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1.
Blood Press ; 33(1): 2326298, 2024 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-38469724

RESUMO

OBJECTIVE: The aim of this study was to describe and compare echocardiographic findings before renal sympathetic denervation (RDN) and 6 and 24 months after the procedure. MATERIALS AND METHODS: Patients with treatment resistant hypertension (TRH) were included in this non-randomised intervention study. RDN was performed by a single experienced operator using the Symplicity Catheter System. Echocardiographic measurements were performed at baseline, and after 6 and 24 months. RESULTS: The cohort consisted of 21 patients with TRH, with a mean systolic office blood pressure (BP) of 163 mmHg and mean diastolic BP 109 mmHg. Mixed model analysis showed no significant change in left ventricular (LV) mass index (LVMI) or left atrium volume index (LAVI) after the RDN procedure. Higher LVMI at baseline was significantly associated with greater reduction in LVMI (p < 0.001). Relative wall thickness (RWT) increased over time (0.48 mm after two years) regardless of change in BP. There was a small but significant reduction in LV end-diastolic (LVIDd) and end-systolic (LVIDs) diameters after RDN, with a mean reduction of 2.6 and 2.4 mm, respectively, after two years. Progression to concentric hypertrophy was observed only in in patients who did not achieve normal BP values, despite BP reduction after RDN. CONCLUSION: There was no reduction of LV mass after RDN. We found a small statistically significant reduction in LVIDd and LVIDs, which together with increase in RWT can indicate progression towards concentric hypertrophy. BP reduction after RDN on its own does not reverse concentric remodelling if target BP is not achieved.


Assuntos
Hipertensão , Humanos , Resultado do Tratamento , Pressão Sanguínea/fisiologia , Simpatectomia/métodos , Ecocardiografia , Hipertrofia/complicações , Rim/diagnóstico por imagem , Rim/cirurgia
2.
Nutr Diabetes ; 14(1): 10, 2024 Mar 12.
Artigo em Inglês | MEDLINE | ID: mdl-38472186

RESUMO

BACKGROUND: The gut microbiota is involved in the pathogenesis of diabetic cardiomyopathy (DCM). Myricetin protects cardiac function in DCM. However, the low bioavailability of myricetin fails to explain its pharmacological mechanisms thoroughly. Research has shown that myricetin has a positive effect on the gut microbiota. We hypothesize that myricetin improves the development of DCM via regulating gut microbiota. METHODS: DCM mice were induced with streptozotocin and fed a high-fat diet, and then treated with myricetin by gavage and high-fat diet for 16 weeks. Indexes related to gut microbiota composition, cardiac structure, cardiac function, intestinal barrier function, and inflammation were detected. Moreover, the gut contents were transplanted to DCM mice, and the effect of fecal microbiota transplantation (FMT) on DCM mice was assessed. RESULTS: Myricetin could improve cardiac function in DCM mice by decreasing cardiomyocyte hypertrophy and interstitial fibrosis. The composition of gut microbiota, especially for short-chain fatty acid-producing bacteria involving Roseburia, Faecalibaculum, and Bifidobacterium, was more abundant by myricetin treatment in DCM mice. Myricetin increased occludin expression and the number of goblet cells in DCM mice. Compared with DCM mice unfed with gut content, the cardiac function, number of goblet cells, and expression of occludin in DCM mice fed by gut contents were elevated, while cardiomyocyte hypertrophy and TLR4/MyD88 pathway-related proteins were decreased. CONCLUSIONS: Myricetin can prevent DCM development by increasing the abundance of beneficial gut microbiota and restoring the gut barrier function.


Assuntos
Diabetes Mellitus , Cardiomiopatias Diabéticas , Flavonoides , Microbioma Gastrointestinal , Animais , Camundongos , Ocludina/farmacologia , Hipertrofia , Camundongos Endogâmicos C57BL , Dieta Hiperlipídica
3.
Int J Mol Sci ; 25(5)2024 Mar 04.
Artigo em Inglês | MEDLINE | ID: mdl-38474216

