Exploring the genetic causal association of TIMP3 on CKD and kidney function: a two-sample mendelian randomization.

Background: Numerous studies have demonstrated a positive association between the level of tissue inhibitor of metalloproteinase 3 (TIMP3) and chronic kidney disease (CKD). Nevertheless, whether those associations reflect causal links still to be determined. This study intended to research the causal relationship of TIMP3 with CKD and markers of kidney function, such as creatinine-based estimated glomerular filtration rate (eGFRcrea), cystatin C-based estimated glomerular filtration rate (eGFRcys), eGFRcrea in diabetics (eGFRcrea (DM)) and eGFRcrea in non diabetics (eGFRcrea (No DM)). Methods: In this study, we investigated the causal relationships between TIMP3 and CKD and kidney function markers using a two-sample Mendelian randomization (MR) technique. We used summary level datasets for TIMP3 and CKD from genome-wide association studies that we were able to access through the study by Suhre K and Pattaro C. Results: We found that TIMP3 had a significant positive causal effect on the risk of CKD (Inverse variance weighted (IVW):odds ratio (OR):0.962, 95% confidence interval (CI): (0.936-0.988),P:0.005). However TIMP3 levels had no significant effect on risk of eGFRcys (PIVW: 0.114),eGFRcrea (PIVW:0.333). After grouping patients based on their diabetes status, we found that genetically higher levels of TIMP3 had a significant impact on eGFRcrea in participants without diabetes (OR:1.003,95%CI (1.001-1.006),P IVW:0.007), but not in participants with diabetes (PIVW = 0.057). Heterogeneity and pleiotropy analyses were carried out to verify the accuracy of the MR findings. Their findings were all not statistically significant. Conclusion: Our study suggests that TIMP3 may be causally associated with CKD and eGFRcrea (No DM)in people of European ancestry. Strategies aimed to increase TIMP3 levels may provide new ways to delay the deterioration of renal function.

MG53 protects against Coxsackievirus B3-induced acute viral myocarditis in mice by inhibiting NLRP3 inflammasome-mediated pyroptosis via the NF-κB signaling pathway.

Pyroptosis, a novel programmed cell death mediated by NOD-like receptor protein 3 (NLRP3) inflammasome, is a critical pathogenic process in acute viral myocarditis (AVMC). Mitsugumin 53 (MG53) is predominantly expressed in myocardial tissues and has been reported to exert cardioprotective effects through multiple pathways. Herein, we aimed to investigate the biological function of MG53 in AVMC and its underlying regulatory mechanism in pyroptosis. BALB/c mice and HL-1 cells were infected with Coxsackievirus B3 (CVB3) to establish animal and cellular models of AVMC. As inflammation progressed in the myocardium, we found a progressive decrease in myocardial MG53 expression, accompanied by a significant enhancement of cardiomyocyte pyroptosis. MG53 overexpression significantly alleviated myocardial inflammation, apoptosis, fibrosis, and mitochondrial damage, thereby improving cardiac dysfunction in AVMC mice. Moreover, MG53 overexpression inhibited NLRP3 inflammasome-mediated pyroptosis, reduced pro-inflammatory cytokines (IL-1ß/18) release, and suppressed NF-κB signaling pathway activation both in vivo and in vitro. Conversely, MG53 knockdown reduced cell viability, facilitated cell pyroptosis, and increased pro-inflammatory cytokines release in CVB3-infected HL-1 cells by promoting NF-κB activation. These effects were partially reversed by applying the NF-κB inhibitor BAY 11-7082. In conclusion, our results suggest that MG53 acts as a negative regulator of NLRP3 inflammasome-mediated pyroptosis in CVB3-induced AVMC, partially by inhibiting the NF-κB signaling pathway. MG53 is a promising candidate for clinical applications in AVMC treatment.

Construction of a prediction model for rebleeding in patients with acute upper gastrointestinal bleeding.

