RESUMO
The choice to postpone treatment while awaiting genetic testing can result in significant delay in definitive therapies in patients with severe pancytopenia. Conversely, the misdiagnosis of inherited bone marrow failure (BMF) can expose patients to ineffectual and expensive therapies, toxic transplant conditioning regimens, and inappropriate use of an affected family member as a stem cell donor. To predict the likelihood of patients having acquired or inherited BMF, we developed a 2-step data-driven machine-learning model using 25 clinical and laboratory variables typically recorded at the initial clinical encounter. For model development, patients were labeled as having acquired or inherited BMF depending on their genomic data. Data sets were unbiasedly clustered, and an ensemble model was trained with cases from the largest cluster of a training cohort (n = 359) and validated with an independent cohort (n = 127). Cluster A, the largest group, was mostly immune or inherited aplastic anemia, whereas cluster B comprised underrepresented BMF phenotypes and was not included in the next step of data modeling because of a small sample size. The ensemble cluster A-specific model was accurate (89%) to predict BMF etiology, correctly predicting inherited and likely immune BMF in 79% and 92% of cases, respectively. Our model represents a practical guide for BMF diagnosis and highlights the importance of clinical and laboratory variables in the initial evaluation, particularly telomere length. Our tool can be potentially used by general hematologists and health care providers not specialized in BMF, and in under-resourced centers, to prioritize patients for genetic testing or for expeditious treatment.
Assuntos
Anemia Aplástica , Doenças da Medula Óssea , Pancitopenia , Humanos , Doenças da Medula Óssea/diagnóstico , Doenças da Medula Óssea/genética , Doenças da Medula Óssea/terapia , Diagnóstico Diferencial , Anemia Aplástica/diagnóstico , Anemia Aplástica/genética , Anemia Aplástica/terapia , Transtornos da Insuficiência da Medula Óssea/diagnóstico , Pancitopenia/diagnósticoRESUMO
Vacuoles, E1 enzyme, X-linked, autoinflammatory, somatic (VEXAS) syndrome is caused by somatic mutations in UBA1 (UBA1mut) and characterized by heterogenous systemic autoinflammation and progressive hematologic manifestations, meeting criteria for myelodysplastic syndrome (MDS) and plasma cell dyscrasias. The landscape of myeloid-related gene mutations leading to typical clonal hematopoiesis (CH) in these patients is unknown. Retrospectively, we screened 80 patients with VEXAS for CH in their peripheral blood (PB) and correlated the findings with clinical outcomes in 77 of them. UBA1mut were most common at hot spot p.M41 (median variant allele frequency [VAF] = 75%). Typical CH mutations cooccurred with UBA1mut in 60% of patients, mostly in DNMT3A and TET2, and were not associated with inflammatory or hematologic manifestations. In prospective single-cell proteogenomic sequencing (scDNA), UBA1mut was the dominant clone, present mostly in branched clonal trajectories. Based on integrated bulk and scDNA analyses, clonality in VEXAS followed 2 major patterns: with either typical CH preceding UBA1mut selection in a clone (pattern 1) or occurring as an UBA1mut subclone or in independent clones (pattern 2). VAF in the PB differed markedly between DNMT3A and TET2 clones (median VAF of 25% vs 1%). DNMT3A and TET2 clones associated with hierarchies representing patterns 1 and 2, respectively. Overall survival for all patients was 60% at 10 years. Transfusion-dependent anemia, moderate thrombocytopenia, and typical CH mutations, each correlated with poor outcome. In VEXAS, UBA1mut cells are the primary cause of systemic inflammation and marrow failure, being a new molecularly defined somatic entity associated with MDS. VEXAS-associated MDS is distinct from classical MDS in its presentation and clinical course.
