IntroductionAmong all barriers to breastfeeding, the need to work has been cited as one of the top reasons for not breastfeeding overall and for early weaning among mothers who seek to breastfeed. We aimed to examine whether extending the duration of paid maternity leave available to new mothers affected early initiation of breastfeeding, exclusive breastfeeding under 6  months and breastfeeding duration in low-income and middle-income countries (LMICs).MethodsWe merged longitudinal data measuring national maternity leave policies with information on breastfeeding related to 992 419 live births occurring between 1996 and 2014 in 38 LMICs that participated in the Demographic and Health Surveys. We used a difference-in-differences approach to compare changes in the prevalence of early initiation and exclusive breastfeeding, as well as the duration of breastfeeding, among treated countries that lengthened their paid maternity leave policy between 1995 and 2013 versus control countries that did not. Regression models included country and year fixed effects, as well as measured individual-level, household-level and country-level covariates. All models incorporated robust SEs and respondent-level sampling weights.ResultsA 1-month increase in the legislated duration of paid maternity leave was associated with a 7.4 percentage point increase (95%  CI 3.2 to 11.7) in the prevalence of early initiation of breastfeeding, a 5.9 percentage point increase (95%  CI 2.0 to 9.8) in the prevalence of exclusive breastfeeding and a 2.2- month increase (95%  CI 1.1 to 3.4) in breastfeeding duration.ConclusionExtending the duration of legislated paid maternity leave appears to promote breastfeeding practices in LMICs. Our findings suggest a potential mechanism to reduce barriers to breastfeeding for working mothers.

BackgroundShenmai injection (SM), as a traditional Chinese medicine injection, is widely used for chronic cor pulmonale heart failure in mainland China. It is essential to systematically assess the efficacy and safety of SM as an adjuvant treatment for chronic cor pulmonale heart failure.MethodsEight English and Chinese electronic databases were searched, from inception to December 2014, to identify randomized controlled trials (RCTs) of SM for chronic cor pulmonale heart failure. The Cochrane Risk of Bias tool was used to evaluate the methodological quality of eligible studies. Meta-analysis was performed by Review Manager 5.2.ResultsTwenty-seven RCTs with 2045 participants were identified. The methodological quality of the included studies was generally low. Only one trial reported data on death. None of the included trials reported quality of life. The meta-analysis indicated that compared to conventional treatment, the combination of SM and conventional treatment was more effective in terms of the New York Heart Association classification (RR, 1.26; 95 % CI, 1.20–1.32; P < 0.00001), Left Ventricular Ejection Fraction (MD, 11.33; 95 % CI, 8.59–14.07; p < 0.00001), partial pressure of oxygen (MD, 1.00; 95 % CI, 0.64–1.36; P < 0.00001) and partial pressure of carbon dioxide (MD, 0.83; 95 % CI, 0.58–1.08; p < 0.00001). In addition, two trials reported that SM plus conventional treatment was superior to the conventional treatment alone to reduce B-type natriuretic peptide. No serious adverse drug events or reactions were reported.ConclusionsSM plus conventional treatment appeared to be effective and relatively safe for chronic cor pulmonale heart failure. However, due to the generally low methodological quality and small sample size, this review didn’t find evidence to support routine use of SM as an adjuvant treatment for chronic cor pulmonale heart failure.Electronic supplementary materialThe online version of this article (doi:10.1186/s12906-015-0939-2) contains supplementary material, which is available to authorized users.

This systematic review was performed to determine the clinical efficacy and safety of total flavonoids from Rhizoma Drynariae (TFRD) for osteoporotic fractures and to provide clear evidence for clinical practice. Eight databases were searched to identify relevant randomized controlled trials (RCTs) until December 2016. Six RCTs involving 846 patients were included. The primary outcomes included fracture recurrence and death. Meta-analysis showed that both the combination therapy and TFRD alone were better than conventional treatments in improving bone mineral density (BMD) value (weighted mean difference [WMD] =3.68, 95% confidence interval [CI]: 0.01 to 0.04, P=0.0002), (WMD =0.14; 95% CI: 0.11 to 0.16; P<0.00001), respectively, and enhancing therapeutic effect (OR =0.25; 95% CI: 0.12 to 0.51; P=0.0002). Thirty-three patients experienced adverse drug reactions (ADRs), none of the ADRs were severe and all were resolved after symptomatic treatments. Gastrointestinal symptoms were the most common ADRs in the usage of TFRD. Overall, the effect of TFRD on osteoporotic fractures was supported by improving BMD and therapeutic effect. Due to the methodological drawbacks of the included studies, the conclusions should be treated with caution for future research. Registration number: CRD42017052797.