RESUMO

Excessive lipid accumulation in adipocytes is a primary contributor to the development of metabolic disorders, including obesity. The consumption of bioactive compounds derived from natural sources has been recognized as being safe and effective in preventing and alleviating obesity. Therefore, we aimed to explore the antilipidemic effects of pennogenin 3-O-ß-chacotrioside (P3C), a steroid glycoside, on hypertrophied 3T3-L1 adipocytes. Oil Red O and Nile red staining demonstrated a P3C-induced reduction in lipid droplet accumulation. Additionally, the increased expression of adipogenic and lipogenic factors, including PPARγ and C/EBPα, during the differentiation process was significantly decreased by P3C treatment at both the protein and mRNA levels. Furthermore, P3C treatment upregulated the expression of fatty acid oxidation-related genes such as PGC1α and CPT1a. Moreover, mitochondrial respiration and ATP generation increased following P3C treatment, as determined using the Seahorse XF analyzer. P3C treatment also increased the protein expression of mitochondrial oxidative phosphorylation in hypertrophied adipocytes. Our findings suggest that P3C could serve as a natural lipid-lowering agent, reducing lipogenesis and enhancing mitochondrial oxidative capacity. Therefore, P3C may be a promising candidate as a therapeutic agent for obesity-related diseases.


Assuntos
Adipogenia , Metabolismo dos Lipídeos , Camundongos , Animais , Adipogenia/genética , Obesidade/metabolismo , Hipertrofia , Lipídeos/farmacologia , Estresse Oxidativo , Células 3T3-L1 , PPAR gama/metabolismo
4.
PeerJ ; 12: e16981, 2024.
Artigo em Inglês | MEDLINE | ID: mdl-38464759

RESUMO

Background: This study examined the epidemiological correlations between secretory otitis media (SOM) and diseases of neighboring organs. We measured changes in disease incidences during the 2020 COVID-19 pandemic using Internet big data spanning from 2011 to 2021. Methods: This study used the Baidu Index (BI) to determine the search volume for the terms "secretory otitis media (SOM)", "tonsillitis", "pharyngolaryngitis", "adenoid hypertrophy (AH)", "nasopharyngeal carcinoma (NPC)", "nasal septum deviation (NSD)", "rhinosinusitis", "allergic rhinitis (AR)", and "gastroesophageal reflux disease (GERD)" in Mandarin from January 2011 to December 2021. The correlations between these terms were analyzed using Spearman's correlation coefficients. The results were compared search data from 2019 and 2021 to assess the effects of isolation on SOM in 2020. Results: The seasonal variations trends of SOM and other diseases coincided well (P < 0.05), except for AR. During the 11-year timeframe, the monthly searches for rhinosinusitis, NSD, tonsillitis, pharyngolaryngitis, and NPC were statistically correlated with SOM (R = 0.825, 0.594, 0.650, 0.636, 0.664, respectively; P < 0.05). No correlation was found between SOM and AR, SOM and AH, or SOM and GERD (R =  - 0.028, R = 0.259, R = 0.014, respectively, P > 0.05). The total search volumes for SOM, rhinosinusitis, NPC, and AH decreased in 2020 compared to 2019. Discussion: SOM exhibited a discernible epidemiological connection with rhinosinusitis, nasal septal deviation (NSD), tonsillitis, pharyngolaryngitis, and nasopharyngeal carcinoma (NPC). A decrease in public gatherings was observed to effectively reduce the incidences of SOM. This underscores the pivotal role of social measures in influencing the prevalence of SOM and emphasizes the intricate interplay between SOM and various associated health factors, with implications for public health strategies.


Assuntos
Refluxo Gastroesofágico , Neoplasias Nasofaríngeas , Otite Média com Derrame , Faringite , Rinite Alérgica , Tonsilite , Humanos , Otite Média com Derrame/epidemiologia , Pandemias , Carcinoma Nasofaríngeo/complicações , Rinite Alérgica/complicações , Hipertrofia/complicações , Faringite/complicações , Tonsilite/complicações , Refluxo Gastroesofágico/complicações , Neoplasias Nasofaríngeas/complicações
5.
J Int Med Res ; 52(3): 3000605241233963, 2024 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-38436326

RESUMO

We herein present a rare case of acute central serous chorioretinopathy (CSC) associated with nonspecific orbital inflammation (NSOI). A 38-year-old woman presented with a 3-day history of ocular pain, reduced vision, periorbital swelling, proptosis, conjunctival chemosis, and restricted eye movements. Optical coherence tomography of the affected eye confirmed signs of CSC. Additionally, a computed tomography scan revealed enlargement of intraconal soft tissues and the lacrimal gland. Ocular ultrasonography detected posterior sclera thickening, indicating posterior scleritis. Following the diagnosis of NSOI, the patient received treatment with systemic corticosteroids, resulting in gradual regression of both the orbital inflammation and CSC. This is the first reported case of localized posterior pole CSC documented in a patient with NSOI. Vigilant monitoring for any ocular disorders is important in patients with orbital inflammation.