BACKGROUND: The incidence of rebleeding in patients with upper gastrointestinal bleeding (UGIB) remains despite advances in intervention approaches. Therefore, early prediction of the risk of rebleeding could help to greatly reduce the mortality rate in these patients. We aim to develop and validate a new prediction model to predict the probability of rebleeding in patients with AUGIB. METHODS: A total of 1170 AUGIB patients who completed the procedure of emergency gastroscopy within 48 h of admission were included. Logistic regression analyses were performed to construct a new prediction model. A receiver operating characteristic curve, a line graph, and a calibration and decision curve were used to assess the predictive performance of our new prediction model and compare its performance with that of the AIMS65 scoring system to determine the predictive value of our prediction model. RESULTS: A new prediction model was constructed based on Lactic acid (LAC), neutrophil percentage (NEUTP), platelet (PLT), albumin (ALB), and D-DIMER. The AUC values and their 95% confidence interval (CI) for the new prediction model and the AIMS65 score were 0.746 and 0.619, respectively, and 0.697-0.795 and 0.567-0.670, respectively. In the training group, the C index values based on the prediction model and the AIMS65 scoring system were 0.720 and 0.610, respectively. In the validation group, the C index values based on the prediction model and the AIMS65 scoring system were 0.828 and 0.667, respectively. The decision and calibration curve analysis also showed that the prediction model was superior to the AIMS65 scoring system in terms of accuracy of prediction, consistency, and net clinical benefit. CONCLUSION: The prediction model can predict the probability of rebleeding in AUGIB patients after endoscopic hemostasis therapy.

Association of serum albumin levels and stroke risk in adults over 40 years: A population-based study.

This study assessed the relationship between serum albumin levels and adult stroke risk. From the 2009 to 2018 National Health and Nutrition Examination Survey, we performed a cross-sectional study with 17,303 participants who were 40 years of age or higher. A multivariate logistic regression model investigated serum albumin levels and stroke. To investigate apparent nonlinear connections, smoothed curve fitting was used. When a nonlinear relationship was discovered, the inflection point was determined using a recursive method. Serum albumin levels were significantly and inversely linked with the risk of stroke after controlling for possible variables [odds ratio 0.02, 95% confidence interval (0.00, 0.18), P = .0003]. An examination of subgroups revealed that the inverse relationship between serum albumin levels and risk of stroke was statistically significant in men, participants under 60 years old, non-diabetic participants, and hypertensive participants. Serum albumin levels and the risk of stroke were negatively correlated. An increased risk of stroke was linked to lower serum albumin levels.

Soluble thrombomodulin alleviates Diquat-induced acute kidney injury by inhibiting the HMGB1/IκBα/NF-κB signalling pathway.

Our research aimed to investigate whether soluble thrombomodulin (sTM) relieved Diquat (DQ)-induced acute kidney injury (AKI) via HMGB1/IκBα/NF-κB signaling pathways. An AKI rat model was constructed using DQ. Pathological changes in renal tissue were detected by HE and Masson staining. Gene expression was determined using qRT-PCR, IHC, and western blotting. Cell activity and apoptosis were analysed using CCK-8 and Flow cytometry, respectively. An abnormal kidney structure was observed in DQ rats. The levels of blood urea nitrogen (BUN), creatinine (CRE), uric acid (UA), oxidative stress, and inflammatory responses in the DQ group increased on the 7th day but decreased on the 14th day, compared with the control group. Additionally, HMGB1, sTM, and NF-kappaB (NF-κB) expression had increased in the DQ group compared with the control group, while the IκKα and IκB-α levels had decreased. In addition, sTM relieved the damaging effects of diquat on renal tubular epithelial cell viability, apoptosis, and the inflammatory response. The levels of HMGB1, TM, and NF-κB mRNA and protein were significantly decreased in the DQ + sTM group compared with the DQ group. These findings indicated that sTM could relieve Diquat-induced AKI through HMGB1/IκBα/NF-κB signaling pathways, which provides a treatment strategy for Diquat-induced AKI.

An immune genes signature for predicting mortality in sepsis patients.

A growing body of evidence indicates that the immune system plays a central role in sepsis. By analyzing immune genes, we sought to establish a robust gene signature and develop a nomogram that could predict mortality in patients with sepsis. Herein, data were extracted from the Gene Expression Omnibus and Biological Information Database of Sepsis (BIDOS) databases. We enrolled 479 participants with complete survival data using the GSE65682 dataset, and grouped them randomly into training (n = 240) and internal validation (n = 239) sets based on a 1:1 proportion. GSE95233 was set as the external validation dataset (n=51). We validated the expression and prognostic value of the immune genes using the BIDOS database. We established a prognostic immune genes signature (including ADRB2, CTSG, CX3CR1, CXCR6, IL4R, LTB, and TMSB10) via LASSO and Cox regression analyses in the training set. Based on the training and validation sets, the Receiver Operating Characteristic curves and Kaplan-Meier analysis revealed that the immune risk signature has good predictive power in predicting sepsis mortality risk. The external validation cases also showed that mortality rates in the high-risk group were higher than those in the low-risk group. Subsequently, a nomogram integrating the combined immune risk score and other clinical features was developed. Finally, a web-based calculator was built to facilitate a convenient clinical application of the nomogram. In summary, the signature based on the immune gene holds potential as a novel prognostic predictor for sepsis.

