Comparative Analysis of Antibiotic Resistance and Biofilm Characteristics of Two Major Enterococcus Species from Poultry Slaughterhouses in South Korea.

The spread of antibiotic-resistant Enterococcus in the poultry industry poses significant public health challenges due to multidrug resistance and biofilm formation. We investigated the antibiotic resistance profiles and biofilm characteristics of E. faecalis and E. faecium isolates from chicken meat in poultry slaughterhouses in South Korea. Ninety-six isolates (forty-eight each of E. faecalis and E. faecium) were collected between March and September 2022. Both species were analyzed using MALDI-TOF, PCR, antibiotic susceptibility testing, and biofilm assays. A high level of multidrug resistance was observed in E. faecalis (95.8%) and E. faecium (93.8%), with E. faecium exhibiting a broader range of resistance, particularly to linezolid (52.1%) and rifampicin (47.9%). All E. faecalis isolates formed biofilm in vitro, showing stronger biofilm formation than E. faecium with a significant difference (p < 0.001) in biofilm strength. Specific genes (cob, ccf, and sprE) were found to be correlated with biofilm strength. In E. faecium isolates, biofilm strength was correlated with resistance to linezolid and rifampicin, while a general correlation between antibiotic resistance and biofilm strength was not established. Through analysis, correlations were noted between antibiotics within the same class, while no general trends were evident in other analyzed factors. This study highlights the public health risks posed by multidrug-resistant enterococci collected from poultry slaughterhouses, emphasizing the complexity of the biofilm-resistance relationship and the need for enhanced control measures.

Protective effect of increased O-GlcNAc cycling against 6-OHDA induced Parkinson's disease pathology.

This study aimed to elucidate the role of O-GlcNAc cycling in 6-hydroxydopamine (6-OHDA)-induced Parkinson's disease (PD)-like neurodegeneration and the underlying mechanisms. We observed dose-dependent downregulation of O-GlcNAcylation, accompanied by an increase in O-GlcNAcase following 6-OHDA treatment in both mouse brain and Neuro2a cells. Interestingly, elevating O-GlcNAcylation through glucosamine (GlcN) injection provided protection against PD pathogenesis induced by 6-OHDA. At the behavioral level, GlcN mitigated motor deficits induced by 6-OHDA, as determined using the pole, cylinder, and apomorphine rotation tests. Furthermore, GlcN attenuated 6-OHDA-induced neuroinflammation and mitochondrial dysfunction. Notably, augmented O-GlcNAcylation, achieved through O-GlcNAc transferase (OGT) overexpression in mouse brain, conferred protection against 6-OHDA-induced PD pathology, encompassing neuronal cell death, motor deficits, neuroinflammation, and mitochondrial dysfunction. These collective findings suggest that O-GlcNAcylation plays a crucial role in the normal functioning of dopamine neurons. Moreover, enhancing O-GlcNAcylation through genetic and pharmacological means could effectively ameliorate neurodegeneration and motor impairment in an animal model of PD. These results propose a potential strategy for safeguarding against the deterioration of dopamine neurons implicated in PD pathogenesis.

Changes in Vertebrobasilar Artery Dissection Visible with High-Resolution Vessel Wall Imaging: A Serial Follow-Up Study.

BACKGROUND: High-resolution vessel wall imaging (HR-VWI) can identify vertebrobasilar artery dissections (VBADs) due to its good intramural hematoma and intimal flap visualization. Although the clinical course of VBADs is known to be benign, changes in VBADs visible using HR-VWI at follow-up are unknown. Thus, this study aimed to assess serial changes in VBADs using HR-VWI at follow-up. MATERIALS AND METHODS: Patients with neurological symptoms from VBADs who had undergone both initial and follow-up HR-VWI examinations were retrospectively enrolled. Enrolled patients with VBADs at the initial HR-VWI after acute symptom onset underwent serial follow-up with HR-VWI at 3, 6, 12, and 24 months. Patients were classified into three groups based on the results of follow-up HR-VWI examinations: type 1 = wall thickness of the dissected artery; type 2 = no interval change; and type 3 = occlusion. RESULTS: Fifteen patients (median age: 50 years, nine males) were enrolled in this study. All patients initially showed an intimal flap and a double lumen. Twelve (80%) patients showed strong wall enhancement. Nine (60%) patients had an intramural hematoma. During serial follow-up, nine (60.0%) patients showed type 1 lesions due to attachment of the intimal flap to the vessel wall, five (33.3%) showed type 2, and one showed type 3. Four patients with BA dissection showed type 2 lesions without change in the intimal flap or the double lumen. CONCLUSIONS: Changes in VBADs in HR-VWI were observed during the follow-up period. Most patients with VBADs showed the healing process, such as the disappearance of the intimal flap and the double lumen.