Assuntos
Hematopoiese Clonal , Dermatite , Humanos , Hematopoiese Clonal/genética , Estudos Prospectivos , Estudos Retrospectivos , MutaçãoRESUMO
After the first report of a graphene-based passive mode-locking ultrafast fiber laser, two-dimensional materials as efficient saturable absorbers offer a new horizon in ultrafast fiber laser. However, the interactions on atomic scale between these two-dimensional materials and fiber and the fiber effect on the carrier dynamics have not been realized. To figure out the exact role of fiber and the carrier dynamics affected by the fiber substrate related to ultrafast photonics, bismuthene, a newly reported 2D quantum material used in a passive mode-locking fiber laser, deposited on α-quartz has been investigated. We surprisingly found that the α-quartz substrate can strongly accelerate the nonradiative electron-hole recombination of bismuthene in theory, and the transient absorption spectra of bismuthene on normal glass and α-quartz further verify the substrate effect on carrier dynamics of bismuthene. The discovery provides new thinking about substrate effect to regulate the performance of ultrafast mode-locking fiber lasers as well as ultrafast photonics.
RESUMO
Gut microbiota communicates bidirectionally with the brain through the nervous, immune, and endocrine systems of the gut. In our preliminary study, the fecal microbiota of volunteers with mild cognitive impairment (Fmci) exhibited a higher abundance of Escherichia fergusonii (NK2001), Veillonella infantium (NK2002), and Enterococcus faecium (NK2003) populations compared with those of healthy volunteers. Therefore, we examined the effects of Fmci, NK2001 (gram-negative), NK2002 (gram-negative-like), and NK2003 (gram-positive) on cognitive impairment-like behavior, neuroinflammation, and colitis in mice with or without antibiotics. Fmci transplantation increased cognitive impairment-like behavior, hippocampal tumor necrosis factor (TNF)-α expression, and the size of toll-like receptor (TLR)4+Iba1+, TLR2+Iba1+, and NF-κB+Iba1+ cell populations independent of antibiotic treatment. Oral gavage of NK2001, NK2002, or NK2003, which induced TNF-α expression in Caco-2 cells, significantly increased cognitive impairment-like behavior and hippocampal TNF-α expression and Iba1-positive cell populations and decreased brain-derived neurotrophic factor (BDNF) expression in mice. Celiac vagotomy significantly decreased NK2001- or NK2002-induced cognitive impairment-like behavior and hippocampal Iba1+ cell population and TNF-α expression and increased NK2001- or NK2002-suppressed hippocampal BDNF expression. However, NK2003-induced cognitive impairment-like behavior and hippocampal Iba1+ cell population and TNF-α expression were partially, but not significantly, attenuated by celiac vagotomy. Furthermore, celiac vagotomy did not affect NK2001-, NK2002-, or NK2003-induced lipopolysaccharide (LPS) levels in the blood and feces and TNF-α expression and NF-κB-positive cell population in the colon. In conclusion, LPS-producing NK2001 and NK2002 and LPS-nonproducing NK2003 may induce NF-κB-mediated neuroinflammation through the translocation of byproducts such as LPS and peptidoglycan into the brain through gut-blood/vagus nerve-brain and gut-blood-brain pathways, respectively, resulting in cognitive impairment.
Assuntos
Disfunção Cognitiva , Escherichia , Lipopolissacarídeos , Veillonella , Humanos , Camundongos , Animais , Lipopolissacarídeos/farmacologia , NF-kappa B/metabolismo , Fator Neurotrófico Derivado do Encéfalo , Fator de Necrose Tumoral alfa/metabolismo , Doenças Neuroinflamatórias , Células CACO-2 , Nervo Vago , Camundongos Endogâmicos C57BLRESUMO
Fecal microbiota transplantation from patients with depression/inflammatory bowel disease (PDI) causes depression with gut inflammation in mice. Here, we investigated the effects of six Lactobacillus reuteri strains on brain-derived neurotropic factor (BDNF), serotonin, and interleukin (IL)-6 expression in neuronal or macrophage cells and PDI fecal microbiota-cultured microbiota (PcM)-induced depression in mice. Of these strains, L6 most potently increased BDNF and serotonin levels in corticosterone-stimulated SH-SY5Y and PC12 cells, followed by L3. L6 most potently decreased IL-6 expression in lipopolysaccharide (LPS)-stimulated macrophages. When L1 (weakest in vitro), L3, and L6 were orally administered in mice with PcM-induced depression, L6 most potently suppressed depression-like behaviors and hippocampal TNF-α and IL-6 expression and increased hippocampal serotonin, BDNF, 5HT7, GABAARα1, and GABABR1b expression, followed by L3 and L1. L6 also suppressed TNF-α and IL-6 expression in the colon. BDNF or serotonin levels in corticosterone-stimulated neuronal cells were negatively correlated with depression-related biomarkers in PcM-transplanted mice, while IL-6 levels in LPS-stimulated macrophage were positively correlated. These findings suggest that IL-6 expression-suppressing and BDNF/serotonin expression-inducing LBPs in vitro, particularly L6, may alleviate gut microbiota-involved depression with colitis in vivo.