Assuntos
Coriorretinopatia Serosa Central , Feminino , Humanos , Adulto , Coriorretinopatia Serosa Central/diagnóstico , Coriorretinopatia Serosa Central/diagnóstico por imagem , Inflamação , Olho , Face , Hipertrofia
7.
Mol Cell Biol ; 44(2): 57-71, 2024.
Artigo em Inglês | MEDLINE | ID: mdl-38483114

RESUMO

Myocyte enhancer factor 2 (MEF2) proteins are involved in multiple developmental, physiological, and pathological processes in vertebrates. Protein-protein interactions underlie the plethora of biological processes impacted by MEF2A, necessitating a detailed characterization of the MEF2A interactome. A nanobody based affinity-purification/mass spectrometry strategy was employed to achieve this goal. Specifically, the MEF2A protein complexes were captured from myogenic lysates using a GFP-tagged MEF2A protein immobilized with a GBP-nanobody followed by LC-MS/MS proteomic analysis to identify MEF2A interactors. After bioinformatic analysis, we further characterized the interaction of MEF2A with a transcriptional repressor, FOXP1. FOXP1 coprecipitated with MEF2A in proliferating myogenic cells which diminished upon differentiation (myotube formation). Ectopic expression of FOXP1 inhibited MEF2A driven myogenic reporter genes (derived from the creatine kinase muscle and myogenin genes) and delayed induction of endogenous myogenin during differentiation. Conversely, FOXP1 depletion enhanced MEF2A transactivation properties and myogenin expression. The FoxP1:MEF2A interaction is also preserved in cardiomyocytes and FoxP1 depletion enhanced cardiomyocyte hypertrophy. FOXP1 prevented MEF2A phosphorylation and activation by the p38MAPK pathway. Overall, these data implicate FOXP1 in restricting MEF2A function in order to avoid premature differentiation in myogenic progenitors and also to possibly prevent re-activation of embryonic gene expression in cardiomyocyte hypertrophy.


Assuntos
Proteômica , Espectrometria de Massas em Tandem , Animais , Fatores de Transcrição MEF2/genética , Miogenina , Cromatografia Líquida , Músculo Esquelético/fisiologia , Hipertrofia
8.
Sci Rep ; 14(1): 6503, 2024 03 18.
Artigo em Inglês | MEDLINE | ID: mdl-38499550

RESUMO

Alterations in thyroid hormones (TH) and thyroid-stimulating hormone levels are frequently found following exposure to chemicals of concern. Dysregulation of TH levels can severely perturb physiological growth, metabolism, differentiation, homeostasis in the adult and developmental processes in utero. A frequently identified mode of action for this interaction is the induction of hepatic detoxification mechanisms (e.g. SULTs and UGTs), which lead to TH conjugation and elimination and therefore interfere with hormonal homeostasis, fulfilling the endocrine disruptors (EDs) definition. A short-term study in rats with dietary exposure to cyproconazole, epoxiconazole and prochloraz was conducted and hepatocyte hypertrophy, hepatic UGT activity and Phase 1/2 gene expression inductions were observed together with changes in TH levels and thyroid follicular hypertrophy and hyperplasia. To test for specific interaction with the thyroid hormone system, in vitro assays were conducted covering thyroidal I-uptake (NIS), TH transmembranal transport via MCT8 and thyroid peroxidase (TPO) function. Assays for iodothyronine deiodinases (DIO1-DIO3) and iodotyrosine deiodinase (DEHAL1) were included, and from the animal experiment, Dio1 and Dehal1 activities were measured in kidney and liver as relevant local indicators and endpoints. The fungicides did not affect any TH-specific KEs, in vitro and in vivo, thereby suggesting hepatic conjugation as the dominant MoA.


