美洛西林与头孢呋辛治疗细菌性感染的成本-效果分析

目的 :探讨不同抗生素治疗细菌性感染所产生的经济效果。方法 :根据文献选择各种细菌性感染的病人 12 0例 ,随机分为美洛西林组和头孢呋辛组分别给予治疗 ,运用药物经济学的成本 效果分析方法进行分析评价。结果 :美洛西林在治疗呼吸道感染和泌尿道感染其成本 /效果比 (治愈率 :51±11和 36± 8;有效率 :39± 8和 2 8± 7)均低于头孢呋辛 (治愈率 :57± 16和 52± 8;有效率 :4 1± 11和 30± 5)。结论 :美洛西林在治疗呼吸道和泌尿道感染方面优于头孢呋辛 ,是一种成本 效果较好的药物。     

Ectopic discharges from injured nerve fibers are highly correlated with tactile allodynia only in early, but not late, stage in rats with spinal nerve ligation

It is widely accepted that ectopic discharges originated from injured sites and dorsal root ganglion (DRG) neurons after peripheral nerve injury contribute to neuropathic pain. However, it has been recently shown that ectopic discharges were not always necessary for neuropathic pain. In the present study, we aim to further examine the role of ectopic discharges in neuropathic pain in a spinal nerve ligation (SNL) model. With teased fiber recordings in vivo, the characteristics of ectopic discharges were observed over 14 days after SNL, and the correlation between ectopic discharges and tactile allodynia was analyzed. It was observed that ectopic discharges have three firing patterns (tonic, bursting, and irregular) after SNL, and proportions of these three patterns changed dynamically over time. The tonic and bursting types were dominant in the first 24 h following SNL, while the irregular type became the only pattern in the late stage (day 14). The average frequencies of ectopic discharges and the percentage of active filaments also changed over time, reaching the peak 24 h after SNL and then declined gradually. Ectopic discharges were highly correlated with tactile allodynia in the first 24 h following SNL, but surprisingly, not in the late stage of days 1 to 14. These findings suggest that ectopic discharges may be crucial in the triggering of neuropathic pain in the early stage, but their importance become more limited over time.     

Differential modulation of nociceptive neural responses in medial and lateral pain pathways by peripheral electrical stimulation: a multichannel recording study

It is well accepted that peripheral electrical stimulation (PES) can produce an analgesic effect in patients with acute and chronic pain. However, the neural basis underlying stimulation-induced analgesia remains unclear. In the present study, we examined the pain-related neural activity modified by peripheral stimulation in rats. The stimulation frequency of pulses applied to needle electrodes in the hindlimb was 2 Hz alternating with 100 Hz, with 0.6 ms pulse width for 2 Hz and 0.2 ms for 100 Hz. The intensity of the stimulation was increased stepwise from 1 to 3 mA with each 1-mA step lasting for 10 min. The nociceptive neural and behavioral responses were examined immediately after the termination of stimulation. Using a multiple-channel recording technique, we simultaneously recorded the activity of many single neurons located in the primary somatosensory and anterior cingulate cortex (ACC), as well as the ventral posterior and medial dorsal thalamus in behaving rats. Our results showed that peripheral electrical stimulation significantly reduced the nociceptive responses in ventroposterior thalamus and somatosensory cortex, indicating an inhibition of nociceptive processing. In contrast, the analgesic stimulation produced a significant increase in mediodorsal thalamus while a less significant decrease in cingulate cortex, reflecting a complicated effect associated with combined antinociceptive activation and nociceptive suppression. These results support the idea that peripheral electrical stimulation can ultimately alter the pain perception by specifically inhibiting the nociceptive transmission in the sensory pathway while mobilizing the antinociceptive action in the affective pathway, thus to produce pain relief.     

Attenuation of mechanical but not thermal hyperalgesia by electroacupuncture with the involvement of opioids in rat model of chronic inflammatory pain

Opioid peptides have been proven effective in reducing the sign of hyperalgesia associated with inflammation. Electroacupuncture (EA) produces antinociception via release of endogenous opioid peptides in normal rats. Moreover, intrathecal injection of dynorphin has antinociceptive effect in rats. The present study was designed to examine whether EA has effect on the thermal and mechanical hyperalgesia in rat model of complete Freund's adjuvant (CFA)-induced inflammatory pain. The results are the following: (1) single session of 100Hz EA (0.5-1.0-1.5 mA, 10 min for each intensity) at both Zusanli (ST 36) and Sanyinjiao acupoints (SP 6) significantly increased mechanical withdrawal threshold determined by von Frey filaments but not with thermal withdrawal latency that is determined by hot plate (52 +/- 0.2 degrees C); (2) 100 Hz EA applied twice a week for 4 weeks and showed a significant decrease in the mechanical hyperalgesia at the third and fourth week, with no effect on thermal hyperalgesia; (3) naloxone (20 mg kg(-1)) had the ability to reverse the inhibition of the mechanical hyperalgesia produced by a single session of EA. In conclusion, the present results indicate that a single or repetitive EA could reduce mechanical hyperalgesia, but not thermal hyperalgesia, in CFA-inflammatory pain rats, and the opioid system might be involved in these effects.     

Cholecystokinin-octapeptide antagonizes morphine analgesia in periaqueductal gray of the rat

The analgesic effect of systemic morphine (5 mg/kg, s.c.) was dose-dependently antagonized by CCK-8 administered to the periaqueductal gray (PAG) of the rat. This effect could be reversed by proglumide, a CCK-receptor antagonist. The effect of morphine analgesia was potentiated by proglumide administered to PAG. These results are compatible with the notion that PAG is a strategic site where CCK-8 exerts an antiopioid activity.     