Assuntos
Microbioma Gastrointestinal , Limosilactobacillus reuteri , Neuroblastoma , Ratos , Humanos , Camundongos , Animais , Interleucina-6/genética , Depressão/terapia , Fator de Necrose Tumoral alfa/genética , Lipopolissacarídeos/toxicidade , Corticosterona/farmacologia , Serotonina/farmacologia , Fator Neurotrófico Derivado do Encéfalo/genética , Fator Neurotrófico Derivado do Encéfalo/metabolismo , Fator Neurotrófico Derivado do Encéfalo/farmacologia , Ansiedade/terapia , Ansiedade/etiologia , Camundongos Endogâmicos C57BLRESUMO
Idiopathic pulmonary fibrosis (IPF) is a chronic progressive interstitial lung disease that seriously threatens the health of patients. The pathogenesis of IPF is still unclear, and there is a lack of effective therapeutic drugs. Myofibroblasts are the main effector cells of IPF, leading to excessive deposition of extracellular matrix (ECM) and promoting the progression of fibrosis. Inhibiting the excessive activation and relieving autophagy blockage of myofibroblasts is the key to treat IPF. PI3K/Akt/mTOR pathway plays a key regulatory role in promoting fibroblast activation and autophagy inhibition in lung fibrosis. Duvelisib is a PI3K inhibitor that can simultaneously inhibit the activities of PI3K-δ and PI3K-γ, and is mainly used for the treatment of relapsed/refractory chronic lymphocytic leukaemia (CLL) and small lymphocytic lymphoma tumour (SLL). In this study, we aimed to examine the effects of Duvelisib on pulmonary fibrosis. We used a mouse model of bleomycin-induced pulmonary fibrosis to evaluate the effects of Duvelisib on pulmonary fibrosis in vivo and further explored the potential pharmacological mechanisms of Duvelisib in lung fibroblasts in vitro. The in vivo experiments showed that Duvelisib significantly alleviated bleomycin-induced collagen deposition and improved pulmonary function. In vitro and in vivo pharmacological experiments showed that Duvelisib dose-dependently suppressed lung fibroblast activation and improved autophagy inhibition by inhibiting the phosphorylation of PI3K, Akt and mTOR. Our results indicate that Duvelisib can alleviate the severity of pulmonary fibrosis and provide potential drugs for the treatment of pulmonary fibrosis.
Assuntos
Fibrose Pulmonar Idiopática , Proteínas Proto-Oncogênicas c-akt , Animais , Camundongos , Bleomicina/toxicidade , Fibroblastos/metabolismo , Fibrose Pulmonar Idiopática/metabolismo , Pulmão/patologia , Recidiva Local de Neoplasia/patologia , Fosfatidilinositol 3-Quinases/metabolismo , Proteínas Proto-Oncogênicas c-akt/metabolismo , Serina-Treonina Quinases TOR/metabolismoRESUMO
The exceptional mechanical, electronic, topological, and optical properties, make bismuthene an ideal candidate for various applications in ultrafast saturation absorption and spintronics. Despite the extensive research efforts devoted to synthesizing this material, the introduction of defects, which can significantly affect its properties, remains a substantial obstacle. In this study, we investigate the transition dipole moment and joint density of states of bismuthene with/without single vacancy defect via energy band theory and interband transition theory. It is demonstrated that the existence of the single defect enhances the dipole transition and joint density of states at lower photon energies, ultimately resulting in an additional absorption peak in the absorption spectrum. Our results suggest that the manipulation of defects in bismuthene has enormous potential for improving the optoelectronic properties of this material.
