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To investigate the protective effect and mechanism of magnesium isoglycyrrhizinate (MgIG) on cisplatin (CDDP) -induced myocardial injury in rats. Methods Twenty-four Wistar rats were randomly divided into the normal control group, the cisplatin model group (CDDP group), the cisplatin + magnesium isoglycyrrhizinate low-dose group (MgIG-L group) and the cisplatin + magnesium isoglycyrrhizinate high-dose group (MgIG-H group), with 6 rats in each group. Changes of body mass of rats were monitored daily. At the end of drug administration, cardiac function indexes including left ventricular ejection fraction (LVEF), left ventricular short-axis narrowing rate (LVFS), left ventricular endsystolic internal diameter (LVESD) and left ventricular end-diastolic internal diameter (LVEDD) were detected by echocardiography. The morphology of myocardial tissue was observed by HE staining. Enzyme-linked immunosorbent assay (ELISA) was used to detect serum levels of creatine kinase isoenzyme MB (CK-MB) and troponin I (cTnI). Levels of superoxide dismutase (SOD), malondialdehyde (MDA), glutathione synthase (GSH), reactive oxygen species (ROS) and ferrous ion (Fe2+ ) in homogenates of myocardial tissue were measured biochemically. The protein expressions of nuclear factor E2-associated factor 2 (Nrf2), long-chain fatty acyl coenzyme A synthase 4 (ACSL4), glutathione peroxidase 4 (GPX4) and ferritin heavy chain 1 (FTH1) protein were detected by Western blot assay. Results The body mass of rats in the control group showed an increasing trend during feeding, and the body mass of rats in the CDDP group showed a decreasing trend. Compared with the CDDP group, the body mass of rats in the MgIG-L group and the MgIG-H group increased after 5 d, 9 d and 13 d of treatment (P＜0.05). Compared with the control group, the CDDP group showed decreased LVEF and LVFS, increased LVESD and LVEDD, disturbed myocardial fiber alignment, myocardial fiber degeneration and fracture, increased serum CK-MB and cTnI levels, increased levels of MDA, Fe2+ and ROS in myocardial tissue, decreased levels of SOD and GSH, and decreased levels of Nrf2, GPX4, and decreased FTH1 protein expression levels and increased ACSL4 protein expression levels in myocardial tissue (P＜0.05). Compared with the CDDP group, the above indicators and myocardial histopathological changes were significantly improved in the MgIG-L group and the MgIG-H group. Conclusion Magnesium isoglycyrrhizinate can ameliorate cisplatin-induced myocardial injury by regulating myocardial oxidative stress and inhibiting cardiomyocyte iron death in rats. [ABSTRACT FROM AUTHOR]

[Objective] The present study aimed to screen candidate genes related to the metabolism of lip pigment in goats with different colors screened by RNA-Seq technology, and the molecular mechanism of the color difference of goat lip mucosa was initially revealed, which provided theoretical basis for the study of animal mucosal pigment metabolism. [Method] The lip mucosa tissues of Youzhou Dark-skin goats (black) and Banjiao goats (pink) with different facial mucosal color were selected as the study objects. The transcriptome sequencing was performed by Illumina Hiseq 2000 sequencing platform. After quality control and assembly, the differentially expressed genes were screened using log, (Fold Change) >1 and q value <0.05 as the criteria. Functional annotation and enrichment analysis of differentially expressed genes were performed. [Result] A total of 249 differentially expressed genes were screened by RNA-Seq technology. Compared with the pink mucosal tissues, 218 up-regulated genes and 31 down-regulated genes were found in the black mucosal tissues. A total of 23 differentially ex- pressed genes were predicted to be classified into 9 TFs families, of which 14 genes were classified into transcription factor families containing zinc finger domains. GO functional enrichment analysis showed that differentially expressed genes were mainly involved in various ion transport-related biological processes and molecular functions. The enrichment results of KEGG metabolic pathways showed that the differentially expressed genes were significantly enriched in oxytocin, calcium, cGMP-PKG signaling pathways, and other 7 signaling pathways related to muscle tissue function, include hypertrophic cardiomyopathy and cardiac muscle contraction, among which calcium and cGMP-PKG signaling pathways were closely related to pigment metabolism. In addition, 12 genes including ASIP were enriched into the core metabolic pathways of pigment such as MAPK signaling pathway, cAMP signaling pathway, and Melanogenesis signaling pathway. Four differentially expressed genes, including CALM16, OXTR, ATP1A2 and ATP1B4 were simultaneously enriched into multiple pathways related to pigment metabolism. qRT-PCR results were consistent with sequencing results, indicating that the sequencing results were reliable. [Conclusion] ASIP gene is preliminarily identified as a candidate gene for pigmentation metabolism of goat lip. Four genes, including CALML6, OXTR, ATP1A2 and ATP1B4, are involved in pigmentation process of goat lip mucosa, which provide theoretical basis for studying the molecular mechanism of pigmentation metabolism of goat mucosa. It also provides reference for exploring the molecular mechanism of abnormal colora- tion of human mucous membranes. [ABSTRACT FROM AUTHOR]

Objective: To investigate the protective effect of dexmedetomidine (DEX) on myocardial ischemia-reperfusion injury in diabetic mice and its possible molecular mechanism. Methods: Sixty 8-week-old SPF C57BL mice were fed with high fat for 6 weeks. At the 7th week, the type 2 diabetes model was established by intraperitoneal injection of streptozotocin (STZ) 45 mg/kg/d once a day for5 days. After modeling, the mice were randomly divided into sham operation group (sham group), ischemia-reperfusion group (I/R group), hypoxia-inducible factor-1α (HIF-1α) inhibitor 2ME2 group (2ME2 group), DEX group and DEX+2ME2 group (DM group), with 12mice in each group. In sham group, the skin was only cut and sutured. In the other four groups, the left anterior descending coronary artery was ligated through thoracotomy, and the ligating wire was released after 60 minutes of ischemia, followed by 120 minutes of reperfusion to establish the ischemia-reperfusion injury model. Blood samples were collected from the abdominal aorta at 120 min of reperfusion for determination of serum concentrations of troponin I (cTnI), interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α)by ELISA. Then the mice were sacrificed and left ventricles were isolated for observation of morphology and structure of myocardium by HE staining. The expression of HIF-1α and NOD-like receptor protein 3 (NLRP3) was detected by Western blot. Cardiac function was assessed by echocardiography at 24 h of reperfusion. Results: Compared with sham group, the concentrations of cTnI, IL-1β and TNF-α were significantly increased, myocardial tissue structure disorder, myocardial fiber rupture, myocardial cell swelling, inflammatory cell infiltration were significantly increased, the expression of NLRP3 in myocardial tissue was significantly increased, and stroke volume (SV), ejection fraction (EF) % and fractional shortening (FS) % were significantly decreased in I/R, 2ME2, DEX and DM groups (P＜0.05).Compared with I/R group, the expression of HIF-1α was significantly increased, the expression of NLRP3 was significantly decreased, the concentrations of cTnI, IL-1β and TNF-α were significantly decreased, myocardial tissue structure was significantly improved, inflammatory cell infiltration was significantly decreased, SV, EF and FS were significantly increased in DEX and DM groups (P＜0.05). Compared with the DEX group, the expression of HIF-1α was significantly decreased, the expression of NLRP3 was significantly increased, the concentrations of cTnI, IL-1β and TNF-α were significantly increased, myocardial tissue structure disorder, myocardial fiber rupture, myocardial cell swelling, inflammatory cell infiltration were significantly increased, SV, EF and FS were significantly decreased in the DM group (P＜0.05). Conclusions: DEX can alleviate myocardial I/R injury in diabetic mice by up-regulating HIF-1α, inhibiting the activation of NLRP3 inflammasome and reducing inflammatory response. [ABSTRACT FROM AUTHOR]

Objective We modified Baoyuan Decoction (ginseng, milkvetch root, liquorice root, cassia bark, and rose-boot) based on the original formula and explored its alleviating effect on physical fatigue. Methods Modified Baoyuan Decoction (MBYD) were analyzed by using HPLC. Altogether 160 ICR mice with SPF grade were divided into 4 parts (n = 40 mice per part), in which were divided into the blank control group (purifed water in the same volume), the modified Baoyuan Decoction low-, mid-, and high-dose groups (1.9, 2., and 2.3 g/kg). All the groups were administered intragatrically once a day for 30 days. The mice were sacrificed and sampled after the last administration. (1) 40 mice were used to get the behavioral indicators. After 21 days of administration, grip strength, back temperature, times of locomotor activity, and fatigue time of rotating rod was measured; while time of weight-loading swimming was measured at the 30th day. (2) 40 mice were used to get liver/muscle glycogen levels. (3) 40 mice were used to get the content of blood lactic acid (BLA) and its area under the curve (AUC). (4) 40 mice were used to get (I) the levels of the metabolic products (blood urea nitrogen, BUN; lactate dehydrogenase, LDH; BLA) ; (II ) activity of the oxidative stress-related enzymes (malondialdehyde, MDA; superoxide dismutase, SOD; catalase, CAT) in the skeletal muscle and the heart; (III) blood oxygen transport capacity (red blood cell, RBC ; hemoglobin, HGB ; mean corpuscular hemoglobin concentration, MCHC) ; (IV) activity of ATP-related enzymes (Na+-K+-ATPase; Ca2+-Mg2+- ATPase; succinate dehydrogenase, SDH; creatine kinase, CK) ; (V) protein expression of phosphorylation alpha-AMP-activated protein kinase (p-AMPK), slient mating type information regulation 2 homolog 1 (SIRT1), peroxisome proliferator activated receptor γ coactivator-1β (PGC-1α) and mitochondrial transcription factor A (TFAM). Results The contents of ginsenoside Rg1 ginsenoside Re, ginsenoside Rb1, salideoside and calycosin in MBYD were 8.15,3. 82,1. 07,0. 41 and 0. 067 g/L. MBYD can significantly improve the activity of Na+-K+-ATPase, Ca2+Mg2+-ATPase, SDH, CAT, and SOD in the heart and skeletal muscles (all P<0.05) ; reduce the MDA levels in the heart and skeletal muscles (both P<0.05) ; reduce the levels of CK and LDH in serum (both P<0.05) ; increase liver glycogen and muscle glycogen reserves(both P < 0.05) ; reduce the BUN level and the AUC of BLA (all P < 0. 05) ; increase the numbers of RBC, HGB, and MCHC in whole blood (all P<0.05) ; and increase the protein expression levels of p-AMPK, SIRT1, PGC-1α, and TFAM in skeletal muscle and heart (all P<0.05). Conclusion Modified Baoyuan Decoction may activate the AMPK/SIRT1/PGC-1α signaling pathway in skeletal muscle and heart, enhance mitochondrial capacity, reduce the accumulation of metabolic products in the body, inhibit oxidative stress, and increase blood oxygen transport capacity, thereby alleviating fatigue. [ABSTRACT FROM AUTHOR]

