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Aims

The aim of this study was to evaluate the effectiveness of a Pilates exercise program with pelvic floor muscle (PFM) contraction compared to a conventional intervention in pregnant women.

Methods

Fifty primiparous women, without gestational alterations, were randomized to the Pilates group (n = 25) and control group (n = 25). Interventions for both groups consisted of twice‐weekly sessions of 1 h each during the period between the 14‐16th and 32‐34th gestational weeks. The Pilates group performed a Pilates exercises program with the addition of voluntary PFM contraction. Mat‐based Pilates exercises were performed involving movement of the upper limbs, lower limbs and trunk in all sessions. The Control group walked for 10 min and performed strengthening exercises of the lower limbs, upper limbs, and trunk with resistance from an elastic band and body weight. Each woman was evaluated by an unblinded physiotherapist before and after intervention for primary (PFM strength using a manometer) and secondary (PFM strength using Oxford Scale, endurance and repeatability) outcomes. Covariance analysis (ANCOVA) was used to compare the groups using the baseline values as a covariate.

Results

Thirty‐six women were included in the analysis. There were no differences between the groups for manometry. An increase in the PFM strength, endurance, and repeatability was only observed in the Pilates group. In addition, the Pilates group showed greater adherence to the intervention.

Conclusion

Pilates exercise program with PFM contraction is not able to change the PFM strength assessed by manometer in pregnant women, but it improved adherence to the intervention.  相似文献   
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A new series of glucosides modified in their saccharide units were synthesized, evaluated against Candida sp., and compared to prototype 1 , an eugenol tetracetyl glucoside previously synthesized and shown to be active against Candida glabrata. Among the new glucosides, benzyl derivative 5 was the most promising, showing fungistatic activity at IC50 18.1  μ m against Candida glabrata (threefold higher than fluconazole) and fungicidal activity with a low IC90 value of 36.2 μm . Moreover, the cytotoxic activity of compound 5 (CC50: 580.9  μ m ), tested in peripheral blood mononuclear cells, suggests its potential as an agent to treat Candida glabrata infections, with a selectivity index of 32. The new eugenol glucoside 5 may be considered as a novel structural pattern in the development of new anti‐Candida drugs.  相似文献   
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Objective

To investigate the potential association of major histocompatibility complex (MHC) markers other than HLA–B27 with ankylosing spondylitis (AS).

Methods

A total of 603 patients with AS and 542 healthy control subjects, all of whom were HLA–B27 positive, were selected for this study based on clinical criteria. First, high‐density genotyping across the MHC region (2,360 single‐nucleotide polymorphisms [SNPs]) was performed in a cohort of 191 patients and 241 control subjects. After a fine‐mapping study, 5 SNPs from the HLA–DPA1/DPB1 region were validated in a second cohort of 412 patients with AS and 301 healthy control subjects.

Results

Seventeen SNPs located within or near the HLA–DPA1 and HLA–DPB1 loci showed association with AS (P = 1.38 × 10−5 to 0.05). In addition, multimarker tests, both linkage disequilibrium and sliding windows, showed association of some groups of adjacent SNPs within the HLA–DPA1/DPB1 region with AS (P = 1.0 × 10−4 to 3.96 × 10−7). We validated the association by genotyping 5 SNPs from the DPA1/DPB1 region in an additional cohort and obtained P values from 6.42 × 10−5 to 0.01 in the analysis of the combined cohorts. Subtyping analysis of HLA–DPA1 and HLA–DPB1 showed that HLA–DPA1*01:03, A1*02:01, and B1*13:01 were the subtypes most susceptible to AS.

Conclusion

HLA markers and linkage disequilibrium blocks near HLA–DPA1 and HLA–DPB1 are statistically associated with AS. We identified a region located around the HLA–DPA1 and HLA–DPB1 loci associated with AS, another region within the MHC that is different from HLA–B27.
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