RESUMO
Previous studies have shown that socioeconomic factors play an important role in multiple myeloma (MM) health outcomes. We postulated that the type of treatment facilities and their volume of cases also affect overall survival, utilization of various therapies including palliative care services in newly diagnosed MM. Using the National Cancer Database (NCDB), we analyzed 174,551 newly diagnosed MM participants from across the country. We found that at high volume facility centers (over 90th percentile of new patient volume from 2004 to 2016), the median overall survival (OS) was 62.3 months versus 35.3 months at lower volume facilities (p <0.001). Similarly, high volume academic cancer centers had an improved median OS of 66.4 months (65.3-67.4 CI) versus 39.2 months (37.9-40.4 months CI) in lower volume academic centers (p <0.001). The odds of utilizing chemotherapy, immunotherapy, and autologous transplants were higher in academic cancer centers compared to community cancer centers, after adjusting for demographic and socioeconomic factors (OR 1.10, 1.23, and 2.06 respectively, all with p<0.001). There was significantly decreased odds of receiving palliative care (OR 0.89, 95% CI 0.85-0.93) in high volume facilities compared to low volume. Palliative care services were more frequently utilized at integrated network cancers and comprehensive community cancer centers compared to community cancer centers, with similar odds of receiving palliative care between community and academic facility types. Our results likely reflect increased provider experience and resources in higher volume and academic facilities. This highlights the need to integrate resources and improve access to community programs.
Assuntos
Mieloma Múltiplo , Humanos , Mieloma Múltiplo/diagnóstico , Mieloma Múltiplo/epidemiologia , Mieloma Múltiplo/terapia , Estudos Retrospectivos , Hospitais , Fatores SocioeconômicosRESUMO
Specific medications to combat cerebellar ataxias, a group of debilitating movement disorders characterized by difficulty with walking, balance and coordination, are still lacking. Notably, cerebellar microglial activation appears to be a common feature in different types of ataxic patients and rodent models. However, direct evidence that cerebellar microglial activation in vivo is sufficient to induce ataxia is still lacking. Here, by employing chemogenetic approaches to manipulate cerebellar microglia selectively and directly, we found that specific chemogenetic activation of microglia in the cerebellar vermis directly leads to ataxia symptoms in wild-type mice and aggravated ataxic motor deficits in 3-acetylpyridine (3-AP) mice, a classic mouse model of cerebellar ataxia. Mechanistically, cerebellar microglial proinflammatory activation induced by either chemogenetic M3D(Gq) stimulation or 3-AP modeling hyperexcites Purkinje cells (PCs), which consequently triggers ataxia. Blockade of microglia-derived TNF-α, one of the most important proinflammatory cytokines, attenuates the hyperactivity of PCs driven by microglia. Moreover, chemogenetic inhibition of cerebellar microglial activation or suppression of cerebellar microglial activation by PLX3397 and minocycline reduces the production of proinflammatory cytokines, including TNF-α, to effectively restore the overactivation of PCs and alleviate motor deficits in 3-AP mice. These results suggest that cerebellar microglial activation may aggravate the neuroinflammatory response and subsequently induce dysfunction of PCs, which in turn triggers ataxic motor deficits. Our findings thus reveal a causal relationship between proinflammatory activation of cerebellar microglia and ataxic motor symptoms, which may offer novel evidence for therapeutic intervention for cerebellar ataxias by targeting microglia and microglia-derived inflammatory mediators.
Assuntos
Ataxia Cerebelar , Camundongos , Animais , Ataxia Cerebelar/induzido quimicamente , Células de Purkinje/fisiologia , Microglia , Fator de Necrose Tumoral alfa/farmacologia , Cerebelo , CitocinasRESUMO
Sarcopenia is closely associated with gut dysbiosis. Probiotics alleviate gut dysbiosis. Therefore, we selected probiotics Lactobacillus paracasei P62 (Lp) and Bifidobacterium bifidum P61 (Bb), which suppressed muscle RING-finger protein-1 (MuRF1) expression and NF-κB activation in C2C12 cells, and examined their effects on muscle mass loss and dysfunction in aged mice. Oral administration of Lp, Bb, or their mix (LB) increased grip strength and treadmill running distance and time. They significantly increased muscle weight in aged mice. They also increased AKT activation, PGC1α, SIRT1, and myosin heavy chain (MyHC) expression, MyHC-positive cell population, and cell size in the gastrocnemius (GA) muscle, while FOXO3a and NF-κB activation, MuRF1, muscle atrophy F-box, and p16 expression, and NF-κB+CD11c+ cell population decreased. Furthermore, they reduced cognitive impairment-like behavior, IL-6 expression, FOXO3a activation, and NF-κB-positive cell population in the hippocampus, GA, and colon, while hippocampal brain-derived neurotropic factor expression increased. They shifted gut microbiota composition in aged mice: they increased Akkermansiaceae and Bacteroidaceae populations, which were positively correlated with total muscle weight and MyHC expression, and decreased Odoribacteraceae and Deferribacteriaceae populations, which were positively correlated with MuRF1 and IL-6 expression. LB alleviated sarcopenia- and cognitive impairment-like symptoms more potently than Lp or Bb alone. Based on these findings, probiotics, particularly Lp, Bb, and LB, can alleviate aging-dependent sarcopenia and cognitive impairment by regulating gut microbiota-mediated AKT, NF-κB, and/or FOXO3a signaling pathways.