Exercise training is effective to improve the quality of life and physical function of patients with chronic heart failure. This paper reviewed the studies on exercise training in rehabilitation of patients with chronic heart failure, in order to provide reference for rehabilitation of patients with chronic heart failure. (运动训练(ET)有助于改善老年慢性心力衰竭患者的生活质量、躯体功能。本研究就国内外慢性心衰患者运动康复研究进展进行综述, 以期为临床制订相关运动护理康复方案提供参考。)

The purpose of this research was to investigate the effects of aging diet supplemented with the new compound antioxidants on growth performance and antioxidant function of meat ducks. A total of 400 one-day-old Cherry Valley ducks were randomly divided into 2 groups with 4 replicates per group and 50 ducks per replicate. The control group were fed the basal diet composed with aging diet, and the treatment group were fed the basal diet composed with aging diet supplemented with 500 mg/kg com‐ pound antioxidants. This experiment lasted for 40 days. The results showed that: ① the treatment group could significantly increase the average daily gain (ADG) of meat ducks aged 1 to 40 days (P<0.05) and significantly decrease the feed/gain (F/G) compared with the control group of meat ducks aged 1 to 40 days and 15 to 40 days（P<0.05), however, there was no significantly effects on ADG、average daily feed intake (ADFI) and F/G between the two groups during the 1 to 14 days (P>0.05). ②Com‐ pared with the control group, the serum and the liver SOD activity and GSH-Px activity of the treatment group were significantly increased(P< 0.05); and the kidney GSH-Px activity, the heart CAT activity and SOD activity were significantly increased (P<0.05); however, the MDA contents of the kidney, heart and chest muscle were signifi‐ cantly decreased (P<0.05). In conclusion, aging diet supplemented with 500 mg/kg the new compound antioxidants can improve the growth performance to a certain extent and improve the antioxidant function of meat ducks. [ABSTRACT FROM AUTHOR]

Objective To investigate the effect of hydrogen on myocardiumapoptosis after limb ischemia-reperfusion in rabbits through inhibition of the tumor necrosis factor-like cytokine 1A (TL1A)/death receptor 3 (DR3) pathway. Methods The gene expression omnibus (GEO) GSE160516 dataset was downloaded and the kyoto encyclopedia of genes and genomes (KEGG) pathway enrichment was performed. Eighteen male New Zealand large-eared white rabbits were randomly divided into control group (Group C), limb ischemia-reperfusion group (Group R), and hydrogen group (Group H) using the random number table method, with six rabbits in each group. The rabbit double hind limb ischemia-reperfusion model was established, and the animals in each group were centrifuged with venous blood to prepare serum, and the hearts were removed. Serum TL1A and DR3 levels were measured by enzyme-linked immunosorbent assay (ELISA). The terminal deoxynucleotidyl transferase UTP mediated nicked end labeling (TUNEL) assay was performed to detect apoptosis rate in myocardium. The relative expression of TL1A, DR3 and cysteine aspartate protease 3 (Caspase3) proteins in myocardium was measured by western blotting (WB). The real-time reverse transcription polymerase chain reaction (RT-qPCR) was performed to determine the relative expression of TL1A, DR3 and Caspase3 mRNA in myocardium. Results KEGG enrichment analysis revealed that gene expression was enriched to Apoptosis signaling pathway, TNF signaling pathway and MAPK signaling pathwayafter myocardium ischemia-reperfusion in mice. It was observed that the expression levels of serum TL1A and DR3 were significantly higher in group R compared with group C (P < 0.01), while the expression levels of serum TL1A and DR3 were significantly lower in group H compared with group R (P < 0.01). Compared with group C, the apoptosis rate of myocardium in group R was significantly higher (P < 0.01) ; compared with group R, the apoptosis rate of myocardium in group H was significantly lower (P < 0.01). The relative expressions of TL1A, DR3 and Caspase3 protein and mRNA in myocardium were significantly increased in group R compared with group C (all P<0.01) ; the relative expressions of TL1A, DR3 and Caspase3 protein and mRNA in myocardium were significantly decreased in group H compared with group R ( P < 0.05, P < 0.01). Conclusion Hydrogen attenuates myocardium apoptosis after limb ischemia-reperfusion by inhibiting the TL1A/DR3 pathway. [ABSTRACT FROM AUTHOR]

BACKGROUND: In recent years, studies on chronic diseases related to aging have attracted wide attention worldwide. As the heart grows with age, premature aging may occur. Exercise is a safe and healthy intervention that can delay its aging. OBJECTIVE: To observe the effect of regular aerobic exercise on the aging of cardiomyocytes and explore its mechanism. METHODS: Healthy male SPF Sprague-Dawley rats aged 3 months (young, n=20), 13 months (middle age, n=24), and 22 months (old, n=24) were randomly divided into youth rest group, youth exercise group, middle age rest group, middle age exercise group, old age rest group, and old age exercise group. The three resting groups did not do aerobic exercise intervention, and the three exercise groups were given a 10-week incremental load aerobic treadmill exercise consisting of 6-week incremental load exercise and 4-week constant load exercise. RT-PCR and immunohistochemical detection were used to detect myocardial Beclin-1, CaMKIIα1, AMPKα1/pAMPKα1, and PI3K/Akt/mTOR pathway-related proteins and genes. RESULTS AND CONCLUSION: After regular aerobic exercises, compared with the three resting groups, the expression levels of Beclin-1 in cardiomyocytes were significantly down-regulated in the three exercise groups. The expression levels of myocardial CaMKIIα1 mRNA were also down-regulated in the three exercise groups. The protein expression levels of pAMPKα1 and AMPKα1 in the three resting groups showed an aging trend, and the expression levels of AMPKα1 in the young, middle age, and old age exercise groups were up-regulated by 16.50% (P < 0.05), 63.09% (P < 0.05), and 31.12% (P < 0.01), respectively. The expression levels of pAMPKα1 were also significantly up-regulated by 131.29% in the young exercise group (P < 0.01), 40.55% in the middle age exercise group (P < 0.01), and 16.77% in the old age exercise group (P < 0.05). Overall, the expression levels of PI3K in the myocardium were down-regulated in the three exercise groups compared with the three resting groups, while the expression levels of AKT1 mRNA were down-regulated in the young and middle age exercise groups. The expression level of mTOR mRNA was slightly down-regulated in the young exercise group, little changed in the middle age exercise group, and significantly upregulated in the old age exercise group. To conclude, aerobic exercise can significantly up-regulate the expression of PI3K, promote the activity of mTOR, downregulate the expression of CaMKIIα1, down-regulate the ratio of pAMPKα1/AMPKα1, decrease the expression of Beclin-1, regulate the level of myocardial autophagy, and make it tend to be normal and stable in aged rats, thereby delaying myocardial aging. [ABSTRACT FROM AUTHOR]

The Qinghai-Tibet Plateau is the highest altitude and largest area in the world. It has a unique geographical environment, with low temperature, low humidity, large temperature difference, strong ultraviolet radiation, low pressure and low oxygen. The heart is an organ that consumes a lot of oxygen, and is very sensitive to hypoxia. Cardiomyocytes are an important tool for studying the pathophysiological mechanism of myocardial structure and function, and cardiomyocyte culture technology has attracted much attention. In recent years, the research on the protection of cardiomyocytes by Chinese Tibetan medicine has become a research hotspot.The article mainly reviews the effects of plateau on myocardial cells and the cultivation and protection of myocardial cells. [ABSTRACT FROM AUTHOR]

