Percutaneous nephrolithotomy in semisupine position: a modified approach for renal calculus

Conventional percutaneous nephrolithotomy (PCNL) is usually performed in a prone position, which compresses the thorax and results in difficulty in rescue during operation. When PCNL is performed in a supine position, the flank renal puncture area is limited, so it is difficult to treat disseminated and complex renal calculi. Herein, we introduce a modified semisupine position for performing PCNL, which has numerous benefits as well as safe and effective. Between May 2002 and May 2009, a total of 452 patients with renal calculi were treated with semisupine PCNL. The patient was placed in 45° semisupine position during the procedure, with the affected flank arched as much as possible. In this series, no one converted to open surgery. The average operating time was (115.2 ± 44.5) min. Single tract PCNL was performed for 80.97% of the cases, two tracts 13.94%, three tracts 4.65%, and four tracts 0.44%. The upper, middle, and lower calix tracts accounted for 12.1, 63.0, and 24.9%, of procedures, respectively. Stone-free rate was 85.7% overall, 92.2% for single calculus (83/90), and 72.9% for staghorn calculi (78/107). Major postoperative complications occurred in 3.3% of the cases. This study demonstrated PCNL in a semisupine position is an effective alternative for treating renal calculi, which combines the advantages of PCNL in a prone position, and PCNL in a supine position. The semisupine position allows easier irrigation of stone fragments, is more comfortable for the patient, and facilitates monitoring of anesthesia.     

低温等离子射频消融治疗腰椎间盘突出症初步探讨

目的评价低温等离子刀射频消融术治疗腰椎间盘突出症的临床疗效。方法 2006年1月～2009年12月应用低温等离子射频消融治疗腰椎间盘突出症共44例,男20例,女24例;年龄30～52岁,平均40岁。局部麻醉,在C型臂引导下操作。共46个椎间隙：单间隙42例,双间隙2例。术后随访近期效果。结果全部病例均获得随访,随访时间6～48个月,平均24个月。VAS评分术前（8.40±0.50）分,术后1周（2.60±0.53）分,末次随访（2.80±0.34）分。Oswestry评分术前（59.00±1.90）分,术后1周（30.00±1.80）分,末次随访（34.00±1.50）分。各指标术后及末次随访时与术前比较有显著性差异（P〈0.05或P〈0.01）,而术后两次随访差异无统计学意义（P〉0.05）。患者满意度80%,无任何并发症。结论经皮低温等离子刀髓核消融术是治疗腰椎间盘突出症行之有效的方法,这种技术简单、微创、安全、疗效肯定。关键是选择合适的适应证。     

The protective role of Smad7 in diabetic kidney disease: mechanism and therapeutic potential

OBJECTIVE

Although Smad3 has been considered as a downstream mediator of transforming growth factor-β (TGF-β) signaling in diabetes complications, the role of Smad7 in diabetes remains largely unclear. The current study tests the hypothesis that Smad7 may play a protective role and has therapeutic potential for diabetic kidney disease.

RESEARCH DESIGN AND METHODS

Protective role of Smad7 in diabetic kidney disease was examined in streptozotocin-induced diabetic mice that have Smad7 gene knockout (KO) and in diabetic rats given Smad7 gene transfer using an ultrasound-microbubble-mediated technique.

RESULTS

We found that mice deficient for Smad7 developed more severe diabetic kidney injury than wild-type mice as evidenced by a significant increase in microalbuminuria, renal fibrosis (collagen I, IV, and fibronectin), and renal inflammation (interleukin-1β [IL-1β], tumor necrosis factor-α [TNF-α], monocyte chemoattractant protein-1 [MCP-1], intracellular adhesion molecule-1 [ICAM-1], and macrophages). Further studies revealed that enhanced renal fibrosis and inflammation in Smad7 KO mice with diabetes were associated with increased activation of both TGF-β/Smad2/3 and nuclear factor-κB (NF-κB) signaling pathways. To develop a therapeutic potential for diabetic kidney disease, Smad7 gene was transferred into the kidney in diabetic rats by an ultrasound-microbubble-mediated technique. Although overexpression of renal Smad7 had no effect on levels of blood glucose, it significantly attenuated the development of microalbuminuria, TGF-β/Smad3-mediated renal fibrosis such as collagen I and IV and fibronectin accumulation and NF-κB/p65-driven renal inflammation including IL-1β, TNF-α, MCP-1, and ICAM-1 expression and macrophage infiltration in diabetic rats.