茅莓总皂苷对局灶性脑缺血再灌注大鼠脑水肿及血-脑脊液屏障变化的影响

目的：研究茅莓总皂苷(TSRP)对局灶性脑缺血再灌注大鼠脑水肿及血脑屏障通透性的影响。方法：采用线栓法制备大鼠局灶性脑缺血再灌注模型,在大鼠脑缺血2 h再灌注6,24,48,72 h分别测定脑含水量和伊文思蓝含量的变化及茅莓总皂苷各剂量组的影响。结果：与模型组比较茅莓总皂苷各剂量组均能不同程度降低脑含水量和伊文思蓝含量。结论：茅莓总皂苷各剂量组显著降低缺血2h再灌注6,24,48,72 h脑水肿和其对血脑屏障通透性,这可能是其减轻I/R时脑水肿的机制之一。     

韩氏穴位神经刺激仪治疗阿片戒断综合征的临床研究

根据电针刺激可促使中枢神经系统释放内源性阿片肽的原理，应用韩氏穴位神经刺激（ＨＡＮＳ），每天刺激一次，每次３０分钟，治疗阿片成瘾者的戒断综合征。首次治疗后便可使过高的心率下降，产生温热感和欣快感，并可使烦躁不安的患者转睡眠状态，缓解戒断症状。４￣５天即可消除“心慌”，明显增加体重，７￣１０天可使阿片成瘾者完全脱瘾。在所进行试验的三种频率（２Ｈｚ、２／１００Ｈｚ、１００Ｈｚ）中，依其有效程度依次为２     

Expression of activity-regulated cytoskeleton-associated protein (Arc/Arg3.1) in the nucleus accumbens is critical for the acquisition, expression and reinstatement of morphine-induced conditioned place preference

Activity-regulated cytoskeleton-associated protein (Arc), also known as activity-regulated gene 3.1 (Arg3.1), is an immediate early gene whose mRNA is selectively targeted to recently activated synaptic sites, where it is translated and enriched. This unique feature suggests a role for Arc/Arg3.1 in coupling synaptic activity to protein synthesis, leading to synaptic plasticity. Although the Arc/Arg3.1 gene has been shown to be induced by a variety of abused drugs and its protein has been implicated in diverse forms of long-term memory, relatively little is known about its role in drug-induced reward memory. In this study, we investigated the potential role of Arc/Arg3.1 protein expression in reward-related associative learning and memory using morphine-induced conditioned place preference (CPP) in rats. We found that (1) intraperitoneal (i.p.) injection of morphine (10 mg/kg) increased Arc/Arg3.1 protein levels after 2 h in the NAc core but not in the NAc shell. (2) In CPP experiments, Arc/Arg3.1 protein was increased in the NAc shell of rats following both morphine conditioning and the CPP expression test compared to rats that received the conditioning without the test or those that did not receive morphine conditioning. (3) Microinjection of Arc/Arg3.1 antisense oligodeoxynucleotide (AS) into the NAc core inhibited the acquisition, expression and reinstatement of morphine CPP; however, intra-NAc shell infusions of the AS only blocked the expression of CPP. These findings suggest that expression of the Arc/Arg3.1 protein in the NAc core is required for the acquisition, context-induced retrieval and reinstatement of morphine-associated reward memory, whereas Arc/Arg3.1 protein expression in the NAc shell is only critical for the context-induced retrieval of memory. As a result, Arc/Arg3.1 may be a potential therapeutic target for the prevention of drug abuse or the relapse of drug use.     

靖江市居民肠道线虫感染及防治知识知晓情况调查

目的调查靖江市居民肠道线虫感染情况及对其认知现状,探索有效控制肠道线虫病的措施。方法在靖江市随机抽取流动人口相对集中的乡镇,以Kato-Katz法检查居民肠道线虫病感染情况,问卷调查防病知识知晓率和卫生行为正确率。结果 2013-2015年共计在靖江市分别调查本地居民和流动人口4 555人和2 278人。本地居民肠道线虫病感染率为0.29%(13例),流动人口为0.75%(17例),差异有统计学意义(χ~2=7.380,P0.01)。本地居民和流动人口性别间肠道线虫病感染率差异均无统计学意义(χ~2=0.010、0.048,P均0.05)。本地居民对肠道线虫病的知晓率高于流动人口,差异有统计学意义(χ~2=9.649~164.533,P均0.01)。结论流动人口是靖江市肠道线虫病的重点防控对象,应对其加强综合干预;健康教育中应加强钩虫病防治相关知识的宣传。     

Association between the brain-derived neurotrophic factor (BDNF) gene and schizophrenia in the Chinese population

Brain-derived neurotrophic factor (BDNF) belongs to a family of the neurotrophin which plays important roles in the development of the brain. BDNF has been suggested as a factor that increases the risk of schizophrenia. In this study, we genotyped three single nucleotide polymorphisms (SNPs) in the BDNF gene using a set sample of Han Chinese subjects consisting of 560 schizophrenes and 576 controls. No significant differences were found for either the genotype or allele distribution of analyzed polymorphisms, nor was any gender-specific association found. Thus, our data suggest that the BDNF gene may not be an important factor in susceptibility to schizophrenia.