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BMC Veterinary Research Jun 2024Hypothyroidism is a common endocrine disruption observed in utero that adversely affects fetal growth and maturation leading to long-term impacts on health; however, the...
BACKGROUND
Hypothyroidism is a common endocrine disruption observed in utero that adversely affects fetal growth and maturation leading to long-term impacts on health; however, the exact molecular mechanisms by which these deleterious effects occur are unknown. We hypothesize that fetal hypothyroidism during late gestation will disrupt cell cycle regulation in a tissue-specific manner. To evaluate this, eight pregnant gilts were dosed with either methimazole or an equivalent negative control during days 85-106 out of 114 days of gestation (n = 4/group). Following treatment, the gilts were humanely euthanized, and tissue samples of fetal heart, ileum, kidney, lung, liver, muscle, spleen, and thymus taken from two male and two female fetuses (n = 32) from each gilt.
RESULTS
The relative expression of three cell cycle promoters (CDK1, CDK2, and CDK4), and one cell cycle inhibitor (CDKN1A) was compared in each tissue to determine the effect of hypothyroidism on the developing fetus. All of the eight tissues examined experienced at least one significant up- or downregulation in the expression of the aforementioned genes as a result of treatment with methimazole. Substantial changes were observed in the liver and muscle, with the latter experiencing significant downregulations of CDK1, CDK2, and CDK4 as a result of treatment. In addition, all tissues were examined for changes in protein content, which further elucidated the impact of hypothyroidism on the fetal liver by the observation of a marked increase in protein content in the methimazole-treated group. Finally, the heart and liver were histologically examined for evidence of cellular hyperplasia and hypertrophy by measuring average nuclei density and size in each tissue, with the results showing a significant decrease in average nuclei size in the liver of hypothyroid fetuses.
CONCLUSIONS
Collectively, these findings indicate the occurrence of organ-specific disruptions in cell cycle progression as a result of in utero hypothyroidism, which may explain the long term and widespread effects of hypothyroidism on fetal development.
Topics: Animals; Female; Methimazole; Hypothyroidism; Pregnancy; Swine; Male; Cell Cycle; Antithyroid Agents; Liver; Swine Diseases; Fetus
PubMed: 38902754
DOI: 10.1186/s12917-024-04102-y -
European Journal of Applied Physiology Jun 2024While muscle mass and skeletal muscle fibers phenotype have been shown atypical in constitutional thinness (CT), force production capacities and its architectural...
PURPOSE
While muscle mass and skeletal muscle fibers phenotype have been shown atypical in constitutional thinness (CT), force production capacities and its architectural determinants have never been explored. The present study compared muscle functionality and architecture between participants with CT and their normal-weight (NW) counterparts.
METHODS
Anthropometry, body composition (Dual-X-ray Absorptiometry), physical activity/sedentary behavior (ActiGraph wGT3X-BT), ultrasound recording of the Vastus Lateralis (2D-ultrasound system), and functional capacities at maximal isometric and isokinetic voluntary contractions (MVC and MVC) during knee extension (isokinetic dynamometer chair Biodex) have been measured in 18 women with CT (body mass index < 17.5 kg/m) and 17 NW women.
RESULTS
A lower fat-free mass (ES: -1.94, 95%CI: -2.76 to -1.11, p < 0.001), a higher sedentary time, and a trend for a lower time spent at low-intensity physical activity, were observed in CT vs NW participants. While absolute MVC, MVC, rate of torque development (RTD), and torque work were all markedly lower in CT, these differences disappeared when normalized to body or muscle mass. Muscle thickness and fascicle length were found lower in CT (ES: -1.29, 95%CI: -2.03 to -0.52, p < 0.001; and ES: -0.87, 95%CI: -1.58 to -0.15, p = 0.02, respectively), while pennation angle was found similar.
CONCLUSION
Despite lower absolute strength capacities observed in CT, present findings support the hypothesis of physiological adaptations to the low body and muscle mass than to some intrinsic contractile impairments. These results call for further studies exploring hypertrophy-targeted strategies in the management of CT.