Objective: To observe whether CAV3 is involved in the physiological process of IMGU and NIMGU. Downregulation of caveolin-3 (CAV3) protein expression by small interference RNAs (iRNA) has been studied. Insulin-mediated glucose uptake (IMGU) is critical in skeletal muscle and cardiac myocytes, but non - insulin -mediated glucose uptake (NIMGU) should not be neglected. Methods: CAV3 siRNAs were designed and transfected in C2C12 cells and H9c2 cells in skeletal muscle and cardiac muscle, respectively, and C2C12 and H9c2 cells were cultured in DMEM medium with and without insulin, respectively. Glucose transporter 4 (GLUT4) protein expression was detected by Western blot, and the glucose uptake rate of cells was measured by biochemical kit. Results: Transfection with CAV3 siRNA successfully down- regulated CAV3 protein expression in C2C12 and H9c2 cells. In the absence of insulin stimulation, GLUT4 expression was decreased (P<0.01) and glucose uptake was reduced (P<0.05) after 48 h of transfection in C2C12 cells, and GLUT4 expression was decreased (P<0.05) and glucose uptake was reduced (P<0.01) after 48 h of transfection in H9c2 cells. In the presence of insulin stimulation, GLUT4 expression was decreased (P<0.01) and glucose uptake was reduced (P<0.01) after 48 hours of transfection in C2C12 cells, and the down-regulation of GLUT4 was not statistically significant and glucose uptake was reduced (P<0.01) after 48 hours of transfection in H9c2 cells. Conclusion: Two different states, IMGU and NIMGU, exist in C2C12 cells and H9c2 cells. Both in the quiet state stimulated by insulin as well as in the absence of insulin stimulation, the cellular uptake of glucose is affected by GLUT4 changes regulated by CAV3. [ABSTRACT FROM AUTHOR]

Copyright of Journal of China Medical University is the property of Journal of China Medical University Editorial Office and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Journal of Shanghai Jiao Tong University (1006-2467) is the property of Journal of Shanghai Jiao Tong University Editorial Office and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Background There is no safe and effective antidote for cardiotoxicity induced by bupivacaine, an extensively used anaesthetic. Our previous research shows that acupoint treatment may partially improve bupivacaine-induced cardiotoxicity, but the mechanism of action needs to be further studied. Objective To observe the effect of acupoint injection of puerarin on mitochondrial energy metabolism in myocardia in bupivacaine-poisoned rats, and to explore its mechanism of action. Methods This experiment was conducted from January to December 2019. Forty 6-month-old male SPF Wistar rats were selected and equally randomized into a blank group (group C) , a model group (group B) , a treatment group (group T) , and a prevention group (group P) . Interventions were given to the groups as follows: Group P received: 0.1 ml puerarin injection injected into bilateral Neiguan acupoints. Then 5 minutes later, bupivacaine-poisoned model was established for three groups (except for group C) using intravenous infusion of 0.5% bupivacaine (10 mg/kg) via femoral vein within 2 minutes. Group C received 0.1 ml of 0.9% sodium chloride solution injected into bilateral Neiguan acpoints. : Immediately after successful modeling, 0.1 ml of 0.9% sodium chloride solution was injected into bilateral Neiguan acupoints for group B, and: 0.1 ml puerarin injection was injected into bilateral Neiguan points for C. The rats in group C were sacrificed at the 8th minute of intravenous infusion of 0.9% sodium chloride solution, and those in groups B, T, and P were sacrificed at the 8th minute of intravenous infusion of bupivacaine, then the left ventricular myocardium of all rats were taken out and cardiomyocyte mitochondria were isolated, the structure of which was observed under the transmission electron microscope. The semi-quantitative analysis of mitochondrial structure was evaluated by Flameng classification system. The activity of mitochondrial adenosine triphosphate synthase (ATPase) was measured by ELISA. The content of adenosine triphosphate (ATP) was measured by colorimetric assay. The mitochondrial membrane potential (MMP) was detected by JC-1 fluorescence staining and colorimetry. The protein levels of myocardial mitochondrial peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α) , nuclear respiratory factor 1 (NRF1) , and mitochondrial transcription factor A (mtTFA) were measured by Western blotting. Results Group C had lower Flameng score than did other three groups (P

Copyright of Practical Pharmacy & Clinical Remedies is the property of Editorial Department of Practical Pharmacy & Clinical Remedies and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Shipin Kexue/ Food Science is the property of Food Science Editorial Department and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Objective To investigate the protective effects and primary mechanism of ginsenoside Rg1 on cardiac muscle of aging mice induced by D-galactose (D-gal). Methods C57BL/6 J mice were randomly divided into normal control, model, Rg1 intervention and negative control groups, with 10 animals in each group. D-gal (200 mg/kg) was injected intraperitoneally to the mice for 42 d to establish the model group, and the mice of the Rg1 intervention group was given 40 mg/kg Rg1 per day for 26 d intraperitoneally from the 16th day of model establishment. The mice of the normal control group were given same amount of normal saline for 42 d, and those of the negative control group were treated with normal saline after model establishment. On the 2nd day after treatment, the hearts were taken to measure the organ index. HE staining and transmission electron microscopy were performed to observe the morphology and micro-structures of the heart tissue from each group. The activities of aspartate aminotransferase (AST), lactate dehydrogenase (LDH), total superoxide dismutase (T-SOD), catalase (CAT) and contents of malondialdehyde (MDA) in the myocardial tissue homogenate were tested by enzyme-labeled colorimetry; The expression levels of Nrf2, Keap1 and HO-1 in the heart tissue were detected by Western blotting. Results Compared with the control group, the model group had significantly increased heart index (P < 0.01); larger amount of deposited collagen fibers between myocardial fibers, disordered myofibril bundles, thicker myocardial fibers, and abnormally swollen mitochondria; enhanced AST and LDH activities, declined T-SOD and CAT activities, and increased MDA content (P < 0.05); remarkably down-regulation of Nrf2 and HO-1 (P < 0.05), and no changed Keap1 level. While in the Rg1 intervention group, all the above phenomena were greatly improved after the intervention, with obviously decreased heart index (P < 0.01), not notable morphological changes with normal control mice, reversed AST, LDH, T-SOD and CAT activities and MDA contents(P < 0.05), and elevated protein levels of Nrf2 and HO-1, and decreased level of Keap1 (P < 0.01). Conclusion Rg1 effectively alleviates the damage of D-gal to the morphology and ultrastructure of mouse myocardium, and its mechanism may be related to the inhibition of oxidative stress and the up-regulation of the Nrf2 antioxidant signal pathway.

Objective To observe the skin ultrastructure change of electric shock death rats and to test the expression changes of hypoxia-inducible factor-2α （HIF-2α） and heart type-fatty acid-binding protein （H-FABP） of myocardial cells, in order to provide basis for forensic identification of electric shock death. Methods The electric shock model of rats was established. The 72 rats were randomly divided into control group, electric shock death group and postmortem electric shock group. Each group was divided into three subgroups, immediate （0 min）, 30 min and 60 min after death. The skin changes of rats were observed by HE staining, the changes of skin ultrastructure were observed by scanning electron microscopy, and the expression of HIF-2α and H-FABP in rats myocardium was tested by immunohistochemical staining. Results The skin in the electric shock death group and postmortem electric shock group had no significant difference through the naked eye or by HE staining. Under the scanning electron microscope, a large number of cellular debris, cells with unclear boundaries, withered cracks, circular or elliptical holes scattered on the cell surface and irregular edges were observed. A large number of spherical foreign body particles were observed. Compared with the control group, the expression of HIF-2α in all electric shock death subgroups increased, reaching the peak immediately after death. In the postmortem electric shock group, HIF-2α expression only increased immediately after death, but was lower than that of electric shock death group （P

BACKGROUND: Studies have confirmed that enalapril can alleviate myocardial injury caused by limb ischemia-reperfusion, but the mechanism of its action has not been reported. OBJECTIVE: To investigate the effect mechanism of enalapril reduction of myocardial injury by ischemia-reperfusion in the rat limb. METHODS: Forty-eight healthy adult male Sprague-Dawley rats were randomly divided into control group, model group, enalapril group and inhibitor group. Except for the normal control group, rats were bundled around the ligation of the posterior limbs with a rubber band for 3 hours, followed by 3-hour reperfusion to establish the model of limb ischemia-reperfusion. Intravenous injection of 0.3 mg/kg LY294002 was given in the inhibitor group 30 minutes before reperfusion. Enalapril group and inhibitor group were given intravenous infusion of enalapril 13 μg/kg/h immediately after reperfusion until the end of reperfusion. An equal amount of normal saline solution was given in the other two groups immediately after reperfusion. After 3 hours of reperfusion, the rats were killed and the myocardial tissue was taken. Myocardial histopathological changes, apoptotic index, apoptosis gene expression and cell conduction pathway protein expression were detected. The study was approved by the Laboratory Animal Ethical Committee of Shenyang Medical College in October 2019 with an approval No. (2019)85. RESULTS AND CONCLUSION: Compared with the model group, myocardial histopathological injury was reduced in the enalapril group. Compared with the enalapril group, myocardial histopathological injury was aggravated in the inhibitor group. Compared with the model group, myocardial apoptosis index (AI) was decreased, Bax expression was downregulated, PI3K, p-Akt and Bcl-2 expression was up-regulated in the enalapril group (P < 0.05). Compared with the enalapril group, myocardial apoptosis index was increased, Bax expression was up-regulated, PI3K, p-Akt and Bcl-2 expression was downregulated in the inhibitor group (P < 0.05). The mechanism by which enalapril reduces limb ischemia-reperfusion caused myocardial injury is related to activating PI3K/Akt signaling pathway and inhibiting cell apoptosis in rats. [ABSTRACT FROM AUTHOR]

In this experiment, 48 5-week-old mice were exposed to arsenic and riboflavin through drinking water. The control group, the arsenic treatment group (20 mg/L As2O3), the riboflavin treatment group (20 mg/L VB2), the arsenic and riboflavin combined group (20 mg/L As2O3+20 mg/L VB2) were set up to explore the alleviating effect of riboflavin on tissue injury caused by arsenic. The results showed that arsenic treatment caused the heart muscle fiber septa widening, fiber bundles bending, myocardial nucleus shedding, alveolar wall thickening and alveolar cavity shrinking compared with the control group. The number of cerebral cortex cells was significantly reduced and disordered, and the nuclei were dissolved and broken. The addition of riboflavin significantly reduced the damage of arsenic to heart, lung and brain. Therefore, this study confirmed that riboflavin intervention has a significant alleviating effect on the structural damage of heart, lung and brain caused by arsenic, it provides new ideas for the toxicological mechanism and prevention of arsenic poisoning. [ABSTRACT FROM AUTHOR]

