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BACKGROUND Lumbar disc herniation (LDH) at L4-L5 impacts paravertebral muscle morphology. Intervertebral disc degeneration is linked to paravertebral muscle changes, affecting LDH treatment outcomes. This study explored L4-L5 LDH paravertebral muscle alterations, specifically in the erector spinae, multifidus, and psoas major, using Michigan State University's classification to guide LDH treatment. MATERIAL AND METHODS The study enrolled 160 patients, including 39 normal patients and 121 L4-L5 LDH patients. Patients with LDH were grouped according to MSU classification and compared to the normal group according to demographics and imaging changes. RESULTS In patients with L4-L5 herniation in Zone B, the FI of the ES muscle at L3-L4 level, L4-L5 level, and L5-S1 level was higher than that of normal people (P=0.018, P=0.043, P=0.010, respectively), and there was no difference between FI of MF and normal people. The Zone B patients also had a smaller CSA of the ES muscle at L4-L5 level than that in the normal group (P=0.049). Patients in the Zone C group were older than those in the normal group (P=0.014). The CSA of the PM of patients with Grade 3 herniation differed from that of the normal group at the L4-L5 and L5-S1 level. They were higher than in normal people at L4-L5 level (P=0.011) and lower at L5-S1 level (P=0.028). CONCLUSIONS In patients with L4-L5 herniation in Zone B, the FI of ES at L3-S1 level was higher than in normal people, and the CSA at L4-L5 level was smaller than in normal people. In patients with Grade3 herniation, PM CSA was larger at L4-L5 level and smaller at L5-S1 level than in normal people.
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Degeneração do Disco Intervertebral , Deslocamento do Disco Intervertebral , Humanos , Michigan , Universidades , Vértebras Lombares , Imageamento por Ressonância Magnética/métodos , Músculos PsoasRESUMO
MicroRNAs (miRNAs) are increasingly reported to have important roles in diverse biological and pathological processes. Changes in abundance of muscle-specific microRNA, miR-1, have been implicated in cardiac disease, including arrhythmia and heart failure. However, the specific molecular targets and cellular mechanisms involved in the miR-1 function in the heart are only beginning to emerge. In this study, we investigated miR-1 expression and its potential role in the mouse model of viral myocarditis (VMC). The expression levels of miR-1 and its target gene Connexin 43 (Cx43) were measured by real-time PCR and western blotting, respectively. The miR-1 expression levels were significantly increased in cardiac myocytes from VMC mice in comparison with control samples (relative expression: 10 ± 2.5 vs. 31 ± 7.6, P < 0.05). Among the target genes of miR-1, the expression Cx43 protein was significantly reduced in such mice while there was no significant difference in the its mRNA levels. Our results revealed an inverse correlation between miR-1 levels and Cx43 protein expression in VMC samples. Using a bioinformatics-based approach, we found two identical potential binding sites were found in mouse miR-1 and Cx43 3'- untranslated region, this confirms a possible regulatory role of miR-1. In cultured, miRNA transfected myocardial cells, we show overexpression of miR-1 accompanied by a decrease in Cx43 protein's expression. There was only a slight (not statistically significant) drop in Cx43 mRNA levels. Our results indicate that miR-1 is involved in VMC via post-transcriptional repression of Cx43, and might constitute potentially valuable data for the development of a new approach in the treatment of this disease.