PubMed: 38900200
DOI: 10.1007/s00421-024-05539-7 -
Journal of Strength and Conditioning... Jul 2024de Lemos Muller, CH, Farinha, JB, Leal-Menezes, R, and Ramis, TR. Aerobic training with blood flow restriction on muscle hypertrophy and strength: systematic review and... (Meta-Analysis)
Meta-Analysis
de Lemos Muller, CH, Farinha, JB, Leal-Menezes, R, and Ramis, TR. Aerobic training with blood flow restriction on muscle hypertrophy and strength: systematic review and meta-analysis. J Strength Cond Res 38(7): 1341-1349, 2024-Integrating strength and endurance training in a single exercise session, even on separate days, can be physically demanding and time-consuming. Therefore, there is a growing interest in identifying efficient training methods that can concurrently enhance cardiovascular and neuromuscular performance through a singular training modality. This study conducted a systematic review and meta-analysis to explore the effects of aerobic training with blood flow restriction (AT + BFR) on muscle hypertrophy and strength gains in healthy individuals. Our study was registered at PROSPERO and used multiple databases (PubMed, Embase, Scopus, and Web of Science), seeking clinical trials that examined AT + BFR influence on muscle hypertrophy and strength gains in individuals aged 18-60 years and comparing with aerobic training without BFR. The risk of bias and method quality were assessed using the ROB2.0 tool and PEDro scale, respectively, and the quality of evidence was evaluated with the GRADE method. A random-effects model was used for meta-analysis, and standardized mean difference (SMD) was calculated for each outcome. Of 4,462 records, 29 full texts were assessed for eligibility, with 7 articles meeting the inclusion criteria. The results indicated that AT + BFR was more beneficial for inducing muscle hypertrophy than aerobic training without BFR (SMD [95% CI] = 0.86 [0.37-1.35]; I2 = 42%). Furthermore, AT + BFR was associated with greater improvements in muscle strength (SMD [95% CI] = 0.41 [0.10-0.72]; I2 = 0%). Despite the generally high risk of bias for both outcomes, these encouraging findings underscore the clinical significance of AT + BFR as a compelling tool for enhancing neuromuscular parameters.
Topics: Humans; Muscle Strength; Muscle, Skeletal; Resistance Training; Exercise; Hypertrophy; Blood Flow Restriction Therapy; Regional Blood Flow; Skeletal Muscle Enlargement
PubMed: 38900180
DOI: 10.1519/JSC.0000000000004800 -
Zhen Ci Yan Jiu = Acupuncture Research Jun 2024To observe the effect of electroacupuncture (EA) at "Neiguan"(PC6) on cardiac function, cardiac morphology and transient receptor potential channel (TRPC) protein...
OBJECTIVES
To observe the effect of electroacupuncture (EA) at "Neiguan"(PC6) on cardiac function, cardiac morphology and transient receptor potential channel (TRPC) protein expressions in myocardial tissue of mice with myocardial hypertrophy, so as to explore its mechanisms underlying improvement of myocardial hypertrophy.
METHODS
Forty-five male C57BL/6 mice were randomly divided into control, model and EA groups (15 mice/group). The myocardial hypertrophy model was established by subcutaneous injection of isoproterenol hydrochloride (15 mg·kg·d) for 14 days. The mice of the control group received subcutaneous injection of same amount of normal saline. The mice of the EA group received EA stimulation (frequency of 2 Hz, intensity of 1 mA) of bilateral PC6 for 20 min each time, once a day for 14 consecutive days. After the intervention, the body weight, tibia length and heart weight were measured. The left ventricular ejection fraction (EF), fractional shortening index (FS), left ventricular end-systolic volume (LVEV), left ventricular end-systolic internal diameter (LVID) and left ventricular posterior wall thickness (LVPW) were measured by using echocardiography for evaluating the cardiac function. The mean number and surface area of myocardial cells was detected by wheat germ agglutinin (WGA) staining, and changes of the cardiac morphology were observed under light microscopy after HE staining. The expression levels of TRPC1, TRPC3, TRPC4 and TRPC6 (TRPC1/3/4/6) in the myocardial tissue were detected by real-time quantitative PCR (qPCR) and Western blot, separately.