Serum Sestrin2 Was Lower in Septic Shock Patients with Cardiomyopathy.

Background: To determine the clinical significance of variations in serum sestrin2 protein levels in the development of septic cardiomyopathy in septic shock patients. Methods: The serum sestrin2 concentrations of each sample were determined using ELISA in a total of 67 control persons and 188 patients with septic shock. Furthermore, using transthoracic echocardiography, septic shock patients were split into two groups based on whether or not cardiomyopathy had developed, and the differences in each index between the two groups were analyzed. We looked at the relationship between serum sestrin2 levels, norepinephrine dosage, and NTproBNP levels. The influencing variables for the prediction of septic cardiomyopathy linked with the development of septic cardiomyopathy and clinical prognosis in septic cardiomyopathy were determined using multivariate binary logistic regression. Results: Assessment of left ventricular systolic function by measurement of LVEF revealed that 61/188 (32.4%) of the 188 patients with septic shock included in the research satisfied the diagnostic criteria for septic cardiomyopathy. (1) Sestrin2 protein levels showed a significant difference between septic shock and healthy controls (p < 0.01). (2) Compared to the group without septic cardiomyopathy, the group with combined septic cardiomyopathy had lower serum sestrin2 protein levels (p < 0.05), lower systolic blood pressure (p < 0.05), and higher plasma NTproBNP levels (p < 0.01) and used greater norepinephrine dosages (p < 0.01). The levels of serum sestrin2 protein revealed a little negative relationship with NTproBNP and norepinephrine dose. However, a binary logistic regression analysis revealed that none of these factors was an independent predictor of septic shock. (3) Age, lactate level, SOFA score, positive bacteremia, and sestrin2 protein were shown to be substantial discrepancies in clinical outcomes in patients with septic cardiomyopathy, becoming variables that impact clinical outcomes. Positive bacteremia (p = 0.031, OR = 5.084), SOFA score (p = 0.021, OR = 1.304), and sestrin2 protein (p = 0.039, OR = 0.897) were revealed to have independent influences in predicting clinical mortality outcome in septic cardiomyopathy using multivariate binary logistic regression. Conclusion: High serum sestrin2 levels clearly distinguish septic shock patients from healthy controls, whereas low serum sestrin2 levels are related with cardiac dysfunction to some extent but are not an independent influence factor for septic cardiomyopathy. Low serum sestrin2 levels were shown to be useful in predicting clinical outcome in patients with septic cardiomyopathy.

Bradykinin postconditioning protects rat hippocampal neurons after restoration of spontaneous circulation following cardiac arrest via activation of the AMPK/mTOR signaling pathway.

Bradykinin (BK) is an active component of the kallikrein-kinin system that has been shown to have cardioprotective and neuroprotective effects. We previously showed that BK postconditioning strongly protects rat hippocampal neurons upon restoration of spontaneous circulation (ROSC) after cardiac arrest. However, the precise mechanism underlying this process remains poorly understood. In this study, we treated a rat model of ROSC after cardiac arrest (induced by asphyxiation) with 150 µg/kg BK via intraperitoneal injection 48 hours after ROSC following cardiac arrest. We found that BK postconditioning effectively promoted the recovery of rat neurological function after ROSC following cardiac arrest, increased the amount of autophagosomes in the hippocampal tissue, inhibited neuronal cell apoptosis, up-regulated the expression of autophagy-related proteins LC3 and NBR1 and down-regulated p62, inhibited the expression of the brain injury marker S100ß and apoptosis-related protein caspase-3, and affected the expression of adenosine monophosphate-activated protein kinase/mechanistic target of rapamycin pathway-related proteins. Adenosine monophosphate-activated protein kinase inhibitor compound C clearly inhibited BK-mediated activation of autophagy in rats after ROSC following cardiac arrest, which aggravated the injury caused by ROSC. The mechanistic target of rapamycin inhibitor rapamycin enhanced the protective effects of BK by stimulating autophagy. Our findings suggest that BK postconditioning protects against injury caused by ROSC through activating the adenosine monophosphate-activated protein kinase/mechanistic target of the rapamycin pathway.

