Molecular and Physiological Effects of 17α-methyltestosterone on Sex Differentiation of Black Rockfish, Sebastes schlegelii.

It is widely known that all-female fish production holds economic value for aquaculture. Sebastes schlegelii, a preeminent economic species, exhibits a sex dimorphism, with females surpassing males in growth. In this regard, achieving all-female black rockfish production could significantly enhance breeding profitability. In this study, we utilized the widely used male sex-regulating hormone, 17α-methyltestosterone (MT) at three different concentrations (20, 40, and 60 ppm), to produce pseudomales of S. schlegelii for subsequent all-female offspring breeding. Long-term MT administration severely inhibits the growth of S. schlegelii, while short term had no significant impact. Histological analysis confirmed sex reversal at all MT concentrations; however, both medium and higher MT concentrations impaired testis development. MT also influenced sex steroid hormone levels in pseudomales, suppressing E2 while increasing T and 11-KT levels. In addition, a transcriptome analysis revealed that MT down-regulated ovarian-related genes (cyp19a1a and foxl2) while up-regulating male-related genes (amh) in pseudomales. Furthermore, MT modulated the TGF-ß signaling and steroid hormone biosynthesis pathways, indicating its crucial role in S. schlegelii sex differentiation. Therefore, the current study provides a method for achieving sexual reversal using MT in S. schlegelii and offers an initial insight into the underlying mechanism of sexual reversal in this species.

Telomere-to-telomere gapless genome assembly of the Chinese sea bass (Lateolabrax maculatus).

Chinese sea bass (Lateolabrax maculatus) is a highly sought-after commercial seafood species in Asian regions due to its excellent nutritional value. With the rapid advancement of bioinformatics, higher standards for genome analysis compared to previously published reference genomes are now necessary. This study presents a gapless assembly of the Chinese sea bass genome, which has a length of 632.75 Mb. The sequences were assembled onto 24 chromosomes with a coverage of over 99% (626.61 Mb), and telomeres were detected on 34 chromosome ends. Analysis using Merqury indicated a high level of accuracy, with an average consensus quality value of 54.25. The ONT ultralong and PacBio HiFi data were aligned with the assembly using minimap2, resulting in a mapping rate of 99.9%. The study also identified repeating elements in 20.90% (132.25 Mb) of the genome and inferred 22,014 protein-coding genes. These results establish meaningful groundwork for exploring the evolution of the Chinese sea bass genome and advancing molecular breeding techniques.

[Experimental study of mitochondrion-targeted small molecule IR-61 ameliorated exhaustive exercise-induced cardiac injury in rats].

