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Purpose: The purpose of this study is to retrospect and summarize clinical efficiency and experience of the free superficial palmar branch of radial artery (SPBRA) flap for soft-tissue reconstruction in distal digital injury. Method: 13 patients with soft-tissue defect of finger, reconstructed by the free superficial palmar branch of radial artery (SPBRA) flap in our department from January 2020 to January 2022, were reviewed. After 6–12 months of follow-up, evaluated the treatment effect of the fingers reconstructed by SPBRA flap. Results: All the flaps in our series application were survival uneventful, and all the donor sites were closed primarily without complications or obvious scarring. The flaps were soft in texture and satisfactory in appearance and function. The flaps with the median nerve palmar cutaneous branch had a good sensation recovery. Measurement of two-point discrimination (TPD) ranged from 6 to 10 mm. All patients were satisfied with the aesthetic appearance. According to the Evaluation Trial Standards of Upper Limb Partial Function of Hand Surgery of Chinese Medical Association, the results were graded as excellent in 11 cases and good in 2 cases. Conclusion: The SPBRA perforator flap has the advantages of simple operation, soft texture, good appearance and function, and is credible and useful for reconstructing various finger injuries. [ABSTRACT FROM AUTHOR]

Background: Composition of the vaginal microbiome is strongly related to a woman's reproductive health and risk of sexually transmitted infections. Ethnoracial, behavioral, and environmental factors can influence microbiome. The Brazilian population is unique in terms of miscegenation of ethnic groups and behavioral characteristics across different regions. We aimed to characterize the vaginal microbiome of women from 5 geographical regions of Brazil.Methods: We sequenced V3-V4 regions of 16S rRNA gene in vaginal samples of 609 reproductive-aged women. We performed logistic regression analyses to estimate odds ratios (OR) and 95% confidence intervals (CI) for the association between sociodemographic and behavioral factors with Lactobacillus-depleted microbiome (community state type [CST] IV).Results: Vaginal samples were grouped into 5 CST: CST I (L. crispatus predominant, 30.5%), CST II (L. gasseri predominant, 4.4%), CST III (Lactobacillus iners predominant, 36.5%), CST IV (Lactobacillus-depleted, 27.4%), and CST V (L. jensenii predominant, 1.2%). Several factors were independently associated with CST IV, such as smoking (OR, 1.80; 95% CI, 1.02-3.18), number of partners (OR, 2.11; 95% CI, 1.20-3.70), and vaginal douching (OR, 2.24; 95% CI, 1.34-3.74). A protective effect was observed for milk/dairy intake (OR, 0.47; 95% CI, 0.27-0.82) and sitz bathing (OR, 0.43; 95% CI, 0.19-0.98).Conclusions: Nearly two thirds of Brazilian women may be at an increased risk for adverse outcomes associated with a vaginal microbiota characterized by the depletion of Lactobacillus or dominance by L. iners, whose protective role has been widely questioned. Several factors related to sexual behavior and intimate hygiene were associated with CST IV. [ABSTRACT FROM AUTHOR]

Background: Femoral neck fractures are one of the problems in clinical treatment. The prognosis is uncertain. Currently, No internal fixation method is superior to other internal fixation methods in the treatment of femoral neck fractures. Therefore, the internal fixation system needs to be further explored. The aim of this study was to compare clinical outcomes of femoral neck dynamic compression locking system (DCLS) and multiple cannulated compression screws(MCCS) in the treatment of femoral neck fractures.Methods: A prospective analysis of 54 cases of femoral neck fractures treated with either a DCLS (n = 28) or MCCS (n = 26) was conducted between December 2015 and November 2017 in authors' hospitals. The perioperative and postoperative parameters of the two groups were recorded and evaluated.Results: Fifty-four patients were followed up for 24-47 months. The etiology was caused by a fall. There was no significant difference in follow-up time, operation time, incision length, surgical blood loss, the incidence of perioperative and postoperative healing complications, and mobility in the two groups (all P > 0.05). The Harris score, fracture healing time, femoral neck shortening, partial weight-bearing time and complete weight-bearing time were significantly better in the DCLS group than in the MCCS group (all P < 0.05). The fracture healing rate in the DCLS group was higher than that in the MCCS group.Conclusions: The DCLS and MCCS might be equally effective in terms of operation time, incision length, surgical blood loss, the incidence of perioperative and postoperative healing complications, and mobility in the treatment of femoral neck fractures. However, the DCLS is superior to the MCCS in Harris score, fracture healing time, femoral neck shortening, weight-bearing time and fracture healing rate. So, DCLS deserves further study. [ABSTRACT FROM AUTHOR]