Identification of Prognostic Factors for Recurrence and Mortality in Patients With Acute Pulmonary Embolism.

BACKGROUND: This study aimed to explore prognostic factors for 1-year recurrence and mortality in patients with acute pulmonary embolism (APE). METHODS: APE patients who attended the Emergency Department of Fujian Provincial Hospital from January 2016 to June 2020 were recruited. Univariate and multivariate logistic regression analyses were carried out to determine the prognostic factors for 1-year recurrence and mortality. RESULTS: A total of 458 APE patients were included, of whom 81 (17.69%) had recurrence, and 97 (21.18%) died. Multivariate logistic regression analyses revealed that smoke (OR: 1.949; 95% CI: 1.094-3.470; P = 0.023), abnormal platelet distribution width (OR: 3.013; 95% CI: 1.574-5.767; P = 0.001), and interrupted maintenance therapy (OR: 18.280; 95% CI: 9.777-34.179; P < 0.001) were significantly associated with an increased risk of 1-year recurrence in APE patients. Age ≥65 years (OR: 3.492; 95% CI: 1.876-6.500; P < 0.001), history of malignancy (OR: 7.190; 95% CI: 3.804-13.587; P < 0.001), history of long-term immobilization (OR: 6.244; 95% CI: 3.472-11.228; P < 0.001), mechanical ventilation (OR: 5.971; 95% CI: 3.154-11.304; P < 0.001), and interrupted maintenance therapy (OR: 2.414; 95% CI: 1.315-4.432; P = 0.004) were independent prognostic factors for 1-year mortality. The AUC of 1-year mortality and recurrence prediction models were 0.852 (95% CI: 0.805-0.898) and 0.868 (95%CI: 0.832-0.905). CONCLUSION: In patients with APE, history of smoking, abnormal PDW, and interrupted maintenance therapy were significantly associated with the risk of 1-year recurrence, while age ≥65 years, history of malignancy, history of long-term immobilization, mechanical ventilation, and interrupted maintenance therapy were independent prognostic factors for 1-year mortality.

[Neuroprotective mechanism of autophagy in bradykinin postconditioning after cardiac arrest in rats].

OBJECTIVE: To explore the protective effects of bradykinin postconditioning on cardiopulmonary resuscitation (CPR) rats, and to assess the underlying mechanisms. METHODS: Forty-eight adult male Sprague-Dawley (SD) rats were randomly divided into four groups according to random number table: Sham operation group, cardiac arrest (CA) group, bradykinin treatment (BK) group, and AMP-activated protein kinase (AMPK) inhibitor Compound C+ bradykinin treatment (CP+BK) group, finally, 8 rats in each group were taken for follow-up experiment. CA was induced by asphyxia. Rats in the Sham group received arteriovenous catheterization, endotracheal intubation, and mechanical ventilation, without CA. Compound C (250 µg/kg) was intraperitoneally injected in CP+BK group 30 minutes before CA, and the same volume of dimethyl sulfoxide (DMSO) was given in the remaining groups. Bradykinin (150 µg/kg) was intraperitoneally injected in BK group and CP+BK group 48 hours after restoration of spontaneous circulation (ROSC), and same volume of saline was given in the remaining groups. The neural function of rats in each group was evaluated with neurological deficit score (NDS) 72 hours after ROSC. Microtubule-associated protein light chain 3 (LC3) and p62 expressions were detected by immunohistochemistry, autophagosomes were observed by transmission electron microscopy, and terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling method (TUNEL) assay was used to assess apoptosis. RESULTS: Compared with the Sham group, the NDS was decreased (60.75±5.80 vs. 80.00±0.00, P < 0.01), the expression levels of LC3 and p62 elevated [LC3 (A value): 1.04±0.64 vs. 0.40±0.14, p62 (A value): 2.75±0.57 vs. 0.36±0.12, both P < 0.05], the number of autophagosomes and apoptotic cells increased in the CA group [(39.00±8.00)% vs. (3.87±1.90)%, P < 0.05]. Compared with the CA group, the NDS (67.75±6.32 vs. 60.75±5.80, P < 0.05), the expression of LC3 (A value: 1.60±0.34 vs. 1.04±0.64, P < 0.05), and the number of autophagosomes increased in the BK group, while the expression of p62 and the rate of apoptotic cells reduced [p62 (A value): 1.51±0.32 vs. 2.75±0.57, apoptotic cells rate: (23.03±1.91)% vs. (39.00±8.00)%, both P < 0.05]. Compared with the BK group, the NDS (59.00±8.19 vs. 67.75±6.32, P < 0.05), the expression of LC3 (A value: 0.62±0.41 vs. 1.60±0.34, P < 0.05) and the number of autophagosomes declined in the CP+BK group, while the expression of p62 and the rate of apoptotic cells elevated [p62 (A value): 3.50±0.47 vs. 1.51±0.32, apoptotic cells rate: (44.53±10.15)% vs. (23.03±1.91)%, both P < 0.05]. CONCLUSIONS: Bradykinin postconditioning played a neuroprotective role in CPR rats by activating autophagy and reducing apoptosis.

