Determination of an Angiotensin II-regulated Proteome in Primary Human Kidney Cells by Stable Isotope Labeling of Amino Acids in Cell Culture (SILAC)

Angiotensin II (AngII), the major effector of the renin-angiotensin system, mediates kidney disease progression by signaling through the AT-1 receptor (AT-1R), but there are no specific measures of renal AngII activity. Accordingly, we sought to define an AngII-regulated proteome in primary human proximal tubular cells (PTEC) to identify potential AngII activity markers in the kidney. We utilized stable isotope labeling with amino acids (SILAC) in PTECs to compare proteomes of AngII-treated and control cells. Of the 4618 quantified proteins, 83 were differentially regulated. SILAC ratios for 18 candidates were confirmed by a different mass spectrometry technique called selected reaction monitoring. Both SILAC and selected reaction monitoring revealed heme oxygenase-1 (HO-1) as the most significantly up-regulated protein in response to AngII stimulation. AngII-dependent regulation of the HO-1 gene and protein was further verified in PTECs. To extend these in vitro observations, we overlaid a network of significantly enriched gene ontology terms from our AngII-regulated proteins with a dataset of differentially expressed kidney genes from AngII-treated wild type mice and AT-1R knock-out mice. Five gene ontology terms were enriched in both datasets and included HO-1. Furthermore, HO-1 kidney expression and urinary excretion were reduced in AngII-treated mice with PTEC-specific AT-1R deletion compared with AngII-treated wild-type mice, thus confirming AT-1R-mediated regulation of HO-1. Our in vitro approach identified novel molecular markers of AngII activity, and the animal studies demonstrated that these markers are relevant in vivo. These interesting proteins hold promise as specific markers of renal AngII activity in patients and in experimental models.     

肱骨近端锁定加压钢板与解剖钢板治疗老年肱骨外科颈骨折的临床疗效

目的:研究肱骨近端锁定加压钢板与解剖钢板治疗老年肱骨外科颈骨折的临床疗效。方法:选取92例老年肱骨外科颈骨折患者作为研究对象。根据数字法随机将患者分成观察组及对照组,各含46例。其中对照组予以解剖钢板术式治疗,观察组则予以肱骨近端的锁定加压钢板术式治疗。对比两组不同治法的疗效,两组患者的手术相关指标,两组患者治疗后的肩关节活动度以及两组患者治疗前后的Constant评分及VAS评分。结果:观察组的优良率是89.13%(41/46),显著高于对照组的76.09%(35/46),差异有统计学意义(P0.05)。观察组的术程、手术出血量以及住院时间和骨折的愈合时间均分别显著少于对照组,差异均有统计学意义(均P0.05)。观察组的肩关节活动度显著大于对照组,差均有统计学意义(P0.05)。治疗后观察组的Constant评分及VAS评分均分别显著高于对照组,差异均有统计学意义(均P0.05)。结论:利用肱骨近端的锁定加压钢板术式治疗FSNH,能够帮助患者获得更为积极的临床预后,值得在临床治疗过程中推广应用。     

腓骨近端截骨术与胫骨高位截骨术治疗内侧间室性膝关节骨关节炎的比较研究

目的:对比内侧间室性膝关节骨关节炎(KOA)患者应用腓骨近端截骨术与胫骨高位截骨术治疗的疗效。方法:选取2016年11月到2017年12月在我院接受治疗的内侧间室性KOA患者32例,采用随机数字表法将所有患者分为腓骨近端截骨组与胫骨高位截骨组各16例,比较两组患者的手术时间、住院时间、术中出血量和住院费用,比较两组患者术前、术后3个月、术后6个月的美国特种外科医院膝关节评分(HSS)、美国膝关节协会评分(KSS)、视觉模拟疼痛评分(VAS)和股胫角(FTA),比较两组患者术后出现的并发症的发生率。结果:腓骨近端截骨组患者的手术时间、住院时间短于胫骨高位截骨组,术中出血量和住院费用均显著少于胫骨高位截骨组(P0.05);术后3个月、术后6个月两组患者的HSS评分、KSS评分均明显高于术前,VAS评分、FTA均明显低于术前(P0.05);术前、术后3个月、术后6个月两组患者的HSS评分、KSS评分、VAS评分、FTA比较均无统计学差异(P0.05);两组患者的并发症发生率比较无统计学差异(P0.05)。结论:腓骨近端截骨术和胫骨高位截骨术均可有效治疗内侧间室性KOA,改善患者的膝关节功能和疼痛感,纠正内翻畸形,但腓骨近端截骨术手术时间和住院时间更短,术中出血量和住院费用更少。     