OBJECTIVE: To investigate the effects of mitochondrion-targeted cyanine fluorescent small molecule IR-61 on cardiac injury induced by exhaustive exercise in rats. METHODS: Thirty-six adult male SD rats were randomly divided into 3 groups(n=12),control group (Ctrl), exhaustive exercise group (EE) and IR-61+ exhaustive exercise group (IR-61+EE). IR-61+EE group were intraperitoneally injected with 2 mg/kg IR-61 at the same time on day 1, 4 and 7. One hour after the end of the last drug administration, the two exhaustive exercise groups were subjected to exhaustive exercise modeling. The rats were placed on an animal treadmill with a slope of 0° at a speed of 10~15 m/min to coordinate their limbs running posture, and then ran at a speed of 25~30 m/min until exhaustion about 15 minutes later. After the animal models established, ECG was recorded by physiological recorder, myocardial injury was observed by light microscope, mitochondrial injury was observed by transmission electron microscope, myocardial cell apoptosis was detected by TUNEL method, markers of myocardial injury were detected by ELISA, and myocardial mitochondrial respiration rate was measured by high-resolution Oxygraph-2K mitochondrial instrument. RESULTS: ① Compared with Ctrl group, heart rate was increased, PR interval was shortened, QRS interval was prolonged, QTc was prolonged and ST segment was depressed significantly in EE group (P＜0.05). In EE group, myocardial fiber fracture and mitochondrial inner chamber swelling were obvious, mitochondrial crest was fuzzy, mitochondrial outer membrane was incomplete, and a large number of mitochondrial rupture and fusion were visible. In EE group, TUNEL staining cells were abundant, chromatin concentration and marginalization, nuclear membrane lysis, chromatin fragmentation into massive apoptotic bodies, apoptosis score increased (P＜0.05). The levels of creatine kinase isoenzyme-MB (CK-MB), cardiac troponin I(cTn-I) and N-terminal B-type natriuretic peptide (NT-proBNP) were increased in EE group (P＜0.05). Basal respiration rate, oxidative respiration rate of fatty acids and respiration rate of complex Ⅰ, Ⅱ and Ⅳ were all decreased (P＜ 0.05). ② Compared with EE group, the heart rate in IR-61+EE group was increased, PR interval was prolonged, QRS interval was shortened, QTc was shortened, ST segment was not significantly depressed (P＜0.05). In IR-61+EE group, myocardial fiber arrangement was loose, no obvious fracture was observed, mitochondrial inner ventricle was swelling, mitochondrial outer membrane was intact, TUNEL stained cells and unstained cells were observed, the overall morphology was more similar to Ctrl group. Apoptosis index was decreased (P＜0.05), the levels of CK-MB and cTn-I were decreased in IR-61+EE group (P＜0.05). The oxidative respiration rate of fatty acids and the respiration rate of complex Ⅱ and Ⅳ were increased (P＜0.05). CONCLUSION: Mitochondrion-targeted cyanine fluorescent small molecule IR-61 can improve cardiac electrical activity, reduce myocardial cell injury and mitochondrial injury, reduce myocardial cell apoptosis, and improve the myocardial mitochondrial energy metabolism condition in exhausted rats.

Optimization of exercise preconditioning duration in protecting from exhausted exercise-induced cardiac injury in rats.

The effect of different duration of exercise preconditioning (EP) on protecting from exhaustive exercise-induced cardiac injury (EECI) has been optimized in rats. Male Sprague-Dawley rats were divided into six groups: the control group, exhaustive exercise (EE) group, EP 20-min + EE group, EP 40-min + EE group, EP 60-min + EE group and EP 80-min + EE group. The EP groups were subjected to treadmill running at the intensity of 74.0% V̇O2 max. Changes of exercise capacity, cardiac pathology, myocardial enzymology, electrocardiogram (ECG), cardiac function, and mitochondrial respiratory function were compared. Compared to the C group, the EE group has shown significant decrease of exercise capacity, elevation of serum N-terminal pro B-type natriuretic peptide (NT-proBNP) and cardiac troponin-I (cTn-I) levels, cardiac morphology change, ECG disturbance, cardiac dysfunction and reduction of myocardial mitochondrial respiration function. Compared to the EE group, the EP groups have shown significant elevation of exercise capacity, decrease of serum NT-proBNP and cTn-I, improvement of cardiac function and myocardial mitochondrial electron transfer pathway complex I, II and IV activity. The correlation analyses showed protection of EP was proportional to EP duration from 20-min to 60-min. EE caused cardiac injury. EP could protect from EECI by alleviating myocardial damage, improving cardiac function and mitochondrial ETP complex I, II and IV activity. EP protection was positively correlated to EP duration from 20-min to 60-min with EP intensity fixed at 74.0% V̇O2 max.

LuxS quorum sensing system mediating Lactobacillus plantarum probiotic characteristics.

Lactobacillus plantarum is one of common probiotics in fermented foods. Quorum sensing (QS) is a common communication way within bacteria. It is not clear whether the probiotic properties of L. plantarum mediated by QS. Here, Lb. plantarum YM-4-3 was examined for resistance of pH, bile, antimicrobial and luxS gene expression pattern. The study found that: (1) the supernatant of YM-4-3 had bacteriostatic effect to Escherichia coli O157:H7, Listeria monocytogenes and Staphylococcus aureus; (2) Lb. plantarum YM-4-3 shown tolerance property to the strongest acid culture that pH value of 3; (3) the bile tolerance of Lb. plantarum YM-4-3 was significant difference with the growth stage, the early exponential phase of the growth culture can tolerate bile of 0.4% (w/v), while the stationary growth stage can only tolerate bile of 0.2%; (4) Lb. plantarum YM-4-3 luxS gene was contrary expression along with the growth. (5) Compared with the wild-type strain, the adhesion ability of Lb. plantarum YM-4-3 ΔluxS was decreased obviously. These results showed that AI-2 LuxS quorum sensing system mediating Lb. plantarum acid, bile tolerance, antimicrobial and adhesion of probiotics.