Assuntos
Glândula Tireoide , Hormônios Tireóideos , Ratos , Animais , Hormônios Tireóideos/metabolismo , Glândula Tireoide/metabolismo , Homeostase , Triazóis/farmacologia , Triazóis/metabolismo , Hipertrofia/metabolismo
10.
Am J Case Rep ; 25: e942706, 2024 Mar 10.
Artigo em Inglês | MEDLINE | ID: mdl-38512480

RESUMO

BACKGROUND Hypertrophic scars occur when there is an excessive wound-healing response in the skin. Fractional, or fractionated, carbon dioxide (CO2) laser therapy uses narrow shafts of light to smooth the skin surface and stimulate dermal collagen, which tightens the skin. This case report describes a 57-year-old woman with a traumatic hypertrophic scar of the face treated with fractional carbon dioxide laser therapy. The purpose of this case report was to highlight the role of fractional CO2 laser therapy in treatment of a facial traumatic hypertrophic scar in a patient after a motor vehicle crash. CASE REPORT A 57-year-old female patient presented with a hypertrophic, rigid, post-traumatic scar on the left side of her face following a motor vehicle crash. For the hypertrophic scar removal, the patient underwent 1 treatment session with fractional CO2 laser using the µ-Scan DOT scanning system. After 1 laser treatment session, the photographic documentation, which permits monitoring the treatment's effectiveness in esthetic improvement, showed a significant improvement in scar texture and color. In addition, a significant reduction in scar height was observed following laser therapy. Fractional laser treatment with the device was very well tolerated by the patient, who reported no pain or discomfort, complications, or adverse effects either during treatment or in the follow-up period (3 months). CONCLUSIONS This report demonstrates the cosmetic application of fractional carbon dioxide laser therapy in a case of hypertrophic scar with the use of an effective therapeutic protocol that did not require the use of suturing.


Assuntos
Cicatriz Hipertrófica , Terapia a Laser , Feminino , Humanos , Pessoa de Meia-Idade , Cicatriz Hipertrófica/radioterapia , Cicatriz Hipertrófica/cirurgia , Cicatriz Hipertrófica/etiologia , Cicatriz/complicações , Dióxido de Carbono , Resultado do Tratamento , Hipertrofia/etiologia , Terapia a Laser/efeitos adversos
11.
J Strength Cond Res ; 38(4): 787-790, 2024 Apr 01.
Artigo em Inglês | MEDLINE | ID: mdl-38513182

RESUMO

ABSTRACT: Nunes, JP, Blazevich, AJ, Schoenfeld, BJ, Kassiano, W, Costa, BDV, Ribeiro, AS, Nakamura, M, Nosaka, K, and Cyrino, ES. Determining changes in muscle size and architecture after exercise training: One site does not fit all. J Strength Cond Res 38(4): 787-790, 2024-Different methods can be used to assess muscle hypertrophy, but the effects of training on regional changes in muscle size can be detected only using direct muscle measurements such as muscle thickness, cross-sectional area, or volume. Importantly, muscle size increases vary across regions within and between muscles after resistance training programs (i.e., heterogeneous, or nonuniform, muscle hypertrophy). Muscle architectural changes, including fascicle length and pennation angle, after resistance and stretch training programs are also region-specific. In this paper, we show that the literature indicates that a single-site measure of muscle shape does not properly capture the effects achieved after exercise training interventions and that conclusions concerning the magnitude of muscle adaptations can vary substantially depending on the muscle site to be examined. Thus, we propose that measurements of muscle size and architecture should be completed at multiple sites across regions between the agonist muscles within a muscle group and along the length of the muscles to provide an adequate picture of training effects.


Assuntos
Músculo Esquelético , Treinamento de Força , Humanos , Músculo Esquelético/fisiologia , Força Muscular/fisiologia , Músculo Quadríceps/fisiologia , Exercício Físico/fisiologia , Treinamento de Força/métodos , Hipertrofia
12.
Endocrinology ; 165(4)2024 Feb 20.
Artigo em Inglês | MEDLINE | ID: mdl-38437158