CONCLUSIONS

Smad7 plays a protective role in diabetic renal injury. Overexpression of Smad7 may represent a novel therapy for the diabetic kidney complication.Diabetic nephropathy is a major complication of diabetes (1–4). Approximately 20–40% of patients with type 1 or type 2 diabetes mellitus (DM) develop diabetic nephropathy (5,6). Diabetic nephropathy is characterized by excessive deposition of extracellular matrix (ECM) proteins in the mesangium and tubulointerstitium, thickness of basement membrane of the glomeruli, and loss of podocytes with the development of microalbuminuria and a decline of renal function (2,3,7). Both in vivo and in vitro studies have demonstrated that renal fibrosis and inflammation play an important role in the pathogenesis of diabetic kidney disease (2–4,7–10). Transforming growth factor-β (TGF-β) family is a crucial mediator in the development of diabetic nephropathy (11–15).It is now clear that after binding to its receptors, TGF-β signals through two critical downstream mediators, Smad2 and Smad3, to exert its biological activities such as ECM production. In addition, TGF-β₁ also induces an inhibitory Smad called Smad7, which negatively regulates activation of Smad2/3 by TGF-β receptor competition and degradation via the ubiquitin-proteasome degradation mechanism (16,17). Recent studies have demonstrated that overexpression of Smad7 is capable of inhibiting renal fibrosis and inflammation by blocking the activation of both TGF-β/Smad and nuclear factor-κB (NF-κB) signaling pathway (18–22). In contrast, deletion of Smad7 promotes renal fibrosis and inflammation (23), suggesting that Smad7 may be a key regulator and a therapeutic agent for renal fibrosis and inflammation (24). Although it has been reported that Smad3 is pathogenic in fibrosis including diabetic kidney disease (25,26), the role of Smad7 in diabetes complications remains unexplored, and it is unknown whether blockade of the TGF-β signaling pathway by Smad7 has therapeutic potential for diabetes complications. Thus, in the current study, we uncovered the role of Smad7 in diabetic kidney disease induced in Smad7 knockout (KO) mice and developed new therapeutic strategy for diabetic kidney complication by targeting the TGF-β/Smad pathway with ultrasound-microbubble-mediated Smad7 gene therapy.     

不同海拔高度青少年最大氧供给和氧利用的特点及影响因素

目的探讨高原青少年最大氧耗量（ＶＯ２ｍａｘ）、最大氧供给量（ＤＯ２ｍａｘ）及氧利用的特点。方法对三个不同海拔高度（２２６０ｍ,３４１７ｍ,４３００ｍ）各１５例健康青少年的氧动力学指标进行测试。用自行车负荷递增法直接测定ＶＯ２ｍａｘ等气体交换指标;耳氧仪同步记录氧饱和度（ＳＯ２）;心阻抗法测定最大心指数（ＣＩｍａｘ）。结果血红蛋白浓度（Ｈｂ）随海拔高度的升高而增大（Ｐ＜０．０５）;ＶＯ２ｍａｘ、ＤＯ２ｍａｘ、ＣＩｍａｘ和ＳＯ２均随海拔升高而下降（Ｐ＜０．０５）;三个海拔高度的最大氧摄取率（ＥＲＯ２）无明显变化;ＶＯ２ｍａｘ和ＤＯ２ｍａｘ在三个海拔高度及总体样本中均呈显著直线相关（ｒ＝０．７７、０．７１、０．７２、０．９８,Ｐ＜０．０５）。结论高原青少年ＶＯ２ｍａｘ降低的原因为ＤＯ２ｍａｘ不足,而非氧利用障碍;ＣＩｍａｘ和ＳＯ２的下降是ＤＯ２ｍａｘ不足的决定因素,同时也是ＶＯ２ｍａｘ降低的主要原因。     

Alfacalcidol treatment increases bone mass from anticatabolic and anabolic effects on cancellous and cortical bone in intact female rats

It has been reported that alfacalcidol had an anticatabolic and anabolic effect on bone in ovariectomized and aged male rat models, but this has not been tested on intact female rats. The current study was to determine the effects of alfacalcidol on cancellous and cortical bone in intact female rats with or without exercise. Seventy-four, 8.5-month-old, intact female rats were orally treated with 0, 0.005, 0.025, 0.05, or 0.1 microg/kg alfacalcidol alone or in combination with raised cage (RC) exercise for 3 months. In vivo peripheral quantitative computerized tomography (pQCT) of the proximal tibial metaphyses (PTM) and ex vivo histomorphometric analyses of the PTM and tibial shaft (TX) were performed. Only the 0.1 microg alfacalcidol/kg dose proved to be anabolic. pQCT analysis showed that this dose increased total and cortical bone mineral content and density and trabecular bone mineral density. Histomorphometrically, it induced an anabolic response by increased trabecular mass and microarchitecture from stimulated cancellous bone and bone bouton formations, and suppressed bone resorption more than bone formation on the trabecular and endocortical surfaces, to produce a positive bone balance. A positive correlation between trabecular connectivity and bone bouton numbers occurred. These findings suggest alfacalcidol treatment augments bone mass by increased cancellous bone mass and improved trabecular architecture through its anticatabolic and anabolic properties in the intact adult female rat. Last, raised cage exercise alone or the combination of raised cage and alfacalcidol was no more effective than alfacalcidol alone.     