RESUMO
Cerasus subhirtella (Miq.) Sok. is a widely used ornamental tree in urban areas around China and has a high ornamental value. From 2018 to 2020, a root rot disease was observed in C. subhirtella in Meitan County, Weng'an County, and Guiyang city of Guizhou, China (106.71 E, 26.57 N). Diseased C. subhirtella trees exhibited wilting with leaf chlorosis accompanied by brown to black root discoloration. In an area of 100 ha in total, with disease incidence ranging from 60 to 80%. Six symptomatic plants with root rot were randomly collected from three locations where disease symptoms were observed for pathogen isolation. Fifty fragments of diseased roots (5×5mm) were disinfected in 3% sodium hypochlorite for 30 s and 75% alcohol for 60 s, rinsed three times in sterile distilled water, plated on potato dextrose agar (PDA; BoWei, Shanghai), and incubated at 28 °C in the dark for 7 days. Eighteen isolates were purified by single spore culturing. Typical Fusarium spp. colonies were obtained from all root samples. On PDA, the colonies showed white and the hyphae were dense, while the colony of isolate YH15 showed pale yellow on the back, radial growth and produced chlamydospores. The macrospores (YH15) were straight to subarcuate, measured 15.3 to 25.1 × 2.5 to 6.2 µm (n=50). The microconidia (YH26) were ellipsoid to ovoid, measured 8.6 to 12.7 × 1.6 to 5.1 µm (n=50). These morphological characteristics were consistent with Fusarium spp., as described recently in Vitullo et al. (2014). To confirm the morphological diagnosis, genomic DNA from the isolates was extracted. The internal transcribed spacer (ITS) (White et al, 1990) region of rDNA and a ß-tubulin (Varga et al, 2011) gene fragment were amplified with the primers ITS1/ITS4 and Bt2a/Bt2b, respectively, and were subsequently sequenced. Maximum likelihood analysis was carried out using MEGA 11.0. BLAST analysis revealed that the ITS and ß-tubulin sequences of isolate YH15 were 100% homologous with F. oxysporum, and the isolate YH26 had a 99.69~100% homology with F. solani. Sequences of isolate YH15 and YH26 were deposited in GenBank (ITS: OQ363005 and OQ363049; ß-tubulin: OQ398187 and OQ398180). The isolate YH15 was thus identified as F. oxysporum by the morphological characteristics and sequences analysis, and the isolate YH26 was identified as F. solani. A reconstructed phylogenetic tree also confirmed their phylogenetic position. The healthy 2-year-old C. subhirtella plants grown in autoclaved acid yellow soil were used for the pathogenicity tests. Then, 50 mL of conidial suspension (2.0×105 conidia/mL, in medium) of 7-day-old isolates YH15 and YH26 were gently applied to the soil in each of the 10 pots as the treatment. A sterilized fungal culture matrix (PDB; BoWei, Shanghai) was applied to each of 10 pots as a control. All pots (30 cm high, 25 cm upper diameter, 15 cm base diameter) were placed in a greenhouse (25 °C, 12 h photoperiod). After 30 days of inoculation, all plants inoculated with the isolates showed wilting symptoms, and the roots showed light-brown to dark-brown lesions. No symptoms were observed in the controls. The pathogen was reisolated from all symptomatic roots and identified as F. oxysporum and F. solani as described above. The pathogenicity test was repeated twice with similar results. Although this fungus was previously reported to cause root disease in many hosts (Li et al., 2020; Gibert et al., 2022), this is the first report of F. oxysporum and F. solani causing root rot in C. subhirtella in China.
