Wyniki leczenia uszkodzenia nerwu strzałkowego na wysokości kolana: doświadczenie oddziału szpitala wo¡skowego

Background and purpose We investigated the management outcome of common peroneal nerve decompression at the knee level between the years 2005 and 2009. Material and methods Thirty consecutive patients with knee-level peroneal nerve injury who underwent decompression surgery and external neurolysis at our institution were evaluated preoperatively and postoperatively by electrophysiological studies and motor examination (Medical Research Council grading). Results Twenty-eight of the cases were male and 2 were female. Mean age was 31.1 for males and 57.5 for females. Physical activity during military training (overstretch/contusion) was the cause of nerve lesion in the majority of the patients (n = 28, 93%). Mean time interval between the diagnosis and the surgery was 5 months. Follow-up time ranged from 3 to 48 months (mean: 14 months). Twenty-nine of 30 (97%) patients recovered totally or near totally in foot/toe dorsiflexion. Conclusions Early decompression and neurolysis of the common peroneal nerve (CPN) at knee level after strenuous physical activity offers excellent functional recovery. Additionally, for knee-level CPN injuries, in order to minimize the postoperative scar, pain and delay in wound healing, we strictly advocate short ‘lazy S-shaped incision’ around the fibular head in supine position unlike the classical extensive opening up to the superior border of the popliteal fossa in prone position.Wstęp i cel pracy Autorzy ocenili wyniki chirurgicznego odbarczenia nerwu strzałkowego wspólnego na wysokości kolana, wykonywanego w latach 2005–2009. Materiał i metody Przedoperacyjnej i pooperacyjnej ocenie klinicznej (w skali Medical Research Council) oraz elektrofizjologicznej poddano 30 kolejnych pacjentów z uszkodzeniem nerwu strzałkowego na wysokości kolana, u których wykonano odbarczenie chirurgiczne z zewnętrzną neurolizą. Wyniki Wśród leczonych było 28 mężczyzn (średnia wieku: 31,1 roku) i dwie kobiety (średnia wieku: 57,5 roku). U zdecydowanej większości pacjentów (n = 28, 93%) przyczyną uszkodzenia nerwu była aktywność fizyczna w czasie szkolenia wojskowego (nadmierne rozciągnięcie/stłuczenie). Średnia czasu od rozpoznania do operacji wyniosła 5 miesięcy. Obserwacja po zabiegu trwała od 3 do 48 miesięcy (średnia: 14 miesięcy). U 29 na 30 chorych (97%) uzyskano pełny lub prawie pełny powrót zgięcia grzbietowego stopy/palców. Wnioski Wczesne chirurgiczne odbarczenie i neuroliza nerwu strzałkowego wspólnego na wysokości kolana w leczeniu urazu powstałego wskutek nadmiernej aktywności fizycznej daje możliwość znakomitej poprawy czynnościowej. Ponadto w przypadku uszkodzeń nerwu strzałkowego wspólnego na wysokości kolana w celu zminimalizowania blizny pooperacyjnej, nasilenia bólu i opóźnienia w gojeniu się rany pooperacyjnej autorzy usilnie zalecają krótkie cięcie w kształcie wydłużonej litery „S” wokół głowy strzałki u chorego w pozycji leżącej na plecach zamiast klasycznego otwarcia aż do górnej granicy dołu podkolanowego w pozycji leżącej na brzuchu

An Ex Vivo Vessel Injury Model to Study Remodeling

Objective: Invasive coronary interventions can fail due to intimal hyperplasia and restenosis. Endothelial cell (EC) seeding to the vessel lumen, accelerating re-endothelialization, or local release of mTOR pathway inhibitors have helped reduce intimal hyperplasia after vessel injury. While animal models are powerful tools, they are complex and expensive, and not always reflective of human physiology. Therefore, we developed an in vitro 3D vascular model validating previous in vivo animal models and utilizing isolated human arteries to study vascular remodeling after injury. Approach: We utilized a bioreactor that enables the control of intramural pressure and shear stress in vessel conduits to investigate the vascular response in both rat and human arteries to intraluminal injury. Results: Culturing rat aorta segments in vitro , we show that vigorous removal of luminal ECs results in vessel injury, causing medial proliferation by Day-4 and neointima formation, with the observation of SCA1 + cells (stem cell antigen-1) in the intima by Day-7, in the absence of flow. Conversely, when endothelial-denuded rat aortae and human umbilical arteries were subjected to arterial shear stress, pre-seeding with human umbilical ECs decreased the number and proliferation of smooth muscle cell (SMC) significantly in the media of both rat and human vessels. Conclusion: Our bioreactor system provides a novel platform for correlating ex vivo findings with vascular outcomes in vivo . The present in vitro human arterial injury model can be helpful in the study of EC-SMC interactions and vascular remodeling, by allowing for the separation of mechanical, cellular, and soluble factors

Mechano-inhibition of endocytosis sensitizes cancer cells to Fas-induced Apoptosis

Abstract The transmembrane death receptor Fas transduces apoptotic signals upon binding its ligand, FasL. Although Fas is highly expressed in cancer cells, insufficient cell surface Fas expression desensitizes cancer cells to Fas-induced apoptosis. Here, we show that the increase in Fas microaggregate formation on the plasma membrane in response to the inhibition of endocytosis sensitizes cancer cells to Fas-induced apoptosis. We used a clinically accessible Rho-kinase inhibitor, fasudil, that reduces endocytosis dynamics by increasing plasma membrane tension. In combination with exogenous soluble FasL (sFasL), fasudil promoted cancer cell apoptosis, but this collaborative effect was substantially weaker in nonmalignant cells. The combination of sFasL and fasudil prevented glioblastoma cell growth in embryonic stem cell-derived brain organoids and induced tumor regression in a xenograft mouse model. Our results demonstrate that sFasL has strong potential for apoptosis-directed cancer therapy when Fas microaggregate formation is augmented by mechano-inhibition of endocytosis

Diagnostic moléculaire des infections neuro-méningées à parechovirus (étude rétrospective sur 5 ans)

PARIS-BIUP (751062107) / SudocSudocFranceF