Melatonin and Exercise Counteract Sarcopenic Obesity through Preservation of Satellite Cell Function.

Sarcopenic obesity (SO) is characterized by atrophic skeletal muscle impairment (sarcopenia) and obesity, which is associated with adverse outcomes of morbidity and mortality in elderly people. We investigated the effects of melatonin and exercise training on SO in 32-week-old senescence-accelerated mouse-prone-8 (SAMP8) mice fed a normal diet or a high-fat diet for 16 weeks. Melatonin, exercise, or melatonin and exercise for 8 weeks displayed reductions in the SO-induced impairment of skeletal muscle function and atrophy. Specifically, a decrease in mitochondrial calcium retention capacity in skeletal muscles observed in the HFD-con group was attenuated in melatonin and/or exercise intervention groups. More importantly, HFD-con mice displayed a lower number of Pax7+ satellite cells (SCs) and higher expression of p16ink than P8ND mice, which were attenuated by melatonin and/or exercise interventions. The cellular senescence in SC-derived primary myoblasts from HFD-con mice was significantly attenuated in myoblasts from the melatonin and/or exercise groups, which was reproduced in a senescence model of H2O2-treated C2C12 myoblasts. Our results suggest that melatonin and exercise training attenuate SO-induced skeletal muscle dysfunction, at least in part, through preserving the SC pool by inhibiting cellular senescence and attenuating mitochondrial dysfunction.

Dynapenic-abdominal obesity as an independent risk factor for chronic kidney disease in postmenopausal women: a population-based cohort study.

OBJECTIVE: Low muscle strength and obesity lead to a higher risk of chronic kidney disease (CKD). Perimenopause is associated with a natural decline in muscle strength and an increase in visceral adiposity. Dynapenic obesity, which is the coexistence of low muscle strength and obesity, is expected to synergistically increase the prevalence of CKD in postmenopausal women. The aim of this study was to determine combined associations of dynapenia and obesity with CKD in postmenopausal women. METHODS: This study used data from the Korean National Health and Nutrition Examination Survey, 2016 to 2019. The study included 4,525 postmenopausal women aged 42 to 80 years that were classified into four groups based on waist circumference (≥85 cm) and hand grip strength (<18 kg): normal, dynapenic, obese, or dynapenic-obese. According to the Kidney Disease: Improving Global Outcomes, we defined CKD as an estimated glomerular filtration rate <60 mL/min per 1.73 m2. Complex sample logistic regression models were conducted to determine the relationships among coexistence of dynapenia, abdominal obesity, and the risk of CKD. RESULTS: Dynapenic-abdominal obese group displayed lower estimated glomerular filtration rate levels than other groups (P < 0.05 for all data). The prevalence rates of CKD were 15.5%, 7.8%, 6.2%, and 2.4% in the dynapenic-abdominal obese, dynapenic, abdominal obese, and normal groups, respectively (P < 0.001). Complex sample logistic regression analyses, after adjusting for age, height, health behaviors, and comorbidities, showed that the odds ratio for CKD with respect to dynapenic-abdominal obesity was 1.82 (95% confidence interval, 1.19-2.79) and to abdominal obesity was 1.54 (95% confidence interval, 1.07-2.22) than in the normal group. CONCLUSIONS: This study demonstrated that dynapenic-abdominal obesity, as determined by low handgrip strength and high waist circumference values, was associated with increased risk of CKD in postmenopausal women.

