外科切口感染危险因素研究

目的：研究术后切口感染危险因素，以降低切口感染率。方法：以１９９４～１９９６年外科手术病人为对象，进行病例对照研究。结果：病例组１３１例切口感染病人和对照组１００例无切口感染病人在手术持续时间、术前抗生素使用种类、免疫抑制剂应用与否以及手术后抗生素使用天数等方面有显著性差异。且随着手术时间延长，术后切口感染的相对危险度呈明显递增趋势。结论：为降低术后切口感染率，必须尽量缩短手术时间，并减少术前术后抗生素使用天数和种类     

KMT2C通过c-Myc/CDK4信号通路调控胃癌细胞的生长与增殖

摘要:目的 探究赖氨酸特异性甲基转移酶2C(lysine specific methyltransferase 2C,KMT2C)在胃癌发生发展中的 作用及机制。方法 通过 TCGA 数据库分析 KMT2C在胃癌与癌旁的表达差异。采用 Western blot检测 KMT2C在胃 癌与癌旁临床样本中的表达差异。通过 Kaplan-Meier Plotter数据库分析 KMT2C 对胃癌患者预后的影响。采用细胞 实验(克隆形成、EdU 及 CCK-8检测)及皮下瘤负荷模型检测 KMT2C 在体内外对胃癌细胞增殖能力的影响。结果 KMT2C在胃癌中高表达。胃癌患者中 KMT2C高表达组相对于 KMT2C低表达组预后较差。敲减 KMT2C在体内外 均有抑制胃癌 细 胞 增 殖 的 作 用。基 因 集 富 集 分 析 (GSEA)发 现 KMT2C 影 响 c-Myc信 号 通 路。敲 减 KMT2C 后, H3K4me1蛋白表达水平降低,同时,CDK4的 mRNA 与蛋白表达水平降低。KMT2C与c-Myc核内结合促进了c-Myc 与 CDK4的启动子区域的结合。结论 KMT2C通过影响c-Myc/CDK4信号通路促进胃癌细胞增殖。     

Comparison of clinical efficacy and toxicity of conventional and optimum biological response modifying doses of interferon alpha-2C in the treatment of hairy cell leukemia: a retrospective analysis of 39 patients

Hairy cell leukemia (HCL) has been shown to be extraordinarily sensitive to treatment with alpha-interferon (IFN). In order to define clinically effective IFN doses associated with minimal toxicity, the therapeutic efficacy and side effects of recombinant IFN-alpha-2C treatment of HCL were compared for two different dose regimens: 18 patients (group A) received conventional doses of recombinant IFN-alpha-2C (2 x 10(6)U/m2) for a median time of 35 weeks (range 26-52 weeks), and 21 patients (group B) received optimum biological response-modifying doses of IFN-alpha-2C (0.2-0.6 x 10(6)U/m2) for a median time of 31 weeks (range 12-52 weeks). Interferon was administered daily subcutaneously for 3 months and then every second or third day. Induction of neopterin excretion was chosen as the marker for definition of biological response. The smallest IFN dose causing maximum in vivo induction of biosynthesis of the GTP-degradation product neopterin was deemed "biologically optimal." Both dose regimens were effective, but the low-dose regimen was almost free of toxicity. Thus, in HCL patients alpha-IFN related toxicity can be separated from its antineoplastic activity. Low doses of alpha-IFN should be considered for treatment of HCL patients who develop toxic side effects and for primary treatment of HCL patients with severe cytopenia.     

Einflüsse von Nahrungsaufnahme und Gewöhnung auf die Verteilung von 8-14C-Coffein bei der Ratte

Zusammenfassung 200 g schwere Ratten erhielten Lösungen von¹⁴C-Coffein entweder nüchtern oder nach vorheriger Verabreichung von Kohlenhydrat, Eiweiß und Fett. Die Nahrungszufuhr bedingte folgende Änderungen der Coffeinverteilung im Organismus gegenüber den nüchternen Tieren: die Coffeinresorption war deutlich verzögert, so daß die¹⁴C-Aktivitätswerte im Serum und Carcass nur langsam anstiegen. Im weiteren Verlauf des Versuches erreichte der Abfall der¹⁴C-Aktivität in Serum und Carcass und ihre Ausscheidung im Harn ein geringeres Ausmaß.Die Coffeinverteilung im Organismus zeigte außerdem bestimmte Änderungen bei Ratten, die im Anschluß an eine 14tägige Gewöhnunsperiode¹⁴C-Coffeinhaltigen Kaffee-Infus erhielten. Im Vergleich zu den nicht an Kaffee gewöhnten Ratten war hierbei die Coffeinresorption deutlich beschleunigt. Die¹⁴C-Aktivitätswerte im Serum stiegen anfangs schneller und höher an, zeigten anschließend aber einen rascheren Abfall. Auf Grund dieser Effekte war die¹⁴C-Ausscheidung durch die Niere erheblich beschleunigt und vermehrt.