Objective To explore the efficacy of nourishing qi (NouQ) and activating blood (ActB) herbal combination at different ratios on diastolic heart failure (DHF) rats by targeting calcium homeastasis. Methods DHF rats were induced by abdominal aortic constriction and grouped into NouQ (AM + CP), NouQ vs ActB = 1:1 (AM + CP vs SM + PP = 1:1), or NouQ vs ActB = 2:1 (AM + CP vs SM + PP = 2:1). Heart function, hemodynamics, cardiomyocytic shortening and calcium transient were measured after 4/12 weeks of treatment. CaMK II, protein kinase A (PKA) and their responding phosphorylation proteins PLB T17 and PLB S16 were examined by using Western blot assay. Results Although all NouQ + ActB groups showed improvements on diastolic function (lower end-diastolic left ventricular pressure (LVEDP) at resting status; shorter time to 50% relaxation of cardiomyocytes) and systolic function (shorter time to 50% contraction of cardiomyocytes), only NouQ vs ActB = 2:1 group decreased E/e ratio, LVEDP under exercise stress and reversed LV remodeling (lower LV anterior wall thickness and LV posterior wall thickness). At cellular level, all treatment groups showed shorter time to 50% contraction, shorter time to 50% relaxation, shorter time to 50% Ca2+ release and reduction of CaMK II expression; all NouQ + ActB treatment groups illustrated additional effects on inhibiting PKA overexpression, but only 2:1 group illustrated shorter time to 50% Ca2+ uptake and reversed hypo-phosphorylation of PLB S16. Conclusion The combination of NouQ herbs (AM + CP) and ActB herbs (SM + PP) at a ratio of 2:1 have a better therapeutic effect than that of a ratio of 1:1 and NouQ herbs on DHF, and this effect may work through regulating Ca2+ handling. [ABSTRACT FROM AUTHOR]

BACKGROUND: Recent studies have found that GPE-AGTshRNA nanocomposite cannot only have better transfection efficiency and lower cytotoxicity to hepatocytes in vitro, and also significantly reduce the expression of angiotensinogen at the gene and protein levels. OBJECTIVE: To observe the effects of angiotensinogen-targeted RNA interference on blood pressure and cardiac protection in spontaneously hypertensive rats, attempting to find a new antihypertensive strategy. METHODS: Spontaneously hypertensive rats were randomly evenly divided into gene therapy group, negative control group and blank control group, and normal Wistar Kyoto rats (WKY) were set as normal blood pressure control group (WKY group). There were nine sessions in total, with 10 days as one session. On the 1st day of each session, administration in each group was given via the rat tail vein: 500 μL of sterile water for injection in the WKY group, 500 μL of GPEAGTshRNA nanocomplex in the gene therapy group, and 500 μL of GPE-NC shRNA nanocomplex in the negative control group, and 500 μL of sterile water in the blank control group. We used real-time PCR and western blot assay respectively to detect hepatic angiotensinogen mRNA and protein levels. The serum levels of angiotensinogen and angiotensin II were measured by ELISA. Systolic blood pressure of the tail artery was measured with tail cuff method. Ventricular function was detected by echocardiography. Myocardial lesion was observed under light microscopy. RESULTS AND CONCLUSION: Angiotensinogen mRNA and protein expression and serum angiotensinogen and angiotensin II levels were significantly lower in the gene therapy group than the negative and blank control groups (P < 0.01). On the 3rd day after the first injection, tail arterial pressure of rats decreased significantly by (28±4) mmHg in the gene therapy group, which was significantly different from that before treatment (P < 0.01). The parameters of left ventricular ejection fraction and left ventricular fractional shortening were significantly increased in the gene therapy group, while the thickness of the left ventricular posterior wall was significantly reduced, and cardiomyocyte hypertrophy were significantly relieved under light microscope. To conclude, angiotensinogen-targeted RNA interference can effectively control blood pressure through downregulation of angiotensinogen, and meanwhile significantly alleviate myocardial hypertrophy and improve ventricular function. [ABSTRACT FROM AUTHOR]

BACKGROUND: Cardiomyocyte direct reprogramming has been a research hotspot in the field of regenerative medicine in recent years. It may become a new way to treat heart disease and has a broad application prospect and development direction. OBJECTIVE: To explore and understand the research process, research hotspots and development trends of cardiomyocyte direct reprogramming through a scientometric and visualization analysis using CiteSpace knowledge map, thereby providing references in relevant research fields. METHODS: Cardiomyocyte direct reprogramming related documents were retrieved in the Web of Science Core Collection using the key words of “direct reprogramming, reprogramming, cardiomyocytes, cardiomyocyte, cardiac muscle cell” on July 29, 2020. CiteSpace was used to visually analyze the authors, institutions and keywords in the included literature. RESULTS AND CONCLUSION: A total of 277 articles were included, which mainly focus on cell biology, bioengineering and applied microbiology. University of California, San Francisco and the University of North Carolina are two main forces in this field. There were nine representative keyword clusters: direct reprogramming, regeneration, pluripotent stem cell, induction, marrow stromal cell, progenitor cell, maturation, transdifferentiation, and induced pluripotent stem cell. The research direction was multi-directional with the development of time. Differentiation of induced stem cells into cardiomyocytes was a research hotspot around 2005, and the direct reprogramming technology gradually attracted wide attention around 2013. This review also suggests that transcription factors, myocyte enhancer factor 2C and heart regeneration may be the research frontiers in the field of direct reprogramming of cardiomyocytes. [ABSTRACT FROM AUTHOR]

[Objective] The present paper aimed to study the effects of Pu’er tea extract and Kuding tea extract on the heart and skeletal muscle of bullfrog and the mechanism of action. [Method] The gastrocnemius muscle of bullfrog was soaked in two tea extracts, and the systolic indexes were recorded.The effects of two tea extracts on the content of acetylcholine（Ach） and the activity of acetylcholinesterase（A-CHE） at the junction of sciatic nerve-gastrocnemius were determined.Two tea extracts of different concentrations were used to irrigate the heart of bullfrog, and the contraction changes were recorded.CaCl2, Ach and high concentration tea extract were selected to co-incubate to observe the effects of frog heart contraction. [Result] The results showed that both tea extracts could promote the contraction and relaxation of skeletal muscle, and the mechanisms were related to the increase of Ca2+ concentration in sarcoplasm by promoting Ca2+ from terminal cisterna into sarcoplasm and the increase of the Ach content by inhibiting the activity of A-CHE at the junction. Two tea extracts all could inhibit the contraction of isolated frog heart, and both could cooperate with the inhibitory effect of Ach on the contraction of isolated frog heart, and inhibit the promoting effect of CaCl2. The mechanisms of action may be related to blocking the ICa-L and activating the M receptors of myocardium membrane, reducing the intracellular cAMP concentration and inhibiting the extracellular Ca2+ influx. [Conclusion] The effects of Pu’er tea on skeletal muscle and myocardium were more obvious than those of Kuding tea. [ABSTRACT FROM AUTHOR]

BACKGROUND: Exercise stimulates skeletal muscle, myocardium and fat tissues to release irisin, and it exerts various effects on muscle and non-muscle tissues through autocrine, paracrine and endocrine pathways. Clinically, serum irisin level is used as an important indicator for diagnosing heart failure and evaluating its severity as well as a potential target for treating heart failure. OBJECTIVE: To explore the mechanism by which exercise-induced irisin exerts myocardial protection from the perspective of receptors. METHODS: SCI, PubMed, and CNKI were searched for relevant documents published from 1990 to 2020. The search terms included “irisin; integrin αV; aerobic exercise; chronic heart failure; myocardial mitochondria” in English and Chinese, respectively. According to the inclusion criteria and exclusion criteria, 68 authoritative and representative literatures were selected for review. RESULTS AND CONCLUSION: Irisin plays an important role in maintaining normal cardiac function, and its cardioprotection is related to the improvement of mitochondrial function. Integrin αV is a novel specific receptor of irisin, which can transmit extracellular signals into cells through outside-in signals. Integrin αV mediates the effects of irisin on myocardial mitochondria, including oxidative stress, biosynthesis and mitophagy, which provides a new therapy for aerobic exercise or irisin to improve heart failure. [ABSTRACT FROM AUTHOR]

Objective To study the myocardial protective mechanism of baicalin in diabetic rats. Methods In July 2019,SD rats were injected with 45mg/kg streptozotocin via tail vein to establish experimental diabetes models,40 diabetes rats were randomly divided into control group (NC group,intraperitoneal injection of normal saline),diabetes mellitus group (DM group,intraperitoneal injection of normal saline),baicalin+diabetes mellitus group [Baicalin+DM,intraperitoneal injection of Baicalin solution 15μmol/L/(kg·d)] and Baicalin+control group [by intraperitoneal injection of Baicalin+NC group,Baicalin solution 15 μmol/L/(kg·d)],with 10 rats in each group. Eight weeks later,blood glucose and cardiac mass index were detected. Masson staining observed myocardial tissue changes in each group,and collagen volume fraction(CVF) was calculated. Western-blotting detected IL- 1β,TNF-α,TLR4,p65 and collagenⅠ. Results Compared with DM groups,blood glucose and cardiac mass index were decreased in Baicalin+DM groups(P <0.05). The myocardial cell was disorganized and the collagen fibers between the muscle fibers proliferated obviously by masson staining method in DM groups. Myocardial cell was organized and collagen fibers hyperplasia decreased obviously of Baicalin+DM groups,CVF was decreased,with statistical significance(P <0.05),Western-blotting showed that IL-1β, TNF-α,TLR4,p65 and collagenⅠin DM groups were significantly higher than those in NC groups. Compared with DM groups,IL- 1β,TNF-α,TLR4,p65 and collagenⅠ were decreased in Baicalin+DM groups,with statistical significance (P <0.05). Conclusion Baicalin has protective effect on myocardium of diabetic rats by inhibiting TLR/NF-κB signaling pathway,reducing myocardial inflammatory response and inhibiting collagen fiber proliferation. [ABSTRACT FROM AUTHOR]