动力髋螺钉与股骨近端髓内钉内固定治疗股骨粗隆间骨折患者的疗效及安全性和关节功能对比观察

目的:比较动力髋螺钉(DHS)与股骨近端髓内钉(PFNA)内固定治疗股骨粗隆间骨折患者的疗效及安全性和关节功能。方法:选取滁州市第一人民医院于2013年3月～2018年4月期间收治的160例股骨粗隆间骨折患者,根据内固定方式的不同将患者分为DHS组(n=80,采用DHS内固定)和PFNA组(n=80,采用PFNA内固定),比较两组临床疗效,采用髋关节功能Harris评分评价所有患者关节功能恢复情况,比较两组患者术前及术后相关指标,并观察患者术后并发症发生情况。结果:PFNA组患者临床总有效率为90.00%,高于DHS组患者的68.75%(P0.05)。两组患者Harris评分的优良率比较差异无统计学意义(P0.05)。PFNA组患者手术时间、卧床时间、骨折愈合时间、切口长度均短于DHS组(P0.05),术中出血量、术后引流量均少于DHS组(P0.05)。两组患者术后并发症总发生率比较无统计学差异(P0.05)。结论:DHS与PFNA内固定治疗股骨粗隆间骨折在术后关节功能恢复、安全性方面效果相当,但与DHS内固定治疗比较,PFNA内固定治疗的临床疗效更佳,手术时间更短,出血量更少,患者术后恢复更快,是治疗股骨粗隆间骨折较理想的手术方式。     

超声引导下髂筋膜神经阻滞联合全麻对老年股骨近端骨折患者术后血清疼痛介质PGE2、SP和认知功能及睡眠质量的影响

摘要 目的：观察超声引导下髂筋膜神经阻滞联合全麻对老年股骨近端骨折患者术后血清疼痛介质前列腺素E₂（PGE₂）、P物质（SP）和认知功能及睡眠质量的影响。方法：选取2018年8月~2021年9月期间我院收治的择期行手术治疗的老年股骨近端骨折患者80例,根据随机数字表法分为对照组（40例,常规全麻方案）和观察组（40例,超声引导下髂筋膜神经阻滞联合全麻方案）,对比两组麻醉效果、血流动力学、疼痛情况、认知功能和睡眠质量,观察不同模式麻醉下的安全性。结果：观察组的苏醒及拔管时间均短于对照组,丙泊酚使用量少于对照组（P<0.05）。两组置入喉罩时（T1）~术毕时（T3）心率（HR）先升高后下降,平均动脉压（MAP）先下降后升高（P<0.05）;观察组T1~T3时点HR低于对照组,MAP高于对照组（P<0.05）。两组术后24 h血清PGE₂、SP水平和视觉疼痛模拟量表（VAS）评分均升高,但观察组低于对照组（P<0.05）。两组术后1 d、2 d、3 d 蒙特利尔认知评估量表（MoCA）评分较术前先下降后升高（P<0.05）;观察组术后2 d、3 d MoCA评分高于对照组（P<0.05）。两组术后1 d、2 d、3 d匹兹堡睡眠质量评估量表（PSQI）评分较术前先升高后下降（P<0.05）;观察组术后1 d、2 d、3 d PSQI评分低于对照组（P<0.05）。两组不良反应发生率对比无差异（P>0.05）。结论：老年股骨近端骨折患者术中选用超声引导下髂筋膜神经阻滞联合全麻,镇痛效果显著,可稳定机体血流动力学,减少对认知功能和睡眠质量的影响,且安全性良好。     