RESULTS
Compared with the control group, the heart-body weight ratio(<0.05) and heart-weight-to-tibia-length ratio (<0.01), LVEV and LVID levels, the relative surface area, left ventricular area ratio, and the expression levels of cardiac TRPC1/3/4/6 were significantly increased (<0.01, <0.05), while the EF, FS, LVPW, number of cardiomyocytes, and the left ventricular posterior wall ratio were obviously decreased (<0.01, <0.05) in the model group. In comparison with the model group, the heart/body weight ratio, heart-weight-to-tibia-length ratio, LVEV and LVID levels, relative surface area, left ventricular area ratio, and the expression levels of cardiac TRPC1/3/4/6 were significantly decreased (<0.01, <0.05), while the EF, FS, LVPW, number of cardiomyocytes and left ventricular posterior wall ratio were significantly increased (<0.01, <0.05) in the EA group. H.E. staining showed disordered arrangement of cardiomyocytes and obvious myocardial interstitial inflammatory cell infiltration in the model group, and evident reduction of degree of cardiac fibrosis and interstitial edema in the EA group.
CONCLUSIONS
EA of PC6 can improve the cardiac function and cardiac morphology in mice with myocardial hypertrophy, which may be related to its functions in down-regulating the expression of transient receptor potential channels.
Topics: Animals; Electroacupuncture; Mice; Mice, Inbred C57BL; Male; Humans; Myocardium; Transient Receptor Potential Channels; Cardiomegaly; Acupuncture Points; TRPC Cation Channels
PubMed: 38897799
DOI: 10.13702/j.1000-0607.20221393 -
Journal of Cellular and Molecular... Jun 2024Cardiac hypertrophy, worldwide known as an adaptive functional compensatory state of myocardial stress, is mainly believed to proceed to severe heart diseases, even to...
Cardiac hypertrophy, worldwide known as an adaptive functional compensatory state of myocardial stress, is mainly believed to proceed to severe heart diseases, even to sudden death. Emerging studies have explored the microRNA alteration during hypertrophy. However, the mechanisms of microRNAs involved in cardiac hypertrophy are still uncertain. We studied young rats to establish abdominal aorta coarctation (AAC) for 4 weeks. With the significant downregulated cardiac function and upregulated hypertrophic biomarkers, AAC-induced rats showed enlarged myocardiocytes and alterations in microRNAs, especially downregulated miR-31-5p. miR-31-5p targets the 3'UTR of Nfatc2ip and inhibits myocardial hypertrophy in vitro and in vivo. Furthermore, we verified that Nfatc2ip is necessary and sufficient for cardiac hypertrophy in neonatal rat cardiomyocytes. Moreover, we found miR-31-5p inhibited the colocalization of Nfatc2ip and hypertrophic gene β-Mhc. Luciferase assay and ChiP-qPCR test demonstrated that Nfatc2ip binded to the core-promoter of β-Mhc and enhanced its transcriptional activity. Above all, our study found a new pathway, mir-31-5p/Nfatc2ip/β-Mhc, which is involved in cardiac hypertrophy, suggesting a potential target for intervention of cardiac hypertrophy.
Topics: MicroRNAs; Animals; Cardiomegaly; NFATC Transcription Factors; Myocytes, Cardiac; Rats; Male; Rats, Sprague-Dawley; Gene Expression Regulation; 3' Untranslated Regions; Disease Models, Animal
PubMed: 38894694
DOI: 10.1111/jcmm.18413 -
International Journal of Molecular... Jun 2024Increased mitochondrial reactive oxygen species (ROS) formation is important for the development of right ventricular (RV) hypertrophy (RVH) and failure (RVF) during...