Exploring the Inhibitory Effect of Low-frequency Magnetic Fields on Epileptiform Discharges in Juvenile Rat Hippocampus.

Stimulation with a low frequency electromagnetic field (LF-EMF) has proven to represent a powerful method for the suppression of seizures, as demonstrated in select clinical and laboratory studies. However, the mechanism by which LF-EMF suppresses seizures remains unclear. The purpose of the present study was to explore the modulatory effect of LF-EMF on epileptiform discharges (EDs) using rat hippocampal slices and investigate the underlying mechanisms that mediate these effects. EDs in hippocampal slices was induced by magnesium-free (zero-Mg2+) artificial cerebrospinal fluid (ACSF) and recorded using an in vitro micro-electrode array (MEA). A small sub-decimeter coil was designed and incorporated in a flexible magnetic stimulation device that allowed electromagnetic fields with different parameters to be delivered to slices. After a stable ED event was recorded, magnetic fields of 0.5 Hz (30 min) with a magnetic intensity of 0.13 mT (5 Vpp voltage input) and 0.25 mT (20 Vpp voltage input) were applied. The results indicated that a high-amplitude 0.5 Hz magnetic field could lead to persistent suppression of ictal discharges (IDs), while low-amplitude magnetic fields did not influence IDs. The persistent suppression of complex ED was prevented if the magnetic fields were applied in the presence of 10 µmol/L bicuculline (BIC), a γ-aminobutyric acid type A (GABAA) receptor antagonist, while the application of BIC subsequent to a magnetic field application led to the reappearance of ID. The addition of BIC resulted in EDs that had previously been inhibited by magnetic fields, reappearing. Low-frequency magnetic stimulation was able to inhibit the conversion from interictal discharges (IIDs) or preictal discharges (PIDs) to IDs. This suppression was attributed to the modulation of GABAA receptor activity.

Study on the time-effectiveness of exercise preconditioning on heart protection in exhausted rats.

To investigate the persistence time and the effectiveness of exercise preconditioning (EP) on myocardial protection in exhausted rats from myocardial enzymes, electrocardiogram (ECG), cardiac function, and mitochondrial respiratory function after cessation of exercise training. One hundred and twelve healthy male Sprague-Dawley rats were randomly divided into seven groups (n = 16): control group (CON), exhaustive exercise (EE) group, EP group, and EE after EP (EP + EE); furthermore, EP + EE group was randomly divided into 1D, 3D, 9D, and 18D groups (1D, 3D, 9D, and 18D) and performed exhaustive treadmill exercise at a speed of 30 m/min on the 1st, 3rd, 9th, and 18th days separately after EP exercise stopped. We detected the serum contents of N-terminal pro B type natriuretic peptide (NT-proBNP) and cardiac troponin I (cTnI) by the enzyme-linked immunosorbent assays method, recorded ECG, detected heart function by pressure volume catheter, measured the respiratory rates of rat myocardial mitochondria state 3 and 4 of complex I, complex II, and IV by high-resolution breathing apparatus. EP could decrease the serum content of NT-proBNP and cTnI, improved the electrical derangement and the left ventricular function in exhausted rats. Moreover, the protective effect was more obvious in the 9th day after EP stopped, whereas it would disappear when EP stopped for more than 18 days. Compared with EE group, the respiratory rate value of myocardial mitochondrial complex increased in 1D, 3D, and 9D groups. Therefore, the protective effect of EP on the heart of exhausted rats decreased with the prolongation of stopping training time, and the effect was significant within 3 days of discontinuing training, then decreased gradually, and completely disappeared in the 18th day. EP enhanced the cardiac function in exhausted rats through raising the nicotinamide adenine diphosphate hydride (NADH) electron transport chain and increased the respiration rates of mitochondrial respiratory complex I and IV state 3, thereby improved myocardial mitochondrial respiratory function and energy metabolism.