Hybrid anisotropic plasmonic metasurfaces with multiple resonances of focused light beams.

Plasmonic metasurfaces supporting collective lattice resonances have attracted increasing interest due to their exciting properties of strong spatial coherence and enhanced light-matter interaction. Although the focusing of light by high-numerical-aperture (NA) objectives provides an essential way to boost the field intensities, it remains challenging to excite high-quality resonances by using high-NA objectives due to strong angular dispersion. Here, we address this challenge by employing the physics of bound states in the continuum (BICs). We design a novel anisotropic plasmonic metasurface combining a two-dimensional lattice of high-aspect-ratio pillars with a one-dimensional plasmonic grating, fabricated by a two-photon polymerization technique and gold sputtering. We demonstrate experimentally multiple resonances with absorption amplitudes exceeding 80% at mid-IR using an NA = 0.4 reflective objective. This is enabled by the weak angular dispersion of quasi-BIC resonances in such hybrid plasmonic metasurfaces. Our results suggest novel strategies for designing photonic devices that manipulate focused light with a strong field concentration.

Dynamic control of magnetization spot arrays with three-dimensional orientations.

We report a new paradigm for achieving magnetization spot arrays with controllable three-dimensional (3D) orientations. Toward this aim, we subtly design a tailored incident beam containing three parts and further demonstrate that the designed incident beam is phase-modulated radial polarization. Based on the raytracing model under tight focusing condition and the inverse Faraday effect on the magneto-optic (MO) film, the magnetization field components along the y-axis and z-axis directions are generated through the focus. In particular, we are able to garner orientation-tunable 3D magnetization under different numerical apertures of the focusing objectives by adjusting the ratios between the three parts of incident beam. Apart from a single magnetization spot, magnetization spot arrays capable of dynamically controlling 3D orientation in each spot can also be achieved by multi-zone plate (MZP) phase filter. Such a robust magnetization pattern is attributed to not only the constructive interferences of three orthogonal focal field components, but also the position translation of each magnetization spot resulting from shifting phase of the MZP phase filter. It is expected that the research outcomes can be beneficial to spintronics, magnetic encryption and multi-value MO parallelized storage.

Bound States in the Continuum in Anisotropic Plasmonic Metasurfaces.

The concept of optical bound states in the continuum (BICs) currently drives the field of dielectric resonant nanophotonics, providing an important physical mechanism for engineering high-quality (high-Q) optical resonances in high-index dielectric nanoparticles and structured dielectric metasurfaces. For structured metallic metasurfaces, realization of BICs remains a challenge associated with strong dissipative losses of plasmonic materials. Here, we suggest and realize experimentally anisotropic plasmonic metasurfaces supporting high-Q resonances governed by quasi-BIC collective resonant modes. Our metasurfaces are composed of arrays of vertically oriented double-pillar meta-molecules covered by a thin layer of gold. We engineer quasi-BIC modes and observe experimentally sharp resonances in mid-IR reflectance spectra. Our work suggests a direct route to boost the resonant field enhancement in plasmonic metasurfaces via combining a small effective mode volume of plasmonic systems with engineered high-Q resonances provided by the BIC physics, with multiple applications to enhance light-matter interaction for nano-optics and quantum photonics.

Bone marrow-derived mesenchymal stem cell transplantation attenuates overexpression of inflammatory mediators in rat brain after cardiopulmonary resuscitation.

