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Objectives
Iatrogenic injury of the Profunda Femoris Artery (PFA) at time of hip fixation surgery can increase morbidity and mortality and prolong the hospital stay. This is an injury that tends to pass unnoticed as a cause of postoperative deterioration despite being frequently reported in the literature. Our study aims to describe the anatomy of the PFA in relation to the medial femoral cortex with specific emphasis on its orientation relative to the position of a sliding hip screw side plate construct. By doing so we are able to present clear guidance to orthopaedic surgeons on how to avoid iatrogenic PFA injury at the time of hip fracture fixation.Methods
Using Computed Tomography Angiographic (CTA) studies, the course of the PFA in relation to the medial femoral cortex was traced in 44 patients (28 males and 16 females) with mean age of 65.6 years. Coronal and axial CT sections were cross-linked to specify the position of the PFA at 1?cm intervals.Results
The course of the artery could be divided into three parts relative to a fixed reference point. Proximal and distal parts of the artery were in a safer position in comparison to the middle part of the artery that was found very close to the femoral cortex and along the coronal axis of the femur (mean angle 2.9° from the femoral coronal axis and 13.8?mm from the medial femoral cortex). Using the commercially available side plate constructs, this part of the artery corresponded to the distal part of the plate (third and fourth holes).Conclusion
Special attention needs to be practiced by the operating surgeon while drilling into the third and fourth holes of the side plate. 相似文献3.
Feng He Yuanjun Ma Shi Li Haozhe Ren Qian Liu Xiaohua Chen Hui Miao Tao Ye Qian Lu Zuge Yang Tianle Li Xin Tong Hongxu Yang Mian Zhang Helin Wang Yazhou Wang Shibin Yu 《Journal of bone and mineral research》2022,37(5):1044-1055
Temporomandibular joint osteoarthritis (TMJOA) is a chronic degenerative disease for which the underlying mechanism still remains unclear. Compared with apoptosis and autophagy, necroptosis causes greater harm to tissue homeostasis by releasing damage-associated molecular patterns (DAMPs). However, the role of necroptosis and downstream key DAMPs in TMJOA is unknown. Here, rodent models of TMJOA were established by the unilateral anterior crossbite (UAC). Transmission electron microscopy (TEM) and immunohistochemistry of receptor interacting protein kinase 3 (RIPK3)/phosphorylation of mixed lineage kinase domain-like protein (pMLKL) were conducted to evaluate the occurrence of necroptosis in vivo. The therapeutic effects of blocking necroptosis were achieved by intra-articularly injecting RIPK3 or MLKL inhibitors and using RIPK3 or MLKL knockout mice. In vitro necroptosis of condylar chondrocyte was induced by combination of tumor necrosis factor alpha (TNFα), second mitochondria-derived activator of caspases (SMAC) mimetics and carbobenzoxy-valyl-alanyl-aspartyl-[O-methyl]- fluoromethylketone (z-VAD-fmk). The possible DAMPs released by necroptotic chondrocytes were screened by quantitative proteomics and blocked by specific antibody. Translucent cytosol, swollen organelles, and ruptured cell membranes, features of necroptosis, were frequently manifested in chondrocytes at the early stage of condylar cartilage degeneration in TMJOA, which was accompanied by upregulation of RIPK3/pMLKL. Inhibiting or knocking out RIPK3/MLKL significantly prevented cartilage degeneration. DAMPs released by necroptotic condylar chondrocytes, such as syndecan 4 (SDC4) and heat shock protein 90 (HSP90), were verified. Furthermore, blocking the function of SDC4 significantly attenuated the expression of TNFα in cartilage and synovium, and accordingly increased cartilage thickness and reduced synovial inflammation. Thus, the necroptotic vicious cycle of TNFα-SDC4-TNFα contributes to cartilage degeneration and synovitis, and can serve as a potential therapeutic target for treating TMJOA. © 2022 American Society for Bone and Mineral Research (ASBMR). 相似文献
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INTRODUCTIONThemicrotubule-associatedprotein蚲ishyperphos-phorylatedandglycosylatedinAlzheimerdisease(AD),andtheseabnormalmodificationsformedthebasisofprogressivelyretrogradeneurofibrillarydegenerationseeninADbrainandtherebythedementia(1,2).ADab-normallyphosphorylated蚲notonlyismicrotubuleas-semblyincompetent,butalsoinhibitsassemblyanddis-assemblesthepreassembledmicrotubulesinvitro(3).Inthetangle-bearingneuronsinADbrain,thenormalcytoskeletonisdisruptedandreplacedwi… 相似文献
6.
目的探讨心房充血分数(AFF)在评价高血压患者左室舒张功能方面的临床应用价值。方法应用声学定量技术(AQ)对40名高血压患者及40名正常人的AAF值,快充血率峰值(PRFR)进行测定,并兼测了二尖瓣口E峰峰值速度与A峰峰值速度比(EV/AV)。结果高血压患者的AFF值明显高于正常人(P<0·001);而PRFR、EV/AV值明显低于正常人(P<0·001~P<0·05)。且所有受试者的AFF值与EV/AV值、PRFR值分别呈负相关(r=-0·51;r=-0·61)。结论AFF能够客观的反映高血压患者的左室舒张功能变化,对鉴别左室舒张功能异常有一定的诊断意义。 相似文献
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M. Perwaiz Iqbal M. Khalid Ashfaq Sarfaraz K. Niazi M. Mahboobali Khalid N. Khawaja 《Biopharmaceutics & drug disposition》1994,15(2):173-177
Pharmacokinetic parameters of two antifolates, trimethoprim and aditoprim, were studied in buffalo calves. The elimination half-life of aditoprim (6.14 h) was nearly twice as long as that of trimethoprim (3.08 h) and compares well with values observed in heifers. This longer half-life of aditoprim is a result of its much larger distribution volume (four to five times larger) because the clearance of aditoprim was about twice as high as that of trimethoprim. The longer half-life of aditoprim is expected to give a longer duration of in vivo bacteriostatic activity than that of trimethoprim. 相似文献
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M Mian A Azzara' D Benetti L Ruocco A Bertelli F Ambrogi 《International journal of tissue reactions》1987,9(6):459-463
Rhein (R: 1,8-dihydroxy-3-carboxyanthraquinone) is the active metabolite of the drug diacetylrhein (DAR), an anthraquinone molecule which has recently been proposed for the long-term treatment of osteoarthrosis. Its action mechanism in rheumatic pathology has not been fully explained. It is known that DAR, while not inhibiting the formation of prostaglandins, inhibits certain proteolytic enzymes, and acts on phlogistic cells by lysosomal enzymic and superoxide-anion modifications. Moreover DAR modifies phagocytic functions and the motility of cells. This paper is a contribution to the clarification of the last point, namely the effect of rhein on cell motility. It reports that in vitro no effect of R on random migration was found, but instead a double inhibiting effect on chemotaxis (i.e. a low-dosage and a high-dosage effect). Furthermore, R did not modify the inhibition or induce modification of chemotaxis by vinblastine. Finally R cancelled the stimulating effect of ionic potassium. The results thus indicate that R acts on the chemotaxis of the leukocytes with a complex action at different doses. The action mechanism is probably due to a membrane effect, since rhein (R) did not modify the chemotaxis-inhibiting activity of vinblastine but did interfere with the stimulating effect of K+. 相似文献