Optimization of different intensities of exercise preconditioning in protecting exhausted exercise induced heart injury in rats.

This study was to optimize the exercise preconditioning (EP) intensity in protecting from exhaustive exercise-induced cardiac injury (EECI). A total of 98 male Sprague-Dawley rats were divided into 7 groups (n â€‹= â€‹14): the control group (C), the exhaustive exercise group (EE) and the EP â€‹+ â€‹EE groups, which include the V10 (53.0%˙O2max), V15 (58.4%˙O2max), V20 (67.0%˙O2max), V26 (74.0%˙O2max) and V30 (80.0%˙O2max) groups. Except the C group, the other groups were subjected to treadmill running. The serum contents of N terminal pro B type natriuretic peptide (NT-proBNP) and cardiac troponin I (cTn-I) were detected by the enzyme-linked immunosorbent assay method, ECG was recorded, heart function was detected by pressure volume catheter and the activities of mitochondrial electron transfer pathway (ET pathway) complexes I, Ⅱ and IV were measured by high-resolution respiration instrument. Compared to the EE group, the EP groups have shown decrease of NT-proBNP and cTn-I, improvement of mitochondrial respiratory function and cardiac function. Compared to other EP groups, the V26 group has shown significant decrease of myocardial enzymes and improvement of mitochondrial function. The correlation analysis showed the EP effect was proportional to EP intensity in the range of 53.0%˙O2max-74.0%˙O2max. High intensity and long duration of exhaustive exercise caused cardiac injury and EP could decrease serum level of NT-proBNP and cTn-I, improve electrical derangement and the left ventricular function, and raise the activities of ET pathway complexes I, Ⅱ and IV. The protection of EP on EECI was improved as the EP intensity was increased from 53.0%˙O2max to 74.0%˙O2max and when EP intensity was 74.0%˙O2max, the effect was the most obvious among all the setting EP groups.

Incidence of de novo autoimmune hepatitis in children and adolescents with increased autoantibodies after liver transplantation: a meta-analysis.

The objective of this meta-analysis was to assess the incidence of de novo autoimmune hepatitis (AIH) in children and adolescents with increased autoantibodies after liver transplantation. We systematically retrieved studies from PubMed, Embase, Central, CNKI, VIP and Wanfang published before February 1, 2020. All analyses were conducted using R-4.0.1 statistical package (Meta). Seven studies with high quality were pooled in our final analysis (N = 251 participants). The incidence of de novo AIH was 9% [95% confidence interval (CI) 1-23%, I2  = 86%]. Subgroup analysis suggested that publications not using the International Autoimmune Hepatitis Group (IAIHG) criteria have marginally significantly higher incidence of de novo AIH than those using IAIHG criteria (P for interaction = 0.08). The incidence of chronic rejection was 8% (95% CI 2-17%, I2  = 72%). Meta-regression indicated significant correlation (P = 0.04; estimate: 1.51) between the incidence of de novo AIH and the rate of increase of antibodies to liver/kidney microsome (anti-LKM). It is still challenging to distinguish de novo AIH and chronic rejection in children and adolescents with increased autoantibodies after liver transplantation. The diagnostic criteria for de novo AIH in children and adolescents and the role of anti-LKM in the development of de novo AIH deserve future investigation.

Tanshinone IIA attenuates atherosclerosis via inhibiting NLRP3 inflammasome activation.

