医疗器械包装设计浅谈

本文介绍了医疗器械之无菌包装系统的设计之关键要素和要求,介绍了目前流行的灭菌方式以及对无菌包装系统的要求和影响。本文最后还列举了常见的医疗器械包装系统。     

胃微小腺癌的组织发生研究

从２１０５例胃癌癌旁组织中找出微小腺癌３１例（〈０．１ｃｍ），观察其组织发生的特征，发现胃腺癌的发生有８种形式：①腺颈部干细胞癌变；②表面上皮癌变；③腺上皮癌变；④肠化生上皮癌变；⑤微腺囊癌变；⑥溃疡边缘上皮癌变；⑦扁平腺瘤癌变；⑧贲门交界处柱状上皮癌变。     

刮治＋自体骨移植术治疗牙源性角化囊肿（附14例报告）

本文总结了１４例应用刮治和自体骨移植术治疗大型牙源性角化囊肿的方法，１４例植骨均成活，４例术后囊肿复发，再次手术，指出：与骨断切除治疗大型角化囊肿的方法比较，此法最大的优点是有利于保持患者面容和咀嚼功能，并对大型角化囊肿的手术原则，自体骨移植问题及手术注意事项进行了讨论。     

NGF prevents the changes induced by monocular deprivation during the critical period in rats

Photic evoked responses were recorded from the striate cortex of Long-Evans hooded intact, monocular visual deprivation (MD) and MD treated with NGF rats. The averaged visual evoked responses (AVER) were obtained from both hemispheres and provided comparison after binocular photic stimuli between the contralateral and the ipsilateral striate cortex with relation to the MD eye. One month of monocular visual deprivation at the critical period of development resulted in marked reduction of the amplitudes of AVER components as compared to the control recordings (P < 0.001). These changes of the AVER could be prevented by NGF infusion to lateral ventricle at the dosage of 2.0–2.4 μg/day for four weeks during the monocular deprivation. In conclusion, the change of AVER amplitudes induced by monocular visual deprivation during the critical period of development can be prevented by NGF infusion to lateral ventricle.     

“90增血剂”对特发性血小板减少性紫裥患者的T细胞亚群的作用

作者根据现代免疫学观点,自1989年起采用自制中药“90增血剂”治疗ITP46例。期间,应用间接免疫荧光技术检测了患者外周血T淋巴细胞亚群,结果表明病例组全T细胞(CD_3)、T辅助/诱导细胞(CD_4)降低,T抑制/细胞毒细胞(CD_8)增高,CD_4/CD_8比值明显降低。治疗后,患者T亚群恢复常态,血小板数上升,骨髓产板型巨核细胞数增加,临床总有效率达91.2%,明显优于激素组(71.4%)。提示中药具有显著的疗效和良好的免疫调节作用。同时,动态观察ITP患者T细胞亚群的变化,对帮助临床判断治疗反应和预后有很大意义。     

Genetic basis of tobacco smoking: strong association of a specific major histocompatibility complex haplotype on chromosome 6 with smoking behavior

The genetic basis for addiction to tobacco smoking--particularly that of the perception of olfactory stimuli that may be important in reinforcing smoking addiction--is largely unknown. A cluster of genes for olfactory receptors is in close proximity to the MHC region on chromosome 6. Polymorphisms of MHC class III genes (RCCX modules, TNFA promoter polymorphisms) were determined in 101 healthy subjects and 232 coronary artery disease (CAD) patients from Hungary with defined tobacco smoking habits. A highly significant association between ever smoking (past + current smokers) and a specific MHC haplotype was observed (odds ratios = 2.14-4.13; P-values = 0.012 to <0.001). This haplotype is characterized by the presence of C4A null alleles and a solitary short C4B gene linked to the TNF2 allele of the promoter for TNFA gene. This haplotype occurred more frequently in the ever smokers than in the never smokers [odds ratio: 4.97 (1.96-12.62); P = 0.001], and such associations were stronger in women (odds ratio = 13.6) than in men (odds ratio = 2.79). An independent study of complement C4 protein polymorphism and smoking habits in Icelandic subjects (n = 351) yielded similar and confirmative results. Considering the documented link between olfactory stimuli and smoking in females, and the presence of a cluster of odorant receptor genes close to the MHC class I region, our findings implicate a potential role of the MHC-linked olfactory receptor genes in the initiation of smoking.     

Dexamethasone alters TNF-alpha expression in retinopathy

TNF-alpha has been found in the retina. Hyperoxia and hypoxia regulate TNF-alpha expression. TNF-alpha is an important factor in inflammation and angiogenesis. Dexamethasone inhibits TNF-alpha production. Changes in TNF-alpha expression in the retina may play an important role in the development of oxygen-induced retinopathy. Oxygen-induced retinopathy was produced in C57BL6 mice by exposure to 75% oxygen at Postnatal Day 7 (P7) for 5 days and the mice recovered in room air until Day 17 (P17). Dexamethasone was administered at 0.5 mg/kg/day once daily subcutaneously during the 5 days of oxygen exposure. TNF-alpha expression was evaluated at Day 7 prior to oxygen exposure, at Day 12 (P12) immediately upon removal from oxygen, and at Day 17, the time of maximal vasoproliferation by RT-PCR. TNF-alpha is developmentally regulated in the retinae of C57BL6 mice. From P7 to P12, there is a 3-fold increase in TNF-alpha expression and from P7 to P17 there is a 2.7-fold increase. There was 2.7-fold suppression in expression immediately following oxygen exposure at P12. The expression was dramatically increased at P17, the time of maximal vasoproliferation. Dexamethasone inhibited the expression of TNF-alpha at P17 by 6.4-fold. At this dose, it also suppressed the baseline TNF-alpha expression in the mouse model. In summary, TNF-alpha is altered in the development of oxygen-induced retinopathy in the mouse. It increased markedly during the vasoproliferative phase and was suppressed by dexamethasone. Modulation of TNF-alpha expression may provide a potential site of action for future therapeutic targets.