RESUMO

Macromastia is an excessive, rapid, or slow growth of breast tissue in 1 or both breasts. While macromastia represents a benign lesion, it may cause breast, shoulder, back, and neck pain, poor posture, infections, and loss of nipple sensation. The pathogenesis of macromastia or hypertrophy of mammary tissue remains poorly understood. The purpose of this study is to investigate the immunohistochemical expression of several hormone receptors that may potentially influence the growth of breast tissue in women with macromastia. Immunohistochemical studies performed on representative sections of breast tissue from 63 patients diagnosed with macromastia included estrogen receptor, progesterone receptor, androgen receptor (AR), prolactin receptor, growth hormone receptor, and vascular endothelial growth factor. The expression of each stain was evaluated separately in the glandular epithelium and adipose tissue and calculated as an H-score. We observed that AR expression in breast glandular and adipose tissue in women with macromastia was significantly lower than benign, nonhypertrophic breast tissue of a control group. Although the analyses were controlled for the age, the fact the mean age and hormonal status differed between the patients and the controls could have affected the results. Additional large studies will be required to further verify this finding and increase the knowledge about the etiology of this condition and then guide pharmacological treatment of juvenile and/or idiopathic gigantomastia.


Assuntos
Mama/anormalidades , Mamoplastia , Fator A de Crescimento do Endotélio Vascular , Feminino , Humanos , Mamoplastia/métodos , Hipertrofia
13.
BMJ Case Rep ; 17(3)2024 Mar 19.
Artigo em Inglês | MEDLINE | ID: mdl-38508598

RESUMO

Liver haemangiomas are the most common benign hepatic tumours, but secondary portal hypertension resulting from haemangiomas is exceedingly uncommon. We present a case of a man in his 50s who presented with a progressively enlarging mass in the right upper abdomen. CT of the liver revealed a large hypodense lesion involving the right lobe, with two smaller lesions in the left lobe. The portal vein was compressed by the tumour, causing portal hypertension. The patient underwent right hepatectomy. Postoperatively, the patient had an uneventful course, and a 3-month follow-up demonstrated resolution of the oesophageal varices, portal gastropathy, with hypertrophy of the left lobe. This case report highlights the successful surgical management of a rare massive hepatic haemangioma causing portal hypertension with surgical resection, emphasising the potential benefits of surgical intervention with minimal complications.


Assuntos
Hemangioma , Hipertensão Portal , Neoplasias Hepáticas , Masculino , Humanos , Neoplasias Hepáticas/complicações , Neoplasias Hepáticas/diagnóstico por imagem , Neoplasias Hepáticas/cirurgia , Hemangioma/complicações , Hemangioma/diagnóstico por imagem , Hemangioma/cirurgia , Hipertensão Portal/etiologia , Hipertensão Portal/cirurgia , Veia Porta/cirurgia , Hepatectomia/métodos , Hipertrofia
14.
Scand J Med Sci Sports ; 34(3): e14608, 2024 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-38515303

RESUMO

PURPOSE: The aim of this study was to determine whether a 9-week resistance training program based on high load (HL) versus low load combined with blood flow restriction (LL-BFR) induced a similar (i) distribution of muscle hypertrophy among hamstring heads (semimembranosus, SM; semitendinosus, ST; and biceps femoris long head, BF) and (ii) magnitude of tendon hypertrophy of ST, using a parallel randomized controlled trial. METHODS: A total of 45 participants were randomly allocated to one of three groups: HL, LL-BFR, and control (CON). Both HL and LL-BFR performed a 9-week resistance training program composed of seated leg curl and stiff-leg deadlift exercises. Freehand 3D ultrasound was used to assess the changes in muscle and tendon volume. RESULTS: The increase in ST volume was greater in HL (26.5 ± 25.5%) compared to CON (p = 0.004). No difference was found between CON and LL-BFR for the ST muscle volume (p = 0.627). The change in SM muscle volume was greater for LL-BFR (21.6 ± 27.8%) compared to CON (p = 0.025). No difference was found between HL and CON for the SM muscle volume (p = 0.178).There was no change in BF muscle volume in LL-BFR (14.0 ± 16.5%; p = 0.436) compared to CON group. No difference was found between HL and CON for the BF muscle volume (p = 1.0). Regarding ST tendon volume, we did not report an effect of training regimens (p = 0.411). CONCLUSION: These results provide evidence that the HL program induced a selective hypertrophy of the ST while LL-BFR induced hypertrophy of SM. The magnitude of the selective hypertrophy observed within each group varied greatly between individuals. This finding suggests that it is very difficult to early determine the location of the hypertrophy among a muscle group.