Copyright of Journal of Forensic Medicine / Fayixue Zazhi is the property of Journal of Forensic Medicine Editorial Office and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

BACKGROUND: In recent years, increasing studies have shown that abnormally activated Hedghog signaling pathway is widely involved in the injury repair of systemic multi-tissue organ diseases, but its related role in myocardial fibrosis is still unclear. OBJECTIVE: To study the effect of blocking Hedgehog-Gli signaling pathway on epithelial-mesenchymal transition of myocardial fibroblasts induced by transforming growth factor-β1 (TGF-β1). METHODS: (1) Animal experiment: The model of myocardial infarction in mice was established by left coronary artery ligature. The pathological changes of myocardial tissue were observed by hematoxylin-eosin staining and Masson staining at 3, 7, and 14 days after infarction. The mRNA, protein and spatiotemporal expressions of Gli1 at different time points were detected by RT-PC, western blot and immunofluorescence. The mRNA and protein expression changes of Gli1 before and after adding inhibitor were detected using RT-PCR and immunofluorescence. (2) Cell experiment: The primary cultured myocardial fibroblasts of neonatal Sprague-Dawley rats were cultured by differential adherent method. The cultured myocardial fibroblasts were cultured with 0, 1, 5, and 10 μg/L TGF-β1 intervention. The expression of Gli1 mRNA and protein was detected by RT-PCR and western blot, respectively. Myocardial fibroblasts were induced by TGF-β1 of 10 μg/L for 24 hours, and the spatio-temporal expression of Gli1 protein and expression of epithelial-mesenchymal transition markers were detected by immunofluorescence. Gli1 and Smo in Hedgehog signaling pathway were specifically blocked by GANT61 and Cyclopamine for 24 hours, respectively, and 10 μg/L TGF-β1 was added. The mRNA expression level of Gli1 was detected by RT-PCR, and the spatio-temporal expression of Gli1 and expression of epithelial-mesenchymal transition markers were detected by immunofluorescence. RESULTS AND CONCLUSION: (1) Results of the animal experiment: As the time after infarction prolonged, the mRNA and protein expression levels of Gli1 in the mouse myocardium gradually increased, but the mRNA and protein expressions of Gli1 in the infarcted tissue decreased after addition of the Hedgehog pathway specific blocker. (2) Results of the cell experiment: After stimulation with TGF-β1, the epithelial mesenchyme of myocardial fibroblasts transformed into myofibroblasts (positive for a-SMA). As the intervention dose of TGF-β1 increased, the mRNA and protein expression of Gli1 gradually increased. After specifically blocking Gli1 and Smo in the Hedgehog signaling pathway for 24 hours, the mRNA and protein expression levels of Gli1 were inhibited, accompanied by the changes in the expression of E-Cadherin and Vimentin during epithelial-mesenchymal transition, indicating the existence of epithelial-mesenchymal transition. By the combination of in vivo and in vitro experiments, this study confirmed that the Hedgehog-Gli signal pathway is involved in the occurrence and development of myocardial fibrosis and myocardial fibroblast transdifferentiation. [ABSTRACT FROM AUTHOR]

BACKGROUND: Exhaustive exercise is a vigorous physical activity performed by an organism beyond its physiological limits, and it causes a series of histological changes in the body. Myocardial exercise-induced oxidative stress injury means that the organism generates free radicals through oxidative stress signal pathway to damage myocardial cells under exhaustive exercise. OBJECTIVE: To explore the mechanism of oxidative stress injury in rat myocardium caused by one-time exhaustive exercise based on the protein kinase C (PKC)/ NOX pathway. METHODS: Thirty adult male Sprague-Dawley rats were randomly divided into a control group, an exhaustive exercise group, and an exhaustive exercise+drug group, with 10 rats in each group. The exhaustive exercise+drug group was injected with PKC inhibitor chelerythrine (5 mg/kg body weight) for 3 consecutive days. Rats in the two exercise groups exercised at a speed of 25 m/min on a 0° incline treadmill until exhaustion. Immediately after exercise, blood sample was collected from each rat, and then the rat’s left ventricle was removed for hematoxylin-eosin staining to observe the morphological changes of myocardial cells. Serum and myocardial malondialdehyde and myocardial reactive oxygen species levels were detected. The protein expressions of PKC, NOX2, NOX4 and 3-NT in rat myocardial tissue were determined by western blot. RESULTS AND CONCLUSION: The myocardial tissues in the exhaustive exercise and exhaustive exercise+drug groups were damaged, but the damage was significantly eased in the exhaustive exercise+drug group compared with the exhaustive exercise group. Compared with the control group, the reactive oxygen species level in the myocardial tissue of the exhaustive exercise group increased significantly (P < 0.05). Compared with the control group, the content of malondialdehyde in the myocardial tissues of the exhaustive exercise and exhaustive exercise+drug groups was significantly increased (P < 0.01), and the concentration of serum malondialdehyde in the exhaustive exercise group was significantly increased (P < 0.05). Compared with the control group, the expression levels of PKC, NOX2, NOX4 and 3-NT proteins in the myocardium of rats after exhaustive exercise were significantly increased (P < 0.01). Compared with the exhaustive exercise group, the expression levels of NOX2 and NOX4 in the myocardial tissue of rats significantly decreased in the exhaustive exercise+drug group (P < 0.01), and the expression of 3-NT significantly decreased (P < 0.05). Therefore, one-time exhaustive exercise can activate PKC and increase its protein expression in rat myocardial cells, which in turn induces an increase in the expression of NOX2 and NOX4 proteins in the myocardium, catalyzes the generation of large amounts of reactive oxygen species, and leads to the excessive production of peroxynitrite anions, thereby causing oxidative damage to the myocardium. [ABSTRACT FROM AUTHOR]

BACKGROUND: NKX2-5 is an important transcriptional regulator during mammalian heart development. Studies from model animals such as rats, mice, and zebrafish have shown that the absence or abnormal function of NKX2-5 affects heart development, leading to pathological manifestations similar to human congenital heart disease. However, the regulatory role and specific mechanisms of NKX2-5 in cardiac development are still unclear. OBJECTIVE: To review the molecular structure, functional effects, and upstream and downstream regulatory molecules of NKX2-5. METHODS: The search terms “NKX2-5, congenital heart disease, CHD, heart development” were used for literature retrieval in the PubMed database (website https://www.ncbi.nlm.nih.gov/pubmed/). The deadline for publication was April 1, 2019. By downloading and reading the retrieved literature, articles irrelevant to NKX2-5 and with duplicate opinions and similar conclusions were excluded. Finally 97 eligible articles were taken for review. RESULTS AND CONCLUSION: (1) NKX2-5 plays a key role in the regulation of cardiac development. Abnormal functions or gene mutations of NKX2-5 can lead to abnormal cardiac development and dysfunction, which are closely related to the occurrence of human congenital heart disease. (2) The function of NKX2-5 depends on its functional domains. NKX2-5 enters the nucleus after transcription and translation, and activates or inhibits downstream regulatory molecules through binding with CO-factors or alone to specific DNA sequences, thereby regulating the proliferation, migration, differentiation and function of cardiac precursor cells and regulating the correct cardiac development process and the normal development and function of the cardiac conduction system. (3) The transcription, translation, nucleation process, transcription activation or inhibition of NKX2-5 is also regulated by various methods. These regulatory factors regulate NKX2-5 from the aspects of chromatin conformation, promoter and enhancer functions, RNA uncoiling, post-transcriptional modification, and nuclear localization. [ABSTRACT FROM AUTHOR]

BACKGROUND: Bone marrow mesenchymal stem cells can be induced into myocardial tissue-like structure in vitro. Myocardial tissue lysates from different parts of the myocardium can be used to construct differential microenvironments. Few studies have investigated the targeted induction efficiency of bone marrow mesenchymal stem cells and the expression of related genes. OBJECTIVE: To investigate the effects of lysates from different parts of the myocardium on the differentiation of bone marrow mesenchymal stem cells into myocardial tissue-like structures and to assess the correlation between the expressions of related genes during induction and myocardial tissue engineering. METHODS: Passage 3 bone marrow mesenchymal stem cells from Sprague-Dawley rats were cultured. Whole heart tissue lysate, atrial muscle tissue lysate, and ventricular muscle tissue lysate were used to construct different microenvironments to induce bone marrow mesenchymal stem cells to differentiate into cardiomyocyte-like cells. The morphological changes and ultrastructure of cells were observed with an inverted phase contrast microscope and transmission electron microscopy. Expression of α-actin and cTnI was detected by immunofluorescence staining. qRT-PCR was used to detect the expression of upstream molecules ANP, HCN4 and downstream molecules MLC-2v in the cAMP/PKA signaling pathway after induction. RESULTS AND CONCLUSION: (1) Each induction cell group followed similar morphological changes: Cardiomyocyte-like cells were capable of autonomic beats, rhythmic contractions and relaxations; under the transmission electron microscope, there were a large number of arranged myofilaments; immunofluorescent staining showed positive expression of α-actin and cTnI. (2) The whole heart tissue lysate was able to induce the differentiation of bone marrow mesenchymal stem cells into rice grain-sized myocardial tissue-like structures with collagen fibers. (3) Atrial muscle tissue lysate could induce bone marrow mesenchymal stem cells to differentiate into atrial muscle-like cells. Autonomic beats appeared earlier, but the beat frequency and duration were shorter. ANP and HCN4 were highly expressed in atrial myocytes. (4) Ventricular muscle tissue lysate induced bone marrow mesenchymal stem cells to differentiate into ventricular muscle-like cells with no secretory granules, and MLC-2v was highly expressed in ventricular muscle-like cells. (5) To conclude, the whole heart tissue lysate can induce bone marrow mesenchymal stem cells to form myocardial tissue-like structures. Atrial muscle tissue lysate can induce bone marrow mesenchymal stem cells to differentiate into atrial muscle-like cells. Ventricular muscle tissue lysate can induce bone marrow mesenchymal stem cells to differentiate into ventricular muscle-like cells. By constructing a specific microenvironment, bone marrow mesenchymal stem cells can be differentiated to cardiomyocytes in different parts, providing laboratory data for the construction of myocardial tissue engineering. [ABSTRACT FROM AUTHOR]

