Acetylcholine exerts cytoprotection against hypoxia/reoxygenation-induced apoptosis, autophagy and mitochondrial impairment through both muscarinic and nicotinic receptors.

Acetylcholine (ACh) has been shown to exert cardioprotection against myocardial ischemia/reperfusion (I/R) injury. However, whether ACh exerts its cardioprotection predominantly through the activation of muscarinic or nicotinic ACh receptors is not fully understood. We investigated the effects of hypoxia/reoxygenation (H/R) in the presence or absence of ACh receptor agonists in H9c2 cells. Cells (2.5 × 105 cells/well) were incubated in the hypoxic chamber with the ischemic solution (30 min) followed by reoxygenation (120 min) with the normal media. ACh or nicotinic ACh receptor agonist (GTS21) was applied 5 min prior to hypoxia, during hypoxia or at reoxygenation onset. Cell viability, apoptosis, ER stress, mitochondrial dynamics and biogenesis were determined. H/R significantly decreased cell viability and mitochondrial biogenesis and increased apoptosis, ER stress, mitochondrial fission and autophagic flux compared with the control. ACh and GTS21 significantly increased cell viability via reducing apoptosis, autophagy, and ER stress. However, ACh and GTS21 increased mitochondrial fusion when applied before or during hypoxia. During reoxygenation onset, only ACh increased mitochondrial biogenesis. Co-treatment with atropine reversed the beneficial effects of ACh and GTS21. Our findings demonstrated that ACh exerted cytoprotection against H/R-induced apoptosis, autophagy and mitochondrial impairment through the activation of both muscarinic and nicotinic receptors.

Targeting mitochondria as a therapeutic anti-gastric cancer approach.

Gastric cancer is regarded as the fifth most common cancer globally but the third most common cancer death. Although systemic chemotherapy is the primary treatment for advanced gastric cancer patients, the outcome of chemotherapy is unsatisfactory. Novel therapeutic strategies and potential alternative treatments are therefore needed to overcome the impact of this disease. At a cellular level, mitochondria play an important role in cell survival and apoptosis. A growing body of studies have shown that mitochondria play a central role in the regulation of cellular function, metabolism, and cell death during carcinogenesis. Interestingly, the impact of mitochondrial dynamics, including fission/fusion and mitophagy, on carcinogenesis and cancer progression has also been reported, suggesting the potential targeting of mitochondrial dynamics for the treatment of cancer. This review not only comprehensively summarizes the homeostasis of gastric cancer cells, but the potential therapeutic interventions for the targeting of mitochondria for gastric cancer therapy are also highlighted and discussed.

Mechanisms and Interventions on Acute Lower Limb Ischemia/Reperfusion Injury: A Review and Insights from Cell to Clinical Investigations.

BACKGROUND: This review aims to highlight mechanistic insights on skeletal muscle ischemia/reperfusion injury (IRI), a potentially life-threatening complication after acute lower limb ischemia. Lower limb IRI produces a wide spectrum of manifestations, ranging from local skeletal muscle necrosis to multi-organ failure. There is increasing evidence from both in vitro and in vivo reports to demonstrate several promising interventions that have successfully reduced IRI in skeletal muscle ischemic models. However, clinical studies to confirm their benefits are still lacking. METHODS: We conducted a comprehensive search of English literature listed in the PubMed database (All related published articles shown in PubMed until September 2020 have been included in this review), using the following keywords: acute limb ischemia, acute arterial occlusion, compartment syndrome, ischemic reperfusion injury, revascularization, and hypoxic reoxygenation. RESULTS: A total of 58 articles pertinent to acute limb ischemia models were identified. The underlying mechanisms associated with IRI in skeletal muscle are due to excessive mitochondrial production of reactive oxygen species (ROS), cellular apoptosis and activation of inflammatory cascades. Several therapeutic interventions including both pharmacological and nonpharmacological treatments have been investigated and some showed promising results. These interventions include anti-oxidation, anti-inflammation, anti-hypertension, controlled-reperfusion, and ischemic preconditioning. Further clinical studies are needed to warrant their use in a clinical setting for lower limb IRI treatment. CONCLUSIONS: This review comprehensively summarizes the mechanisms underlying IRI in lower limb ischemia. The reports currently available regarding the potential therapeutic interventions against lower limb IRI from in vitro, in vivo and clinical studies are presented and discussed. These findings may provide mechanistic insights for devising the strategies to improve the clinical outcomes in IRI patients in the near future. Further clinical studies are needed to warrant their use in a clinical setting for lower limb IRI treatment.

