Correlation between physical activity and adolescent idiopathic scoliosis: a systematic review.

BACKGROUND: The multifactorial aetiology of scoliosis is well known. Physical activity is considered both a treatment and causative factor for idiopathic scoliosis; however, evidence for a causal relationship between physical activity levels and idiopathic scoliosis in adolescents is conflicting. Therefore, we aimed to summarise the current evidence regarding the association between adolescent idiopathic scoliosis and physical activity and further to assess whether the relationship is dose dependent. METHODS: PubMed, Cochrane, Scopus, and Web of Science databases were searched from 1991 to July 2022 using the following main keywords: adolescent idiopathic scoliosis, physical activity, and risk factors, supplemented with manual searches, secondary citations, and reference searches. The quality of the included literature was evaluated using the Scale for Reporting Observational Studies in Enhanced Epidemiology guidelines. RESULTS: Eight studies were included in this review, of which six reported an association between adolescent idiopathic scoliosis and physical activity levels and two reported no association. One British study reported reduced physical function early in life as a new risk factor for scoliosis onset. CONCLUSIONS: Physical activity is strongly associated with adolescent idiopathic scoliosis. Physical activity should be encouraged as it plays an important role in the prevention of adolescent idiopathic scoliosis. Further research is needed to determine the dose-dependent relationship between physical activity and prevention of adolescent idiopathic scoliosis.

Updated findings of skin flap thickness and residual breast tissue after mastectomy for breast cancer: a systematic review of the literature.

BACKGROUND: There is limited evidence on the ideal retention thickness of skin flap in mastectomy. Residual breast tissue (RBT) after mastectomy still represents an unknown risk for local recurrence or new breast cancer lesions. We made this systematic review to identify the optimal flap after mastectomy with minimal complications and better oncological safety. METHODS: A systematic review was performed using MEDLINE search in PubMed, Embase, and Cochrane Library with the search terms relevant to skin flap thickness and residual breast tissue in breast cancer patients undergoing mastectomy. RESULTS: Twenty-one studies were included of which fifteen studies enrolled 3814 patients who received mastectomy, and additional six studies were based on cadavers or breast specimens. Four studies confirmed the presence of the superficial fascial layer (Camper's fascia) which can theoretically be used as an anatomical marker for flap retention during mastectomy. Two other studies confirmed Camper's fascia deficiency to a greater or lesser extent. The flap thickness ranged from 3.8 mm to 23 mm in 2692 patients of 7 studies, which was related to BMI, breast size, and examination modalities. Two retrospective and one prospective studies confirmed flaps exceeding 5 mm could significantly increase postoperative complications. Nine studies including 1122 patients explored the association among flap thickness, RBT, and complications, 3 studies of which confirmed excessive flap thickness could cause a significant increase in RBT, which proved to be a potential risk factor for local recurrence in 3 studies. Flaps beyond 5 mm were also found to significantly increase the chance of local recurrence in 4 studies. CONCLUSION: Camper's fascia can serve as an ideal demarcation between fat and breast tissue based on most current studies. 5 mm thickness of the flap retention in mastectomy is recommended if Camper's fascia is absent or obscure, through which better cosmetic outcomes and less RBT can be achieved.

Extracellular signal-regulated kinase inhibition prevents venous adaptive remodeling via regulation of Eph-B4.

OBJECTIVES: Vein graft adaptation (VGA) is a process that vein as a vascular graft conduits in arterial reconstructive surgery; VGA can lead to postoperative vein graft stenosis (VGS) and complications after coronary artery bypass graft and other peripheral artery bypass surgeries. VGA is characterized by vein graft loss the venous features without exhibiting arterial features; furthermore, the activation of ERK inhibited the maintenance of venous properties of the vein graft. We hypothesized that ERK inhibition can affect vein VGS through regulating the expression of EphB4. METHODS: Rat vein transplantation model was established using wild-type and EphB4+/- Sprague-Dawley rats. Hematoxylin-eosin, Masson, Verhoeff, actin staining, and immunohistochemistry were applied to observe the structure of the vein grafts. Vascular smooth muscle cells (VSMCs) were isolated from the vein and vein grafts. Western blotting was used to determine the expression of p-ERK1/2 and EphB4, and immunofluorescence was applied to detect the expression and location of EphB4. Cell wound scratch assay and CCK8 assay were used to determine the migration and proliferation of VSMCs. Real-time polymerase chain reaction was used to determine the mRNA expression of EphB4. RESULTS: Western blotting in vein sample and vein graft sample detected p-ERK1/2 and ERK1/2 expression in both EphB4+/+ and EphB4+/- rats. The expression of p-ERK was increased in vein graft compared to vein. Immunofluorescence in VSMCs form EphB4+/+ and EphB4+/- rats detected EphB4 expression in both cells, and the expression of EphB4 was increased in VSMCs form EphB4+/+ rats. SCH772984 reduces the proliferation and migration of VSMCs. Inhibition of ERK suppressed the increase of vein graft wall thickness, and the expression of collagen fibers, elastic fibers, and α-actin was decreased. Vein graft from EphB4+/- rats reduces the expression of EphB4, and SCH772984 suppressed the decrease of EphB4 in vivo. Vein graft from EphB4+/- rats increased the expression of EphB4, and SCH772984 suppressed the increase of EphB4 in vivo. CONCLUSIONS: The inhibition of ERK1/2 suppressed the process of VGS by decreasing the proliferation of VSMCs. The ERK-inhibitor SCH772984 suppressed the level of VGS by extending the time of EphB4 expression during the process of VGA, thus maintaining the venousization of vein graft. The mechanism may be that the inhibitor SCH772984 suppresses the level of VGS by extending the time of EphB4 expression during the process of VGA. Therefore, our research provides a new target of VGS treatment by inhibiting the expression of ERK1/2 through the process of VGA.

WITHDRAWN: Endovascular Repair with Stent-Graft of Symptomatic Tuberculous Aortic Pseudoaneurysm

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