As a therapy for AB, TRQ has potentially beneficial effect in improving effective rates, reducing the time to resolution of fever, cough, crackles and absorption of shadows on X-ray. However, due to the limitations of methodological quality of the included trials, it is difficult to make a conclusive recommendation about TRQ treating patients with AB. Further rigorous clinical trials are warranted to evaluate the efficacy and safety of TRQ.

Neuronal death and inflammatory response are two common pathological hallmarks of acute central nervous system injury and chronic degenerative disorders, both of which are closely related to cognitive and motor dysfunction associated with various neurological diseases. Neurological diseases are highly heterogeneous; however, they share a common pathogenesis, that is, the aberrant accumulation of misfolded/unfolded proteins within the endoplasmic reticulum (ER). Fortunately, the cell has intrinsic quality control mechanisms to maintain the proteostasis network, such as chaperone-mediated folding and ER-associated degradation. However, when these control mechanisms fail, misfolded/unfolded proteins accumulate in the ER lumen and contribute to ER stress. ER stress has been implicated in nearly all neurological diseases. ER stress initiates the unfolded protein response to restore proteostasis, and if the damage is irreversible, it elicits intracellular cascades of death and inflammation. With the growing appreciation of a functional association between ER stress and neurological diseases and with the improved understanding of the multiple underlying molecular mechanisms, pharmacological and genetic targeting of ER stress are beginning to emerge as therapeutic approaches for neurological diseases.

The aim of this meta-analysis was to evaluate the efficacy of Tai chi (TC) as an adjuvant treatment for osteopenia and primary osteoporosis. Methods: We went through eight databases to identify relevant randomized controlled trials that compared TC with a control group. The primary outcome was osteoporosis-related fractures (fracture incidence). Meta-analyses and trial sequential analyses (TSA) were conducted using RevMan 5.3 and TSA 0.9. Results: Fifteen randomized controlled trials involving a total of 857 patients were included in the analyses. No trials reported primary outcome; however, bone mineral density (BMD) values differed significantly in subgroup 1 (TC vs no treatment; weighted mean difference [WMD] =0.05 g/cm 2 , 95% CI 0.03 to 0.07; P,0.00001; P for heterogeneity =0.22, I 2 =22%) and subgroup 2 (TC vs conventional treatments; WMD =0.16 g/cm 2 , 95% CI 0.11 to 0.21; P,0.00001; P for heterogeneity =0.008, I 2 =75%). In addition, two trials compared TC with conventional treatments, which found a significant difference in bone gla protein (standardized mean difference =-1.18, 95% CI-1.66 to-0.70; P,0.00001; P for heterogeneity =0.58, I 2 =75%). The results of the BMD were confirmed by TSA. Also, TC may have a certain effect on the relief of osteoporotic pain (WMD =-2.61, 95% CI-3.51 to-1.71; WMD =-1.39, 95% CI-2.01 to-0.77). However, it did not promote the quality of life, level of serum calcium, serum phosphorus, and also had no effect on bone turnover markers. Conclusion: Although there is no study monitoring fracture incidence, TC may be beneficial for patients in improving BMD values, level of bone gla protein, and relieving osteoporotic pain. However, due to the low methodological quality, current evidence for treating osteopenia and primary osteoporosis through TC is insufficient.

