中日友好医院分型股骨头坏死腓骨植入治疗的三维有限元分析

文题释义：股骨头坏死中日友好医院分型的有限元分析：根据李子荣等提出的中日友好医院分型，建立股骨头坏死三维模型，分为 M型(内侧型)、C型(中央型)和 L型(外侧型)，其中 L型包括L1型(次外侧型)、L2型(极外侧型)和 L3型(全头型)。通过对建立的模型进行有限元分析，为该分型的保髋治疗提供了一定力学依据，显示外侧柱的存留是精准预防塌陷的重要因素，为进一步实现个体化治疗提供力学基础。 腓骨支撑坏死股骨头保髋手术：是对于早中期股骨头坏死需要保留股骨头患者进行的一种手术方式。首先需对股骨头进行髓芯减压，清除一定坏死骨，空腔填塞松质骨(髂骨为主)，打压结实后植入腓骨(异体或自体)支撑，给坏死区的提供力学支撑及生物学修复，预防股骨头进一步坏死及塌陷。 背景：研究报道股骨头坏死的保髋疗效与外侧柱存留密切相关，中日友好医院分型是根据三柱结构确立的，对股骨头塌陷的预测准确性高。 目的：建立股骨头坏死中日友好医院分型各分型仿真的三维有限元模型，通过有限元分析各分型腓骨植入的力学变化，探讨外侧柱存留对保髋疗效的意义，为该分型的塌陷精准预测提供基础。 方法：建立正常股骨头、中日友好医院分型(M型、C型、L1型、L2型、L3型)股骨头坏死及其腓骨植入3组11种三维有限元模型，运用ANSYS软件进行有限元分析计算，观察各组模型的最大应力值、最大位移值及股骨头内部载荷传递模式。 结果与结论：①坏死组位移最大，应变最大，且因坏死分型不同而位移不同，位移变化如下：M型相似文献   

Intravenous Iloprost: A New Therapeutic Option for Patients with Post-Transplant Distal Limb Syndrome (PTDLS)

The purpose of this study was to investigate the application of intravenous iloprost as a novel therapy for the treatment of post-transplant distal limb syndrome (PTDLS). PTDLS is a benign but disabling complication in the first year after renal transplantation. It is characterized by bilateral, often incapacitating pain in the feet and or knees on motion and a significant rise in alkaline phosphatase levels on laboratory evaluation. On MRI, bone marrow edema of the affected bone regions can be demonstrated. PTDLS differs from steroid induced osteonecrosis of the hip in terms of localization, an average cumulative steroid dosage within expected limits, and a benign outcome, as PTDLS does not progress to overt cell necrosis. From August 2003 to April 2005 we treated 10 patients with MRI-proven diagnosis of PTDLS following a standardized regimen of intravenous iloprost over 5 days. Iloprost led to prompt pain relief measured on a visual analogous scale (VAS) ranging from 1 to 10 (5.6 +/- 1.5 before vs. 2.1 +/- 1.3 after treatment, p = 0.0004). PTDLS represents a benign but disabling complication following renal transplantation. Intravenous iloprost might be a promising therapeutic concept leading to a quick relief of symptoms without relevant side effects.     

皮(肌)瓣治疗小腿长段骨坏死实验研究与临床应用

[目的] 探讨皮（肌）瓣治疗骨坏死的可行性。[方法]应用新西兰大白兔48只，随机分为对照组、实验组。按实验方法将胫骨制成骨坏死模型。对照组用游离皮片覆盖坏死骨；实验组用腓肠肌皮瓣覆盖坏死骨。术后2、4、8、12周行ECT、X线片、骨钙素（BGT）、组织切片检查。临床应用436例。[结果]ECT显示实验组动脉相放射摄入值及延迟相放射摄入值明显高于对照组（P〈0．02）；血清BGP水平实验组各时段均比对照组高（P〈0．001）；组织学检查4周实验组髓腔中可见增生的血管，大量骨细胞；X线片12周实验组的胫前皮质骨接近正常骨，而对照组皮质骨仍为坏死、骨质硬化。临床应用小腿外观好，足部肿胀消退，创面感染治愈，坏死骨成活，骨髓腔再通。[结论]用血运丰富的皮（肌）瓣覆盖坏死胫骨段后，血运改善，坏死骨可以成活。     

Diving physiology and pathophysiology

Summary. Divers have worked at 500 m depth in the sea and have reached 700 m in simulated chamber dives. A prerequisite for this has been extensive physiological studies of the body's reactions to pressure and pressure changes. This paper reviews such physiological and pathophysiological studies with emphasis on recent developments.     

血管束植入骨内的形态学研究

选用32只(64后肢)体重在11～18.5kg成年健康杂种狗,随机分为三组,每组10～11只。实验组将血管束植入源于肋骨、胫骨段的骨块内,并埋置肌间,对侧骨为无血管束植入的对照组。术后60～180天作大体观测、X线检查和组织学观察。在半数动物作骨缺血坏死模型实验的骨块,采用热灼法、蒸煮游离骨和硅膜包骨法,在不同时间内进行观察,其中以硅膜包骨的骨缺血坏死模型最为满意。实验证明,在血管束植入骨内后,可以重建血供,血管长入,骨细胞再生,发现有很多密集的成骨细胞、骨软骨母细胞、胶原纤维、新骨小梁和黄骨髓等组织,而无血管束植入的对照骨块均成为死骨。     

Medication-Related Osteonecrosis of the Jaw (MRONJ): Are Antiresorptive Drugs the Main Culprits or Only Accomplices? The Triggering Role of Vitamin D Deficiency