RESUMO
Due to the limitation of frequency resolution and the spectrum leakage caused by signal windowing, the spectrums of harmonic and interharmonic components with close frequencies overlap each other. When the dense interharmonic (DI) components are close to the harmonic spectrum peaks, the harmonic phasor estimation accuracy is seriously reduced. To address this problem, a harmonic phasor estimation method considering DI interference is proposed in this paper. Firstly, based on the spectral characteristics of the dense frequency signal, the phase and amplitude characteristics are used to determine whether DI interference exists in the signal. Secondly, an autoregressive model is established by using the autocorrelation of the signal. Data extrapolation is performed on the basis of the sampling sequence to improve the frequency resolution and eliminate the interharmonic interference. Finally, the estimated values of harmonic phasor, frequency and rate of change of frequency are obtained. The simulation and some experimental results demonstrate that the proposed method can accurately estimate the parameters of harmonic phasors when DIs exist in the signal, and has a certain anti-noise capability and dynamic performance.
RESUMO
Patients with severe aplastic anaemia (SAA) are often not vaccinated against viruses due to concerns of ineffective protective antibody response and potential for pathogenic global immune system activation, leading to relapse. We evaluated the impact of COVID-19 vaccination on haematological indices and disease status and characterized the humoural and cellular responses to vaccination in 50 SAA patients, who were previously treated with immunosuppressive therapy (IST). There was no significant difference in haemoglobin (p = 0.52), platelet count (p = 0.67), absolute lymphocyte (p = 0.42) and neutrophil (p = 0.98) counts prior to and after completion of vaccination series. Relapse after vaccination, defined as a progressive decline in counts requiring treatment, occurred in three patients (6%). Humoural response was detectable in 90% (28/31) of cases by reduction in an in-vitro Angiotensin II Converting Enzyme (ACE2) binding and neutralization assay, even in patients receiving ciclosporin (10/11, 90.1%). Comparison of spike-specific T-cell responses in 27 SAA patients and 10 control subjects revealed qualitatively similar CD4+ Th1-dominant responses to vaccination. There was no difference in CD4+ (p = 0.77) or CD8+ (p = 0.74) T-cell responses between patients on or off ciclosporin therapy at the time of vaccination. Our data highlight appropriate humoural and cellular responses in SAA previously treated with IST and true relapse after vaccination is rare.
Assuntos
Anemia Aplástica , COVID-19 , Humanos , Anemia Aplástica/tratamento farmacológico , Ciclosporina/uso terapêutico , Vacinas contra COVID-19/uso terapêutico , SARS-CoV-2 , Imunossupressores/uso terapêutico , COVID-19/prevenção & controle , Recidiva , Imunidade , VacinaçãoRESUMO
BACKGROUND: Childhood obesity is more likely to increase the chance of many adult health problems. Numerous studies have shown obese children to be more prone to elevated blood pressure (BP) and hypertension. It is important to identify an obesity anthropometric index with good discriminatory power for them in pediatric population. METHODS: MEDLINE/PubMed, Web of Science, and Cochrane databases were retrieved comprehensively for eligible studies on childhood obesity and hypertension/elevated BP through June 2021. The systematic review and meta-analysis of studies used receiver operating characteristics (ROC) curves for evaluating the discriminatory power of body mass index (BMI), waist circumference (WC), and waist-to-height ratio (WHtR) in distinguishing children with elevated BP and hypertension. RESULTS: 21 cross-sectional studies involving 177,943 children and 3-19 years of age were included in our study. Meta-analysis showed that the pooled area under the reporting receiver-operating characteristic curves (AUC) and 95% confidence intervals (CIs) for BMI, WC, and WHtR to detect hypertension of boys were 0.68 (0.64, 0.72), 0.69 (0.64, 0.74), 0.67 (0.63, 0.71), for elevated BP, the pooled AUCs and 95% CIs were 0.67 (0.61, 0.73), 0.65 (0.58, 0.73), 0.65 (0.61, 0.71). The pooled AUCs and 95% CIs for BMI, WC and WHtR of predicting hypertension were 0.70 (0.66, 0.75), 0.69 (0.64, 0.75), 0.67 (0.63, 0.72) in girls, the pooled AUCs and 95% CIs of predicting elevated BP were 0.63 (0.61, 0.65), 0.62 (0.60, 0.65), 0.62 (0.60, 0.64) respectively. There was no anthropometric index was statistically superior in identifying hypertension and elevated BP, however, the accuracy of BMI predicting hypertension was significantly higher than elevated BP in girls (P < 0.05). The subgroup analysis for the comparison of BMI, WC and WHtR was performed, no significant difference in predicting hypertension and elevated BP in pediatric population. CONCLUSIONS: This systematic review showed that no anthropometric index was superior in identifying hypertension and elevated BP in pediatric population. While compared with predicting elevated BP, all the indicators showed superiority in predicting hypertension in children, the difference was especially obvious in girls. A better anthropometric index should be explored to predict children's early blood pressure abnormalities.
