Objective To evaluate the midterm results of the cementless S‐ROM modular femoral stem used with subtrochanteric transverse shortening osteotomy for the treatment of high hip dislocation secondary to hip pyogenic arthritis. Methods We retrospectively reviewed the data of 49 patients (49 hips) with an average infection quiescent period of 37.4 years who underwent cementless total hip arthroplasty (THA) with simultaneous subtrochanteric transverse shortening osteotomy from July 2008 to June 2012. There were 23 men and 26 women with a mean age of 44.3 years at the time of surgery. The following clinical outcomes were evaluated: the Western Ontario and McMaster Universities Arthritis Index (WOMAC) score, Harris hip score (HSS), modified Merle d'Aubigne‐Postel hip (MAP) score, low back pain visual analog scale score, 12‐item short‐form health survey questionnaire score, limp, and Trendelenburg sign. Radiographic outcomes and complications were also evaluated. Results The mean follow‐up period was 8.7 years (range, 5.5–10 years). No infection recurrence was observed after THA. The average HSS significantly improved from 45.0 to 84.8. The WOMAC score improved from 70.1 ± 3.5 (range, 65–76) to 43.1 ± 13.4 (range, 21–67). The modified MAP score improved from 5.9 ± 1.9 (range, 3–9) to 14.3 ± 2.4 (range, 11–18). The low back pain visual analog scale score, 12‐item short‐form health survey questionnaire score, limp, and Trendelenburg sign also improved significantly. The average limb length discrepancy decreased from 39.6 mm (range, 30–55 mm) to 7.2 mm (range, 0–22 mm). Two patients had temporary sciatic nerve paralysis but recovered within 6 months without any functional defects; one had an intraoperative fracture fixed by cerclage wires. One hip required revision surgery because of femoral stem aseptic loosening. Conclusions The cementless S‐ROM modular femoral stem used with subtrochanteric transverse shortening osteotomy is safe and effective for high hip dislocation secondary to pyogenic arthritis and provides satisfactory midterm results. Significant improvements in clinical function were observed, as were high rates of stable fixation of the cementless implant, restoration of more normal limb lengths, and a low incidence of complications.

Blood-brain barrier (BBB) disruption following ischemic stroke (IS) contributes to hemorrhagic transformation, brain edema, increased neural dysfunction, secondary injury, and mortality. Brain endothelial cells form a para and transcellular barrier to most blood-borne solutes via tight junctions (TJs) and rare transcytotic vesicles. The prevailing view attributes the destruction of TJs to the resulting BBB damage following IS. Recent studies define a stepwise impairment of the transcellular barrier followed by the paracellular barrier which accounts for the BBB leakage in IS. The increased endothelial transcytosis that has been proven to be caveolae-mediated, precedes and is independent of TJs disintegration. Thus, our understanding of post stroke BBB deficits needs to be revised. These recent findings could provide a conceptual basis for the development of alternative treatment strategies. Presently, our concept of how BBB endothelial transcytosis develops is incomplete, and treatment options remain limited. This review summarizes the cellular structure and biological classification of endothelial transcytosis at the BBB and reviews related molecular mechanisms. Meanwhile, relevant transcytosis-targeted therapeutic strategies for IS and research entry points are prospected.

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Background and Purpose: Blood-brain barrier (BBB) disruption following ischemic stroke (IS) contributes to hemorrhagic transformation, brain edema, increased neural dysfunction, secondary injury, and mortality. The prevailing view attributes the destruction of tight junction proteins (TJs) to the resulting BBB damage following IS. However, recent studies define a stepwise impairment of the transcellular barrier followed by the paracellular barrier which accounts for the BBB leakage in IS. The increased endothelial transcytosis that has been proven to be caveolae-mediated, preceding and independent of TJs disintegration. Emerging experimental investigations suggested Storax attenuates BBB damage after stroke. This study aimed to test our hypothesis that Storax inhibits caveolae-mediated transcytosis at BBB after ischemic stroke in rats.Methods: Male Wistar rats (250–300 g) were subjected to transient middle cerebral artery occlusion (t-MCAO). Brain water content and the cerebral infarction size were assessed by brain tissue drying-wet method and 2,3,5-triphenyltetrazolium chloride (TTC) staining. BBB permeability was detected by the leakage of Evans blue and Albumin-Alexa594. The ultrastructure of BBB was examined by transmission electron microscopy (TEM). Cav-1 and Mfsd2a were quantified by western blotting and immunofluorescence staining, AQP4, PDGFR-β, ZO-1 and Occludin were quantified by western blotting.Results: Storax treatment of 0.1 g/kg had no significant effects on brain lesions. Storax treatment of 0.2, 0.4, and 0.8 g/kg led to a significant decrease in infarction size, and the Storax 0.4, 0.8 g/kg groups displayed a significant reduction in brain water content. Storax treatment of 0.8 g/kg showed mild toxic reactions. Thus, 0.4 g/kg Storax was selected as the optimal dose for subsequent studies. Storax significantly inhibited the fluorescent albumin intensity in the brain parenchyma and the number of caveolae in ECs, alongside attenuating the ultrastructural disruption of BBB at 6 h after stroke. Meanwhile, Storax significantly increased the expression of Mfsd2a and PDGFR-β, and decrease the expression of Cav-1 and AQP4, corresponding to the significantly decreased Cav-1 positive cells and increased Mfsd2a positive cells. However, Storax has no significant effects on Evan blue leakage or the expression ZO-1, Occludin.Conclusion: Our experimental findings demonstrate Storax treatment inhibits caveolae-mediated transcytosis at BBB in the focal stroke model of rats. We also speculate that regulation of Cav-1, Mfsd2a, AQP4, and PDGFR-β expressions might be associated with its beneficial pharmacological effect, but remain to define and elucidate in future investigation.