Copyright of Journal of Modern Laboratory Medicine is the property of Journal of Modern Laboratory Medicine Editorial Department and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

BACKGROUND: Our previous experimental results have shown that hyaluronic acid(HA) hydrogel can act as a vehicle for bone marrow mesenchymal stem cell(BMSC) delivery to improve the cardiac function of rats with myocardial infarction. OBJECTIVE: To explore the effects of BMSCs encapsulated in HA hydrogel on histological changes of the rat myocardium after myocardial infarction. METHODS: BMSCs from male Sprague-Dawley rats were isolated and cultured, and then HA-encapsulated BMSCs were cultured in vitro in the three-dimensional manner. A model of myocardial infarction was made by ligating the left anterior descending artery of female Sprague-Dawley rats. After 1 week, the model rats were screened by ultrasonic testing and then eligible ones were randomly divided into four groups: PBS group(n=8), HA group(n=8), BMSCs group(n=29), and HA-encapsulated BMSCs group(n=29). At 1 week after ligation, the model rats underwent the secondary thoracotomy followed by corresponding injections into the infarcted region and its marginal zone. At 4 week after injection, cardiovascular regeneration, myocardial protection, and ventricular remodeling were evaluated using hematoxylin-eosin staining, Masson’s staining and immunohistochemical staining, respectively. RESULTS AND CONCLUSION: At 4 weeks after transplantation, compared with the PBS group, the infarcted ventricular wall was thickened in the HA group, cardiomyocyte hypertrophy was relieved and neovascularization was increased in the BMSCs group, and the largest benefits were indicated in the HA-encapsulated BMSCs group by reversing cardiac remodeling, increasing neovascularization and viable myocardium tissues in the infarct zone. Therefore, the HA-encapsulated BMSCs can achieve the best effect in the treatment of myocardial infarction. [ABSTRACT FROM AUTHOR]

BACKGROUND: Poly(glycerol sebacate) holds excellent and good biocompatibility, flexibility and degradability, which is widely used in soft tissue replacement and tissue engineering, drug delivery carrier, wound dressing, and bone-cartilage regeneration. OBJECTIVE: To summarize the research progress in the optimal synthesis and medical application of poly(glycerol sebacate) and Its compsites. METHODS: PubMed, Elsevier, CNKI and WanFang databases were retrieved. The key words were "poly(glycerol sebacate), synthesis, cardiac muscle, blood vessels, nerves, skin, drug delivery carrier, wound dressing, bone regeneration" in English and Chinese, respectively. Finally, 43 articles eligible for the inclusion criteria were obtained RESULTS AND CONCLUSION: In recent years, poly(glycerol sebacate) has attracted much attention because of its many excellent properties. Many basic scientific studies and animal experiments have confirmed that it is suitable for tissue engineering. Conventional poly(glycerol sebacate) curing process requires high temperature, high vacuum and long duration, which prevents the polymer from binding directly to cells or temperature-sensitive molecules, resulting in some limitations in its application. The composite scaffold material synthesized with a variety of other materials can make up for the corresponding shortcomings of its application in myocardial and vascular tissue engineering, drug delivery carrier, nerve guiding materials, skin and wound dressing, and bone-cartilage tissue engineering. At present, most of the studies on poly(glycerol sebacate) composites focus on the cytobiology level, and few studies focus on the mechanism of action in vivo. Further study may develop an important material for tissue replacement. [ABSTRACT FROM AUTHOR]

Copyright of China Mechanical Engineering is the property of Editorial Board of China Mechanical Engineering and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Objective To study the expression pattern of brain natriuretic peptide （BNP） in myocardial tissue from forensic routine cases and to explore its application value in the forensic determination of sudden cardiac death （SCD）. Methods The data of 96 autopsy cases accepted by the center of Medico-legal Investigation of China Medical University between December 2008 to May 2014 were collected. There were 62 cases in SCD group cardiac and 34 cases in non-SCD group. The myocardial tissues were taken from left and right ventricular wall, respectively. The expressions of BNP protein and BNP mRNA in myocardial tissue were detected by HE staining, immunohistochemical staining, Western blotting and quantitative real-time reverse transcription-polymerase chain reaction （RT-qPCR）, etc. Results The immunohistochemical staining of myocardial tissue showed diffusely positive staining in SCD group, and patchily or diffusely positive staining in non-SCD group with lighter degree. The result of Western blotting showed that the expression of BNP protein elevated in left ventricular wall of SCD group. The result of RT-qPCR showed a positive correlation between the BNP mRNA expressions in bilateral ventricular walls and the heart weight, bilateral lung weight, and N-terminal prohormone of brain natriuretic peptide （NT-proBNP） concentration. There were large differences between the BNP mRNA concentrations in SCD group and non-SCD group, and the former was statistically higher （P

Objective To observe the expression changes of hypoxia inducible factor-1α（HIF-1α） and vascular endothelial growth factor-A （VEGF-A） in rats with arrhythmias, and to explore the differences of the expression pattern in the two indicators of acute myocardial ischemia caused by arrhythmias and coronary insufficiency. Methods The arrhythmia was induced by CaCl2, and the expression changes of HIF-1α and VEGF-A were detected by immunohistochemistry, Western blotting and real-time PCR within 6 h after the arrhythmia in rats. Results The expression of HIF-1α and VEGF-A showed diffuse in the myocardial tissue of rats died from arrhythmias. Both of them increased in the early arrhythmia, then decreased. Extensive myocardial ischemia happened at the beginning of arrhythmia occurrence and its range didn’t expand with time. Conclusion The expressions of HIF-1α and VEGF-A in myocardium of the rats with arrhythmia can provide evidence for the differential diagnosis of acute myocardial ischemia caused by fatal arrhythmia and coronary insufficiency.

Cardiovascular complications are the leading cause of death in diabetic patients. Among them, diabetic cardiomyopathy (DCM) is a type of specific cardiomyopathy excluding myocardial damage caused by hypertension and coronary heart disease. It is characterized by abnormal metabolism of cardiomyocytes and gradual decline of cardiac function. The clinical manifestations of DCM are impaired diastolic function in early stage and impaired systolic function in late stage. Eventually it developed into heart failure. Mitochondria are the main organelles that provide energy in cardiomyocytes. Mitochondrial dynamics refers to the dynamic process of mitochondrial fusion and fission, which is an important approach for mitochondrial quality control. Mitochondrial dynamics plays a crucial role in maintaining mitochondrial homeostasis and cardiac function. The proteins that regulate mitochondrial fission are mainly Drp1 and its receptors, Fis1, MFF, MiD49 and MiD51. The protein that performs mitochondrial outer membrane fusion is Mfn1/2, and the inner membrane fusion protein is Opa1. This paper reviews recent progress on mitochondrial dynamics in DCM. The main contents are as follows: mitochondrial dynamics imbalance in both type 1 and 2 DCM is manifested as increased fission and inhibited fusion. The molecular mechanism of the former is mainly associated with up-regulated Drp1 and down-regulated Opa1, while the molecular mechanism of the latter is mainly associated with up-regulated Drp1 and down-regulated Mfn1/2. Increased mitochondrial fission and inhibited fusion can lead to mitochondrial dysfunction and promote the development of DCM. The active ingredients of the traditional Chinese medicine such as punicalagin, paeonol and endogenous substance melatonin can improve mitochondrial function and alleviate the symptoms of DCM by inhibiting mitochondrial fission or promoting mitochondrial fusion. This article is helpful to further understand the role and mechanism of mitochondrial dynamics in DCM, and provide new treatment methods and intervention strategies for clinical DCM patients based on mitochondrial dynamics.