The impact of genetic polymorphisms on weight regain after successful weight loss.

Obesity is associated with an increased risk of various diseases and mortality. Although nearly 50 % of adults have been reported trying to lose weight, the prevalence of obesity has increased. One factor that hinders weight loss-induced decrease in obesity prevalence is weight regain. Although behavioural, psychological and physiological factors associated with weight regain have been reviewed, the information regarding the relationship between weight regain and genetics has not been previously summarised. In this paper, we comprehensively review the association between genetic polymorphisms and weight regain in adults and children with obesity after weight loss. Based on this information, identification of genetic polymorphism in patients who undergo weight loss intervention might be used to estimate their risks of weight regain. Additionally, the genetic-based risk estimation may be used as a guide for physicians and dietitians to provide each of their patients with the most appropriate strategies for weight loss and weight maintenance.

Vagus nerve stimulation exerts cardioprotection against myocardial ischemia/reperfusion injury predominantly through its efferent vagal fibers.

Vagus nerve stimulation (VNS) has been shown to exert cardioprotection against myocardial ischemia/reperfusion (I/R) injury. However, whether the cardioprotection of VNS is mainly due to direct activation through its ipsilateral efferent fibers (motor) rather than indirect effects mediated by the afferent fibers (sensory) have not been clearly understood. We hypothesized that VNS exerts cardioprotection predominantly through its efferent vagal fibers. Thirty swine (30-35 kg) were randomized into five groups: I/R no VNS (I/R), and left mid-cervical VNS with both vagal trunks intact (LC-VNS), with left vagus nerve transection (LtVNX), with right vagus nerve transection (RtVNX) and with atropine pretreatment (Atropine), respectively. VNS was applied at the onset of ischemia (60 min) and continued until the end of reperfusion (120 min). Cardiac function, infarct size, arrhythmia score, myocardial connexin43 expression, apoptotic markers, oxidative stress markers, inflammatory markers (TNF-α and IL-10) and cardiac mitochondrial function, dynamics and fatty acid oxidation (MFN2, OPA1, DRP1, PGC1α and CPT1) were determined. LC-VNS exerted cardioprotection against myocardial I/R injury via improvement of mitochondrial function and dynamics and shifted cardiac fatty acid metabolism toward beta oxidation. However, LC-VNS and LtVNX, both efferent vagal fibers are intact, produced more profound cardioprotection, particularly infarct size reduction, decreased arrhythmia score, oxidative stress and apoptosis and attenuated mitochondrial dysfunction compared to RtVNX. These beneficial effects of VNS were abolished by atropine. Our findings suggest that selective efferent VNS may potentially be effective in attenuating myocardial I/R injury. Moreover, VNS required the contralateral efferent vagal activities to fully provide its cardioprotection.

Revisiting the Cardioprotective Effects of Acetylcholine Receptor Activation against Myocardial Ischemia/Reperfusion Injury.