New Glycoprotein-Associated Amino Acid Transporters

The L-type amino acid transporter LAT1 has recently been identified as being a disulfide-linked ``light chain' of the ubiquitously expressed glycoprotein 4F2hc/CD98. Several LAT1-related transporters have been identified, which share the same putative 12-transmembrane segment topology and also associate with the single transmembrane domain 4F2hc protein. They display differing amino acid substrate specificities, transport kinetics and localizations such as, for instance, y⁺LAT1 which is localized at the basolateral membrane of transporting epithelia, and the defect of which causes lysinuric protein intolerance. The b^0,+AT transporter which associates with the 4F2hc-related rBAT protein to form the luminal high-affinity diamino acid transporter defective in cystinuria, belongs to the same family of glycoprotein-associated amino acid transporters (gpaATs). These glycoprotein-associated transporters function as amino acid exchangers. They extend the specificity range of vectorial amino acid transport when located in the same membrane as carriers that unidirectionally transport one of the exchanged substrates. gpaATs belong to a phylogenetic cluster within the amino acid/polyamine/choline (APC) superfamily of transporters. This cluster, which we designate the LAT family (named after its first vertebrate member), includes some members from nematodes, yeast and bacteria. The latter of these proteins presumably lack association with a second subunit. In this review, we focus on the animal members of the LAT cluster that form, together with some of the nematode members, the family of glycoprotein-associated amino acid transporters (gpaAT family). Received: 20 July 1999/Revised: 7 September 1999     

Ulltrastructural and trace metal studies on radiographers’ hair and nails

Scalp hair and fingernail samples of 42 medical radiographers and 42 nonradiographers (control) with matching age groups and food habits were collected for this study. Trace metal estimation by atomic absorption spectrometry (AAS) has indicated a significant increase (P < 0.001) in Zn, Cu, and Cd contents in the radiographers’ hair and nails. Scanning electron microscopy (SEM) reveled structural changes in the hair and nails of radiographers. Significant alterations in the Zn and Cd contents along with extensive structural damage in the hair and nails probably indicate that low-dose Χ-radiation imposes stress on these radiation workers.     

Hypothermia causes a marked injury to rat proximal tubular cells that is aggravated by all currently used preservation solutions

Cold preservation results in cell death via iron-dependent formation of reactive oxygen species, leading to apoptosis during rewarming. We aimed to study cold-induced damage (i.e., injury as a consequence of hypothermia itself and not cold ischemia) in proximal tubular cells (PTC) in various preservation solutions presently applied and to clarify the role of mitochondria in this injury. Primary cultures of rat PTC were incubated at 4 degrees C for 24 h in culture medium, UW, Euro-Collins or HTK solution with and without the iron chelator desferal and rewarmed at 37 degrees C in culture medium. Cell damage, morphology, and apoptosis were studied and mitochondrial membrane potential was assessed by fluorescence microscopy. Cold incubation of PTC in culture medium followed by rewarming caused marked cell damage compared to warm incubation alone (LDH release 39+/-10% vs. 1.6+/-0.3%). Cold-induced damage was aggravated in all preservation solutions (LDH release 85+/-2% for UW; similar in Euro-Collins and HTK). After rewarming, cells showed features suggestive for apoptosis. Desferal prevented cell injury in all solutions (e.g., 8+/-2% for UW). Mitochondrial membrane potential was lost during rewarming and this loss could also be inhibited by desferal. Trifluoperazine, which is known to inhibit mitochondrial permeability transition (MPT), was able to prevent cold-induced injury (LDH 85+/-5% vs. 12+/-2%). We conclude that cold-induced injury occurs in PTC and is aggravated by UW, Euro-Collins, and HTK solution. Iron-dependent MPT is suggested to play a role in this damage. Strategies to prevent cold-induced injury should aim at reducing the availability of "free" iron.