Objective: To explore the application value of quantitative flow ratio (QFR) in the hemodynamic evaluation of myocardial bridge and to preliminarily evaluate the correlation and related influencing factors between deformation quantitative flow ratio (D-QFR) and QFR. Methods: This is a cross-sectional study. Patients with CAG-confirmed simple myocardial bridge of the middle anterior descending coronary artery from June 2012 to June 2022 at the Air Force Medical Center were retrospectively included in this study. Systolic stenosis of mural coronary arteries (MCA) and myocardial bridge length were measured using quantitative coronary angiography. The patients were divided into mild stenosis group (<50% systolic stenosis) and moderate-to-severe stenosis group (≥50% systolic stenosis) according to the Nobel grading criteria. At different time periods (systolic and diastolic), the QFR values were measured at 3 locations (1 to 2 cm before the MCA entrance, the middle segment of the MCA, and 1 to 2 cm after the MCA exit), denoted as QFRa, QFRb, and QFRc, respectively, and the D-QFR values, incorporating vessel deformation information, were recorded. The MCA distal QFR≤0.8 in either stage was defined as an abnormal QFR value. QFR values were compared between the two groups at different locations and within each group. Factors associated with abnormal QFR values were analysed using multifactorial logistic regression. Spearman rank correlation analysis was used to examine the correlation between D-QFR values and systolic and diastolic QFR values.Multiple linear regression was used to analyse the factors associated with D-QFR. Results: A total of 83 patients were enrolled, including 58 males, aged (57.1±13.1) years. There were 48 cases in the mild stenosis group and 35 cases in the moderate-to-severe stenosis group, and the differences in systolic and diastolic QFRb and QFRc values between the two groups were statistically significant (all P <0.05). Within-group comparisons showed the values of QFRb and QFRc in the systolic phase were lower than those in the diastolic phase; QFRb and QFRc were both lower than QFRa during the same period (all P <0.05). Multifactorial logistic regression analysis showed that MCA systolic stenosis ( OR =1.225, 95% CI 1.093-1.372, P <0.001) was an influential factor for abnormal QFR. D-QFR values were positively correlated with both systolic and diastolic QFR values (correlation coefficients were 0.849 and 0.675, respectively, both P <0.01). Multiple linear regression analysis showed that D-QFR values were negatively correlated with age ( β =-0.208, P =0.029), systolic stenosis ( β =-0.500, P <0.001), and myocardial bridge length ( β =-0.211, P =0.036). Conclusions: The QFR values in middle and distal of myocardial bridge decrease. The systolic stenosis rate of myocardial bridge is an important factor affecting QFR value. D-QFR is positively correlated with both systolic and diastolic QFR values. Age, myocardial bridge systolic stenosis rate and length are factors influencing the D-QFR values.

Objective: To investigate the correlation between 6-phosphofructo-2-kinase/fructose-2, 6-biphosphatase 3 (PFKFB3) and the inflammatory activation of polymorphonuclear myeloid-derived suppressor cell (PMN-MDSC) in acute myocardial infarction (AMI), and to evaluate the effect of intervention targeting PFKFB3 on the inflammatory activation of PMN-MDSC during AMI., Methods: (1) Clinical trial section: a observational study was conducted. The patients with acute coronary syndrome (ACS) admitted to Zhenjiang Fourth People's Hospital were enrolled, and they were divided into AMI group and non-AMI group according to clinical diagnosis. The peripheral venous blood of the two groups was collected to detect the proportion of PMN-MDSC, and the expression of PFKFB3 gene in mononuclear cells was detected by real-time quantitative polymerase chain reaction (RT-qPCR). (2) Basic experiment section: a total of 30 male C57 mice (aged 6-8 weeks) were divided into normal control group (n = 5), Sham group (n = 5), AMI model group (n = 10) and PFKFB3 inhibitor PKF-15 intervention group (n = 10) according to random number table method. The AMI model of mice was reproduced by left anterior descending coronary artery (LADCA) ligation, and the mice in the Sham group did not attach the artery after thoracotomy. The PKF-15 intervention group was intraperitoneally injected with PKF-15 (20 μg/g) at the same time of LADCA ligation. Normal control mice did not receive any treatment. Peripheral venous blood and myocardial tissue of mice were collected 24 hours after modeling. Both the circulating PMN-MDSC ratio and the infiltration of PMN-MDSC in myocardial tissue were detected. After staining with hematoxylin-eosin (HE), the degree of inflammatory damage in mouse myocardial tissue was observed under light microscopy. PMN-MDSC were isolated from mice with flow cytometry, and the gene expressions of PFKFB3 and inflammatory factors were measured by RT-qPCR., Results: (1) Clinical trial section: the circulating PMN-MDSC ratio of patients in the AMI group (n = 25) was significantly higher than that in the non-AMI group [n = 20; (8.53±0.96)% vs. (1.13±0.39)%, P < 0.01], and PFKFB3 gene expression in the peripheral blood mononuclear cells was also increased (2 -ΔΔCt : 1.18±0.19 vs. 0.96±0.16, P < 0.01). Pearson correlation analysis showed that circulating PMN-MDSC ratio was positively correlated with PFKFB3 gene expression in mononuclear cells in AMI patients (r = 0.608, P = 0.001). (2) Basic experimental section: the circulating PMN-MDSC ratio and the infiltration of PMN-MDSC in myocardial tissue of AMI mice were significantly higher than those in the normal control group and Sham group. PFK-15 intervention could reduce the ratio of PMN-MDSC in the peripheral blood and myocardial tissue of AMI mice [(26.33±5.27)% vs. (75.12±5.02)% in peripheral blood, (20.87±2.97)% vs. (35.28±4.36)% in myocardial tissue, both P < 0.01]. Under light microscopy, the myocardial cells in the AMI modal group were disordered and a large number of inflammatory cells infiltrated. PFK-15 intervention could maintain a normal arrangement of cardiomyocytes and reduce the infiltration of inflammatory cells. The gene expression levels of PFKFB3 in the peripheral blood and myocardial tissue as well as the inflammatory factors in the myocardial tissue of AMI mice were significantly higher than those in the normal control group and Sham group. PKF-15 intervention could effectively reduce the gene expression levels of PFKFB3 in the peripheral blood and myocardial tissue as well as the inflammatory factors in the myocardial tissue of AMI mice [PFKFB3 mRNA (2 -ΔΔCt ): 1.01±0.09 vs. 1.40±0.12 in peripheral blood, 0.95±0.09 vs. 1.47±0.10 in myocardial tissue; myocardial tissue tumor necrosis factor-α (TNF-α) mRNA (2 -ΔΔCt ) was 14.55±3.99 vs. 29.66±3.90, interleukin-1β (IL-1β) mRNA (2 -ΔΔCt ) was 8.72±1.35 vs. 18.53±2.43, IL-6 mRNA (2 -ΔΔCt ) was 11.87±2.97 vs. 19.82±4.32, all P < 0.01]., Conclusions: The activation of PFKFB3 is closely related to the inflammatory activation of PMN-MDSC during AMI. Inhibition of PFKFB3 activity can inhibit the inflammatory activation of PMN-MDSC and reduce myocardial inflammatory injury.

Objective To investigate the correlation between serum E-selectin (ES) and soluble intercellular adhesion molecule-1 (sICAM-1 ) and myocardial injury in children with mycoplasma pneumonia (MPP). Methods A total of 130 children with MPP admitted to Henan Children's Hospital from January 2016 to January 2018 were divided into non myocardial injury group (96 cases) and myocardial injury group (34 cases) according to whether myocardial injury occurred during hospitalization. General clinical data and laboratory test indexes of children with MPP were collected, and their relations hip with myocardial injury in MPP children was analyzed. Results The duration of fever, the time of macrolide administration, MP antibody titer, Creactive protein (CRP), interleukin 6(IL-6),tumor necrosis factor-α(TNF-α), creatine kinase isoenzyme, cardiac troponin I (cTnD, ES and sICAM-1 levels in myocardial injury group were significantly higher than those in non myocardial injury group (P< 0. 05). Spearman correla tionanalysis showed that ES were positively correlated with WBC, CRP, IL-6, TNF-α, cTnI and sICAMl (r = 0. 344, 0. 428, 0. 560, 0. 362, 0. 475, P< 0. 05), and sICAM-1 were positively correlated with WBC, IL-6, TNF-α, creatine kinase isoenzyme and cTnI (r = 0. 372, 0. 394, 0. 401, 0. 408, 0. 401, P <0. 05). ROC curve analysis showed that the AUC of ES and sICAM-1 in diagnosis of myocardial injury were 0. 782 and 0. 859, with sensitivity of 61. 76 % and 73 . 53 %, specificity of 88. 54% and 81. 25 %, respectively. Multivariate logistic regression analysis showed that sICAM-1 was an independent risk factor for myocardial injury in children with MPP. Conclusion Serum ES and sICAM-1 levels may be the influencing factors of myocardial injury in children with MPP, and s ICAM-1 is an independent influencing factor, which can be used as a clinical index for the diagnosis of myocardial injury in children with MPP. [ABSTRACT FROM AUTHOR]

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Objective To observe the influence of tip root acupoint combination pretreatment on calcium homeostasis, myocardial oxidative stress and inflammatory cytokines in diabetic rats with myocardial ischemia reperfusion (l/R) injury, analyze the mechanism from the aspect of p38MAPK signaling pathway and provide a new theoretical discussion and experimental basis for prevention and treatment of cardiovascular diseases in clinic. Methods All rats (n = 50) were randomly divided into 5 groups: sham operation group, model group, electro-acupuncture retreatment group, inhibitor pretreatment group and electro acupuncture + inhibitor pretreatment group (each n = 10). The sham operation group was not given other treatment after opening chest to expose heart, model group was given in vivo myocardial l/R operation, electro acupuncture retreatment group was given needling in Neiguan (PC6) and Zusanli (ST36) one week before modeling, inhibitor pretreatment group was given injection of SB203580 (inhibitor of p38MAPK signaling pathway) before modeling, and electro acupuncture + inhibitor pretreatment group was given injection of SB203580 one week after electro acupuncture retreatment and before modeling. All rats in 5 groups were treated and executed for collecting samples. The indexes related to calcium homeostasis, myocardial oxidative stress and inflammatory cytokines were detected in all groups. Results The difference in Na+ -K+ -ATPase, Mg2+ ATase, Ca2+ ATPase, superoxide dismutase , malondialdehyde < MDA> and tumor necrosis factor-a (TNPa) were significant between sham operation group and model group (P<0.05). There difference in the above mentioned indexes had statistical significance compared among inhibitor pretreatment group and electro acupuncture inhibitor pretreatment group. Conclusion The pretreatment of tip root acupoint combination aims at maintaining cardiom yocyte calcium homeostasis, improving ability of scavenging oxygen free radicals, inhibiting myocardial inflammation, and alleviating significantly damage of heart function due to l/R in diabetic rats with l/R injury. [ABSTRACT FROM AUTHOR]