Acute myocardial infarction (AMI) is the most common cause of acute myocardial injury and its most clinically significant form. The most effective treatment for AMI is to restore an adequate coronary blood flow to the ischemic myocardium as quickly as possible. However, reperfusion of an ischemic region can induce cardiomyocyte death, a phenomenon termed "myocardial ischemia/reperfusion (I/R) injury". Disruption of cardiac parasympathetic (vagal) activity is a common hallmark of a variety of cardiovascular diseases including AMI. Experimental studies have shown that increased vagal activity exerts cardioprotective effects against myocardial I/R injury. In addition, acetylcholine (ACh), the principle cardiac vagal neurotransmitter, has been shown to replicate the cardioprotective effects of cardiac ischemic conditioning. Moreover, studies have shown that cardiomyocytes can synthesize and secrete ACh, which gives further evidence concerning the importance of the non-neuronal cholinergic signaling cascades. This suggests that the activation of ACh receptors is involved in cardioprotection against myocardial I/R injury. There are two types of ACh receptors (AChRs), namely muscarinic and nicotinic receptors (mAChRs and nAChRs, respectively). However, the effects of AChRs activation in cardioprotection during myocardial I/R are still not fully understood. In this review, we summarize the evidence suggesting the association between AChRs activation with both electrical and pharmacological interventions and the cardioprotection during myocardial I/R, as well as outline potential mechanisms underlying these cardioprotective effects.

Acetylcholine Attenuates Hydrogen Peroxide-Induced Intracellular Calcium Dyshomeostasis Through Both Muscarinic and Nicotinic Receptors in Cardiomyocytes.

BACKGROUND/AIMS: Oxidative stress induced intracellular Ca2+ overload plays an important role in the pathophysiology of several heart diseases. Acetylcholine (ACh) has been shown to suppress reactive oxygen species generation during oxidative stress. However, there is little information regarding the effects of ACh on the intracellular Ca2+ regulation in the presence of oxidative stress. Therefore, we investigated the effects of ACh applied before or after hydrogen peroxide (H2O2) treatment on the intracellular Ca2+ regulation in isolated cardiomyocytes. METHODS: Single ventricular myocytes were isolated from the male Wistar rats for the intracellular Ca2+ transient study by a fluorimetric ratio technique. RESULTS: H2O2 significantly decreased both of intracellular Ca2+ transient amplitude and decay rate. ACh applied before, but not after, H2O2 treatment attenuated the reduction of intracellular Ca2+ transient amplitude and decay rate. Both atropine (a muscarinic acetylcholine receptor blocker) and mecamylamine (a nicotinic acetylcholine receptor blocker) significantly decreased the protective effects of acetylcholine on the intracellular Ca2+ regulation. Moreover, the combination of atropine and mecamylamine completely abolished the protective effects of acetylcholine on intracellular Ca2+ transient amplitude and decay rate. CONCLUSION: ACh pretreatment attenuates H2O2-induced intracellular Ca2+ dyshomeostasis through both muscarinic and nicotinic receptors.

Protective effects of garlic extract on cardiac function, heart rate variability, and cardiac mitochondria in obese insulin-resistant rats.

PURPOSE: Garlic has been shown to exhibit antioxidant effects and cardioprotective properties. However, the effects of garlic extract on the heart in insulin resistance induced by long-term high-fat-diet consumption are not well defined. Therefore, we sought to determine the effects of garlic extract in the obese insulin-resistant rats. METHODS: Male Wistar rats (180-200 g) were divided into two groups: normal-diet or high-fat-diet (n = 24/group) fed for 12 weeks. Rats in each groups were divided into three subgroups (n = 8 each): vehicle or garlic extract (250 or 500 mg/kg/day, respectively) treated for 28 days. At the end of the treatment, the metabolic parameters, heart rate variability (HRV), cardiac function, and cardiac mitochondrial function were determined. RESULTS: Rats that received a high-fat-diet for 12 weeks had increased body weight, visceral fat, plasma insulin levels, total cholesterol, oxidative stress levels, depressed HRV, and cardiac mitochondrial dysfunction. Garlic extract at both concentrations significantly decreased the plasma insulin, total cholesterol, homeostasis model assessment index, and oxidative stress levels. Furthermore, garlic extract at both doses restored the HRV, cardiac function, and cardiac mitochondrial function. CONCLUSION: We concluded that garlic extract at both concentrations exerted cardioprotective effects against cardiac dysfunction and mitochondrial dysfunction in obese insulin-resistant rats.

Continuous positive airway pressure therapy for obstructive sleep apnea reduces interictal epileptiform discharges in adults with epilepsy.