Traumatic brain injury (TBI) is one of the leading causes of trauma-induced mortality and disability, and emerging studies have shown that endoplasmic reticulum (ER) stress plays an important role in the pathophysiology of TBI. Tauroursodeoxycholic acid (TUDCA), a hydrophilic bile acid, has been reported to act as an ER stress inhibitor and chemical chaperone and to have the potential to attenuate apoptosis and inflammation. To study the effects of TUDCA on brain injury, we subjected mice to TBI with a controlled cortical impact (CCI) device. Using western blotting, we first examined TBI-induced changes in the expression levels of GRP78, an ER stress marker, p-PERK, PERK, p-eIF2a, eIF2a, ATF4, p-Akt, Akt, Pten, Bax, Bcl-2, Caspase-12 and CHOP, as well as changes in the mRNA levels of Akt, GRP78, Caspase-12 and CHOP using RT-PCR. Neuronal cell death was assessed by a terminal deoxynucleotidyl transferase (TdT)-mediated dUTP nick end-labeling (TUNEL) assay, and CHOP expression in neuronal cells was detected by double-immunofluorescence staining. Neurological and motor deficits were assessed by modified neurological severity scores (mNSS) and beam balance and beam walking tests, and brain water content was also assessed. Our results indicated that ER stress peaked at 72 h after TBI and that TUDCA abolished ER stress and inhibited p-PERK, p-eIF2a, ATF4, Pten, Caspase-12 and CHOP expression levels. Moreover, our results show that TUDCA also improved neurological function and alleviated brain oedema. Additionally, TUDCA increased p-Akt expression and the Bcl-2/Bax ratio. However, the administration of the Akt inhibitor MK2206 or siRNA targeting of Akt abolished the beneficial effects of TUDCA. Taken together, our results indicate that TUDCA may attenuate early brain injury via Akt pathway activation.

IntroductionThe spectrum of critical illness-related corticosteroid insufficiency (CIRCI) in severe traumatic brain injury (TBI) is not fully defined and no effective treatments for TBI-induced CIRCI are available to date. Despite growing interest in the use of stress-dose hydrocortisone as a potential therapy for CIRCI, there remains a paucity of data regarding its benefits following severe TBI. This study was designed to investigate the effects of stress-dose hydrocortisone on CIRCI development and neurological outcomes in a rat model of severe traumatic brain injury.MethodsRats were subjected to lateral fluid percussion injury of 3.2-3.5 atmosphere. These rats were then treated with either a stress-dose hydrocortisone (HC, 3 mg/kg/d for 5 days, 1.5 mg/kg on day 6, and 0.75 mg on day 7), a low-dose methylprednisolone (MP, 1 mg/kg/d for 5 days, 0.5 mg/kg on day 6, and 0.25 mg on day 7) or control saline solution intraperitoneally daily for 7 days after injury.ResultsWe investigated the effects of stress-dose HC on the mortality, CIRCI occurrence, and neurological deficits using an electrical stimulation test to assess corticosteroid response and modified neurological severity score (mNSS). We also studied pathological changes in the hypothalamus, especially in the paraventricular nuclei (PVN), after stress-dose HC or a low dose of MP was administered, including apoptosis detected by a TUNEL assay, blood–brain barrier (BBB) permeability assessed by brain water content and Evans Blue extravasation into the cerebral parenchyma, and BBB integrity evaluated by CD31 and claudin-5 expression. We made the following observations. First, 70% injured rats developed CIRCI, with a peak incidence on post-injury day 7. The TBI-associated CIRCI was closely correlated with an increased mortality and delayed neurological recovery. Second, post-injury administration of stress-dose HC, but not MP or saline increased corticosteroid response, prevented CIRCI, reduced mortality, and improved neurological function during the first 14 days post injury dosing. Thirdly, these beneficial effects were closely related to improved vascular function by the preservation of tight junctions in surviving endothelial cells, and reduced neural apoptosis in the PVN of hypothalamus.ConclusionsOur findings indicate that post-injury administration of stress-dose HC, but not MP reduces CIRCI and improves neurological recovery. These improvements are associated with reducing the damage to the tight junction of vascular endothelial cells and blocking neuronal apoptosis in the PVN of the hypothalamus.