Potential roles of the interactions between gut microbiota and metabolites in LPS-induced intrauterine inflammation (IUI) and associated preterm birth (PTB).

BACKGROUND: Prenatal exposure to intrauterine inflammation (IUI) is a crucial event in preterm birth (PTB) pathophysiology, increasing the incidence of neurodevelopmental disorders. Gut microbiota and metabolite profile alterations have been reported to be involved in PTB pathophysiology. METHOD AND RESULTS: In this study, IUI-exposed PTB mouse model was established and verified by PTB rate and other perinatal adverse reactions; LPS-indued IUI significantly increased the rates of PTB, apoptosis and inflammation in placenta tissue samples. LPS-induced IUI caused no significant differences in species richness and evenness but significantly altered the species abundance distribution. Non-targeted metabolomics analysis indicated that the metabolite profile of the preterm mice was altered, and differential metabolites were associated with signaling pathways including pyruvate metabolism. Furthermore, a significant positive correlation between Parasutterella excrementihominis and S4572761 (Nb-p-coumaroyltryptamine) and Mreference-1264 (pyruvic acid), respectively, was observed. Lastly, pyruvic acid treatment partially improved LPS-induced IUI phenotypes and decreased PTB rates and decreased the apoptosis and inflammation in placenta tissue samples. CONCLUSION: This study revealed an association among gut microbiota dysbiosis, metabolite profile alterations, and LPS-induced IUI and PTB in mice models. Our investigation revealed the possible involvement of gut microbiota in the pathophysiology of LPS-induced IUI and PTB, which might be mediated by metabolites such as pyruvic acid. Future studies should be conducted to verify the findings through larger sample-sized animal studies and clinical investigations.

TRIOBP modulates ß-catenin signaling by regulation of miR-29b in idiopathic pulmonary fibrosis.

Idiopathic pulmonary fibrosis (IPF) is a fatal and devastating lung disease of unknown etiology, described as the result of multiple cycles of epithelial cell injury and fibroblast activation. Despite this impressive increase in understanding, a therapy that reverses this form of fibrosis remains elusive. In our previous study, we found that miR-29b has a therapeutic effect on pulmonary fibrosis. However, its anti-fibrotic mechanism is not yet clear. Recently, our study identified that F-Actin Binding Protein (TRIOBP) is one of the target genes of miR-29b and found that deficiency of TRIOBP increases resistance to lung fibrosis in vivo. TRIOBP knockdown inhibited the proliferation of epithelial cells and attenuated the activation of fibroblasts. In addition, deficiency of Trio Rho Guanine Nucleotide Exchange Factor (TRIO) in epithelial cells and fibroblasts decreases susceptibility to lung fibrosis. TRIOBP interacting with TRIO promoted abnormal epithelial-mesenchymal crosstalk and modulated the nucleocytoplasmic translocation of ß-catenin. We concluded that the miR-29b‒TRIOBP-TRIO-ß-catenin axis might be a key anti-fibrotic axis in IPF to regulate lung regeneration and fibrosis, which may provide a promising treatment strategy for lung fibrosis.

[Mechanism of salidroside in inhibiting proliferation, migration and promoting phenotypic switching of arterial smooth muscle cells].