Obstructive sleep apnea (OSA) is highly prevalent, affecting 25% of men and 10% of women. We recently reported a prevalence of OSA of 30% among 130 adults with epilepsy unselected for sleep disorder complaints, including 16% with moderate-to-severe disease, rates that markedly exceed general population estimates. Treatment of OSA with continuous positive airway pressure (CPAP) therapy or upper airway surgery reduces seizures in many cases. A single study reported a reduction in interictal spike rate with CPAP in 6 patients with OSA. We explored the effect of CPAP therapy on spike rate in 9 adults with epilepsy and OSA. Interictal epileptiform discharges were quantified during a diagnostic polysomnogram (PSG) and a second PSG using therapeutic CPAP. Spike rates were calculated for each recording during wake and sleep stages. Continuous positive airway pressure therapy was associated with significant reductions in median (quartiles) spike rate overall (77.9 [59.7-90.7] %), in wakefulness (38.5 [0.3-55] %), and in sleep (77.7 [54.8-94.7] %) but not in REM sleep. Continuous positive airway pressure therapy also produced a significant improvement in oxygen saturation and arousals. Our work extends a single prior observation demonstrating beneficial effects of CPAP therapy on interictal EEG in patients with epilepsy with comorbid OSA and supports the hypothesis that sleep fragmentation due to OSA contributes to epileptogenicity.

Effect modification of diabetic status on the association between exposure to particulate matter and cardiac arrhythmias in a general population: A systematic review and meta-analysis.

Particulate matter (PM) has various health effects, including cardiovascular diseases. Exposure to PM and a diagnosis of diabetes mellitus (DM) have been associated with an increased risk of cardiac arrhythmias. However, no comprehensive synthesis has been conducted to examine the modifying effect of DM on the association between PM and arrhythmia events. Thus, the objectives of this review were to investigate whether the association of PM is linked to cardiac arrhythmias and whether DM status modifies its effect in the general population. The search was conducted on PubMed/MEDLINE and Embase until January 18, 2023. We included cohort and case-crossover studies reporting the effect of PM exposure on cardiac arrhythmias and examining the role of diabetes as an effect modifier. We used the DerSimonian and Laird random-effects model to calculate the pooled estimates. A total of 217 studies were found and subsequently screened. Nine studies met the inclusion criteria, and five of them were included in the meta-analysis. The participants numbered 4,431,452, with 2,556 having DM. Exposure to PM of any size showed a significant effect on arrhythmias in the overall population (OR 1.10, 95% CI 1.04-1.16). However, the effect modification of DM was not significant (OR 1.18 (95% CI 1.01-1.38) for DM; OR 1.08 (95% CI 1.02-1.14) for non-DM; p-value of subgroup difference = 0.304). Exposure to higher PM concentrations significantly increases cardiac arrhythmias requiring hospital or emergency visits. Although the impact on diabetic individuals is not significant, diabetic patients should still be considered at risk. Further studies with larger sample sizes and low bias are needed.

Effects of glyphosate-based herbicides and glyphosate exposure on sex hormones and the reproductive system: From epidemiological evidence to mechanistic insights.

Glyphosate-based herbicides (GBHs) containing glyphosate as the active component are extensively used worldwide. Concerns have arisen about their potential risk to human, as glyphosate has been detected in human body fluids. Current controversies surround the endocrine-disrupting properties and transgenerational inheritance of diseases and germline epimutations resulting from exposure to GBHs and glyphosate. This review discusses evidence from in vitro, in vivo, and clinical studies on their impact on sex hormone regulation and reproductive system. Evidence suggests that they act as endocrine-disrupting chemicals, which altering sex hormone levels. Mechanistically, they interfere with hormone signaling pathways by disrupting proteins involved in hormone transport and metabolism. Pathological changes have been observed in male and female reproductive systems, potentially leading to reproductive toxicity. Prenatal exposure may lead to transgenerational inheritance of pathologies and sperm epimutations. However, due to the complexity of glyphosate formulations containing adjuvants identifying higher risk components in environmental exposure becomes challenging.