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Conexina 43/metabolismo , Infecções por Coxsackievirus/genética , MicroRNAs/genética , Miocardite/genética , Miocardite/virologia , Miócitos Cardíacos/metabolismo , Animais , Células Cultivadas , Conexina 43/genética , Infecções por Coxsackievirus/metabolismo , Enterovirus Humano B , Masculino , Camundongos , Camundongos Endogâmicos BALB C , MicroRNAs/metabolismo , Miocardite/metabolismo , Miócitos Cardíacos/patologia , Miócitos Cardíacos/virologia , RNA Mensageiro/genética , RNA Mensageiro/metabolismo , RatosRESUMO
OBJECTIVE: To explore the relationship between beta-actin mRNA degradation in SD rat's brain, heart and kidney and early postmortem interval (PMI) in order to find new markers for estimating early PMI. METHODS: Rats were sacrificed and kept in the place at a temperature of 20 degrees C. The total RNA were extracted from the brain, heart and kidney at different PMI points. Real time RT-PCR was applied to determine beta-actin mRNA levels in total RNA and the results were given in the form of Ct values. Linear relationships between PMI and Ct values were obtained and the functions of linear regression were established. RESULTS: The great decrease of beta-actin mRNA level were observed in the three organs. The degradation rate was obviously higher in 24 hours after death in the heart and kidney. However, there were no significant changes in the brain. The changes of Ct values and PMI showed a good linear relationship. CONCLUSION: beta-actin mRNA in rat's brain, heart and kidney degrades obviously after death and can be used for estimating early PMI by its degradation rules.
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Actinas/metabolismo , Encéfalo/metabolismo , Rim/metabolismo , Miocárdio/metabolismo , Mudanças Depois da Morte , RNA Mensageiro/metabolismo , Actinas/genética , Animais , Medicina Legal/métodos , Masculino , Estabilidade de RNA , RNA Mensageiro/genética , Ratos , Ratos Sprague-Dawley , Reação em Cadeia da Polimerase Via Transcriptase Reversa/métodos , Fatores de TempoRESUMO
Employing a first-principles method, we have studied the stability, diffusivity, and permeation properties of hydrogen (H) and its isotopes in bcc vanadium (V). A single H atom is found to favor the tetrahedral interstitial site (TIS) in V. The charge density distribution exhibits a strong interaction between H and its neighbor V atoms. Analysis of DOS and Bader charge reveals that the occupation number of H-induced low energy states is directly associated with the stability of H in V. Further, H is shown to diffuse between the neighboring TISs with a diffusion barrier of 0.07 eV. Diffusion coefficients and permeabilities of H isotopes in V are estimated with empirical theory. At a typical temperature of 800 K, the diffusion coefficient and the permeability of H are 2.48 × 10(-4) cm(2) s(-1) and 2.19 × 10(-9) mol m(-1) s(-1) Pa(- 1/2), respectively.
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Hidrogênio/química , Modelos Químicos , Vanádio/química , Difusão , Cinética , Teoria Quântica , TemperaturaRESUMO
Bacteria often sequentially utilize coexisting carbohydrates in environment and firstly select the one (frequently glucose) easiest to metabolize. This phenomenon is known as carbon catabolite repression (CCR). In existing Chinese teaching materials of molecular biology and related courses, unclear or even wrong interpretations are given about CCR mechanism. A large number of studies have shown that rather than the existence of intracellular glucose, CCR is mainly caused by the glucose transport process coupling with glucose phosphorylation via the phosphoenolpyruvate: carbohydrate phosphotransferase system PTS. The transport process leads to accumulation of dephosphorylated form of EAGlc.This form of EAGlc can bind the membrane-localized LacY protein to block the uptake of lactose inducer. cAMP functions in activation of key genes involved in PTS system to strengthen the role of inducer exclusion. In addition, dephosphorylated form of EBGlc and Yee bind global transcription repressor Mlc to ensure the expression of key genes involved in the PTS system. This review summarizes the current advancement in mechanism of Escherichia coli carbon catabolite repression.