This study aims to examine the effect of salidroside(SAL) on the phenotypic switching of human aortic smooth muscle cells(HASMC) induced by the platelet-derived growth factor-BB(PDGF-BB) and investigate the pharmacological mechanism. Firstly, the safe concentration of SAL was screened by the lactate dehydrogenase release assay. HASMC were divided into control, model, and SAL groups, and the cells in other groups except the control group were treated with PDGF-BB for the modeling of phenotypic switching. Cell proliferation and migration were detected by the cell-counting kit(CCK-8) assay and Transwell assay, respectively. The cytoskeletal structure was observed by F-actin staining with fluorescently labeled phalloidine. The protein levels of proliferating cell nuclear antigen(PCNA), migration-related protein matrix metalloprotein 9(MMP-9), fibronectin, α-smooth muscle actin(α-SMA), and osteopontin(OPN) were determined by Western blot. To further investigate the pharmacological mechanism of SAL, this study determined the expression of protein kinase B(Akt) and mammalian target of rapamycin(mTOR), as well as the upstream proteins phosphatase and tensin homologue(PTEN) and platelet-derived growth factor receptor ß(PDGFR-ß) and the downstream protein hypoxia-inducible factor-1α(HIF-1α) of the Akt/mTOR signaling pathway. The results showed that the HASMCs in the model group presented significantly increased proliferation and migration, the switching from a contractile phenotype to a secretory phenotype, and cytoskeletal disarrangement. Compared with the model group, SAL weakened the proliferation and migration of HASMC, promoted the expression of α-SMA(a contractile phenotype marker), inhibited the expression of OPN(a secretory phenotype marker), and repaired the cytoskeletal disarrangement. Furthermore, compared with the control group, the modeling up-regulated the levels of phosphorylated Akt and mTOR and the relative expression of PTEN, HIF-1α, and PDGFR-ß. Compared with the model group, SAL down-regulated the protein levels of phosphorylated Akt and mTOR, PTEN, PDGFR-ß, and HIF-1α. In conclusion, SAL exerts a protective effect on the HASMCs exposed to PDGF-BB by regulating the PDGFR-ß/Akt/mTOR/HIF-1α signaling pathway.

Customizing Bonding Affinity with Multi-Intermediates via Interfacial Electron Capture to Boost Hydrogen Evolution in Alkaline Water Electrolysis.

Developing efficient and earth-abundant alkaline HER electrocatalysts is pivotal for sustainable energy, but co-regulating its intricate multi-step process, encompassing water dissociation, OH- desorption, and hydrogen generation, is still a great challenge. Herein, we tackle these obstacles by fabricating a vertically integrated electrode featuring a nanosheet array with prominent dual-nitride metallic heterostructures characterized by impeccable lattice matching and excellent conductivity, functioning as a multi-purpose catalyst to fine-tune the bonding affinity  with alkaline HER intermediates. Detailed structural characterization and theoretical calculation elucidate that charge redistribution at the heterointerface creates electron-accumulating W-W sites, which reduces the O p-W d and H s-W d interactions vs. single nitride, thereby enhancing OH- transfer and H2 release. As anticipated, the resulting WN-NiN/CFP catalyst demonstrates a gratifying low overpotential of 36.8 mV at 10 mA/cm² for alkaline HER, while concurrently maintaining operational stability for 1300 h at 100 mA/cm² for overall water splitting. This work presents an effective approach to meticulously optimize multiple site-intermediate interactions in alkaline HER, laying the foundation for efficient energy conversion.

ELMO1 Deficiency Reduces Neutrophil Chemotaxis in Murine Peritonitis.

Peritoneal inflammation remains a major cause of treatment failure in patients with kidney failure who receive peritoneal dialysis. Peritoneal inflammation is characterized by an increase in neutrophil infiltration. However, the molecular mechanisms that control neutrophil recruitment in peritonitis are not fully understood. ELMO and DOCK proteins form complexes which function as guanine nucleotide exchange factors to activate the small GTPase Rac to regulate F-actin dynamics during chemotaxis. In the current study, we found that deletion of the Elmo1 gene causes defects in chemotaxis and the adhesion of neutrophils. ELMO1 plays a role in the fMLP-induced activation of Rac1 in parallel with the PI3K and mTORC2 signaling pathways. Importantly, we also reveal that peritoneal inflammation is alleviated in Elmo1 knockout mice in the mouse model of thioglycollate-induced peritonitis. Our results suggest that ELMO1 functions as an evolutionarily conserved regulator for the activation of Rac to control the chemotaxis of neutrophils both in vitro and in vivo. Our results suggest that the targeted inhibition of ELMO1 may pave the way for the design of novel anti-inflammatory therapies for peritonitis.

Experimental measurement of electro-chemo-mechanical properties of a composite silicon electrode in lithium ion batteries.