旋转臂自锁式髓内钉治疗股骨干骨折

目的 探讨旋转臂自锁式髓内钉(RBSN)治疗股骨干骨折的临床效果.方法 对32例股骨干骨折采用切开复位RBSN内固定.结果 患者均获随访,时间10～30(16.2±1.4)个月.全部骨性愈合,时间为12～26(21.3±2.1)周.采用HSS膝关节评分标准评价疗效:优30例,良1例,可1例,优良率96.9%.结论 RBSN治疗股骨干骨折创伤小,操作简便,固定牢固,疗效确切.     

肝移植术后肺部真菌感染的诊断和治疗

目的探讨肝移植术后肺部真菌感染的早期诊断及治疗方法。方法回顾分析20例肝移植术后肺部真菌感染患者的临床资料,分析其原发病、免疫状态、感染真菌的种类及抗真菌药物的应用。结果20例患者念珠菌感染17例,死亡2例,曲霉菌感染3例,死亡2例。氟康唑、伊曲康唑、两性霉素B治疗有效率70％,伏立康唑、卡泊芬净治疗有效率100％。结论肝移植术后真菌感染高发,以危重患者为主要目标人群,发生早,病情重。诊断分三级,达到临床诊断即应及早治疗。治疗以伏立康唑为首选,严重感染者联合应用卡泊芬净效果良好。     

Lichtenstein法无张力疝修补术治疗120例成人腹股沟疝体会

目的总结Lichtenstein法治疗成人腹股沟疝的疗效。方法120例腹股沟疝患者,采用Lichtenstein法行无张力疝修补术,其中斜疝93例（包括复发性斜疝14例,双侧斜疝3例）;直疝27例。结果120例患者手术过程顺利,手术时间平均50（45-60）min,术后住院5-7 d。伤口感染1例,经抗生素治疗及局部换药痊愈;阴囊积液4例,经阴囊穿刺1-2次治愈;局部疼痛2例,术后1-3月逐渐好转。术后96例获随访,平均14个月,无一例复发。结论Lichtenstein法治疗成人腹股沟疝效果确切,符合解剖生理特点,操作简单,术后并发症少,值得推广。     

局部肺循环临时阻断在复杂肺切除术中的应用

目的探讨局部肺循环临时阻断在复杂肺切除术中的应用价值和技术细节。方法接受局部肺循环临时阻断条件下的肺切除手术24例,12例接受支气管、肺动脉、静脉联合成形术,其中4例为支气管肺动脉“双袖”成形术;10例肺动脉成形或同时联合肺静脉成形（其中1例联合左心房成形术）;2例单纯肺动脉、静脉阻断切除肺叶或全肺。在“双袖”成形术中采用左房血反流氧合残肺。结果术后30 d内死亡2例,死亡原因分别为右全肺切除术后呼吸衰竭和肺动脉成形术后急性肺动脉栓塞。4例接受“双袖”成形术的患者术后均产生不同程度的残肺水肿,术后14-18 d完全恢复。发生脓胸1例（4.2%）,肺炎6例（25.0%）,漏气3例（12.5%）。Ⅰ-Ⅱ期肺癌患者中位生存期为36个月,ⅢA期患者中位生存期为18个月。结论局部肺循环临时阻断在复杂肺切除术中的应用能降低术中风险,简化操作程序,达到最大限度保留健康肺组织和最大限度切除癌肿的目的,有临床实用价值。     

原发性肝癌手术后种植灶的治疗

目的：探讨原发性肝癌术后种植性转移的发生和治疗.方法:分析35例原发性肝癌手术后腹腔和(或)腹壁种植性转移患者的临床特征、治疗方式及预后.结果:肝癌手术后种植性转移发生率为1.03%,再次手术率为94.29%,首次肝癌切除术后1年、2年和3年的生存率分别是90.52%、66.79%和40.20%,平均生存期为38.28个月,中位生存期为32个月;种植灶切除术后1年、2年和3年的生存率分别是70.60%、48.06%和29.63%,平均生存期为29.59个月,中位生存期为24个月.结论:肝癌术后种植性转移与包膜侵犯、肿瘤破裂、相对根治性手术、肿瘤侵犯程度以及围手术期输血密切相关.及时行手术切除治疗,可延长生存期,甚至达到治愈的疗效.