Mechanical behavior of spiral reinforcement recycled aggregate concrete round columns under axial compression after spraying water at high temperatures

Spiral hoops can effectively enhance the load-bearing capacity of recycled aggregate concrete columns, and the mechanical performance of such a member after experiencing fire and a fire sprinkler is very important for its application and promotion. Aiming at this problem, the mechanical behavior of spiral reinforcement recycled aggregate concrete round columns under axial compression after spraying water at high temperatures cooling was investigated. Three parameters including recycled coarse aggregate replacement ratio, temperature, and pitch of screw stirrups were taken into consideration. 26 specimens were designed for static loading test. The failure modes of regenerated concrete columns with spiral reinforcement were observed after cooling by high-temperature water spraying. The mechanical properties of specimens under different cooling modes after high temperatures were obtained and analyzed. The results indicate that the effect of the recycled aggregate replacement ratio on the performance of the specimens was mainly in terms of peak displacement. And the reduction in the spiral stirrup spacing increases the peak load and ductility coefficient of the specimens. The high temperature above 600°C has a obvious effect on the mechanical properties of the specimens. Water spray cooling can reduce the appearance of small cracks on the surface of the specimens and their peak displacement. The calculation method of bearing capacity of regenerated spiral reinforced concrete columns cooled by high-temperature water spraying was discussed

Targeting mitophagy for depression amelioration: a novel therapeutic strategy

Major depressive disorder is a global psychiatric condition characterized by persistent low mood and anhedonia, which seriously jeopardizes the physical and mental well-being of affected individuals. While various hypotheses have been proposed to explicate the etiology of depression, the precise pathogenesis and effective treatment of this disorder remain elusive. Mitochondria, as the primary organelles responsible for cellular energy production, possess the ability to meet the essential energy demands of the brain. Research indicated that the accumulation of damaged mitochondria is associated with the onset of depression. Mitophagy, a type of cellular autophagy, specifically targets and removes excess or damaged mitochondria. Emerging evidence demonstrated that mitophagy dysfunction was involved in the progression of depression, and several pharmacological interventions that stimulating mitophagy exerted excellent antidepressant actions. We provided an overview of updated advancements on the regulatory mechanism of mitophagy and the mitophagy abnormality in depressed patients and animals, as well as in cell models of depression. Meanwhile, various therapeutic strategies to restore mitophagy for depression alleviation were also discussed in this review

HMGB1-RAGE Axis Makes No Contribution to Cardiac Remodeling Induced by Pressure-Overload.

High-mobility group box1 (HMGB1) exerts effects on inflammation by binding to receptor for advanced glycation end products (RAGE) or Toll-like receptor 4. Considering that inflammation is involved in pressure overload-induced cardiac hypertrophy, we herein attempted to investigate whether HMGB1 plays a role in myocardial hypertrophy in RAGE knockout mice as well as in the growth and apoptosis of cardiomyocytes. The myocardial expression of RAGE was not significantly changed while TLR4 mRNA was upregulated in response to transverse aortic constriction (TAC) for 1 week. The myocardial expression of HMGB1 protein was markedly increased in TAC group when compared to the sham group. Heart weight to body weight ratio (HW/BW) and lung weight to body weight ratio (LW/BW) were evaluated in RAGE knockout (KO) and wild-type (WT) mice 1 week after TAC. Significant larger HW/BW and LW/BW ratios were found in TAC groups than the corresponding sham groups, but no significant difference was found between KO and WT TAC mice. Similar results were also found when TAC duration was extended to 4 weeks. Cultured neonatal rat cardiomyocytes were treated with different concentrations of recombinant HMGB1, then cell viability was determined using MTT and CCK8 assays and cell apoptosis was determined by Hoechst staining and TUNEL assay. The results came out that HMGB1 exerted no influence on viability or apoptosis of cardiomyocytes. Besides, the protein expression levels of Bax and Bcl2 in response to different concentrations of HMGB1 were similar. These findings indicate that HMGB1 neither exerts influence on cardiac remodeling by binding to RAGE nor induces apoptosis of cardiomyocytes under physiological condition

Effect of rHMGB1 on apoptosis of cardiomyocytes.

<p>Neonatal rat <b>c</b>ardiomyocytes were stimulated with different concentrations of rHMGB1 for 24h. (A) Hoechst staining assay of cardiomyocyte apoptosis. Scale bar, 50 μm. (B) Quantitative analysis of Hoechst-staining positive cells. (C) Examples of TUNEL staining pictures. (D) Quantitative analysis of TUNEL-assay positive cells. Results in histograms are mean ± SEM. Each experiment was repeated at least three times.</p

rHMGB1 exerted no effect on protein expression of Bax and Bcl2 in neonatal rat cardiomyocytes.

<p>(A) Western blot analysis of cytosolic Bax (cyto-Bax) in the presence of rHMGB1. (B)Total cellular protein expression of Bax. (C) Total cellular protein expression of Bcl2. β-actin served as a loading control. Results are means ± SEM. Each experiment was repeated three times.</p

Effect of RAGE deletion on cardiac hypertrophy induced by TAC for 1 week.

<p>(A) Results of Real-time PCR for gene expression of receptor for advanced glycation end products (RAGE) and Toll like receptor 4 (TLR4) in mice subjected to sham or transverse aortic constriction (TAC). (B) Western blot of high-mobility group box1 (HMGB1) expression in response to sham or TAC. *<i>P</i> < 0.05 compared with sham, n = 5 in each group for panel A and B. (C) Genotyping results. RAGE −/− (homozygote, HO) and RAGE +/+ (wildtype, WT) mice for experiments were generated by mating RAGE + / − (heterozygote, HE) mice with each other. (D) H&E and Azan staining to evaluate cardiomyocyte hypertrophy and myocardial fibrosis, respectively. Scale bar = 50 μm. (F) Lung weight/body weight (LW/BW) ratio was similar in WT and KO (RAGE knockout) TAC mice. (G) Heart weight/body weight (HW/BW) ratio in response to sham or TAC. *<i>P</i> < 0.01 compared with the corresponding sham group. Results in histograms are mean ± SEM, n = 10 in WT sham and WT TAC groups, and n = 7 and 6 in KO sham and KO TAC group, respectively.</p

Effect of RAGE deletion on heart failure induced by TAC for 4 weeks evaluated by echocardiography, invasive hemodynamic measurements and morphological analysis.

<p>(A) Echocardiographic left ventricular end-diastolic diameter (LVEDd). (B) Echocardiographic LV posterior wall thickness at diastole (LVPWd). (C) Echocardiographic LV fractional shortening (LVFS). (D) LV systolic pressure (LVSP). (E) LV end-diastolic pressure (LVEDP). (F) LV dp/dt max and min. (G) Examples of LV pressure and dp/dt curves recoding. (H) Heart weight to body weight ratio (HW/BW). (I) Lung weight to body weight ratio (LW/BW). Results are mean ± SEM, n = 6–8 in each group, *<i>P</i> < 0.05 vs. the corresponding sham group.</p

Effect of rHMGB1 on cell viability.

<p>Neonatal rat cardiomyocytes were exposed to recombinant HMGB1 (rHMGB1). (A) Effect of rHMGB1 on p-ERK1/2. (B) Cell viability was detected with MTT assay. (C) Cell proliferation detected with CCK8 assay. (D) Cell surface area in response to rHMGB1 in the absence/presence of anti-RAGE neutralizing antibody. Results are means ± SEM. n = 6 in each dose group in panel A-C, n = 50 cells in each group and *<i>P</i> <0.05 vs. 1^st bar in panel D.</p