Role of exercise in estrogen deficiency-induced sarcopenia.

A decline in estrogen levels during menopause is associated with the loss of muscle mass and function, and it can accelerate sarcopenia. However, with the growing number of postmenopausal women due to the increase in life expectancy, the effects of estrogen on skeletal muscle are not completely understood. This article reviews the relationship between estrogen deficiency and skeletal muscle, its potential mechanisms, including those involving mitochondria, and the effects of exercise on estrogen deficiency-induced skeletal muscle impairment. In particular, mitochondrial dysfunction induced by estrogen deficiency accelerates sarcopenia via mitochondrial dynamics, mitophagy, and mitochondrial-mediated apoptosis. It is well known that exercise training is essential for health, including for the improvement of sarcopenia. This review highlights the importance of exercise training (aerobic and resistance exercise) as a therapeutic intervention against estrogen deficiency-induced sarcopenia.

Exercise Training Attenuates Ovariectomy-Induced Alterations in Skeletal Muscle Remodeling, Apoptotic Signaling, and Atrophy Signaling in Rat Skeletal Muscle.

PURPOSE: The effects of aerobic exercise training on soleus muscle morphology, mitochondria-mediated apoptotic signaling, and atrophy/hypertrophy signaling in ovariectomized rat skeletal muscle were investigated. METHODS: Female Sprague-Dawley rats were divided into control (CON), ovariectomy (OVX), and ovariectomy plus exercise (OVX+EX) groups. After ovarian excision, exercise training was performed using a rat treadmill at 20 m/min, 50 min/day, 5 days/week for 12 weeks. Protein levels of mitochondria-mediated apoptotic signaling and atrophy/hypertrophy signaling in the skeletal muscle (soleus) were examined through western immunoblot analysis. RESULTS: The number of myocytes and myocyte cross-sectional area (CSA) were increased and the extramyocyte space was decreased in the OVX group compared to those in the CON group. However, aerobic exercise training significantly increased myocyte CSA and decreased extramyocyte space in the OVX+EX group compared to those in the OVX group. The protein levels of proapoptotic signaling and muscle atrophy signaling were significantly increased, whereas the protein levels of muscle hypertrophy signaling were significantly decreased in the OVX group compared to that in the CON group. Aerobic exercise training significantly decreased the protein levels of proapoptotic signaling and increased the protein level of antiapoptotic protein in the OVX+EX group compared to that in the OVX group. Aerobic exercise training significantly increased the protein levels of hypertrophy signaling and decreased protein levels of atrophy signaling in the OVX+EX group compared to those in the OVX group. CONCLUSION: Treadmill exercise improved estrogen deficiency-induced impairment in skeletal muscle remodeling, mitochondria-mediated apoptotic signaling, and atrophy/hypertrophy signaling in skeletal muscle.

A Case Report for Myopericarditis after BNT162b2 COVID-19 mRNA Vaccination in a Korean Young Male.

Mass vaccination with the Pfizer-BioNTech coronavirus disease 2019 (COVID-19) vaccine (BNT162b2) in Korea has resulted in many reported adverse effects. These side effects are the object of much scrutiny in the medical community. We report the case of a 29-year-old male who was diagnosed with myopericarditis after his second dose of Pfizer-BioNTech COVID-19 vaccine. This patient is the second recognized case of Pfizer-BioNTech COVID-19 vaccine induced myopericarditis in Korea and the first to have recovered from it. He originally presented with chest discomfort and exertional chest pain. Lab tests revealed elevated cardiac marker levels and echocardiographic findings displayed minimal pericardial effusion, prompting diagnosis as myopericarditis. We decided on two weeks of outpatient treatment with non-steroidal anti-inflammatory drugs (NSAIDs) due to the patient's mild symptoms and his occupation in the military. When this proved insufficient, we shifted to combination therapy with low dose corticosteroids and NSAIDs. After two weeks of treatment, the patient's symptoms and pericardial effusion had improved, and he was recovered completely 37 days after the onset.

