A Pilot Study on Real-time Monitoring of Heart Rate and Movement Speed in Middle-distance Race of Physical Education Classes

In Chinese universities, students need to participate in the middle-distance-race. Normally, female students are required to participate in the race of 800 meters, while male students are required to participate in the race of 1000 meters. However, it is difficult for teachers to grasp the real time information of students during the race. And there is a lack of timely communications between the teachers and students. Focusing on this issue, this study, with the use of POLAR heart rate sensor and other modern information technologies, expands the original function of the sensor to achieve a concurrent operation of detecting heart rates and automatically measuring the movement speed. The researchers have successfully designed a micro system to monitor the process of middle-distance race. Moreover, the study also engages in a preliminary experiment verification so as to provide object and effective reference and basis for the middle-distance race physical education teaching in universities

Thioredoxin-1 maintains mechanistic target of rapamycin (mTOR) function during oxidative stress in cardiomyocytes

Thioredoxin 1 (Trx1) is a 12-kDa oxidoreductase that catalyzes thiol-disulfide exchange reactions to reduce proteins with disulfide bonds. As such, Trx1 helps protect the heart against stresses, such as ischemia and pressure overload. Mechanistic target of rapamycin (mTOR) is a serine/threonine kinase that regulates cell growth, metabolism, and survival. We have shown previously that mTOR activity is increased in response to myocardial ischemia-reperfusion injury. However, whether Trx1 interacts with mTOR to preserve heart function remains unknown. Using a substrate-trapping mutant of Trx1 (Trx1C35S), we show here that mTOR is a direct interacting partner of Trx1 in the heart. In response to H2O2 treatment in cardiomyocytes, mTOR exhibited a high molecular weight shift in non-reducing SDS-PAGE in a 2-mercaptoethanol-sensitive manner, suggesting that mTOR is oxidized and forms disulfide bonds with itself or other proteins. The mTOR oxidation was accompanied by reduced phosphorylation of endogenous substrates, such as S6 kinase (S6K) and 4E-binding protein 1 (4E-BP1) in cardiomyocytes. Immune complex kinase assays disclosed that H2O2 treatment diminished mTOR kinase activity, indicating that mTOR is inhibited by oxidation. Of note, Trx1 overexpression attenuated both H2O2-mediated mTOR oxidation and inhibition, whereas Trx1 knockdown increased mTOR oxidation and inhibition. Moreover, Trx1 normalized H2O2-induced down-regulation of metabolic genes and stimulation of cell death, and an mTOR inhibitor abolished Trx1-mediated rescue of gene expression. H2O2-induced oxidation and inhibition of mTOR were attenuated when Cys-1483 of mTOR was mutated to phenylalanine. These results suggest that Trx1 protects cardiomyocytes against stress by reducing mTOR at Cys-1483, thereby preserving the activity of mTOR and inhibiting cell death

An alternative mitophagy pathway mediated by Rab9 protects the heart against ischemia

Energy stress, such as ischemia, induces mitochondrial damage and death in the heart. Degradation of damaged mitochondria by mitophagy is essential for the maintenance of healthy mitochondria and survival. Here, we show that mitophagy during myocardial ischemia was mediated predominantly through autophagy characterized by Rab9-associated autophagosomes, rather than the well-characterized form of autophagy that is dependent on the autophagy-related 7 (Atg) conjugation system and LC3. This form of mitophagy played an essential role in protecting the heart against ischemia and was mediated by a protein complex consisting of unc-51 like kinase 1 (Ulk1), Rab9, receptor-interacting serine/ thronine protein kinase 1 (Rip1), and dynamin-related protein 1 (Drp1). This complex allowed the recruitment of transGolgi membranes associated with Rab9 to damaged mitochondria through S179 phosphorylation of Rab9 by Ulk1 and S616 phosphorylation of Drp1 by Rip1. Knockin of Rab9 (S179A) abolished mitophagy and exacerbated the injury in response to myocardial ischemia, without affecting conventional autophagy. Mitophagy mediated through the Ulk1/Rab9/Rip1/Drp1 pathway protected the heart against ischemia by maintaining healthy mitochondria

Comparative Analysis of mRNA Isoform Expression in Cardiac Hypertrophy and Development Reveals Multiple Post-Transcriptional Regulatory Modules