Assuntos
Hipertensão , Obesidade Infantil , Adulto , Pressão Sanguínea , Índice de Massa Corporal , Criança , Estudos Transversais , Feminino , Humanos , Hipertensão/epidemiologia , Masculino , Obesidade Infantil/diagnóstico , Curva ROC , Fatores de Risco , Circunferência da Cintura , Razão Cintura-EstaturaRESUMO
Hypertrophic scar causes serious functional and cosmetic problem, but no treatment method is known to achieve a satisfactory therapeutic effect. However, mesenchymal stem cells show a possible cure prospect. Here, we investigated the effect of interleukin-10-modified adipose-derived mesenchymal stem cells (IL-10-ADMSC) on the formation of hypertrophic scar. In vitro, IL-10-ADMSC could highly express IL-10 and exhibited stronger inhibition of hypertrophic scar fibroblasts (HSFs) proliferation, migration, and extracellular matrix synthesis (the expression of collagen I, collagen III, FN, and α-SMA protein) than ADMSC. In vivo, we found that IL-10-ADMSC speeded up wound healing time and reduced scar area and scar outstanding height. Same as in vitro, IL-10-ADMSC also exhibited stronger inhibition of extracellular matrix synthesis (the expression of collagen I, collagen III protein) in wound than ADMSC. In addition, we also found that IL-10-ADMSC is also a stronger inhibitory effect on inflammation in wound than ADMSC, and IL-10-ADMSC inhibited TGF-ß/Smads and NF-κB pathway. In conclusion, IL-10-ADMSC demonstrated the ability to prevent hypertrophic scar formation. And its possible molecular mechanism might be related to IL-10-ADMSC inhibiting the proliferation and migration of the synthesis of extracellular matrix of HSFs, and IL-10-ADMSC inhibited the inflammation during the wound healing.
Assuntos
Cicatriz Hipertrófica , Interleucina-10 , Transplante de Células-Tronco Mesenquimais , Células-Tronco Mesenquimais , Cicatriz Hipertrófica/metabolismo , Cicatriz Hipertrófica/patologia , Cicatriz Hipertrófica/prevenção & controle , Colágeno Tipo I/metabolismo , Fibroblastos/metabolismo , Humanos , Inflamação/metabolismo , Interleucina-10/metabolismo , Células-Tronco Mesenquimais/metabolismoRESUMO
Aiming to solve the problem of dense-frequency signals in the power system caused by the growing proportion of new energy, this paper proposes a dense-frequency signal-detection method based on the primal-dual splitting method. After establishing the Taylor-Fourier model of the signal, the proposed method uses the sparse property of the coefficient matrix to obtain the convex optimization form of the model. Then, the optimal solution of the estimated phasor is obtained by iterating over the fixed-point equation, finally acquiring the optimal estimation result for the dense signal. When representing the Taylor-Fourier model as a convex optimization form, the introduction of measuring-error entropy makes the solution of the model more rigorous. It can be further verified through simulation experiments that the estimation accuracy of the primal-dual splitting method proposed in this paper for dense signals can meet the M-class PMU accuracy requirements.