The applications of silicon (Si)-based electrodes in lithium ion batteries have been impeded by mechanical degradation caused by lithiation/delithiation-induced volume changes. Understanding the evolution of mechanical behavior and properties of Si composite electrodes during electrochemical cycling is indispensable to develop coping strategies and predict battery life. In this study, we optimized an in situ method for measuring electro-chemo-mechanical properties, including partial molar volume, elastic modulus, and electrochemical reaction-induced stress, based on the curvature changes of cantilever electrodes. We found that the swell strain and partial molar volume of Si electrodes increase with the Li concentration. The elastic modulus generally decreases with the Li concentration. The in-plain stress transforms from tensile stress to compressive stress and showed an increasing tendency during further lithiation, while it shows a reverse trend during delithiation. The stress evolution correlates well with the "opening" and "closing" of micro-cracks in Si composite electrodes during cycling. These findings provide not only input parameters for battery modeling but also help understand the capacity fading of Si electrodes. Furthermore, the in situ measurement methodology developed in this study is readily applied to other battery electrodes.

Dual Role of Mitophagy in Cardiovascular Diseases.

ABSTRACT: Mitophagy is involved in the development of various cardiovascular diseases, such as atherosclerosis, heart failure, myocardial ischemia/reperfusion injury, and hypertension. Mitophagy is essential for maintaining intracellular homeostasis and physiological function in most cardiovascular origin cells, such as cardiomyocytes, endothelial cells, and vascular smooth muscle cells. Mitophagy is crucial to ensuring energy supply by selectively removing dysfunctional mitochondria, maintaining a balance in the number of mitochondria in cells, ensuring the integrity of mitochondrial structure and function, maintaining homeostasis, and promoting cell survival. Substantial research has indicated a "dual" effect of mitophagy on cardiac function, with inadequate and increased mitochondrial degradation both likely to influence the progression of cardiovascular disease. This review summarizes the main regulatory pathways of mitophagy and emphasizes that an appropriate amount of mitophagy can prevent endothelial cell injury, vascular smooth muscle cell proliferation, macrophage polarization, and cardiomyocyte apoptosis, avoiding further progression of cardiovascular diseases.

Neurodevelopmental outcomes of healthy Chinese term infants fed infant formula enriched in bovine milk fat globule membrane for 12 months - A randomized controlled trial.

BACKGROUND AND OBJECTIVES: Human milk fat globule membrane (MFGM) has multifunctional health benefits. We evaluated neurodevelopment and growth of healthy term infants fed bovine milk-derived MFGM-enriched formula (MF) over 12 months. METHODS AND STUDY DESIGN: A prospective, multi-center, double-blind, randomized trial was conducted in Fuzhou, China. Healthy term infants (n=212), aged <14 days, were assigned randomly to be fed MF or a standard formula (SF) for 6 months and then switched to stage 2 MF and SF formula until 12 months. A reference group (n=206) contained healthy breastfed infants (BFR). Neurodevelopment was assessed with Bayley-III Scales. RESULTS: At 12 months, the composite social emotional (+3.5) and general adaptive behaviour (+5.62) scores were significantly higher in MF than SF (95% CIs 0.03 to 6.79 and 1.78 to 9.38; p=0.048 and 0.004, respectively). Mean cognitive (+2.86, 95% CIs -1.10 to 6.80, p=0.08), language (+0.39, 95% CIs -2.53 to 3.30, p=0.87) and motor (+0.90, 95% CIs -2.32 to 4.13, p=0.49) scores tended to be higher in MF than SF, but the differences between the two groups were not significant. BFR scored higher on Bayley-III than either MF or SF at 6 and 12 months. Cognitive scores were significantly higher in BFR than SF (95% CI 0.05 to 7.20; p=0.045), but not MF (p=0.74) at 6 months. Short-term memory was significantly higher in MF than SF at 12 months (95% CI 1.40 to 12.33; p=0.002). At 4 months, serum gangliosides were significantly higher in MF and BFR than SF (95% CI 0.64 to 13.02; p=0.025). Milk intake, linear growth, body mass and head circumference were not significantly different between formula-fed groups. CONCLUSIONS: MFGM supplementation in early life supports adequate growth, increased serum gangliosides concentration and improves some measures of cognitive development in Chinese infants.

Alterations and potential roles of microbial population of pregnant mouse saliva and amniotic fluid.