Experiences of Changes in Eating Habits and Eating Behaviors of Women First Diagnosed with Gestational Diabetes.

As gestational diabetes, which is increasing steadily around the world, can cause complications in the mother and fetus, it is essential to change eating habits and eating behavior to prevent this. According to the 2020 American Diabetes Association recommendations, the food plan should be designed for the adequate calorie intake to achieve glycemic goals and consequently promote maternal and fetal health. Thus, the following study has used the qualitative theme analysis method to assess what it means for 28 South Korean women, who were diagnosed with gestational diabetes for the first time, to change their eating habits and behaviors. As a result, themes were derived related to reflection on daily life, formation of new relationships in the same group, efforts that must be made, rediscovery of couples, and lifestyles reborn as new roles. Based on the results of the study, it is shown that the study participants recovered the peace in their mental state after the crisis of gestational diabetes to pursue relaxation and ultimately higher quality of life by following the plan to fulfill healthy achievements, such as changing their eating habits and behaviors. Therefore, future research and support measures to help the healthy behaviors should be sought by comprehensively exploring the effects of women's experiences in changing their eating habits and behaviors.

Personalized Healthcare for Dementia.

Dementia is one of the most common health problems affecting older adults, and the population with dementia is growing. Dementia refers to a comprehensive syndrome rather than a specific disease and is characterized by the loss of cognitive abilities. Many factors are related to dementia, such as aging, genetic profile, systemic vascular disease, unhealthy diet, and physical inactivity. As the causes and types of dementia are diverse, personalized healthcare is required. In this review, we first summarize various diagnostic approaches associated with dementia. Particularly, clinical diagnosis methods, biomarkers, neuroimaging, and digital biomarkers based on advances in data science and wearable devices are comprehensively reviewed. We then discuss three effective approaches to treating dementia, including engineering design, exercise, and diet. In the engineering design section, recent advances in monitoring and drug delivery systems for dementia are introduced. Additionally, we describe the effects of exercise on the treatment of dementia, especially focusing on the effects of aerobic and resistance training on cognitive function, and the effects of diets such as the Mediterranean diet and ketogenic diet on dementia.

Moderate aerobic exercise training ameliorates impairment of mitochondrial function and dynamics in skeletal muscle of high-fat diet-induced obese mice.

The purpose of this study is to determine whether moderate aerobic exercise training improves high-fat diet-induced alterations in mitochondrial function and structure in the skeletal muscle. Male 4-week-old C57BL/6 mice were randomly divided into four groups: control (CON), control plus exercise (CON + EX), high-fat diet (HFD), and high-fat diet plus exercise (HFD + EX). After obesity was induced by 20 weeks of 60% HFD, treadmill exercise training was performed at 13-16 m/min, 40-50 min/day, and 6 days/week for 12 weeks. Mitochondrial structure, function, and dynamics, and mitophagy were analyzed in the skeletal muscle fibers from the red gastrocnemius. Exercise training increased mitochondrial number and area and reduced high-fat diet-induced obesity and hyperglycemia. In addition, exercise training attenuated mitochondrial dysfunction in the permeabilized myofibers, indicating that HFD-induced decrease of mitochondrial O2 respiration and Ca2+ retention capacity and increase of mitochondrial H2 O2 emission were attenuated in the HFD + EX group compared to the HFD group. Exercise also ameliorated HFD-induced imbalance of mitochondrial fusion and fission, demonstrating that HFD-induced decrease in fusion protein levels was elevated, and increase in fission protein levels was reduced in the HFD + EX groups compared with the HFD group. Moreover, dysregulation of mitophagy induced by HFD was mitigated in the HFD + EX group, indicating a decrease in PINK1 protein level. Our findings demonstrated that moderate aerobic exercise training mitigated obesity-induced insulin resistance by improving mitochondrial function, and reversed obesity-induced mitochondrial structural damage by improving mitochondrial dynamics and mitophagy, suggesting that moderate aerobic exercise training may play a therapeutic role in protecting the skeletal muscle against mitochondrial impairments and insulin resistance induced by obesity.