RESUMO
ABSTRACT: Mandibular angle osteotomy with outer cortex grinding has become the preferred cosmetic procedure for correcting square faces. After surgery, bone hyperplasia at the mandibular angle affects the operation result. This study evaluated the effect of the masticatory muscles on bone repair. From January 2016 to January 2019, patients who underwent mandibular angle osteotomy with outer cortex grinding were retrospectively reviewed. Computed tomography data of these patients were collected, and the bone volume of the mandibular angle changes and its correlation with masticatory muscle morphology were analyzed. Computed tomography data measurement results showed that a large amount of bone in the mandibular angle area was removed by the operation; however, the long-term follow-up results showed that there was bone hyperplasia in the mandibular angle areas. Compared with the immediate postoperative bone volume, the difference was statistically significant (Pâ<â0.01). The thickness and cross-sectional area of the masseter muscle were significantly related to bone regeneration (Pâ<â0.01). This study suggests that mandibular angle osteotomy with outer cortex grinding could ablate the symptoms of a prominent mandibular angle; however, muscle-related bone hyperplasia in the mandibular angle area after surgery was a non-negligible event, which may significantly compromise surgical outcomes.
Assuntos
Músculo Masseter , Osteotomia , Regeneração Óssea , Humanos , Mandíbula/diagnóstico por imagem , Mandíbula/cirurgia , Músculos da Mastigação/diagnóstico por imagem , Estudos RetrospectivosRESUMO
ABSTRACT: This study evaluated age-associated morphology changes in the cranial base, facial development, and upper airway of patients with Treacher Collins syndrome (TCS). A total of 33 preoperative computed tomographic images (TCS, nâ=â14; control, nâ=â19) were included in the study and divided into three age-related subgroups (2-6âyears, 7-18âyears, and older than 18âyears). Linear, angular cephalometric measurements and upper airway volumes were collected. All measurements were analyzed using ProPlan CMF software (version 3.0; Materialize, Leuven, Belgium). The association between aging and upper airway morphology was analyzed. Compared to control subjects, TCS patients had a smaller cranial base, maxilla, and nose; they also had reduced upper airway volume compared to control subjects. The observed differences were most significant in patients between the ages of 7 and 18âyears. This study used computed tomography-based three-dimensional analyses to provide a detailed description of age-related changes that occur in craniofacial measurements and upper airway volumes in children, adolescents, and young adult patients with TCS in China. These data can be used to evaluate individual patients with TCS and to select treatment to improve the growth of the craniofacial region.
Assuntos
Disostose Mandibulofacial , Adolescente , Cefalometria , Criança , Humanos , Mandíbula , Disostose Mandibulofacial/diagnóstico por imagem , Maxila , Base do CrânioRESUMO
Based on density functional theory, we have systematically investigated the geometric, magnetic, and electronic properties of fluorographene with three types of vacancy defects. With uneven sublattice, the partial defect structures are significantly spin-polarized and present midgap electronic states. The magnetic moment is mainly contributed by the adjacent C atoms of vacancy defects. Furthermore, the strain dependence of the bandgap is analyzed and shows a linear trend with applied strain. This defect-induced tunable narrow bandgap material has great potential in electronic devices and spintronics applications.
RESUMO
Liver fibrosis is a disease caused by long-term damage that is related to a number of factors. The current research on the treatment of liver fibrosis mainly focuses on the activation of hepatic stellate cell, in addition to protecting liver cells. byakangelicin has certain anti-inflammatory ability, but its effect on liver fibrosis is unclear. This study aims to explore whether byakangelicin plays a role in the development of liver fibrosis and to explore its mechanism. We determined that byakangelicin has a certain ability to resist fibrosis and reduce liver cell damage in a model of carbon tetrachloride-induced liver fibrosis in mice. Thereafter, we performed further verification in vitro. The signalling pathways of two important pro-fibrotic cytokines, transforming growth factor-ß and platelet-derived growth factor, were studied. Results showed that byakangelicin can inhibit related pathways. According to the hepatoprotective effect of byakangelicin observed in animal experiments, we studied the effect of byakangelicin on 4-HNE-induced hepatocyte (HepG2) apoptosis and explored its related pathways. The results showed that byakangelicin could attenuate 4-HNE-induced hepatocyte apoptosis via inhibiting ASK-1/JNK signalling. In conclusion, byakangelicin could improve carbon tetrachloride-induced liver fibrosis and liver injury by inhibiting hepatic stellate cell proliferation and activation and suppressing hepatocyte apoptosis.