PROBLEM: Prenatal exposure to intrauterine inflammation (IUI) is a crucial event in PTB pathophysiology. However, the relationship between microflora and PTB is not fully elucidated. METHOD OF STUDY: In this study, we established an intrauterine inflammation mouse model via LPS intrauterine injection. The saliva and amniotic fluid were collected for 16s RNA gene sequencing. The levels of TNF-α and IL-1ß in mouse amniotic fluid were determined by ELISA assays. RESULTS: Up to 60% of the operational taxonomic units (OTUs) in the saliva and amniotic fluid of PBS-treated mice were overlapped. LPS treatment-induced changes in the abundance of oral and amniotic fluid microorganisms. Both immune-associated probiotics, salivarius and mastitidis, were still detected in saliva (at significantly increased levels) after LPS-induced intrauterine inflammation and almost no probiotics of any type were detected in amniotic fluid, suggesting that the uterine cavity seems to be more susceptible to LPS compared to the oral cavity. Moreover, the abundance of pathogenic bacteria Escherichia coli was increased in both saliva and amniotic fluid after LPS treatment. The level of TNF-α and IL-1ß in amniotic fluid is positively related to the amniotic fluid E. coli abundance. CONCLUSIONS: The microbial composition of saliva and amniotic fluid of pregnant mice was similar. LPS-induced intrauterine inflammation decreased the consistency of microbial composition in mouse saliva and amniotic fluid, increased the abundance of E. coli in saliva and amniotic fluid, and decreased the abundance of immune-associated probiotics, especially in amniotic fluid.

Diffusion-Induced Stress in Commercial Graphite Electrodes during Multiple Cycles Measured by an In Situ Method.

The cyclic stress evolution induced by repeated volume variation causes mechanical degradation and damage to electrodes, resulting in reduced performance and lifetime of LIBs. To probe the electro-chemo-mechanical coupled degradation, we conducted in situ measurements of Young's modulus and stress evolution of commercial used graphite electrodes during multiple cycles. A bilayer graphite electrode cantilever is cycled galvanostatically in a custom cell, while the bending deformation of the bilayer electrode is captured by a CCD optical system. Combined with a mechanical model, Li-concentration-dependent elastic modulus and stress are derived from the curvature of the cantilever electrode. The results show that modulus, stress and strain all increase with the lithium concentration, and the stress transforms from compression to tension in the thickness direction. During multiple cycles, the modulus decreases with an increase in the cycle number at the same concentration. The maximum stress/strain of each cycle is maintained at almost same level, exhibiting a threshold that results from the co-interaction of concentration and damage. These findings provide basic information for modeling the degradation of LIBs.

An Improved Experiment for Measuring Lithium Concentration-Dependent Material Properties of Graphite Composite Electrodes.

The in situ curvature measurement of bilayer beam electrodes is widely used to measure the lithium concentration-dependent material properties of lithium-ion battery electrodes, and further understand the mechano-electrochemical coupling behaviors during electrochemical cycling. The application of this method relies on the basic assumption that lithium is uniformly distributed along the length and thickness of the curved active composite layer. However, when the electrode undergoes large bending deformation, the distribution of lithium concentration in the electrolyte and active composite layer challenges the reliability of the experimental measurements. In this paper, an improved experiment for simultaneously measuring the partial molar volume and the elastic modulus of the graphite composite electrode is proposed. The distance between the two electrodes in the optical electrochemical cell is designed and graphite composite electrodes with four different thickness ratios are measured. The quantitative experimental data indicate that the improved experiment can better satisfy the basic assumptions. The partial molar volume and the elastic modulus of the graphite composite electrode evolve nonlinearly with the increase of lithium concentration, which are related to the phase transition of graphite and also affected by the other components in the composite active layer. This improved experiment is valuable for the reliable characterization of the Li concentration-dependent material properties in commercial electrodes, and developing next-generation lithium batteries with more stable structures and longer lifetimes.

Two-rope method for dissecting esophagus in McKeown MIE.

