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In order to effectively solve the problems of independent construction of various systems in the existing coal industry, lack of sharing of multi-system data, low utilization of intelligent analysis and data mining, this paper uses the Internet of Things, big data, artificial intelligence and other information technologies, and on the basis of in-depth integration of coal mine safety management business, we proposed the construction scheme of the whole process traceable coal mine safety intelligent management and control cloud platform, focusing on the analysis of risk management and control, hidden danger trouble shooting, team task processing business processes such as violation correction. The platform realizes the storage, integration and analysis of multi-source heterogeneous monitoring data through the data center, integrates the nine subsystems involved in coal mine safety management into the safety intelligent management and control platform, and uses the data to share a chart for collaborative management and control and effective analysis and display of data. The application results show that the platform has realized coal mine data fusion, collaborative control, business linkage and decision-making, and has a good effect in improving safety control efficiency, reducing control costs and maximizing enterprise interests.

IGF-I rescues diabetic heart defects and oxidative stress, although the underlying mechanism of action remains poorly understood. This study was designed to delineate the beneficial effects of IGF-I with a focus on RhoA, Akt, and eNOS coupling. Echocardiography was performed in normal or diabetic Friend Virus-B type (FVB) and IGF-I transgenic mice. Cardiomyocyte contractile properties were evaluated using peak shortening (PS), time-to-90% relengthening ([TR.sub.90]), and intracellular [Ca.sup.2+] rise and decay. Diabetes reduced fraction shortening, PS, and intracellular [Ca.sup.2+]; it increased chamber size, prolonged [TR.sub.90], and intracellular [Ca.sup.2+] decay. Levels of RhoA mRNA, active RhoA, and [O.sup.-.sub.2] were elevated, whereas nitric oxide (NO) levels were reduced in diabetes. Diabetes-induced [O.sup.-.sub.2] accumulation was ablated by the NO synthase (NOS) inhibitor nitro-Larginine methyl ester (L-NAME), indicating endothelial NOS (eNOS) uncoupling, all of which except heart size were negated by IGF-I. The IGF-I-elicited beneficial effects were mimicked by the Rho kinase inhibitor Y27632 and BH4. Diabetes depressed expression of [Kv.sub.1.2] and dihydrofolate reductase (DHFR), increased [beta]-myosin heavy-chain expression, stimulated p38 MAPK, and reduced levels of total Akt and phosphorylated Akt/eNOS, all of which with the exception of myosin heavy chain were attenuated by IGF-I. In addition, Y27632 and the eNOS coupler folate abrogated glucose toxicity-induced PS decline, [TR.sub.90] prolongation, while it increased [O.sup.-.sub.2] and decreased NO and [Kv.sub.1.2] levels. The DHFR inhibitor methotrexate impaired myocyte function, NO/[O.sup.-.sub.2] balance, and rescued Y27632-induced cardiac protection. These results revealed that IGF-I benefits diabetic hearts via Rho inhibition and antagonism of diabetes-induced decrease in pAkt, eNOS uncoupling, and [K.sup.+] channel expression. heart; Akt; [K.sup.+] channel; cardiomyocytes; nitric oxide; intracellular [Ca.sup.2+]

Women with functional ovaries have a lower cardiovascular risk than men and postmenopausal women. However, estrogen replacement therapy remains controversial. This study examined the effect of ovarian hormone deficiency and estrogen replacement on ventricular myocyte contractile function and PKB/Akt activation. Nulliparous female rats were subjected to bilateral ovariectomy (Ovx) or sham operation (sham). A subgroup of Ovx rats received estrogen ([E.sub.2]) replacement (40 [micro]g*[kg.sup.-1]* [day.sup.-1]) for 8 weeks. Mechanical and intracellular [Ca.sup.2+] properties were evaluated including peak shortening (PS), time to PS (TPS), time to 90% relengthening (T[R.sub.90]), maximal velocity of shortening/relengthening ([+ or -]dL/dt), fura 2 fluorescence intensity (FFI), and decay rate. Levels of sarco(endo)plasmic reticulum [Ca.sup.2+]-ATPase (SERCA2a), phospholamban (PLB), and Akt were assessed by Western blot. Ovx promoted body weight gain associated with reduced serum [E.sub.2] and uterine weight, all of which were abolished by [E.sub.2]. Ovx depressed PS and [+ or -] dL/dt, prolonged TPS, T[R.sub.90], and decay rate, and enhanced resting FFI, all of which, with the exception of TPS, were restored by [E.sub.2]. Ovx did not alter the levels of SERCA2a, PLB, and total Akt, but significantly reduced Akt activation [phosphorylated Akt (pAkt)], pAkt/Akt, and the SERCA2a-to-PLB ratio. These alterations in protein expression were restored by [E.sub.2]. [E.sub.2] enhanced PS and +dL/dt in vitro, which was abolished by the [E.sub.2] receptor antagonist ICI-182780. Ovx reduced myocyte [Ca.sup.2+] responsiveness and lessened stimulating frequency-induced decline in PS, both ablated by [E.sub.2]. These data suggest that mechanical and protein functions of ventricular myocytes are directly regulated by [E.sub.2]. ovariectomy; cardiac myocyte; contraction, intracellular [Ca.sup.2+]