Does Cell-Type-Specific Silencing of Monoamine Oxidase B Interfere with the Development of Right Ventricle (RV) Hypertrophy or Right Ventricle Failure in Pulmonary Hypertension?
Increased mitochondrial reactive oxygen species (ROS) formation is important for the development of right ventricular (RV) hypertrophy (RVH) and failure (RVF) during pulmonary hypertension (PH). ROS molecules are produced in different compartments within the cell, with mitochondria known to produce the strongest ROS signal. Among ROS-forming mitochondrial proteins, outer-mitochondrial-membrane-located monoamine oxidases (MAOs, type A or B) are capable of degrading neurotransmitters, thereby producing large amounts of ROS. In mice, MAO-B is the dominant isoform, which is present in almost all cell types within the heart. We analyzed the effect of an inducible cardiomyocyte-specific knockout of MAO-B (cmMAO-B KO) for the development of RVH and RVF in mice. Right ventricular hypertrophy was induced by pulmonary artery banding (PAB). RV dimensions and function were measured through echocardiography. ROS production (dihydroethidium staining), protein kinase activity (PamStation device), and systemic hemodynamics (in vivo catheterization) were assessed. A significant decrease in ROS formation was measured in cmMAO-B KO mice during PAB compared to Cre-negative littermates, which was associated with reduced activity of protein kinases involved in hypertrophic growth. In contrast to littermates in which the RV was dilated and hypertrophied following PAB, RV dimensions were unaffected in response to PAB in cmMAO-B KO mice, and no decline in RV systolic function otherwise seen in littermates during PAB was measured in cmMAO-B KO mice. In conclusion, cmMAO-B KO mice are protected against RV dilatation, hypertrophy, and dysfunction following RV pressure overload compared to littermates. These results support the hypothesis that cmMAO-B is a key player in causing RV hypertrophy and failure during PH.
Topics: Animals; Hypertrophy, Right Ventricular; Monoamine Oxidase; Hypertension, Pulmonary; Mice; Mice, Knockout; Reactive Oxygen Species; Myocytes, Cardiac; Heart Failure; Male; Disease Models, Animal; Heart Ventricles; Ventricular Dysfunction, Right
PubMed: 38892401
DOI: 10.3390/ijms25116212 -
International Journal of Molecular... May 2024The association between vitamin D deficiency and cardiovascular disease remains a controversial issue. This study aimed to further elucidate the role of vitamin D...
Ablation of Vitamin D Signaling in Cardiomyocytes Leads to Functional Impairment and Stimulation of Pro-Inflammatory and Pro-Fibrotic Gene Regulatory Networks in a Left Ventricular Hypertrophy Model in Mice.
The association between vitamin D deficiency and cardiovascular disease remains a controversial issue. This study aimed to further elucidate the role of vitamin D signaling in the development of left ventricular (LV) hypertrophy and dysfunction. To ablate the vitamin D receptor (VDR) specifically in cardiomyocytes, VDR mice were crossed with Mlcv2-Cre mice. To induce LV hypertrophy experimentally by increasing cardiac afterload, transverse aortic constriction (TAC) was employed. Sham or TAC surgery was performed in 4-month-old, male, wild-type, VDR, Mlcv2-Cre, and cardiomyocyte-specific VDR knockout (VDR) mice. As expected, TAC induced profound LV hypertrophy and dysfunction, evidenced by echocardiography, aortic and cardiac catheterization, cardiac histology, and LV expression profiling 4 weeks post-surgery. Sham-operated mice showed no differences between genotypes. However, TAC VDR mice, while having comparable cardiomyocyte size and LV fibrosis to TAC VDR controls, exhibited reduced fractional shortening and ejection fraction as measured by echocardiography. Spatial transcriptomics of heart cryosections revealed more pronounced pro-inflammatory and pro-fibrotic gene regulatory networks in the stressed cardiac tissue niches of TAC VDR compared to VDR mice. Hence, our study supports the notion that vitamin D signaling in cardiomyocytes plays a protective role in the stressed heart.