Osteonecrosis of the jaw (ONJ) is a severe clinical condition characterized mostly but not exclusively by an area of exposed bone in the mandible and/or maxilla that typically does not heal over a period of 6–8 weeks. The diagnosis is first of all clinical, but an imaging feedback such as Magnetic Resonance is essential to confirm clinical suspicions. In the last few decades, medication-related osteonecrosis of the jaw (MRONJ) has been widely discussed. From the first case reported in 2003, many case series and reviews have appeared in the scientific literature. Almost all papers concerning this topic conclude that bisphosphonates (BPs) can induce this severe clinical condition, particularly in cancer patients. Nevertheless, the exact mechanism by which amino-BPs would be responsible for ONJ is still debatable. Recent findings suggest a possible alternative explanation for BPs role in this pattern. In the present work we discuss how a condition of osteomalacia and low vitamin D levels might be determinant factors.     

增骨健步汤预防激素性股骨头坏死的实验研究

目的：探讨增骨健步汤防治激素性骨头坏死的作用机理。方法：将24只健康兔随机分为3组：激素组、中药组及正常对照组。激素组和中药组分别给予醋酸强的松龙肌注造模型,中药组同时喂服增骨健步汤,激素组喂服等量生理盐水。10周后全部动物处死取血,行血液流变检测和取股骨头进行形态组织学观察。结论：增骨健步汤能显著降低血粘度、血脂水平,改善肌骨头血运、防治激素性肌骨头坏死。     

激素性股骨头坏死血管新生相关基因的鉴定及其靶向中药成分筛选验证

目的 基于生物信息学分析筛选激素性股骨头坏死（steroid induced osteonecrosis of femoral head,SONFH）中涉及血管生成相关的基因,进一步探讨其作用机制并筛选靶向中药活性成分。方法 通过Perl语言和R软件处理GEO数据,获得SONFH的关键差异基因,使用David工具进行基因本体（gene ontology,GO）和京都基因与基因组百科全书（Kyoto encyclopedia of genes and genomes,KEGG）分析。然后使用STRING平台和Cytoscape软件分析蛋白互作关系,用MCODE和CytoHubba插件识别重要基因簇模块和核心基因,并进一步验证。使用CTD数据库搜索靶向核心基因的中药活性成分并用autodock vina软件进行分子对接,以及探索核心基因与SONFH的相互作用。利用激素诱导人股骨头骨微血管内皮细胞（bone microvascular endothelial cells,BMECs）,通过CCK-8、细胞划痕实验和Transwell实验观察白藜芦醇对细胞增殖及迁移的影响,通过Western ...     

CircCDR1as Suppresses Bone Microvascular Endothelial Cell Activity and Angiogenesis Through Targeting miR‐135b/ FIH‐1 Axis

ObjectiveThe current study investigated the role of CircCDR1as on angiogenesis of bone microvascular endothelial cells (BMECs) isolated from non‐traumatic ONFH.MethodsForty corticosteroid‐induced ONFH patients received THA were enrolled in our study. Expressions of CircCDR1as, miR‐135b, and FIH‐1 were detected by qRT‐PCR in affected necrosis tissue and non‐affected normal tissue. Bone microvascular endothelial cells (BMEC) were isolated from six patients and treated with 0.1 mg/mL hydrocortisone to establish a GC‐damaged model of BMECs. Circ CDR1as plasmid and miR‐135b mimic were transfected into BMECs. BMEC proliferation was assessed using MTT assays. The migration ability of cells was detected by scratch‐wound assays. Matrigel assay was performed to detect angiogenesis in vitro. Western blot assay was used to detect HIF‐1α, VEGF, and FIH‐1 expressions. FISH, RNA pull down, RIP, and luciferase assay were carried out to determine the interaction of CircCDR1as, miR‐135b, and FIH‐1.ResultsCircCDR1as was upregulated(2.02 ± 0.30 vs. 1.00 ± 0.10,P < 0.001) whereas miR‐135b was downregulated (0.55 ± 0.12 vs. 1.00 ± 0.10,P < 0.001) in affected tissues than in non‐affected tissues. Expression of CircCDR1as and FIH‐1 were negatively associated with miR‐135b in affected tissues (CircCDR1as with miR‐135b: r = −0.506, P < 0.001; FIH‐1 with miR‐135b r = −0.510, P < 0.001). Total blood tubule density was increased when CircCDR1as was silenced compared with NC (P < 0.01 vs. NC). The number of migrated BMECs were significantly increased in CircCDR1as silencing group compared with NC group (P < 0.05 vs. NC). In addition, CircCDR1as plasmids transfection increased the protein expressions of FIH‐1 (P < 0.05 vs. NC) and reduced the HIF‐1α as well as VEGF expression compared with NC group (P < 0.05 vs. NC). FISH, RNA pull down, RIP, and luciferase assay identified that FIH‐1 was a target of miR‐135b and could be modulated by CircCDR1as.ConclusionCircCDR1as decreases angiogenesis and proliferation of BMECs by sponging miR‐135b and upregulate FIH‐1.     

Disseminated Bartonella henselae disease mimicking Langerhans’ cell histiocytosis

Bartonella henselae, the causative agent of cat‐scratch disease, has been recognized to be responsible for a broad range of clinical syndromes. We report the case of a patient with disseminated B. henselae infection mimicking Langerhans cell histiocytosis at presentation and its successful management with neurosurgery, prolonged antibacterial therapy, and observation.