Exercise as a Therapeutic Strategy for Sarcopenia in Heart Failure: Insights into Underlying Mechanisms.

Sarcopenia, a syndrome commonly seen in elderly populations, is often characterized by a gradual loss of skeletal muscle, leading to the decline of muscle strength and physical performance. Growing evidence suggests that the prevalence of sarcopenia increases in patients with heart failure (HF), which is a dominant pathogenesis in the aging heart. HF causes diverse metabolic complications that may result in sarcopenia. Therefore, sarcopenia may act as a strong predictor of frailty, disability, and mortality associated with HF. Currently, standard treatments for slowing muscle loss in patients with HF are not available. Therefore, here, we review the pathophysiological mechanisms underlying sarcopenia in HF as well as current knowledge regarding the beneficial effects of exercise on sarcopenia in HF and related mechanisms, including hormonal changes, myostatin, oxidative stress, inflammation, apoptosis, autophagy, the ubiquitin-proteasome system, and insulin resistance.

Aging Promotes Mitochondria-Mediated Apoptosis in Rat Hearts.

Aging represents a major risk for developing cardiac disease, including heart failure. The gradual deterioration of cell quality control with aging leads to cell death, a phenomenon associated with mitochondrial dysfunction in the heart. Apoptosis is an important quality control process and a necessary phenomenon for maintaining homeostasis and normal function of the heart. However, the mechanism of mitochondria-mediated apoptosis in aged hearts remains poorly understood. Here, we used male Fischer 344 rats of various ages, representing very young (1 month), young (4 months), middle-aged (12 months), and old (20 months) rats, to determine whether mitochondria-mediated apoptotic signals and apoptosis in the left ventricle of the heart are altered notably with aging. As the rats aged, the extramyocyte space and myocyte cross-sectional area in their left ventricle muscle increased, while the number of myocytes decreased. Additionally, mitochondrion-mediated apoptotic signals and apoptosis increased remarkably during aging. Therefore, our results demonstrate that aging promotes remarkable morphological changes and increases the degree of mitochondrion-mediated apoptosis in the left ventricle of rat hearts.

Re-Setting the Circadian Clock Using Exercise against Sarcopenia.

Sarcopenia is defined as the involuntary loss of skeletal muscle mass and function with aging and is associated with several adverse health outcomes. Recently, the disruption of regular circadian rhythms, due to shift work or nocturnal lifestyle, is emerging as a novel deleterious factor for the development of sarcopenia. The underlying mechanisms responsible for circadian disruption-induced sarcopenia include molecular circadian clock and mitochondrial function associated with the regulation of circadian rhythms. Exercise is a potent modulator of skeletal muscle metabolism and is considered to be a crucial preventative and therapeutic intervention strategy for sarcopenia. Moreover, emerging evidence shows that exercise, acting as a zeitgeber (time cue) of the skeletal muscle clock, can be an efficacious tool for re-setting the clock in sarcopenia. In this review, we provide the evidence of the impact of circadian disruption on skeletal muscle loss resulting in sarcopenia. Furthermore, we highlight the importance of exercise timing (i.e., scheduled physical activity) as a novel therapeutic strategy to target circadian disruption in skeletal muscle.

Palladium-Catalyzed Decarboxylative Coupling of Alkynyl Carboxylic Acids and Alkenyl Tosylates for the Synthesis of Enynones.

A palladium-catalyzed decarboxylative coupling reaction was developed for the synthesis of 3-(1-alkynyl)-2-cyclohexen-1-ones. A variety of alkynyl carboxylic acids were coupled with 3-oxocyclohexenyl tosylates to afford the corresponding enynones in good to excellent yields. The developed catalytic system is phosphine free and showed good tolerance toward various functionalities such as chloride, cyano, nitro, ester, aldehyde, and alcohol groups. In addition, phenylpropiolic acid exhibited higher reactivity in the reaction with alkenyl toslyate than phenyl acetylene.