Tanshinone IIA (Tan IIA) possesses potent anti-atherogenic function, however, the underlying pharmacological mechanism remains incompletely understood. Previous studies suggest that oxidized LDL (oxLDL)-induced NLRP3 (NOD-like receptor (NLR) family, pyrin domain-containing protein 3) inflammasome activation in macrophages plays a vital role in atherogenesis. Whether the anti-atherogenic effect of Tan IIA relies on the inhibition of the NLRP3 inflammasome has not been investigated before. In this study, we found that Tan IIA treatment of high-fat diet fed ApoE-/- mice significantly attenuated NLRP3 inflammasome activation in vivo. Consistently, Tan IIA also potently inhibited oxLDL-induced NLRP3 inflammasome activation in mouse macrophages. Mechanically, Tan IIA inhibited NF-κB activation to downregulate pro-interleukin (IL) -1ß and NLRP3 expression, and decreased oxLDL-induced expression of lectin-like oxidized LDL receptor-1 (LOX-1) and cluster of differentiation 36 (CD36), thereby attenuating oxLDL cellular uptake and subsequent induction of mitochondrial and lysosomal damage - events that promote the NLRP3 inflammasome assembly. Through regulating both the inflammasome 'priming' and 'activation' steps, Tan IIA potently inhibited oxLDL-induced NLRP3 inflammasome activation, thereby ameliorating atherogenesis.

Effect of priming low-frequency magnetic fields on zero-Mg2+ -induced epileptiform discharges in rat hippocampal slices.

During the process of seizures, the addition of low-frequency magnetic fields has been proved to be an effective method to suppress epileptic discharges. However, whether adding magnetic fields before the appearance of epileptic discharges can produce this inhibition has not been studied. In the present study, we first constructed epilepsy models on brain slices by perfusing them with Mg2+-free artificial cerebrospinal fluid (aCSF). The events of seizures evolved from inter-ictal epileptiform discharges (IIDs) to inter-epileptiform discharges (IDs). Combined with the multi-electrode array platform, we designed a flexible moving coil to generate a 0.5 Hz magnetic field on the brain slices. Using this method, we added the magnetic fields to brain slices for 30 min before epileptiform discharges were induced. The experimental results demonstrated that although the priming magnetic fields could not completely inhibit epileptiform discharges, they can significantly reduce the frequency of IDs and increase the frequency of IIDs in the CA3 region of the hippocampal slices. In the control group, the rates of IDs and IIDs were 0.0024 ± 0.0006 Hz and 0.0138 ± 0.0043 Hz, respectively, while in the magnetic stimulation group, the rates were 0.0012 ± 0.0004 Hz and 0.0251 ± 0.0067 Hz. Moreover, the results indicated that changing the frequency of interictal discharges did not affect ictogenesis. The results demonstrated that the priming magnetic fields had a certain weakening effect on the frequency of IDs, which was achieved by reducing the signal propagation speed and increasing the excitability threshold of hippocampal neurons.

Different Intensity Exercise Preconditions Affect Cardiac Function of Exhausted Rats through Regulating TXNIP/TRX/NF-ĸBp65/NLRP3 Inflammatory Pathways.

OBJECTIVE: To investigate whether exercise preconditioning (EP) improves the rat cardiac dysfunction induced by exhaustive exercise (EE) through regulating NOD-like receptor protein 3 (NLRP3) inflammatory pathways and to confirm which intensity of EP is better. METHOD: Ninety healthy male Sprague Dawley rats were randomly divided into five groups: a control group (CON), exhaustive exercise group (EE), low-, middle-, and high-intensity exercise precondition and exhaustive exercise group (LEP + EE, MEP + EE, HEP + EE group). We established the experimental model by referring to Bedford's motion load standard to complete the experiment. Then, the pathological changes of the myocardium were observed under a light microscope. Biomarker of myocardial injury in serum and oxidative stress factor in myocardial tissue were evaluated by ELISAs. The cardiac function parameters were detected using a Millar pressure and volume catheter. The levels of thioredoxin-interacting protein (TXNIP), thioredoxin protein (TRX), nuclear transcription factor kappa Bp65 (NF-ĸBp65), NLRP3, and cysteinaspartate specific proteinase 1 (Caspase-1) protein in rats' myocardium were detected by western blotting. RESULTS: 1. The myocardial structures of three EP + EE groups were all improved compared with EE groups. 2. The levels of the creatine phosphating-enzyme MB (CK-MB), reactive oxygen species (ROS), interleukin-6 (IL-6), C-reactive protein (CRP), and tumor necrosis factor alpha (TNF-α) in three EP + EE groups were all increased compared with CON but decreased compared with the EE group (P < 0.05). 3. Compared with the CON group, slope of end-systolic pressure volume relationship (ESPVR), ejection fraction (EF), and peak rate of the increase in pressure (dP/dt max) all dropped to the lowest level in the EE group (P < 0.05), while the values of cardiac output (CO), stroke volume (SV), end-systolic volume (Ves), end-diastolic volume (Ved), and relaxation time constant (Tau) increased in the EE group (P < 0.05). 4. Compared with the CON group, the expression levels of TXNIP, NF-ĸBp65, NLRP3, and Caspase-1 all increased obviously in the other groups (P < 0.05); meanwhile, they were all decreased in three EP + EE groups compared with the EE group (P < 0.05). 5. NLRP3 was positively correlated with heart rate, IL-6, and ROS, but negatively correlated with EF (P < 0.01). CONCLUSION: EP protects the heart from EE-induced injury through downregulating TXNIP/TRX/NF-ĸBp65/NLRP3 inflammatory signaling pathways. Moderate intensity EP has the best protective effect.

