RPH、外剥内扎术联合肛垫悬吊及皮桥整形术治疗中老年女性脱垂性环状痔的临床观察

目的探讨以自动痔疮套扎术(RPH)、外剥内扎术(M-M)为基础的肛垫悬吊及皮桥整形术治疗中老年女性脱垂性环状痔的临床疗效。方法选取2018年1月—2019年1月于遂宁市中心医院就诊的124例中老年女性脱垂性环状痔患者,随机分为对照组和观察组,每组62例。对照组患者采用RPH、M-M治疗,观察组患者采用RPH、M-M联合肛垫悬吊、皮桥整形术治疗。观察两组患者手术时间、术中出血量及住院时间等手术相关指标;比较两组患者术后第4天便时出血、创面疼痛、肛缘水肿评分等临床症状;比较两组患者术后1个月治疗有效率;比较两组患者术后3个月肛缘皮赘形成、肛门直肠狭窄、肛门形态。结果观察组手术时间较对照组长(P<0.05)。观察组创面疼痛、便时出血、肛门坠胀、肛缘水肿评分较对照组低(P<0.05)。观察组治疗总有效率较对照组高(P<0.05)。观察组肛缘皮赘形成、肛门形态评分较对照组低(P<0.05)。结论RPH、M-M联合肛垫悬吊、皮桥整形术可显著减轻老年女性脱垂性环状痔患者黏膜及外痔脱垂症状,降低患者便时出血、创面疼痛及肛缘水肿程度,减少术后肛缘皮赘形成,适合临床推广。

便秘状态下肠道菌群变化对脂代谢的影响

肠道菌群的稳定在维持机体健康中发挥重要作用,当便秘引起肠道菌群失衡时,它通过干扰胆汁酸(bile acids,BAs)的合成影响脂质消化、吸收过程;肠道菌群代谢物短链脂肪酸(short chain fatty acids,SCFAs)减少可破坏肠道黏膜屏障的完整性,且SCFAs的受体不能被激活,此外,氧化三甲胺(trimethylamine oxide,TMAO)产生量增多影响脂质代谢过程中关键酶的表达,进一步影响脂质转运、清除过程.本文就便秘状态下肠道菌群通过BAs、SCFAs、TMAO的变化介导脂代谢紊乱的机制作一综述.

Nogo-A expression dynamically varies after spinal cord injury

The mechanism involved in neural regeneration after spinal cord injury is unclear. The my-elin-derived protein Nogo-A, which is speciifc to the central nervous system, has been identiifed to negatively affect the cytoskeleton and growth program of axotomized neurons. Studies have shown that Nogo-A exerts immediate and chronic inhibitory effects on neurite outgrowth.In vivo, inhibitors of Nogo-A have been shown to lead to a marked enhancement of regenerative axon extension. We established a spinal cord injury model in rats using a free-falling weight drop device to subsequently investigate Nogo-A expression. Nogo-A mRNA and protein expression and immunoreactivity were detected in spinal cord tissue using real-time quantitative PCR, immu-nohistochemistry and western blot analysis. At 24 hours after spinal cord injury, Nogo-A protein and mRNA expression was low in the injured group compared with control and sham-operated groups. The levels then continued to drop further and were at their lowest at 3 days, rapidly rose to a peak after 7 days, and then gradually declined again after 14 days. These changes were observed at both the mRNA and protein level. The transient decrease observed early after injury followed by high levels for a few days indicates Nogo-A expression is time dependent. This may contribute to the lack of regeneration in the central nervous system after spinal cord injury. The dynamic varia-tion of Nogo-A should be taken into account in the treatment of spinal cord injury.

Fabrication and thermal conductivity of copper matrix composites reinforced by tungsten-coated carbon nanotubes

Carbon nanotubes （CNTs） were coated by tungsten using metal organic chemical vapor deposition. Magnetic stirring was employed to disperse the W-coated CNTs （W-CNTs） in a Cu matrix, and then, the mixed powders were consolidated by spark plasma sintering. The W-CNTs obtained a uniform dispersion within the Cu matrix when the W-CNT content was less than 5.0vo1%, but high content of W-CNTs （10vol%） resulted in the presence of clusters. The W-CNT/Cu composites containing low content of W-CNTs （〈5.0vol%） exhibited a higher thermal conductivity than the sintered pure Cu, while the CNT/Cu composites exhibited no increase in thermal conductivity after the incorporation of uncoated CNTs. The W-CNT content was found to play a crucial role in determining the thermal conductivity of the W-CNT/Cu composites. The thermal conductivity of the W-CNT/Cu composites increased first and then decreased with the W-CNT content increasing. When the W-CNT content was 2.5vo1%, the W-CNT/Cu composite obtained the maximum value of thermal conductivity. The thermal resistance of the （W-CNT）-Cu interface was predicted in terms of Maxwell-Gamett effective medium approximation, and its calculated value was about 3.0× 10-9 m2.K.W-l.

Effects of the microstructure of twin roll cast and hot rolled plates on the surface quality of presensitized plates

The effect of the microstructure of plates fabricated both in the traditional process, involving casting, hot rolling and cold rolling （HR）, and in the novel twin roll casting ＋ cold rolling （TRC） process on the surface quality of presensitized （PS） plates was analyzed by optical microscopy （OM）, scanning electron microscopy （SEM）, and energy-dispersive X-ray spectroscopy （EDXS）. The formation of pores on the surface of the electrolyzed HR plate could be attributed to the presence of approximately 1-μm-sized large Al-Fe precipitates in the HR plate compared to the smaller precipitates in the TRC plate. Moreover, residual graphite lubricants used during the TRC process were entrapped on the surface of the TRC plate during the subsequent rolling process. The entrapped pollutants tended to further deteriorate the formation of pores on the surface of the TRC plate, and no residual carbon was detected on the surface of the HR plate. Furthermore, the surface quality of the TRC plate can be improved by surface cleaning before the cold rolling process, which could dramatically lower the residual graphite on the surface.

rhe Mitochondrion-Targeted PENTATRICOPEPTIDE REPEAT78 Protein Is Required for nad5 Mature mRNA Stability and Development in Maize

Pentatricopepetide repeat （PPR） proteins are a large family of RNA-binding proteins involved in RNA meta- bolism in plant organelles. Although many PPR proteins have been functionally studied, few of them are identified with a function in mitochondrial RNA stability. By using a reverse genetic approach, we characterized the role of the mitochondrion-targeted PPR78 protein in nad5 mature mRNA stability and maize （Zea mays） seed development. Loss of PPR78 function leads to a dramatic reduction in the steady-state level of mitochondrial nad5 mature mRNA, blocks the assembly of complex I in the electron transport chain, and causes an arrest in embryogenesis and endosperm development. Characterization of a second strong allele confirms the function of PPR78 in nad5 mRNA accumulation and maize seed development. The generation of mature nad5 requires the assembly of three distinct precursor RNAs via transsplicing reactions, and the accumulation ofnad5T1 precursor is reduced in the ppr78 mutants. However, it is the instability of mature nad5 rather than nad5T1 causing loss of the full-length nad5 transcript, and degradation of nad5 losing both translation start and stop codons is enriched in the mutant. Our data imply the assembly of mature nad5 mRNA precedes the protection of PPR78.