Li13Mn(SeO3)8: Lithium-Rich Transition Metal Selenite Containing Jahn-Teller Distortive Cations.

A novel lithium-rich transition metal selenite, Li13Mn(SeO3)8, that is composed of a Jahn-Teller distortive cation, Mn3+, in the high spin d4 state, and a second-order Jahn-Teller (SOJT) distortive lone pair cation, Se4+, has been synthesized via hydrothermal and high temperature solid state reactions. The selenite is classified as a molecular compound consisting of MnO6 octahedra, SeO3 trigonal pyramids, and Li+ cations. Considering the Li-O interactions, the structure of Li13Mn(SeO3)8 may be described as a pseudo-three-dimensional framework as well. The title compound is thermally stable up to 500 °C and starts decomposing above the temperature attributable to the volatilization of SeO2. While the MnO6 octahedra in Li13Mn(SeO3)8 exhibit six identical Mn-O bond distances at room temperature due to the dynamic Jahn-Teller effect, a clear elongation of two Mn-O bonds along a specific direction is observed at 100 K. A series of isostructural selenites with different transition metals, i.e., Li13M(SeO3)8 (M = Sc, Cr, and Fe), have been also successfully obtained in phase pure forms using similar synthetic methods. Magnetic properties, spectroscopic characterizations, and local dipole moments calculations for all the synthesized selenites are presented.

Airway fire injury during rigid bronchoscopy in a patient with a silicon stent -A case report-.

Therapeutic bronchoscopy is widely employed as an effective first-line treatment for patients with central airway obstructions. Airway fires during rigid bronchoscopy are rare, but can have potentially devastating consequences. Pulmonologist and anesthesiologist undertaking this type of procedure should be aware of this serious problem and be familiar with measures to avoid this possibly fatal complication. We report the case of a 24-year-old patient with a silicone stent who experienced an electrocautery-induced airway fire during rigid bronchoscopy.

Serial cloning of pigs by somatic cell nuclear transfer: restoration of phenotypic normality during serial cloning.

Somatic cell nuclear transfer (scNT) is a useful way to create cloned animals. However, scNT clones exhibit high levels of phenotypic instability. This instability may be due to epigenetic reprogramming and/or genomic damage in the donor cells. To test this, we produced transgenic pig fibroblasts harboring the truncated human thrombopoietin (hTPO) gene and used them as donor cells in scNT to produce first-generation (G1) cloned piglets. In this study, 2,818 scNT embryos were transferred to 11 recipients and five G1 piglets were obtained. Among them, a clone had a dimorphic facial appearance with severe hypertelorism and a broad prominent nasal bridge. The other clones looked normal. Second-generation (G2) scNT piglets were then produced using ear cells from a G1 piglet that had an abnormal nose phenotype. We reasoned that, if the phenotypic abnormality of the G1 clone was not present in the G2 and third-generation (G3) clones, or was absent in the G2 clones but reappeared in the G3 clones, the phenotypic instability of the G1 clone could be attributed to faulty epigenetic reprogramming rather than to inherent/accidental genomic damage to the donor cells. Blastocyst rates, cell numbers in blastocyst, pregnancy rates, term placenta weight and ponderal index, and birth weight between G1 and G2 clones did not differ, but were significantly (P < 0.05) lower than control age- and sex-matched piglets. Next, we analyzed global methylation changes during development of the preimplantation embryos reconstructed by donor cells used for the production of G1 and G2 clones and could not find any significant differences in the methylation patterns between G1 and G2 clones. Indeed, we failed to detect the phenotypic abnormality in the G2 and G3 clones. Thus, the phenotypic abnormality of the G1 clone is likely to be due to epigenetic dysregulation. Additional observations then suggested that expression of the hTPO gene in the transgenic clones did not appear to be the cause of the phenotypic abnormality in the G1 clones and that the abnormality was acquired by only a few of the G1 clone's cells during its gestational development.