Topics: Animals; Myocytes, Cardiac; Mice; Hypertrophy, Left Ventricular; Receptors, Calcitriol; Vitamin D; Gene Regulatory Networks; Fibrosis; Signal Transduction; Male; Disease Models, Animal; Mice, Knockout; Inflammation
PubMed: 38892126
DOI: 10.3390/ijms25115929 -
Aesthetic Plastic Surgery Jun 2024To investigate the postoperative effect of double-lid blepharoplasty based on the histological difference in the upper eyelid of Asian patients.
OBJECTIVE
To investigate the postoperative effect of double-lid blepharoplasty based on the histological difference in the upper eyelid of Asian patients.
MATERIAL AND METHODS
A total of 76 patients with poor bilateral upper eyelid morphology or a single eyelid were included in this study. Different techniques of double-eyelid blepharoplasty were performed based on the thickness of the palpebral tissue. The improved PARK method (group A: 15 participants) was employed for patients with orbicularis oculi muscle being thinner, and the fat bulge of orbital septum was less. The improved traditional method (group B: 52 participants) was employed for patients with hypertrophy of the eyelid skin, orbicularis oculi muscle, and fat bulge in the orbital septum.
RESULTS
All 76 patients achieved satisfactory outcomes in a single surgical procedure. Postoperative follow-up ranged from 3 to 6 months. In group A, there was no obvious swelling of flap near the palpebral margin and the double blepharon line becomes shallow. Although some patients in group B experienced varying degrees of bruising in the early postoperative period, all patients returned to a more natural shape 1-3 months after surgery. Furthermore, after 3-6 months postoperatively, there were no obvious scar adhesion and ladder sensation in the both sides of the incision.
CONCLUSION
Preoperative analysis of the thickness of the upper eyelid tissue is essential to determine the appropriate surgical technique for double-eyelid blepharoplasty. The improved traditional method is recommended for patients with hypertrophy of the upper eyelid tissue (group A), as it minimizes scar adhesion and reduces the stair-step sensation in the lower eyelid tissue during long-term follow-up. For patients with thin upper eyelid tissue, the improved PARK method should be employed to avoid issues such as tissue accumulation, double eyelid crease became shallower, or disappearance. In order to obtain natural and long-term surgical results, different surgical methods should be provided according to the patient's eye tissue condition.
LEVEL OF EVIDENCE II
This journal requires that authors assign a level of evidence to each article. For a full description of these Evidence-Based Medicine ratings, please refer to the Table of Contents or the online Instructions to Authors www.springer.com/00266 .
PubMed: 38890159
DOI: 10.1007/s00266-024-04051-9 -
Revue Neurologique Jun 2024
PubMed: 38890053
DOI: 10.1016/j.neurol.2024.06.001 -
The Journal of Sports Medicine and... Jun 2024The aim of this study is to evaluate the influence of implementation of the BFR training on the hypertrophy and strength of the lower limb muscles in combat sports...
BACKGROUND
The aim of this study is to evaluate the influence of implementation of the BFR training on the hypertrophy and strength of the lower limb muscles in combat sports fighters, using common and easy to perform both training and control methods.
METHODS
Design as a randomized control trial (RCT). The study included 30 men, MMA fighters since at least a year. They were divided into two groups: (A, a control group; B, men with the BFR training). The training lasted 8 weeks (3 times a week) and consisted of performing a set of specific exercises with a load of 20% 1RM.
RESULTS
The Wilcoxon analyzing test showed important changes in muscle girth (P<0.01) and lower limb muscular strength (P<0.05). These changes were to be seen in the tested group only, not in the control group.
CONCLUSIONS
Occlusion training is effective in increasing strength and hypertrophy of lower limb muscles in martial arts fighters.
PubMed: 38888559
DOI: 10.23736/S0022-4707.24.15782-9