Assuntos
Músculos Isquiossurais , Treinamento de Força , Humanos , Músculos Isquiossurais/diagnóstico por imagem , Força Muscular/fisiologia , Hipertrofia , Tendões , Treinamento de Força/métodos , Fluxo Sanguíneo Regional/fisiologia , Músculo Esquelético/fisiologia
15.
Elife ; 122024 Mar 11.
Artigo em Inglês | MEDLINE | ID: mdl-38466320

RESUMO

An increase in mechanical loading, such as that which occurs during resistance exercise, induces radial growth of muscle fibers (i.e. an increase in cross-sectional area). Muscle fibers are largely composed of myofibrils, but whether radial growth is mediated by an increase in the size of the myofibrils (i.e. myofibril hypertrophy) and/or the number of myofibrils (i.e. myofibrillogenesis) is not known. Electron microscopy (EM) can provide images with the level of resolution that is needed to address this question, but the acquisition and subsequent analysis of EM images is a time- and cost-intensive process. To overcome this, we developed a novel method for visualizing myofibrils with a standard fluorescence microscope (fluorescence imaging of myofibrils with image deconvolution [FIM-ID]). Images from FIM-ID have a high degree of resolution and contrast, and these properties enabled us to develop pipelines for automated measurements of myofibril size and number. After extensively validating the automated measurements, we used both mouse and human models of increased mechanical loading to discover that the radial growth of muscle fibers is largely mediated by myofibrillogenesis. Collectively, the outcomes of this study offer insight into a fundamentally important topic in the field of muscle growth and provide future investigators with a time- and cost-effective means to study it.


Approximately 45% of human body mass is made of skeletal muscle. These muscles contract and relax to provide the mechanical forces needed for breathing, moving, keeping warm and performing many other essential processes. Both sedentary and active adults lose approximately 30-40% of this muscle mass by the age of 80, increasing their risk of disease, disability and death. As a result, there is much interest in developing therapies that can restore, maintain and increase muscle mass in older individuals. Muscles are made of multiple fibers that are in turn largely composed of smaller units known as myofibrils. Previous studies have shown that performing resistance training or other exercise that increases the mechanical loads placed on muscles stimulates muscle growth. This growth is largely due to increased girth of the existing muscle fibers. However, it remained unclear whether this was due to myofibrils growing in size, increasing in number, or a combination of both. To address this question, Jorgenson et al. developed a fluorescence imaging method called FIM-ID to count the number and measure the size of myofibrils within cross-sections of skeletal muscle. Using FIM-ID to study samples of mouse and human muscle fibers then revealed that increasing mechanical loads on muscles increased the number of myofibrils and this was largely responsible for muscle fiber growth. FIM-ID mostly relies on common laboratory instruments and free open-source software is used to count and measure the myofibrils. Jorgenson et al. hope that this will allow as many other researchers as possible to use FIM-ID to study myofibrils in the future. A better understanding of how the body controls the number of myofibrils may lead to the development of therapies that can mimic the effects of exercise on muscles to maintain or even increase muscle mass in human patients.


Assuntos
Músculo Esquelético , Miofibrilas , Humanos , Animais , Camundongos , Fibras Musculares Esqueléticas , Hipertrofia , Imagem Óptica
16.
J Pak Med Assoc ; 74(2): 394-397, 2024 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-38419245

RESUMO

Sturge- Weber syndrome (SWS), is a rare neuro-cutaneous angiomatosis which affects male and females alike. The clinical manifestations include angiomas, haemangiomas of the lips, tongue and palatine region. The oral manifestations are usually unilateral and are susceptible to bleed. Patients can also present with macroglossia and maxillary bone hypertrophy which can lead to malocclusion of the oral cavity. Food accumulation due to occlusion can cause growth of bacteria which can intensify infections and can cause gingival hyperplasia. A case of a middle-aged 39 year old female was reported in the Ziauddin Hospital, Karachi on 2nd of February,2022 with the presenting complaints of intermittent fever and drowsiness for 10 days. On examination she had massive tongue enlargement, drooling, malocclusion, difficulty in eating and breathing. She was a known case of Sturgeweber syndrome. Based on the clinical and radiological findings, she was managed along the lines of prelaryngeal soft tissue and submandibular infection.