Functional roles of orexin in obstructive sleep apnea: From clinical observation to mechanistic insights.

Obstructive sleep apnea is the most common sleep-related breathing disorder. Repetitive episodes of the obstructive respiratory events lead to arousal, sleep fragmentation, and excessive daytime sleepiness. Orexin, also known as hypocretin, is one of the most important neurotransmitters responsible for sleep and arousal regulation. Deficiency of orexin has been shown to be involved in the pathogenesis of narcolepsy, which shares cardinal symptoms of sleep apnea and excessive daytime sleep with obstructive sleep apnea. However, the relationship between orexin and obstructive sleep apnea is not well defined. In this review, we summarize the current evidence, from in vitro, in vivo, and clinical data, regarding the association between orexin and obstructive sleep apnea. The effects of orexin on sleep apnea, as well as how the consequences of obstructive sleep apnea affect the orexin system function are also discussed. Additionally, the contrary findings are also included and discussed.

Melatonin and metformin ameliorated trastuzumab-induced cardiotoxicity through the modulation of mitochondrial function and dynamics without reducing its anticancer efficacy.

Trastuzumab has an impressive level of efficacy as regards antineoplasticity, however it can cause serious cardiotoxic side effects manifested by impaired cardiac contractile function. Although several pharmacological interventions, including melatonin and metformin, have been reported to protect against various cardiovascular diseases, their potential roles in trastuzumab-induced cardiotoxicity remain elusive. We hypothesized that either melatonin or metformin co-treatment effectively attenuates trastuzumab-mediated cardiotoxicity through attenuating the impaired mitochondrial function and mitochondrial dynamics. Male Wistar rats were divided into control (normal saline, n = 8) and trastuzumab group (4 mg/kg/day for 7 days, n = 24). Rats in the trastuzumab group were subdivided into 3 interventional groups (n = 8/group), and normal saline, or melatonin (10 mg/kg/day), or metformin (250 mg/kg/day) were orally administered for 7 consecutive days. Cardiac parameters were determined, and biochemical investigations were carried out on blood and heart tissues. Trastuzumab induced left ventricular (LV) dysfunction by increasing oxidative stress, inflammation, and apoptosis. It also impaired cardiac mitochondrial function, dynamics, and autophagy. Treatment with either melatonin or metformin equally attenuated trastuzumab-induced cardiac injury, indicated by a marked reduction in inflammation, oxidative damage, cardiac mitochondrial injury, mitochondrial dynamic imbalance, autophagy dysregulation, and apoptosis, leading to improved LV function, as demonstrated by increased LV ejection fraction. Melatonin and metformin conferred equal levels of cardioprotection against trastuzumab-induced cardiotoxicity, which may provide novel and promising approaches for management of cardiotoxicity induced by trastuzumab.

Phosphoinositide binding differentially regulates NHE1 Na+/H+ exchanger-dependent proximal tubule cell survival.

Tubular atrophy predicts chronic kidney disease progression, and is caused by proximal tubular epithelial cellcaused by proximal tubular epithelial cell (PTC) apoptosis. The normally quiescent Na(+)/H(+) exchanger-1 (NHE1) defends against PTC apoptosis, and is regulated by PI(4,5)P(2) binding. Because of the vast array of plasma membrane lipids, we hypothesized that NHE1-mediated cell survival is dynamically regulated by multiple anionic inner leaflet phospholipids. In membrane overlay and surface plasmon resonance assays, the NHE1 C terminus bound phospholipids with low affinity and according to valence (PIP(3) > PIP(2) > PIP = PA > PS). NHE1-phosphoinositide binding was enhanced by acidic pH, and abolished by NHE1 Arg/Lys to Ala mutations within two juxtamembrane domains, consistent with electrostatic interactions. PI(4,5)P(2)-incorporated vesicles were distributed to apical and lateral PTC domains, increased NHE1-regulated Na(+)/H(+) exchange, and blunted apoptosis, whereas NHE1 activity was decreased in cells enriched with PI(3,4,5)P(3), which localized to basolateral membranes. Divergent PI(4,5)P(2) and PI(3,4,5)P(3) effects on NHE1-dependent Na(+)/H(+) exchange and apoptosis were confirmed by selective phosphoinositide sequestration with pleckstrin homology domain-containing phospholipase Cδ and Akt peptides, PI 3-kinase, and Akt inhibition in wild-type and NHE1-null PTCs. The results reveal an on-off switch model, whereby NHE1 toggles between weak interactions with PI(4,5)P(2) and PI(3,4,5)P(3). In response to apoptotic stress, NHE1 is stimulated by PI(4,5)P(2), which leads to PI 3-kinase activation, and PI(4,5)P(2) phosphorylation. The resulting PI(3,4,5)P(3) dually stimulates sustained, downstream Akt survival signaling, and dampens NHE1 activity through competitive inhibition and depletion of PI(4,5)P(2).