Objective: Minimally invasive McKeown esophagectomy (McKeown MIE) is performed at many hospitals in esophageal cancer(EC) treatment. However, secure and quick methods for dissecting the esophagus and dissecting lymph nodes in this surgery are lacking. This study introduces a simple, secure and feasible esophagus dissecting technique named two-rope method. Two mobile traction ropes are placed around the esophagus and we tow these ropes to free the esophagus, dissect the lymph nodes, and decrease the operative trauma. Materials and Methods: Retrospective analysis was performed on 112 patients who underwent McKeown MIE in our center from January 2019 to September 2021. They were assigned into two groups based on the method of dissecting the esophagus: Group A (two-rope method, 45 cases) and Group B (regular method, 67 cases). Operation time, thoracic operation time, the number of dissected thoracic lymph nodes, and postoperative complications were compared between the two groups after propensity score matching. Results: Using 1:1 nearest neighbor matching, we successfully matched 41 pairs of patients. Operation time, thoracic operation time, and the duration (ac to as) was significantly shorter and the size of the abdominal incision was significantly smaller in the Group A than Group B (p < 0.05). There was no statistically significant difference in the number of dissected thoracic lymph nodes, pulmonary infection, anastomotic leak, recurrent laryngeal (RLN) injury, and chylothorax between the two groups (p > 0.05). Conclusions: Two-rope method to free the esophagus and dissect thoracic lymph nodes in McKeown MIE has significant advantages compared with the regular method. The technique is, therefore suitable for widespread adoption by surgeons.

Long non-coding RNAs: Modulators of phenotypic transformation in vascular smooth muscle cells.

Long non-coding RNA (lncRNAs) are longer than 200 nucleotides and cannot encode proteins but can regulate the expression of genes through epigenetic, transcriptional, and post-transcriptional modifications. The pathophysiology of smooth muscle cells can lead to many vascular diseases, and studies have shown that lncRNAs can regulate the phenotypic conversion of smooth muscle cells so that smooth muscle cells proliferate, migrate, and undergo apoptosis, thereby affecting the development and prognosis of vascular diseases. This review discusses the molecular mechanisms of lncRNA as a signal, bait, stent, guide, and other functions to regulate the phenotypic conversion of vascular smooth muscle cells, and summarizes the role of lncRNAs in regulating vascular smooth muscle cells in atherosclerosis, hypertension, aortic dissection, vascular restenosis, and aneurysms, providing new ideas for the diagnosis and treatment of vascular diseases.

Research Progress on Catalpol as Treatment for Atherosclerosis.

Coronary atherosclerotic heart disease, cerebrovascular disease, and peripheral artery disease are common diseases with high morbidity and mortality rates and must be addressed. Their most frequent complications, including myocardial infarction and stroke, are caused by spontaneous thrombotic occlusion and are the most frequent cause of death worldwide. Atherosclerosis (AS) is the most widespread underlying pathological change for the above diseases. Therefore, drugs that interfere with this pathophysiological process must be incorporated in the treatment. Chinese traditional and herbal drugs can effectively treat AS. With the development of traditional Chinese medicine, the active ingredients in common Chinese medicinal materials must be thoroughly purified prior to their application in western medicine. Various proprietary Chinese medicine preparations with remarkable effects have been used in AS treatment. Catalpol, the active component of Rehmannia glutinosa, belongs to iridoid terpene and has anti-inflammatory, antioxidant, insulin resistance improvement, and other related effects. Several reviews have been conducted on this compound and its actions against osteoporosis, neurodegenerative diseases, Alzheimer's disease (AD), Parkinson's disease (PD) and diabetes and its complications. The current review focused on catalpol's effect on atherosclerotic plaque formation in different animal models. The potential mechanisms of catalpol to ameliorate AS were also summarized in terms of oxidative stress, inflammation, cell aging, apoptosis, and activation of the silent information regulator factor 2-related enzyme 1 (SIRT1) pathway.

Perioperative safety and short-term efficacy of functional minimally invasive esophagectomy.