Cardiac hypertrophy is enlargement of the heart in response to physiological or pathological stimuli, chiefly involving growth of myocytes in size rather than in number. Previous studies have shown that the expression pattern of a group of genes in hypertrophied heart induced by pressure overload resembles that at the embryonic stage of heart development, a phenomenon known as activation of the “fetal gene program”. Here, using a genome-wide approach we systematically defined genes and pathways regulated in short- and long-term cardiac hypertrophy conditions using mice with transverse aortic constriction (TAC), and compared them with those regulated at different stages of embryonic and postnatal development. In addition, exon-level analysis revealed widespread mRNA isoform changes during cardiac hypertrophy resulting from alternative usage of terminal or internal exons, some of which are also developmentally regulated and may be attributable to decreased expression of Fox-1 protein in cardiac hypertrophy. Genes with functions in certain pathways, such as cell adhesion and cell morphology, are more likely to be regulated by alternative splicing. Moreover, we found 3′UTRs of mRNAs were generally shortened through alternative cleavage and polyadenylation in hypertrophy, and microRNA target genes were generally de-repressed, suggesting coordinated mechanisms to increase mRNA stability and protein production during hypertrophy. Taken together, our results comprehensively delineated gene and mRNA isoform regulation events in cardiac hypertrophy and revealed their relations to those in development, and suggested that modulation of mRNA isoform expression plays an importance role in heart remodeling under pressure overload

The Effects of Estrogen Receptor -Alpha, Estrogen and Phytoestrogen on Global Myocardial Ischemia -Reperfusion Injury

250 p.Thesis (Ph.D.)--University of Illinois at Urbana-Champaign, 2000.The effects of estrogen receptor-alpha on myocardial ischemia-reperfusion injury were investigated in male estrogen receptor-alpha knockout (ERKO) and wild-type control mice (Control). The effects of estrogen and phytoestrogen were investigated in 6 control mice (Control). The effects of estrogen and phytoestrogen were investigated in 6 groups of female rats. One group was a sham-operated control for ovariectomy and fed a diet free of phytoestrogen (SHAM group). One group was ovariectomized and fed a diet containing no phytoestrogen (OVX group). One group was ovariectomized, fed a phytoestrogen-free diet and was implanted a 17 beta-estradiol capsule subcutaneously (OVX+E2 group). One group was ovariectomized and fed a diet containing 49.39 mg isoflavones/g protein (HPE group). One group was ovariectomized, fed the same diet as the HPE group and treated with ICI 182780 (HPE+ICI group). The last group was ovariectomized and fed a diet containing 3.32 mg isoflavones/g protein (LPE group). Mouse hearts were subjected to 45 minutes of global ischemia followed by 180 minutes of reperfusion. Rat hearts were subjected to 30 minutes of ischemia followed by 120 minutes of reperfusion. The hearts were excised, cannulated, and maintained in a chilled (4°C) cardioplegia solution until warm (37°C), oxygenated Krebs-Henseleit bicarbonate buffer was perfused through the coronary arteries. All hearts were allowed to beat spontaneously. ERKOs started beating later and had a higher incidence of ventricular arrhythmias than the Controls. The OVX and the HPE+ICI groups had significantly lower left ventricular dP/dtmax. Coronary flow rate was significantly lower in ERKO hearts and the OVX group of rat hearts. Myocardial calcium ion accumulation was significantly greater in ERKOs and the OVX and LPE groups. Nitrite production was significantly less in ERKOs in the OVX the HPE+ICI and LPE groups. Mitochondrial respiratory function was significantly lower in experimental ERKOs the OVX the HPE+ICI and the LPE groups. Marked myocardial damage was seen in Hematoxylin and Eosin stained sections, Hematoxylin basic fuchsin picric acid stained sections and ultra-thin sections from ERKOs and the OVX and HPE+ICI groups.U of I OnlyRestricted to the U of I community idenfinitely during batch ingest of legacy ETD

Pharmacological modulation of autophagy during cardiac stress.

Autophagy is an evolutionarily conserved intracellular mechanism for degradation of long-lived proteins and organelles. Accumulating lines of evidence indicate that autophagy is deeply involved in the development of cardiac disease. Autophagy is upregulated in almost all cardiac pathological states, exerting both protective and detrimental functions. Whether autophagy activation is an adaptive or maladaptive mechanism during cardiac stress seems to depend upon the pathological context in which it is upregulated, the extent of its activation, and the signaling mechanisms promoting its enhancement. Pharmacological modulation of autophagy may therefore represent a potential therapeutic strategy to limit myocardial damage during cardiac stress. Several pharmacological agents that are able to modulate autophagy have been identified, such as mammalian target of rapamycin inhibitors, adenosine monophosphate-dependent kinase modulators, sirtuin activators, myo-inositol-1,4,5-triphosphate and calcium-lowering agents, and lysosome inhibitors. Although few of these modulators of autophagy have been directly tested during cardiac stress, many of them seem to have high potential to be efficient in the treatment of cardiac disease. We will discuss the potential usefulness of different pharmacological activators and inhibitors of autophagy in the treatment of cardiac diseases. © 2012 by Lippincott Williams & Wilkins