Assuntos
Hemangioma , Macroglossia , Macroglossia/congênito , Má Oclusão , Síndrome de Sturge-Weber , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Adulto , Síndrome de Sturge-Weber/complicações , Síndrome de Sturge-Weber/diagnóstico , Macroglossia/etiologia , Hipertrofia
17.
J Nanobiotechnology ; 22(1): 72, 2024 Feb 19.
Artigo em Inglês | MEDLINE | ID: mdl-38374072

RESUMO

Osteoarthritis (OA) is one of the most prevalent chronic musculoskeletal diseases among the elderly population. In this study, macrophage-derived exosomes were isolated and identified. Exosomes were subjected to microRNA (miRNA) sequencing and bioinformatic analysis, and differentially expressed miRNAs were verified. miR-26b-5p target genes were confirmed through target-site mutation combined with a dual-luciferase reporter assay. The effects of miR-26b-5p on macrophage polarization and chondrocyte hypertrophy were assessed in vitro. miR-26b-5p agomir was applied to mice with OA induced by anterior cruciate ligament transection (ACLT). The therapeutic effects of miR-26b-5p were evaluated via pain behavior experiments and histological observations. In vitro, miR-26b-5p repolarized M1 macrophages to an anti-inflammatory M2 type by targeting the TLR3 signaling pathway. miR-26b-5p could target COL10A1, further inhibiting chondrocyte hypertrophy induced by M1 macrophage-conditioned medium (M1-CM). In vivo, miR-26b-5p agomir ameliorated gait abnormalities and mechanical allodynia in OA mice. miR-26b-5p treatment attenuated synovitis and cartilage degeneration, thereby delaying OA progression. In conclusion, M2 macrophage-derived exosomal miR-26b-5p could protect articular cartilage and ameliorate gait abnormalities in OA mice by targeting TLR3 and COL10A1. miR-26b-5p further affected macrophage polarization and chondrocyte hypertrophy. Thus, this exosomal miR-26b-5p-based strategy might be a potential method for OA treatment.


Assuntos
MicroRNAs , Osteoartrite , Idoso , Animais , Humanos , Camundongos , Condrócitos/metabolismo , Hipertrofia/metabolismo , Hipertrofia/patologia , Macrófagos/metabolismo , MicroRNAs/genética , MicroRNAs/metabolismo , Osteoartrite/metabolismo , Receptor 3 Toll-Like/metabolismo , Colágeno Tipo X/genética , Colágeno Tipo X/metabolismo , Exossomos/genética
18.
Biomed Pharmacother ; 172: 116253, 2024 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-38359490

RESUMO

Ventricular remodeling refers to the structural and functional changes of the heart under various stimuli or disease influences and may also be accompanied by myocardial fibrosis, where an excessive amount of fibrous tissue appears in the myocardial tissue, affecting the heart's normal contraction and relaxation. Hypertension is posing the potential risk of causing myocardial injury and remodeling. The significance of the renin-angiotensin-aldosterone system (RAAS) in myocardial remodeling cannot be overlooked. Drug targeting of RAAS can effectively lower blood pressure and reduce left ventricular mass. Studies have shown that ginsenoside Rh4 can inhibit oxidative stress and inflammatory responses. In this study, a myocardial remodeling model was established using angiotensin (Ang) II, and the inhibitory effect of RH4 on myocardial hypertrophy and remodeling induced by Ang II was investigated using pathological staining and quantitative polymerase chain reaction (qPCR). Immunofluorescence and qPCR demonstrated that Rh4 causes myocardial hypertrophy and the generation of reactive oxygen species (ROS) in vitro. The Rh4 target was identified using transcriptomics. The findings indicated that RH4 could inhibit myocardial hypertrophy, inflammatory fibrosis, and oxidative stress induced by Ang II, suggesting potential cardiovascular protection effects. In vitro experiments have shown that Rh4 inhibits myocardial hypertrophy. Transcriptomics revealed that nuclear factor interleukin-3 (NFIL3) is a downstream regulator of Rh4. By constructing AAV9-NFIL3 and injecting it into mice, it was found that NFIL3 overexpression interfered with anti-Ang II-induced myocardial remodeling of Rh4. These results indicate that Rh4 demonstrates potential therapeutic effects on myocardial hypertrophy and fibrosis.