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Summary Rats weighing 200 g obtained¹⁴C-caffeine solution either after starvation or after feeding carbohydrate, proteine or fat. The following differences in caffeine distribution in the fed rats compared with the starved ones were confirmed: caffeine absorption was clearly decreased, resulting in slow increase in¹⁴C-activity in the serum and the carcass. During the course of the experiment it was observed that the decline of¹⁴C-activity in serum and carcass was delayed and its excretion in the urine was decreased. Additionally caffeine distribution in the rat body showed certain changes which were accompanied by caffeine habituation in the animals after administration of¹⁴C-caffeine contained in coffee infusion for 14 days. In the coffee habituated animals the caffeine absorption was noticeably accelerated.¹⁴C-activity in serum increased initially quicker but finally showed a quicker decline. Governed by these effects the¹⁴C-excretion via kidney was increased and its rate was accelerated.

     

Cerebellar damage impairs automaticity of a recently practiced movement

It has been suggested that the cerebellum plays a critical role in learning to make movements more "automatic" (i.e., requiring less attention to the details of a movement). We hypothesized that cerebellar damage compromises learning of movement automaticity, resulting in increased attentional demands for movement control. The purpose of our study was to determine whether cerebellar damage disrupts the ability to make a practiced movement more automatic. We developed a dual task paradigm using two tasks that did not have overlapping sensory or motor requirements for execution. Our motor task required subjects to maintain an upright posture while performing a figure-8 movement using their arm. This motor task was chosen to simulate requirements of everyday movements (e.g., standing while reaching for objects), but it was novel enough to require practice for improvement. Our secondary task was an auditory vigilance task where subjects listened to letter sequences and were asked to identify the number of times a target letter was heard. We tested controls and people with cerebellar damage as they practiced the movement task alone and then performed it with the auditory task. We recorded 3D position data from the arm, trunk, and leg during the movement task. Errors were recorded for both the movement and the letter tasks. Our results show that cerebellar subjects can improve the movement to a very limited extent with practice. Unlike controls, the motor performance of cerebellar subjects deteriorates to prepractice levels when attention is focused away from the movement during dual task trials. Control subjects' insensitivity to dual task interference after practice was due to learned movement automaticity and was not a reflection of better dual task performance generally. Overall, our findings suggest that the cerebellum may be important for shifting movement performance from an attentionally demanding (unpracticed) state to a more automatic (practiced) state.     

Localization of corticotropin-releasing activity in the rat hypothalamus

Hypothalamic nuclei were removed from frozen sections of rat brain and examined for their corticotropin-releasing activity. The highest concentration was measured in the median eminence. In addition there was significantly more activity detected in the nuclei paraventricularis, supraopticus, suprachiasmaticus and arcuatus than in the other nuclei.     

蛙类肠系膜内微小动脉的压力检测

根据Wiederhielm的阻抗平衡压力检测原理,设计了一个改进的伺服零微血管测压系统。利用该系统检测了蟾蜍及蛙肠系膜内微小动脉的压力、获得了各管径级的压力和脉压的参数,并观察了药物的作用,探讨了微动脉内压力的波动特性以及应激情况下压力的骤变式与脉动式的交替,为微循环研究提供一些有价值的现象。     

Cell shrinkage stimulates bradykinin-induced cell membrane potential oscillations in NIH 3T3 fibroblasts expressing the ras-oncogene

In NIH 3T3 fibroblasts expressing the Ha-ras oncogene (+ras) bradykinin leads to sustained oscillations of cell membrane potential due to oscillations of intracellular Ca²⁺ with subsequent activation of Ca²⁺-sensitive K⁺ channels. In cells not expressing the oncogene (-ras), bradykinin leads only to a single transient hyperpolarization of the cell membrane. The present study has been performed to elucidate the possible interaction of cell volume, intracellular pH and bradykinin-induced oscillations of the cell membrane potential. Bradykinin leads to cell shrinkage and intracellular alkalinization of both +ras cells and –ras cells. Inhibition of Na⁺/H⁺ exchanger by HOE 694 abolishes the bradykinin-induced alkalinization but does not significantly interfere with the bradykinin-induced oscillations of cell membrane potential. In contrast, prevention of bradykinin-induced cell shrinkage by simultaneous reduction of extracellular osmolarity blunts the oscillations. Thus, cell shrinkage stimulates bradykinin-induced oscillations of cell membrane potential. On the other hand, cell shrinkage alone does not elicit oscillations unless, in addition, Ca²⁺ entry is stimulated by ionomycin.