BACKGROUND: Standard minimally invasive McKeown three-field esophagectomy (SMIE) results in high perioperative risk and poor postoperative quality of life owing to considerable surgical damage and numerous postoperative complications. We created a modified procedure, functional minimally invasive esophagectomy (FMIE), which preserves the azygos arch, bronchial artery, pulmonary branch of the vagus nerve, and the mediastinal pleura. Our aim was to evaluate the efficacy and safety of FMIE and to determine whether it has limited invasiveness. METHODS: Between 2018 and 2020, FMIE was performed for 48 patients who were compared with 76 SMIE cases; 44 paired cases were matched using propensity score matching. RESULTS: Operation time, extubation time, and postoperative hospital stay were significantly lower in the FMIE group. FMIE was also associated with fewer pulmonary infections. Postoperative drainage volume on postoperative day (POD) 1 and POD 2, and white blood cell counts on POD 2 and POD 4 were also significantly lower in the FMIE group. There was no statistically significant difference in the number of dissected lymph nodes, short-term recurrence, metastasis rates, or survival rate between the two groups. CONCLUSIONS: FMIE is a less invasive procedure and may be a suitable alternative for lower and early middle esophageal carcinoma.

Oxygen-Reconstituted Active Species of Single-Atom Cu Catalysts for Oxygen Reduction Reaction.

Identification of an active center of catalysts under realistic working conditions of oxygen reduction reaction (ORR) still remains a great challenge and unclear. Herein, we synthesize the Cu single atom embedded on nitrogen-doped graphene-like matrix electrocatalyst (abbreviated as SA-Cu/NG). The results show that SA-Cu/NG possesses a higher ORR capability than 20% Pt/C at alkaline solution while the inferior activity to 20% Pt/C at acidic medium. Based on the experiment and simulation calculation, we identify the atomic structure of Cu-N2C2 in SA-Cu/NG and for the first time unravels that the oxygen-reconstituted Cu-N2C2-O structure is really the active species of alkaline ORR, while the oxygen reconstitution does not happen at acidic medium. The finding of oxygen-reconstituted active species of SA-Cu/NG at alkaline media successfully unveils the bottleneck puzzle of why the performance of ORR catalysts at alkaline solution is better than that at acidic media, which provides new physical insight into the development of new ORR catalysts.

Celastrol Alleviates Aortic Valve Calcification Via Inhibition of NADPH Oxidase 2 in Valvular Interstitial Cells.

This study sought to investigate whether reactive oxygen species (ROS)-generating reduced nicotinamide adenine dinucleotide phosphate oxidase 2 (Nox2) contributes to calcific aortic valve disease (CAVD) or whether celastrol, a natural Nox2 inhibitor, may provide potential therapeutic target for CAVD. CAVD is an active and cellular-driven fibrocalcific process characterized by differentiation of aortic valvular interstitial cells (AVICs) toward an osteogenic-like phenotype. ROS levels increase in calcified aortic valves, while the sources of ROS and their roles in the pathogenesis of CAVD are elusive. The roles of Nox2 and the effects of celastrol were studied using cultured porcine AVICs in vitro and a rabbit CAVD model in vivo. Nox2 proteins were significantly upregulated in human aortic valves with CAVD. In vitro, Nox2 was markedly induced upon stimulation of AVICs with osteogenic medium, along with the increases in ROS production and calcium nodule formation. Celastrol significantly decreased calcium deposition of AVICs by 35%, with a reduction of ROS generation. Knockdown of endogenous Nox2 substantially suppressed AVIC calcification by 39%, the inhibitory effect being similar to celastrol treatment. Mechanistically, either celastrol treatment or knockdown of Nox2 significantly inhibited glycogen synthase kinase 3 beta/ß-catenin signaling, leading to attenuation of fibrogenic and osteogenic responses of AVICs. In a rabbit CAVD model, administration of celastrol significantly reduced aortic valve ROS production, fibrosis, calcification, and severity of aortic stenosis, with less left ventricular dilatation and better preserved contractile function. Upregulation of Nox2 is critically involved in CAVD. Celastrol is effective to alleviate CAVD, likely through the inhibition of Nox2-mediated glycogen synthase kinase 3 beta/ß-catenin pathway in AVICs.

Neuregulin-1ß Partially Improves Cardiac Function in Volume-Overload Heart Failure Through Regulation of Abnormal Calcium Handling.