Assuntos
Angiotensina II , Ginsenosídeos , Interleucina-3 , Animais , Camundongos , Miocárdio , Hipertrofia
19.
Free Radic Biol Med ; 214: 206-218, 2024 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-38369076

RESUMO

Benzoylaconitine is a natural product in the treatment of cardiovascular disease. However, its pharmacological effect, direct target protein, and molecular mechanisms for the treatment of heart failure are unclear. In this study, benzoylaconitine inhibited Ang II-induced cell hypertrophy and fibrosis in rat primary cardiomyocytes and rat fibroblasts, while attenuating cardiac function and cardiac remodeling in TAC mice. Using the limited proteolysis-mass spectrometry (LiP-MS) method, the angiotensin-converting enzyme 2 (ACE2) was confirmed as a direct binding target of benzoylaconitine for the treatment of heart failure. In ACE2-knockdown cells and ACE2-/- mice, benzoylaconitine failed to ameliorate cardiomyocyte hypertrophy, fibrosis, and heart failure. Online RNA-sequence analysis indicated p38/ERK-mediated mitochondrial reactive oxygen species (ROS) and nuclear factor kappa B (NF-κB) activation are the possible downstream molecular mechanisms for the effect of BAC-ACE2 interaction. Further studies in ACE2-knockdown cells and ACE2-/- mice suggested that benzoylaconitine targeted ACE2 to suppress p38/ERK-mediated mitochondrial ROS and NF-κB pathway activation. Our findings suggest that benzoylaconitine is a promising ACE2 agonist in regulating mitochondrial ROS release and inflammation activation to improve cardiac function in the treatment of heart failure.


Assuntos
Aconitina/análogos & derivados , Insuficiência Cardíaca , NF-kappa B , Ratos , Camundongos , Animais , NF-kappa B/genética , NF-kappa B/metabolismo , Enzima de Conversão de Angiotensina 2/genética , Espécies Reativas de Oxigênio/metabolismo , Peptidil Dipeptidase A/metabolismo , Angiotensina II/metabolismo , Insuficiência Cardíaca/tratamento farmacológico , Insuficiência Cardíaca/genética , Miócitos Cardíacos/metabolismo , Fibrose , Hipertrofia
20.
Am J Case Rep ; 25: e942418, 2024 Feb 17.
Artigo em Inglês | MEDLINE | ID: mdl-38366584

RESUMO

BACKGROUND The adenoids are lymphatic tissue located in the nasopharynx and play a role in upper-airway immunity. Inflammation of the adenoids is called adenoiditis, which can cause a variety of symptoms. This is a common condition and is due to acute viral or bacterial infection. Most patients experience mild symptoms of upper-respiratory tract infection with a self-limiting course. CASE REPORT A 5-year-old female patient was brought into the clinic by her parents with concerns regarding hearing and sleep. Clinical assessment was consistent with persistent otitis media with effusion and sleep-disordered breathing. She was scheduled for surgery, including nasendoscopy, adenoidectomy, and bilateral grommet insertion. During surgery, direct visualization of the postnasal space showed complete obstruction by hypertrophic, inflamed adenoids covered in a thick, white film. A biopsy was taken, which detected herpes virus cytopathic effect. A diagnostic workup excluded a neoplastic process and other bacterial or fungal infections. A trial of oral antiviral medication was successful and follow-up nasendoscopy showed resolution of adenoid hypertrophy. CONCLUSIONS Direct visualization of the postnasal space, with a transoral mirror or 120-degree endoscope, prior to adenoidectomy can aid diagnosis. Adenoiditis may be caused by a wide range of organisms, including herpes virus. Active mucopurulent discharge should raise concern for infection by bacteria, fungi, or virus. Previous research on viral infection of the adenoids have been in asymptomatic patients with presumed latent infection and undergoing elective adenoidectomy. To our knowledge, this is the first paper to report on successful treatment with antiviral medication alone.


Assuntos
Tonsila Faríngea , Otite Média , Pré-Escolar , Feminino , Humanos , Adenoidectomia , Tonsila Faríngea/microbiologia , Tonsila Faríngea/patologia , Tonsila Faríngea/cirurgia , Antivirais/uso terapêutico , Hipertrofia , Nasofaringe/patologia
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