Objective: To study the effect of GATA4 gene H435Y mutation on the heart function of mice and its possible mechanisms. Methods: Our research included in 2 groups: Wild type (WT) mice group and Gata4 H435Y mutant(Gata4 H435Y) mice group, 6 mice in each group. The heart function and the ratio of heart weight to body weight (HW/BW) were compared between 2 groups; the myocardial morphology was observed by Masson staining; the mRNA and protein expressions of GATA4, Sox9, Scleraxis, Tenascin and Aggrecan were determined by RT-PCR and Western blot analysis. Results: Compared with the WT mice, GATA4 H435Y mice group showed decreased LVEF, LV fraction shortening and increased left ventricular internal diameter at end-systole (LVESD)(P<0.05). The BWand ratio of HW/BWof GATA4 H435Y mice were obviously lower (P<0.05), the heart weight showed no significant difference between 2 groups (P>0.05). Masson staining showed that there was no significant difference in the myocardial fibers between the two groups, but the collagen fibers of myocardiumin WT group were deeper. The mRNA and protein expressions of GATA4, Sox9 and Scleraxis were decreased in GATA4 H435Y mice (P<0.05), Tenascin and Aggrecan showed no significant difference between 2 groups(P>0. 05). Conclusion: GATA4 gene H435Y mutation may affect the expression of extracellular matrix genes in cardiac muscle by reducing the expression of GATA4 and downstreamgenes, thereby impairing the cardiac function of mice. [ABSTRACT FROM AUTHOR]

Background 131I-metaiodobenzylguanidine (131I-MIBG), which can be taken by cardiac sympathetic postganglionic fibers, is an imaging agent to assess the cardiac sympathetic nerve function. The present study is to assess the cardiac sympathetic nerve function of patients with Parkinson's disease (PD) by 131I-MIBG myocardial scintigraphy and preliminarily explore its applications in the early diagnosis of PD. Methods Twenty-one eligible PD patients (16 early PD and 5 late PD) and 9 normal controls were enrolled in the study. Unified Parkinson's Disease Rating Scale (UPDRS) and Hoehn-Yahr stage were used to evaluate the severity of PD. Planar images of chest were obtained at different time points (15 min, 4 h and 24 h) after injection of 3 mCi 131I-MIBG, and then the 131I-MIBG myocardial uptake ratios were calculated. Results 1) The 131I-MIBG myocardial uptake ratios in PD group at 15 min (1.67 ± 0.38), 4 h (1.53 ± 0.47) and 24 h (1.35 ± 0.42) after injection were lower than those in the normal control group respectively (P = 0.000, 0.000, 0.000), and the 131I-MIBG myocardial uptake ratios in the PD group reduced over time (P = 0.002, 0.000, 0.000). 2) The 131I-MIBG myocardial uptake ratios in the early and late PD groups at 15 min [(1.73 ± 0.40) and (1.50 ± 0.30)], 4 h [(1.58 ± 0.51) and (1.37 ± 0.31)], 24 h [(1.39 ± 0.46) and (1.24 ± 0.29)] after injection were lower than those in the normal control group respectively (early PD: P = 0.000, 0.000, 0.000; late PD: P = 0.000, 0.000, 0.000), and the 131I-MIBG myocardial uptake ratios in the early and late PD groups reduced over time (early PD: P = 0.012, 0.000, 0.000; late PD: P = 0.039, 0.001, 0.024). Conclusions Cardiac sympathetic nerve damage could occur in PD patients, even at an early stage of PD. 131I-MIBG myocardial scintigraphy may help in the early diagnosis of PD. DOI: 10.3969/j.issn.1672-6731.2016.06.008

Objective: To define differentially expressed N6-adenylate methylation (m6A) genes in the myocardial tissue of mice with myocardial infarction (MI) and explore its potential impact on the pathological process of MI. Methods: The random number table method was used to divide the eighteen SPF C57BL/6J male mice aged from 8 to 10 weeks into MI group (MI group, n =9) and control group (control group, n =9). Modified m6A genes from the myocardial tissue were detected via methylated RNA immunoprecipitation with the next generation sequencing (MeRIP-seq). We explored methylation modified characteristics, verified mRNA expression and m6A modified level by bioinformatics analysis, qPCR and MeRIP-qPCR. Results: The Heatmap revealed that 901 differentially modified m6A genes between MI and control group, of which 537 genes were upregulated, and 364 genes were downregulated. The principal component analysis affirmed that two groups could be distinguished significantly in terms of m6A gene modification. The characteristic sequence of m6A modification was GGACU and mainly concentrated in the coding sequence. According to the conjoint analysis with RNA-seq and MeRIP-seq, 119 genes expressed simultaneous m6A modification difference and mRNA expression difference. The Venn diagram exhibited the positive and negative correlation between m6A modification and mRNA expression. Besides, the GO enrichment analysis indicated that the genes with m6A differential modification in MI group were mainly involved in heart development and other processes. qPCR verified that Gbp6 was up-regulated, while Dnaja1 and Dnajb1 were down-regulated. MeRIP-qPCR revealed that the m6A modification level of Hspa1b was downregulated. Conclusion: Myocardial infarction induces differential modification of m6A in the mice model. In addition, the genes with m6A modification may be affected by methylation related enzymes, thus participating the pathogenesis of MI by regulating apoptosis and inflammation.

Heart failure (HF),a chronic progressive disease,is a global health problem and the leading cause of deaths in the global population.The pathophysiological abnormalities of HF mainly include abnormal cardiac structure (myocardium and valves),disturbance of electrophysiological activities,and weakened myocardial contractility.In addition to drug therapy and heart transplantation,interventional therapies can be employed for advanced-stage HF,including transcatheter interventions and mechanical circulatory assist devices.This article introduces the devices used for advanced HF that have been marketed or certified as innovative or breakthrough devices around the world and summarizes the research status and prospects the trend in this field.As diversified combinations of HF devices are used for the treatment of advanced HF,considerations regarding individualized HF therapy,risk-benefit evaluation on device design,medical insurance payment,post-market supervision system,and protection of intellectual property rights of high-end technology are needed,which will boost the development of the technology and industry and benefit the patients.

Objective To analyze and summarize the clinical data of children with myocardial densification（NVM） combined with congenital heart disease，explore the best treatment for the disease. Methods 48 children with NVM combined with congenital heart disease were collected admitted to the hospital from September 2007 to June 2017. According the treat⁃ ment plan，the 48 cases divided into 3 groups：interventional group（9 cases），surgical group（11cases）and drugs group（28 cases）. The clinical manifestations, pregnancy status, previous medical history, family history, auxiliary examination, treatment plan and prognosis of the three groups were analyzed, and the clinical efficacy of the three groups was compared.Results In the 48 cases children，43 cases had pneumonia，38 cases had heart failure，16 cases had arrhythmias，no one had thrombosis.According to the quantity of cases，the combined heart disease were ASD，pulmonary hypertension，the disease of tricuspid valve，the disease of mitral valve，PDA，VSD.In the interventional group，6 cases had no NVM，2 case got better.In the surgical group，3 cases were dead，1 case was given up，and in the live children，5 cases had no NVM.In the drugs group，1 case was dead，2 cases were given up，and in the live children ，2 cases had no NVM，9 cases had no significant changes. The improvement rate of NVM after treat⁃ ment for congenital heart disease in the interventional group and the surgical group were significantly higher than that in the drug group，the differences were statistically significant（P<0.05）. Conclusion Comparing with drugs group，the NVM of the cases of interventional group and surgical group improve obviously after treatment for congenital heart disease. [ABSTRACT FROM AUTHOR]

Objective To systematically evaluate the effect of dexmedetomidine on myocardial injury in the patients with sepsis. Methods The databases such as Pubmed，Cochrane Library，Embase，Web of Science，CNKI，VIP database， Wangfang Database and CMCC were retrieved by computer，and the unpublished and on-going clinical trials were also re- trieved. Meanwhile all the related study literatures were retrieved. The retrieval contents were the clinical study literatures on the impact of dexmedetomidine and other sedative drugs on myocardial injury in the patients with sepsis. The retrieval time was up to December 2017.The literatures were carefully read and the related trials were included strictly according to the inclusion and excluding criteria. Then extracted data were performed the meta analysis by using the Revman5.3 software. Results Five randomized controlled trials（RCT）were finally included，involving 337 cases of sepsis. One hundred and seventy cases（study group）adopted the dexmedetomidine intervention and 167 cases（control group）adopted other sedative drugs. The ultra-TnI level after 24 h sedation in the study group was significantly lower than that in the control group，the NT-proBNP level after 24， 48，72 h sedation in the study group was still significantly lower than that in the control group，the differences were statistically significant（P<0.05）.The ICU hospitalization duration，28 d fatality rate，and acute physical and chronic health evaluation （APACHEⅡ）score had no statistical difference between the two groups（P>0.05）. Conclusion Dexmedetomidine can effec- tively improve the myocardial function in the aspect of treating myocardial injury in septic patients. [ABSTRACT FROM AUTHOR]