Emerging evidence suggests that bone marrow-derived mesenchymal stem cell transplantation improves neurological function after cardiac arrest and cardiopulmonary resuscitation; however, the precise mechanisms remain unclear. This study aimed to investigate the effect of bone marrow-derived mesenchymal stem cell treatment on expression profiles of multiple cytokines in the brain after cardiac arrest and cardiopulmonary resuscitation. Cardiac arrest was induced in rats by asphyxia and cardiopulmonary resuscitation was initiated 6 minutes after cardiac arrest. One hour after successful cardiopulmonary resuscitation, rats were injected with either phosphate-buffered saline (control) or 1 × 106 bone marrow-derived mesenchymal stem cells via the tail vein. Serum S100B levels were measured by enzyme-linked immunosorbent assay and neurological deficit scores were evaluated to assess brain damage at 3 days after cardiopulmonary resuscitation. Serum S100B levels were remarkably decreased and neurological deficit scores were obviously improved in the mesenchymal stem cell group compared with the phosphate-buffered saline group. Brains were isolated from the rats and expression levels of 90 proteins were determined using a RayBio Rat Antibody Array, to investigate the cytokine profiles. Brain levels of the inflammatory mediators tumor necrosis factor-α, interferon-γ, macrophage inflammatory protein-1α, macrophage inflammatory protein-2, macrophage inflammatory protein-3α, macrophage-derived chemokine, and matrix metalloproteinase-2 were decreased ≥ 1.5-fold, while levels of the anti-inflammatory factor interleukin-10 were increased ≥ 1.5-fold in the mesenchymal stem cell group compared with the control group. Donor mesenchymal stem cells were detected by immunofluorescence to determine their distribution in the damaged brain, and were primarily observed in the cerebral cortex. These results indicate that bone marrow-derived mesenchymal stem cell transplantation attenuates brain damage induced by cardiac arrest and cardiopulmonary resuscitation, possibly via regulation of inflammatory mediators. This experimental protocol was approved by the Institutional Animal Care and Use Committee of Fujian Medical University, China in January 2016 (approval No. 2016079).

Dirac potential in a rotational dissipative quantum system.

This study proposes the usage of an effective potential to investigate a dissipative quantum system with rotational velocity. After gauge transformation, a Doebner- Goldin equation (DGE) that describes the dissipative quantum system with a Dirac potential is obtained. The DGE is solved based on constraint of vertical relation between the rotational velocity field and density gradient when a harmonic oscillator model is considered. It is observed that the dissipative quantum system is directly equivalent to a monopole system and that the two gauge potentials that are given by Wu and Yang in the north and south hemispheres can be reproduced. Furthermore, a set of gauge-invariant parameters is obtained to discuss the dissipation characteristics of the system.

Characterization of Staphylococcus aureus isolated from patients with burns in a regional burn center, Southeastern China.

BACKGROUND: S.aureus is a predominant pathogen that causes infection in critically ill patients, but little information exists regarding the characterization of S. aureus from different sources in burn patients in southeastern China. METHODS: We enrolled 125 patients with S. aureus infection in burns center between Jan 2014 and Dec 2015. S. aureus isolates were characterized by antimicrobial susceptibility test, toxin gene detection, and molecular typing with multilocus sequence type, staphylococcal protein A (spa) type, and staphylococcal cassette chromosome mec (SCCmec) type. RESULTS: Sixty-eight MRSA were isolated from SSTI and 31 from non-SSTI patients, respectively. Overall, the drug-resistant ability of S. aureus isolated from SSTI was higher than that from non-SSTI groups. SCCmecIII-CC239-t030 was the most common clone (38 from SSTIs, and 8 from non-SSTIs). Seg was the most common enterotoxin gene (21 from SSTIs and 33 from non-SSTIs). Isolates from SSTIs was more likely to carry seb (P = 0.04), while those from non-SSTIs tended to carry sea and seg (P = 0.002 and 0.01, respectively). Although isolates carried four hemolysin genes, there was no significant difference between them (P > 0.05). CONCLUSION: SCCmecIII-CC239-t030 was the most common clone in Jiangxi burns center, China. The molecular characterization of S. aureus was quite different between SSTI and non-SSTI groups.

Time Circular Birefringence in Time-Dependent Magnetoelectric Media.