Physiological and ecological characteristics of Periploca sepium Bunge under drought stress on shell sand in the Yellow River Delta of China.

This study investigated the physiological and ecological changes in P. sepium Bunge and elucidated the physiological regulatory mechanisms underlying the adaptation of P. sepium to drought stress in shell sand. Drought stress led to a significant decrease in the net photosynthesis rate (Pn) and respiration rate of leaves and a decrease in low-intensity light-use efficiency (LUE) and light ecological amplitude. An increase in drought stress led to a considerable decrease in the photosynthetic electron transport rate in the P. sepium leaves and a significant increase in the amount of light energy dissipated as heat. In addition, the photosynthesis process suffered from severe photoinhibition. P. sepium plants counteracted the effects of drought stress primarily by increasing their peroxidase (POD) activity and by regulating membrane lipid peroxidation by secreting greater numbers of osmotic adjustment substances (proline (Pro) and soluble sugars (Ss)) and malondialdehyde (MDA). As drought stress increased, both the stem sap flow rate and the cumulative sap flow of P. sepium decreased considerably. P. sepium Bunge adapts to drought stress through interregulatory activity between photosynthesis, water-related physiological activities, and physiological and biochemical processes, and this species exhibits relatively high adaptive plasticity to drought.

Validation of the long-term prognostic capability of the SYNTAX score II in patients undergoing biodegradable polymer-based Sirolimus-eluting stents: 2-year outcomes from the PANDA III trial.

BACKGROUND: This study aimed to assess the prognostic ability of SYNTAX (Synergy Between Percutaneous Coronary Intervention with Taxus and Cardiac Surgery) Score II (SS-II) in LM and/or TVD patients undergoing biodegradable polymer-based drug-eluting stents (BP-DES) in the multi-central randomized PANDA III trial. METHODS: A total of 723 patients in PANDA III population were enrolled in this study. According to SS-II tertiles, patients were stratified as follow: SS-II ≤ 23 (n = 224), 23 < SS II ≤ 31 (n = 255), SS II > 31 (n = 244). The predictive abilities for 2-year cardiac death were compared between angiographic scores and scores combining both angiographic and clinical variables. RESULTS: Mean anatomic SS was 20.6 ± 9.4, SS-II for PCI was 28.7 ± 8.6. During 2-year follow up, cardiac death (0.00% vs. 1.7% vs. 4.3%, p = 0.003) and target lesion failure (5.9% vs. 9.1% vs. 13.6%, p = 0.020) was significantly higher in the upper tertile group than in intermedian and low tertile. At multivariate analysis, SS-II for PCI was an independent risk factor of cardiac death (Hazard ratio: 2.41, 95%CI: 1.47-3.97, p < 0.005) and TLF (Hazard ratio: 1.29, 95%CI: 1.01-1.65, p = 0.040). The ROC curve analysis showed that SS-II for PCI had better ability than other SYNTAX scoring systems to predict cardiac death (AUC: 0.746, 95%CI:0.63-0.87, p = 0.010). CONCLUSIONS: The SS-II had superiority than other SYNTAX scoring systems in predicting 2-year cardiac death in LM and/or TVD patients undergoing PCI with biodegradable polymer drug-eluting stents.