IL-13 dysregulation plays a critical role in the pathogenesis of a variety of inflammatory and remodeling diseases. In these settings, STAT6 is believed to be the canonical signaling molecule mediating the tissue effects of IL-13. Signaling cascades involving MAPKs have been linked to inflammation and remodeling. We hypothesized that MAPKs play critical roles in effector responses induced by IL-13 in the lung. We found that Tg IL-13 expression in the lung led to potent activation of ERK1/2 but not JNK1/2 or p38. ERK1/2 activation also occurred in mice with null mutations of STAT6. Systemic administration of the MAPK/ERK kinase 1 (MEK1) inhibitor PD98059 or use of Tg mice in which a dominant-negative MEK1 construct was expressed inhibited IL-13-induced inflammation and alveolar remodeling. There were associated decreases in IL-13-induced chemokines (MIP-1alpha/CCL-3, MIP-1beta/CCL-4, MIP-2/CXCL-1, RANTES/CCL-5), MMP-2, -9, -12, and -14, and cathepsin B and increased levels of alpha1-antitrypsin. IL-13-induced tissue and molecular responses were noted that were equally and differentially dependent on ERK1/2 and STAT6 signaling. Thus, ERK1/2 is activated by IL-13 in the lung in a STAT6-independent manner where it contributes to IL-13-induced inflammation and remodeling and is required for optimal IL-13 stimulation of specific chemokines and proteases as well as the inhibition of specific antiproteases. ERK1/2 regulators may be useful in the treatment of IL-13-induced diseases and disorders. [ABSTRACT FROM AUTHOR]

Hyperoxic acute lung injury (HALI) is characterized by a cell death response with features of apoptosis and necrosis that is inhibited by IL-11 and other interventions. We hypothesized that Bfl-1/A1, an antiapoptotic Bcl-2 protein, is a critical regulator of HALI and a mediator of IL-11-induced cytoprotection. To test this, we characterized the expression of A1 and the oxygen susceptibility of WT and IL-11 Tg(+) mice with normal and null A1 loci. In WT mice, 100% O(2) caused TUNEL(+) cell death, induction and activation of intrinsic and mitochondrial-death pathways, and alveolar protein leak. Bcl-2 and Bcl-xl were also induced as an apparent protective response. A1 was induced in hyperoxia, and in A1-null mice, the toxic effects of hyperoxia were exaggerated, Bcl-2 and Bcl-xl were not induced, and premature death was seen. In contrast, IL-11 stimulated A1, diminished the toxic effects of hyperoxia, stimulated Bcl-2 and Bcl-xl, and enhanced murine survival in 100% O(2). In A1-null mice, IL-11-induced protection, survival advantage, and Bcl-2 and Bcl-xl induction were significantly decreased. VEGF also conferred protection via an A1-dependent mechanism. In vitro hyperoxia also stimulated A1, and A1 overexpression inhibited oxidant-induced epithelial cell apoptosis and necrosis. A1 is an important regulator of oxidant-induced lung injury, apoptosis, necrosis, and Bcl-2 and Bcl-xl gene expression and a critical mediator of IL-11- and VEGF-induced cytoprotection. [ABSTRACT FROM AUTHOR]

IL-13 potently stimulates eosinophilic and lymphocytic inflammation and alveolar remodeling in the lung, effects that depend on the induction of various matrix metalloproteinases (MMPs). Here, we compared the remodeling and inflammatory effects of an IL-13 transgene in lungs of wild-type, MMP-9-deficient, or MMP-12-deficient mice. IL-13-induced alveolar enlargement, lung enlargement, compliance alterations, and respiratory failure and death were markedly decreased in the absence of MMP-9 or MMP-12. Moreover, IL-13 potently induced MMPs-2, -12, -13, and -14 in the absence of MMP-9, while induction of MMPs-2, -9, -13, and -14 by IL-13 was diminished in the absence of MMP-12. A deficiency in MMP-9 did not alter eosinophil, macrophage, or lymphocyte recovery, but increased the recovery of total leukocytes and neutrophils in bronchoalveolar lavage (BAL) fluids from IL-13 transgenic mice. In contrast, a deficiency in MMP-12 decreased the recovery of leukocytes, eosinophils, and macrophages, but not lymphocytes or neutrophils. These studies demonstrate that IL-13 acts via MMPs-9 and -12 to induce alveolar remodeling, respiratory failure, and death and that IL-13 induction of MMPs-2, -9, -13, and -14 is mediated at least partially by an MMP-12-dependent pathway. The also demonstrate that MMPs-9 and -12 play different roles in the generation of IL-13-induced inflammation, with MMP-9 inhibiting neutrophil accumulation and MMP-12 contributing to the accumulation of eosinophils and macrophages. [ABSTRACT FROM AUTHOR]