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Metabolismo dos Carboidratos , Escherichia coli/metabolismo , AMP Cíclico/fisiologia , Proteína Receptora de AMP Cíclico/fisiologia , Sistema Fosfotransferase de Açúcar do Fosfoenolpiruvato/fisiologiaRESUMO
We have investigated the structure, solution and diffusion behavior of carbon (C) in tungsten (W) based on first-principles calculations. The single C atom is energetically favorable sitting at the octahedral interstitial site (OIS) with a solution energy of 0.78 eV in W. Double C atoms tend to be paired up at the two neighboring OISs along the (210) direction with a distance of â¼ 3.57 Å and a binding energy of + 0.50 eV. This suggests that a positive attractive interaction between C atoms exists, which might lead to a local higher concentration of C in W and form carbide. Kinetically, the C and vacancy diffusion co-efficients as a function of temperature have been determined, and are 1.32 × 10(-19) m(2) s(-1) and 3.11 × 10(-23) m(2) s(-1) at a typical temperature of 600 K, respectively.
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We perform first-principles computational tensile and compressive tests (FPCTT and FPCCT) to investigate the intrinsic bonding and mechanical properties of a γ-TiAl intermetallic compound (L 1(0) structure) using a first-principles total energy method. We found that the stress-strain relations and the corresponding theoretical tensile strengths exhibit strong anisotropy in the [001], [100] and [110] crystalline directions, originating from the structural anisotropy of γ-TiAl. Thus, γ-TiAl is a representative intermetallic compound that includes three totally different stress-strain modes. We demonstrate that all the structure transitions in the FPCTT and FPCCT result from the breakage or formation of bonds, and this can be generalized to all the structural transitions. Furthermore, based on the calculations we qualitatively show that the Ti-Al bond should be stronger than the Ti-Ti bond in γ-TiAl. Our results provide a useful reference for understanding the intrinsic bonding and mechanical properties of γ-TiAl as a high-temperature structural material.
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We perform a first-principles computational tensile test (FPCTT) on a ZnO single crystal based on density functional theory to systematically investigate structural transitions, mechanical, and intrinsic bonding properties in the three representative directions, [Formula: see text], [0001], and [Formula: see text]. Stress as a function of tensile strain shows that the ideal tensile strengths in the three directions are 16.2 GPa, 22.4 GPa, and 19.0 GPa, corresponding to strains of 0.20, 0.16, and 0.16, respectively. The [0001] is the strongest direction due to the strongest bonding between the most closely packed Zn and O(0001) layers. We demonstrate that different structures in these three directions lead to different structural transitions, i.e. from a wurtzite (WZ) to a body-centered tetragonal (BCT) structure for [Formula: see text], to a graphite-like (GP-like) structure for [0001], and to a quasi-hexagonal (quasi-HX) structure for [Formula: see text], respectively. Bond length and charge density evolution under tension indicate the occurrence of bond formation and disassociation during these structure transitions. New O-Zn bonds form in the WZ [Formula: see text] BCT and WZ [Formula: see text] quasi-HX transitions, and the original O-Zn bonds break in the WZ [Formula: see text] GP-like transition.
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L-amino acid oxidases (LAOs) are one of the major components of snake venoms, which possess numerous biological functions. However, little is known of the influence of LAOs on organ lesions. In the present study, a unique LAO from Agkistrodon blomhoffii ussurensis snake venom named ABU-LAO was purified by Heparin-Sepharose FF chromatography followed by an ion-exchange chromatography procedure. The purified ABU-LAO appears a dimer with a molecular mass of approximately 108.8kDa. Kinetics studies showed that ABU-LAO is very active towards its substrates L-Asn, L-Phe, L-Tyr, L-Leu, L-Ile and L-Trp. The most striking observation in the present study is that ABU-LAO causes severe pneumorrhagia, pulmonary interstitial edema, fusion of pulmonary alveoli, cardiac interstitial edema and bleeding when being intravenously injected into BALB/c mice. ABU-LAO also induces liver cell necrosis and release of cytokines including IL-6, IL-12 and IL-2 from highly purified human peripheral blood monocytes and T cells, respectively. In conclusion, ABU-LAO potently induces lesions in lungs and livers. The ability of ABU-LAO will contribute to the understanding of the pathogenesis of snakebite wound.