The effects of doxorubicin on cardiac calcium homeostasis and contractile function.

Cancer is one of the leading causes of death globally and the number of cancer deaths is rising as a result of increased longevity. Doxorubicin (DOX) is one of the most effective anti-neoplastic drugs used to treat various forms of cancer. However, its therapeutic utility is limited by its associated cardiotoxicity, specifically cardiac contractile dysfunction. Current evidence indicates that interference with cardiac intracellular calcium (Ca2+) homeostasis is one of the major causes among the molecular and cellular determinants of DOX-induced cardiotoxicity. This contributes to the development of cardiac contractile dysfunction, which remains a major concern and obstacle in clinical applications. This review comprehensively summarizes the effects of DOX on cardiac Ca2+ homeostasis and contractile function from in vitro, ex vivo, and in vivo studies. It also highlights the information essential for the potential interventions which may support the therapeutic effectiveness in clinical practice for the attenuation of cardiotoxicity in DOX-treated patients.

Sexual dimorphism in cardiometabolic and cardiac mitochondrial function in obese rats following sex hormone deprivation.

OBJECTIVE: Our study aims to test the hypothesis that poorer function of cardiac mitochondria in males, under sex hormone-deprived and obese-insulin-resistant conditions, is responsible for a worse cardiometabolic function than females. METHODS: One hundred and forty-four rats were subjected to receive either 12 weeks of normal diet (ND) or a high-fat diet (HFD) consumption following the induction of sex hormone deprivation. Temporal evaluations of metabolic parameters, cardiac autonomic modulation, left ventricular (LV) contractile, and mitochondrial functions were measured after starting each feeding protocol for 4, 8, and 12 weeks. RESULTS: After HFD feeding for 8 weeks, increased plasma insulin and HOMA index were initially observed in male HFD-fed sham-operated rats (M-HFS), male HFD-fed orchiectomized rats (M-HFO), female ND-fed ovariectomized rats (F-OVX), female HFD-fed sham-operated rats (F-HFS), and female HFD-fed ovariectomized rats (F-HFO) groups. In addition, as early as week 4, male ND-fed orchiectomized rats (M-ORX) and M-HFO exhibited impaired cardiac autonomic balance, LV contractile and mitochondrial functions, whereas M-HFS and F-HFO developed these impairments at week 8 and F-OVX and F-HFS exhibited them at week 12. CONCLUSION: We concluded that sex hormone-deprived females are prone to develop metabolic impairments, whereas males are more likely to have cardiac autonomic impairment, LV contractile and mitochondrial dysfunction even in the absence of obese-insulin-resistant condition. However, under estrogen-deprived condition, these impairments were further accelerated and aggravated by obese-insulin resistance.

Repurposing metformin as a potential treatment for inflammatory bowel disease: Evidence from cell to the clinic.