Transforming growth factor ß1 is a differentially expressed candidate protein of congestive heart failure with Qi-deficiency-blood-stasis syndrome.

OBJECTIVE: To investigate the role of tongue coating fluid protein in regulation of congestive heart failure (CHF) in Qi-deficiency-blood-stasis syndrome. METHODS: We studied patients with CHF (3 patients with Qi-deficiency-blood-stasis syndrome and 3 without Qi-deficiency-blood-stasis syndrome) to investigate differentially expressed proteins. We also included a control group. A biotin label-based antibody array was used for testing tongue coating fluid samples from patients. Network analysis of these differentially expressed proteins was conducted using the STRING database, which can predict the relations between differentially expressed proteins and CHF with Qi-deficiency-blood-stasis syndrome. RESULTS: A total of seven differentially expressed proteins were identified, and among these, transforming growth factor ß1 (TGF-ß1) gets a?particular?attention for us has drawn specific attention. Network analysis showed a homologous relationship of TGF-ß1 with bone morphogenetic protein 15, which is associated with myocardial fibrosis. CONCLUSION: Occurrence and development of CHF may result from certain DE-proteins and associated signaling pathways. TGF-ß1 protein may be a candidate marker for assessing the risk of CHF in Qi-deficiency-blood-stasis syndrome.

Exercise Preconditioning Plays a Protective Role in Exhaustive Rats by Activating the PI3K-Akt Signaling Pathway.

OBJECTIVE: To investigate whether exercise preconditioning (EP) protects the rat heart from exhaustive exercise- (EE-) induced injury by inducing the PI3K-Akt signaling pathway. METHODS: 84 male Sprague-Dawley rats were randomly divided into 6 groups (n = 14 rats per group): control group (Con), exhaustive exercise group (EE), exercise preconditioning group (EP), exercise preconditioning + exhaustive exercise group (EP + EE), LY294002 (PI3K inhibitor) + exercise preconditioning + exhaustive exercise group (LY + EP + EE), and LY294002 group (LY). The Con and LY did not exercise. The remaining groups were subjected to treadmill running. The structure of myocardial tissue and serum biomarkers of myocardial injury were observed. Hemodynamic parameters were recorded with a pressure-volume catheter. TUNEL assay was used to detect the apoptosis of cardiac myocytes, and the level of mitochondrial membrane permeability transforming pore (mPTP) in myocardium was evaluated using ELISA. Pathway and apoptosis-related proteins in myocardium were assessed using western blotting. RESULTS: Compared to the Con group, the EE group showed remarkable myocardial injury, such as cardiac dysfunction and myocardial apoptosis. Compared to the EE group, the injuries in the EP + EE group were improved. EP increased the PI3K-Akt signaling pathway and regulated Bcl-2 family to decrease the mPTP openness level. However, the cardioprotective effects of EP were attenuated when pretreated with the LY294002. CONCLUSIONS: EP protected the heart from EE-induced injury, and it may improve the cardiac function and reduce the cardiomyocyte apoptosis by activating the PI3K-Akt signaling pathway.

Exploring the form- And time-dependent effect of low-frequency electromagnetic fields on maintenance of hippocampal long-term potentiation.

Low-frequency electromagnetic field (LF-EMF) stimulation is an emerging neuromodulation tool that is attracting more attention because of its non-invasive and well-controlled characteristics. However, the effect of different LF-EMF features including the forms and the time of addition on neuronal activity has not been completely understood. In this study, we used multi-electrode array (MEA) systems to develop a flexible in vitro magnetic stimulation device with plug-and-play features that allows for real-time delivery of LF-EMFs to biological tissues. Crucially, the method enables different forms of LF-EMF to be added at any time to a long-term potentiation (LTP) experiment without interrupting the process of LTP induction. We demonstrated that the slope of field excitatory postsynaptic potentials (fEPSPs) decreased significantly under post or priming uninterrupted sine LF-EMFs. The fEPSPs slope would continue to decline significantly when LF-EMFs were added two times with a 20-min interval. Paired-pulse ratio (PPR) was analyzed and the results reflected that LF-EMFs induced LTP was expressed postsynaptically. The results of pharmacological experiments indicated that AMPA receptor activity was involved in the process of LTP loss caused by post-LF-EMFs. Moreover, the effect of priming sine or Quadripulse stimulation (QPS)-patterned LF-EMFs depended on the time interval between the end of LF-EMF and the beginning of baseline recording. Interestingly, the effect of sine LF-EMFs on LTP would not disappear within 120 min, while the impact of QPS-patterned LF-EMFs on LTP might disappear after 90 min. These results indicated that LF-EMF might have a form- and time-dependent effect on LTP.