This study characterized the cardiac contractile function and IGF-I response in a transgenic diabetic mouse model. Mechanical properties were evaluated in cardiac myocytes from OVE26 diabetic and FVB wild-type mice, including peak shortening (PS), time to PS (TPS), time to 90% relengthening (T[R.sub.90]) and maximal velocity of shortening/relengthening ([+ or -]dL/dt). Intracellular [Ca.sup.2+] was evaluated as [Ca.sup.2+]-induced [Ca.sup.2+] release [difference in fura 2 fluorescent intensity ([DELTA]FFI)] and fluorescence decay rate ([tau]). Sarco(endo)plasmic reticulum [Ca.sup.2+]-ATPase (SERCA)2a, phospholamban (PLB), [Na.sup.+]-[Ca.sup.2+] exchanger (NCX), GLUT4, and the serine-threonine kinase Akt were assessed by Western blot. RhoA and IGF-I/IGF-I receptor mRNA levels were determined by RT-PCR and Northern blot. OVE26 myocytes displayed decreased PS, [+ or -]dL/dt, and ([DELTA]FFI associated with prolonged TPS, T[R.sub.90], and [tau]. SERCA2a, NCX, and Akt activation were reduced, whereas PLB and RhoA were enhanced in OVE26 hearts. GLUT4 was unchanged. IGF-I enhanced PS and [DELTA]FFI in FVB but not OVE26 myocytes. IGF-I mRNA was increased, but IGF-I receptor mRNA was reduced in OVE26 hearts and livers. These results validate diabetic cardiomyopathy in OVE26 mice due to reduced SERCA2, NCX, IGF-I response, and Akt activation associated with enhanced RhoA level, suggesting a therapeutic potential for Akt and RhoA. diabetic mouse; ventricular myocyte; excitation-contraction coupling; insulin-like growth factor I; sarco(endo)plasmic reticulum [Ca.sup.2+]-ATPase; sodium-calcium exchanger

Diabetic cardiomyopathy is characterized by impaired ventricular contraction and altered function of insulin-like growth factor I (IGF-I), a key factor for cardiac growth and function. Endogenous IGF-I has been shown to alleviate diabetic cardiomyopathy. This study was designed to evaluate exogenous IGF-I treatment on the development of diabetic cardiomyopathy. Adult rats were divided into four groups: control, control + IGF-I, diabetic, and diabetic + IGF-I. Streptozotocin (STZ; 55 mg/kg) was used to induce experimental diabetes immediately followed by a 7-wk IGF-I (3 mg*[kg.sup.-1]*[day-1] ip) treatment. Mechanical properties were assessed in ventricular myocytes including peak shortening (PS), time-to-PS (TPS), time-to-90% relengthening ([TR.sub.90]) and maximal velocities of shortening/relengthening ([+ or -] dL/dt). Intracellular [Ca.sup.2+] transients were evaluated as [Ca.sup.2+]-induced [Ca.sup.2+] release and [Ca.sup.2+] clearing constant. Levels of sarco(endo)plasmic reticulum [Ca.sup.2+]-ATPase (SERCA), phospholamban (PLB), and glucose transporter (GLUT4) were assessed by Western blot. STZ caused significant weight loss and elevated blood glucose, demonstrating the diabetic status. The diabetic state is associated with reduced serum IGF-I levels, which were restored by IGF-I treatment. Diabetic myocytes showed reduced PS and [+ or -] dL/dt as well as prolonged TPS, [TR.sub.90], and intracellular [Ca.sup.2+] clearing compared with control. IGF-I treatment prevented the diabetes-induced abnormalities in PS, [+ or -] dL/dt, [TR.sub.90], and [Ca.sup.2+] clearing but not TPS. The levels of SERCA and GLUT4, but not PLB, were significantly reduced in diabetic hearts compared with controls. IGF-I treatment restored the diabetes-induced decline in SERCA, whereas it had no effect on GLUT4 and PLB levels. These results suggest that exogenous IGF-I treatment may ameliorate contractile disturbances in cardiomyocytes from diabetic animals and could provide therapeutic potential in the treatment of diabetic cardiomyopathy. diabetic cardiomyopathy; insulin-like growth factor I; ventricular myocytes; sarco(endo)plasmic reticulum [Ca.sup.2+]-ATPase; glucose transporter 4