Inflammatory bowel disease (IBD) comprises a group of intestinal disorders, including ulcerative colitis and Crohn's disease. Currently, the incidence and prevalence of IBD are increasing globally. Although both biologic agents and small molecule drugs have been available for treatment of IBD patients, approximately one third of treated patients do not respond to these treatments. Therefore, novel therapy or repurposing of drugs have been extensively studied to obtain an effective therapy for IBD patients. Among these drugs, metformin has been reported to exert beneficial effects in many organs via its anti-inflammatory effect. Additionally, evidence from cellular to clinical models of IBD demonstrated significant positive effects of metformin on inflammatory pathways, oxidative stress, gut barrier integrity, and gut microbiota. In this review, the beneficial effects of metformin on IBD are comprehensively summarized and discussed using the results of in vitro, in vivo, and clinical studies. Increased understanding of these protective effects and the underlying mechanisms may pave the way for effective use of metformin in IBD patients.

The morphometric study of the moderator band in Thais.

A moderator band, also known as the septomarginal trabecula, is a group of muscle bundles located in the ventricle of almost all human hearts. The morphology of the moderator band has various forms and several studies have focused mostly on its structure. Thus, in the present study, we sought to study the morphology and morphometry of the moderator band and tried to rearrange the criteria based on the previous studies to classify the moderator band in Thais. The study investigated 67 formalin-fixed human hearts of both sexes obtained from Thai donors aged 24-101 years with mean age at death 69.92 years. The moderator band was evident in 66 of the 67 specimens (98.51%). The moderator band had the mean or median of overall length, thickness, distance to the base of the tricuspid valve, distance to the base of the pulmonary valve, distance to the apex of the right ventricle, the angle at the septal connection, and angle of the papillary, which were 18.9 ± 6.4 mm, 3.17 (2.04-4.55) mm, 33.0 ± 7.97 mm, 38.8 ± 9.62 mm, 56.4 ± 8.09 mm, 50 (30-105)°, 73.9 ± 30.1°, respectively. The mean distance originating point from the supraventricular crest to the anterior papillary muscle was 0.396 ± 0.07 of the distance from the base of the tricuspid valve to the apex of the right ventricle. Our present classification found that crest-like and thick moderator band with complex secondary branching at high origin (type IVc), and low origin (type IVd) were the most common subtypes. This study provided both anatomical and clinical information that should be useful in cardiac surgery, radiology, and cardiac electrophysiological interventions.

Effect of intensive weekend mindfulness-based intervention on BDNF, mitochondria function, and anxiety. A randomized, crossover clinical trial.

Background: The previous metanalysis found that Mind-body intervention (MBI) improves neuropsychologic well-being and may increase brain-derived growth factor (BDNF). BDNF is a neurotrophic factor related to neuroplasticity. Objective: To evaluate the effect of the short intensive MBI compared to control-relaxation on Site on BDNF and examine if this change is related to mitochondria function or stress-related neurohormonal activity. Methods: Randomized, controlled, two-period cross-over trial conducted in a medical center in Thailand. Healthy-meditation naive Nurse and Occupational Therapy Students, 23 assigned randomly to MBI, and 24 relaxations at the site for 8 h during the weekend. The wash-out period was three months between the two periods. All volunteers took the blood test for BDNF, mitochondrial oxidative phosphorylation (OXPHOS), Cortisol, and Heart rate variability (HRV) measurement before and Visual Analogue Scale for Anxiety (VAS-A), forward and backward digit span after each period. Results: A total of 40 participants finished the trials. The cross over trial analysis showed a significant treatment effect between MBI and Relaxation on-site for the mean VAS-A as 9.89 (95% CI 4.81 to 19.47; P = 0.001), serum BDNF as 1.24 (95% CI 0.16 to 2.32; P = 0.04), and OXPHOS complex-1 was decreased 0.41 (95% CI 0.03-0.29 p = 0.03). There were no significant differences for digit span, cortisol, and HRV. Conclusion: In healthy meditation naïve females, even a short period of MBI may increase serum BDNF and reduce anxiety more than relaxation on-site. The more reduction of OXPHOS complex-1 in the mindfulness group suggests oxidative stress may be a more sensitive indicator than stress-related neurohormonal activity.