Identification and characterization of a novel short-type peptidoglycan recognition protein in Apostichopus japonicus.

Peptidoglycan recognition proteins (PGRPs) are pattern recognition molecules of the innate immune system via specific recognizing peptidoglycan, a unique component of bacterial cell wall. In the present study, a homologous gene encoding PGRP-S was identified and characterized from Apostichopus japonicus and designated as AjPGRP-S. The open reading frame of AjPGRP-S is 756 bp encoding a polypeptide of 251 amino acids (aa) with a signal peptide (1-24 aa) and a typical PGRP domain (37-178 aa). Phylogenetic analysis and sequence alignment revealed that AjPGRP-S is a member of the PGRP-S family. In healthy sea cucumbers, AjPGRP-S was expressed in all examined tissues with the highest distribution in body wall, muscle, and intestine. In Vibrio splendidus-infected sea cucumbers, AjPGRP-S was remarkably induced in coelomocytes. The recombinant AjPGRP-S (rAjPGRP-S) was shown to possess the highly amidase activity in the presence of Zn2+. Moreover, rAjPGRP-S exhibited agglutination abilities and strong bacteriostatic activities against V. splendidus, V. harveyi, V. parahaemolyticus, Staphylococcus aureus, and Micrococcus luteus. Furthermore, the agglutination ability can be enhanced in the presence of Zn2+. In conclusion, our results suggested that AjPGRP-S serves as a pattern recognition molecule involved in the immune response towards various pathogenic infections.

Two-year safety evaluation of a biodegradable polymer sirolimus-eluting stent with increased drug elution and polymer absorption kinetics in complex patient and lesion cohort.

OBJECTIVES: The aim of the present report was to compare 2-year safety outcomes of two biodegradable polymer (BP) sirolimus-eluting stents (SESs) with different drug eluting and polymer absorption kinetics in a subgroup of complex patients and lesions. BACKGROUND: The previously published PANDA III study showed the BuMA BP SES, with faster drug elution and polymer absorption, was non-inferior to the Excel SES in target lesion failure (TLF). METHODS: In PANDA III trial, patients who fulfilled one or more of the following criteria were included: Small vessel disease (reference vessel diameter ≤ 2.5 mm); long lesion (lesion length ≥ 20 mm); chronic total occlusion lesion; and diabetic patients. RESULTS: Among 2,348 patients randomly assigned to treatment with BuMA (n = 1,174) or Excel SES (n = 1,174) in the PANDA III study, 858 in the BuMA group and 855 in the Excel group satisfied the inclusion criteria. At 2-year follow-up, the incidence of definite/probable stent thrombosis (ST) was significantly lower with BuMA SES as compared with Excel SES (0.7% vs. 1.9%, p = 0.03). This difference was mainly caused by decreased subacute stent thrombosis rate (0% vs. 0.6%, p = 0.03). In patients who did not fulfill the complex patient and lesion criteria, there were no between-group difference in ST (0.7% vs. 0%, p = 0.50). Myocardial infarction and TLF rates were similar (5.7% vs. 6.0%, p = 0.79 and 8.8% vs. 7.5%, p = 0.34, respectively), whereas patient-oriented composite endpoint was higher with BuMA SES mainly due to high risk of revascularization (15.6% vs. 11.4%, p = 0.01; 8.4% vs. 4.6%, p < 0.01). CONCLUSIONS: Two-year subgroup analysis of the all-comer PANDA III trial revealed the increased safety benefit of the BuMA SES is more prominently seen in complex patient and lesion population. CLINICAL TRIAL: ClinicalTrial.gov, Identifier-NCT02017275.