聚合酶在DNA修复过程中的功能打下基础。     

海南三沙市某岛蛇害调查与防控

对三沙市某蛇岛采用现场随机走访和问卷调查相结合的方法调查蛇害,鉴定蛇种为舟山眼镜蛇,岛上气候、植被、食源、设施等因素适合蛇类繁育。人群中蛇年遇见率为85.6%,77.6%的人恐惧蛇,对蛇咬伤急救知识缺乏。该岛存在毒蛇咬伤风险,开展宣教培训及防控措施研究很有必要。     

全营养素混合液对早产儿血清渗透压及血糖的影响

为观察全营养素混合液（TNA）对早产儿血清渗透压的影响，按6ml·kg－1·h-1的速度给早产儿静脉输入TNA，测定输注前及输注过程中的血钠、血糖、BUN和血清渗透压，并计算渗透压间隙（OG）。结果显示输注前及输注过程中血清渗透压、OG及血糖无显著性差异，提示TNA液在一定速度内输注对早产儿血清渗透压及血糖无明显影响。     

儿童锌缺乏敏感指标的评价

为评价反映儿童锌缺乏的敏感指标.方法 我们对300名3～6岁儿童进行膳食调查与体格检查,同时测定了锌缺乏组和对照组儿童的尿锌与尿肌酐比值,血清ALP活性,血清胆固醇水平及锌缺乏儿童补锌治疗前后上述指标的变化.结果 锌缺乏组与对照组尿锌与尿肌酐比值,血清ALP活性有显著性差异.锌缺乏组儿童血浆锌,尿锌与尿肌酐比值,血清ALP活性,血清胆固醇水平在补锌治疗前后有显著性差异.结论 血浆锌和血清ALP同时降低可以预示儿童体内锌缺乏,需要补锌治疗;尿锌与尿肌酐比值能较敏感地反映儿童的锌营养状况;胆固醇与锌营养之间的关系值得进一步研究.     

Dasatinib and interferon alpha synergistically induce pyroptosis-like cell death in philadelphia chromosome positive acute lymphoblastic leukemia

Philadelphia chromosome-positive acute lymphoblastic leukemia (Ph+ALL) is a high-risk disease subtype with a dismal prognosis. Inhibiting BCR-ABL kinase alone is insufficient to eradicate Ph+ALL clones, and alternative BCR-ABL-dependent and -independent pathways need to be targeted as an effective strategy. Our study revealed that the combination of dasatinib and interferon-α showed synergistic activity against Ph+ALL, inducing mitochondrial dysfunction and causing necrosis-like cell lysis. Mechanistic studies showed that the induced cell death was caspase-3-independent. Canonical necroptosis signals, such as RIP1 and MLKL, were not activated; instead, the pyroptosis executor Gasdermin D was upregulated expression and activated. The expression levels of extracellular ATP and IL-1β were also upregulated, both of which are markers of pyroptotic cell death. In a murine Ph+ALL model, the dual drug treatment prolonged the survival of tumor-bearing mice. More importantly, we incorporated the dual drugs to maintenance therapy in 39 patients who were unfit for allogeneic stem cell transplantation (allo-HSCT). The median follow-up was 28.5 months, the 4-year disease-free survival and overall survival rates were 52.2% and 65.2%, respectively. Our data suggest that the combination of dasatinib and interferon-α has potential synergistic activity against Ph+ALL and shows promise as a maintenance therapy for Ph+ALL patients who are unfit for allo-HSCT.     

The FLT3 Y842D mutation may be highly sensitive to midostaurin: a case report

A Y842D mutation within the activation loop of fms-like tyrosine kinase 3 (FLT3) has been shown to confer strong resistance to sorafenib in vitro. Whether this type of mutation exerts clinically significant effects in patients with acute myeloid leukaemia (AML) remains unclear. Here, a novel Y842D activating mutation within the kinase domain of FLT3, in a pregnant patient with de novo hyperleucocyte acute myeloid leukaemia, is described. Following induction failure with standard dose idarubicin and cytarabine (IA), the patient received re-induction combined with midostaurin, a promising agent targeting mutant-FLT3, and IA regimen. Fortunately, morphological remission was achieved. During the period of midostaurin treatment, the patient exhibited a symptom that was characteristic of differentiation syndrome, which disappeared following treatment with methylprednisolone. The present case revealed that Y842D, an uncommon activating mutation in the activation loop of FLT3, may be a midostaurin-sensitive mutation type in patients with acute myeloid leukaemia.