Alcoholic cardiomyopathy is characterized by impaired ventricular function although its toxic mechanism is unclear. This study examined the impact of cardiac overexpression of alcohol dehydrogenase (ADH), which oxidizes ethanol into acetaldehyde (ACA), on ethanol-induced cardiac contractile defect. Mechanical and intracellular [Ca.sup.2+] properties were evaluated in ventricular myocytes from ADH transgenic and wild-type (FVB) mice. ACA production was assessed by gas chromatography. ADH myocytes exhibited similar mechanical properties but a higher efficiency to convert ACA compared with FVB myocytes. Acute exposure to ethanol depressed cell shortening and intracellular [Ca.sup.2+] in the FVB group with maximal inhibitions of 23.3% and 23.4%, respectively. Strikingly, the ethanol-induced depression on cell shortening and intracellular [Ca.sup.2+] was significantly augmented in the ADH group, with maximal inhibitions of 43.7% and 40.6%, respectively. Pretreatment with the ADH inhibitor 4-methylpyrazole (4-MP) or the aldehyde dehydrogenase inhibitor cyanamide prevented or augmented the ethanol-induced inhibition, respectively, in the ADH but not the FVB group. The ADH transgene also substantiated the ethanol-induced inhibition of maximal velocity of shortening/relengthening and unmasked an ethanol-induced prolongation of the duration of shortening/relengthening, which was abolished by 4-MP. These data suggest that elevated cardiac ACA exposure due to enhanced ADH expression may play an important role in the development of alcoholic cardiomyopathy. transgene; acetaldehyde; shortening; intracellular calcium ion transient

This study was designed to evaluate the effects of a novel phytoestrogen, α-zearalanol (α-ZAL), and estradiol benzoate (B-E2), on c-myc, c-fos, and EGFR expression in normal human breast tissues implanted into nude mice. A xenograft-model, pieces of normal human breast tissue implanted subcutaneously into 9–10-week-old athymic nude mice, was established. The mice were divided into five groups subjected to the following treatments: normal saline (Controls); α-ZAL at 1 and 5 mg/kg; and estradiol benzoate (B-E2) at 1 and 5 mg/kg. Treatment was given every other day, and human breast tissues were removed for experiments after treatment for 30 days. The expression of c-myc, c-fos, and EGFR mRNAs were determined by in situ hybridization. α-ZAL decreased expression of c-myc ( p < 0.05). About 1 mg/kg α-ZAL increased EGFR expression ( p < 0.05) and two dosage of α-ZAL increased c-fos expression ( p < 0.01) compared with control. B-E2 significantly increased expression of c-myc, c-fos, and EGFR mRNAs expression compared with controls ( p < 0.01). The extents of the increases in EGFRmRNA expression induced by α-ZAL and in c-fos mRNA by 5 mg/kg α-ZAL were lower than those induced by B-E2 ( p < 0.01). These data suggest that the phytoestrogen α-ZAL may be safer than estrogen on breast. [ABSTRACT FROM AUTHOR]

Abstract: Although estrogen replacement therapy may improve dampened endothelial function in postmenopausal women, the associated risk of breast and ovarian cancer has limited its long-term use. Identifying effective alternative remedy with less carcinogenicity is in serious demand. This study was designed to examine the effect of the phytoestrogen α-zearalanol (α-ZAL) on homocysteine-induced endothelin-1 (ET-1) induction, reactive oxygen species (ROS) production and transcription pathways in human umbilical vein endothelial cells (HUVECs). ROS was measured by DCF fluorescent microscopy. Homocysteine-induced expression of ET-1 mRNA, ERK, pERK and c-jun/AP-1 protein was measured using RT-PCR and Western blot analysis, respectively. ET-1 secretion was determined by the enzymatic immunoassay. Transcriptional factor AP-1 expression in response to α-ZAL, homocysteine or both was evaluated by transient transfection assay. Our data revealed that α-ZAL ablated homocysteine-elicited ET-1 secretion, upregulated ET-1 mRNA and homocysteine-induced ROS accumulation without any effects by itself. α-ZAL also nullified homocysteine-induced increase in c-Jun/AP-1 expression/activity without eliciting any effect by itself. Collectively, our data indicated that α-ZAL may antagonize homocysteine-induced ET-1 gene induction, ROS accumulation, activation of ERK signaling pathway and AP-1 transcriptional factor, all of which may contribute to α-ZAL-induced beneficial effect on endothelial function. [Copyright &y& Elsevier]