Background: Neuregulin (NRG-1), an essential stress-mediated paracrine growth factor, has a cardioprotective effect in failing heart. However, the underlying mechanism remains unclear. The role of NRG-1ß in heart failure (HF) rats was examined. Methods and Results: Volume-overload HF rat model was created by aortocaval fistula surgery. The sham-operated (SO) rats received the same surgical intervention without the fistula. Thirty-five HF rats were injected with NRG-1ß (NRG, 10 µg/kg·d) via the tail vein for 7 days, whereas 35 HF rats and 20 SO rats were injected with the same dose of saline. The echocardiographic findings showed left ventricular dilatation, systolic and diastolic dysfunction, and QTc interval prolongation in HF rats. The NRG-1ß treatment attenuated the ventricular remodeling and shortened the QTc interval. Patch clamp recordings showed ICa-L was significantly decreased in the HF group, and NRG-1ß treatment attenuated the decreased ICa-L. No significant differences in the kinetic properties of ICa-L were observed. The expressions of Cav1.2 and SERCA2a were significantly reduced, but the expression level of NCX1 was increased dramatically in the HF group. NRG-1ß treatment could partially prevent the decrease of Cav1.2 and SERCA2a, and the increase of NCX1 in HF rats. Conclusions: NRG-1ß could partly attenuate the heart function deterioration in the volume-overload model. Reduced function and expression of calcium transportation-related proteins might be the underlying mechanism.

Amorphous Cobalt Iron Borate Grown on Carbon Paper as a Precatalyst for Water Oxidation.

The key to improving water oxidation is to develop efficient and earth-abundant catalysts for the oxygen evolution reaction (OER). Herein, a new amorphous cobalt iron borate supported on 3D carbon paper integrated electrode is reported as a precatalyst for the OER, which was synthesized by using a one-pot hydrothermal method. An optimum OER activity was obtained at 25 % Fe doping by screening the compositions of the Co and Fe. The best synthesized catalyst needs an overpotential of 227 mV to deliver a current density of 10 mA cm-2 and also exhibits a long-term durability of 24 h. Impressively, we find that CoFe oxyhydroxide was formed in situ in the OER process, which serves as the real catalytic active species for OER. Moreover, the direct conversion from CoFe borate to CoFe oxyhydroxide is reported for the first time in metal borate OER catalysts. The discovery in this work, that is, that metal borate as a precursor can efficiently catalyze the OER in alkaline media, significantly widens the family of OER catalysts.

Effects of cisplatin on surgically induced endometriosis in a rat model.

Research has strongly suggested that the features of endometriosis serve as a precursor lesion of ovarian cancer. Cisplatin (CDDP) is the preferred drug against these cancer types. The present study investigated the effects of CDDP on surgically induced endometriosis in a rat model. Endometriosis was surgically induced by the autologous transplantation of endometrial tissue. A total of 36 model rats were randomly divided into three groups. The rats in Group 1 (control group, n=12) received no medication. The rats in Group 2 (n=12) and Group 3 (n=12) were administered 35 mg/m2 CDDP and 70 mg/m2 CDDP, respectively, every four days. All rats were treated for a total of 24 days. The growth and histologic scores of the implants were calculated. The expression of protein markers, including vascular endothelial growth factor (VEGF), aromatase P450 (P450arom), transforming growth factor-ß (TGF-ß) and matrix metalloproteinase (MMP)-2, were assessed using immunohistochemistry, an enzyme-linked immunosorbent assay and western blot analysis. Following CDDP treatment, the mean implant sizes were significantly reduced in Groups 2 and 3 compared with the control group (P=0.01). The mean histologic scores were also significantly lower in Groups 2 and 3. Furthermore, the protein expression of VEGF, P450arom, TGF-ß and MMP-2 was significantly lower in Groups 2 and 3 when compared with the control group. A loss of hair was observed in 4 rats, which only occurred in Group 3. A dose-dependent effect was observed in the two CDDP-treated groups. In conclusion, the expression of proliferation- and angiogenesis-associated proteins was significantly lower following treatment with CDDP. CDDP caused a significant regression in the size of the endometriotic implants and induced atrophy of these lesions in rats.