Light traveling in time-dependent media has many extraordinary properties which can be utilized to convert frequency, achieve temporal cloaking, and simulate cosmological phenomena. In this paper, we focus on time-dependent axion-type magnetoelectric (ME) media, and prove that light in these media always has two degenerate modes with opposite circular polarizations corresponding to one wave vector , and name this effect "time circular birefringence" (TCB). By interchanging the status of space and time, the pair of TCB modes can appear simultaneously via "time refraction" and "time reflection" of a linear polarized incident wave at a time interface of ME media. The superposition of the two TCB modes causes the "time Faraday effect", namely the globally unified polarization axes rotate with time. A circularly polarized Gaussian pulse traversing a time interface is also studied. If the wave-vector spectrum of a pulse mainly concentrates in the non-traveling-wave band, the pulse will be trapped with nearly fixed center while its intensity will grow rapidly. In addition, we propose an experimental scheme of using molecular fluid with external time-varying electric and magnetic fields both parallel to the direction of light to realize these phenomena in practice.

Arecoline inhibits epithelial cell viability by upregulating the apoptosis pathway: implication for oral submucous fibrosis.

Oral submucous fibrosis (OSF) is a chronic inflammatory disease characterized by the accumulation of excess collagen, and areca nut chewing has been proposed as a significant etiological factor for disease manifestation. However, the underlying molecular mechanisms regarding areca nut chewing-induced OSF are only partially understood. Herein, we reported that arecoline markedly induced morphologic change in HaCaT epithelial cells, but had no obvious effect on Hel fibroblast cells. MTS assay revealed that arecoline significantly suppressed HaCaT cell viability. Moreover, flow cytometric analysis indicated that arecoline substantially promoted HaCaT cell, but not Hel cell apoptosis in a dose-dependent manner. Furthermore, arecoline-induced HaCaT cell apoptosis was found to be associated with increased expression and activation of cleaved-Bid, cleaved-PARA and cleaved-caspase-3. Collectively, our results suggest that HaCaT epithelial cells are more sensitive than Hel fibroblast cells to arecoline-induced cytotoxicity, which may be involved in the pathogenesis of OSF.

Arecoline suppresses HaCaT cell proliferation through cell cycle regulatory molecules.

Betel nut chewing is the most common cause of oral submucous fibrosis (OSF). Arecoline is the main component of the betel nut, and is associated with the occurrence and development of OSF through cytotoxicity, genotoxicity and DNA damage. Similar types of stimuli elicit differential responses in different cells. In the present study, we investigated the effects of arecoline on the HaCaT epithelial and Hel fibroblast cell lines. The data showed that arecoline affected HaCaT cell morphology. MTT assay revealed that arecoline suppressed HaCaT cell proliferation. Furthermore, we found that arecoline induced the cell cycle arrest of HaCaT cells. In comparison with the untreated control cells, following treatment with ≥75 µg/ml arecoline an increased percentage of HaCaT cells remained at the G0/G1 phase of the cell cycle, accompanied by a reduced percentage of cells in the S phase. However, arecoline treatment did not significantly alter Hel cell cycle distribution. In the HaCaT epithelial cells, arecoline downregulated expression of the G1/S phase regulatory proteins cyclin D1, CDK4, CDK2, E2F1 as determined by reverse transcription-PCR analysis and western blotting. In summary, arecoline inhibits HaCaT epithelial cell proliferation and survival, in a dose-dependent manner, and cell cycle arrest in the G1/S phase, while this is not obvious in the Hel fibroblast cells. Potentially, our findings may aid in the prevention of arecoline-associated human OSF.

Therapeutic benefits of mild hypothermia in patients successfully resuscitated from cardiac arrest: A meta-analysis.

BACKGROUND: Good neurological outcome after cardiac arrest (CA) is hard to achieve for clinicians. Experimental and clinical evidence suggests that therapeutic mild hypothermia is beneficial. This study aimed to assess the effectiveness and safety of therapeutic mild hypothermia in patients successfully resuscitated from CA using a meta-analysis. METHODS: We searched the MEDLINE (1966 to April 2012), OVID (1980 to April 2012), EMBASE (1980 to April 2012), Chinese bio-medical literature & retrieval system (CBM) (1978 to April 2012), Chinese medical current contents (CMCC) (1995 to April 2012), and Chinese medical academic conference (CMAC) (1994 to April 2012). Studies were included if 1) the study design was a randomized controlled trial (RCT); 2) the study population included patients successfully resuscitated from CA, and received either standard post-resuscitation care with normothermia or mild hypothermia; 3) the study provided data on good neurologic outcome and survival to hospital discharge. Relative risk (RR) and 95% confidence interval (CI) were used to pool the effect. RESULTS: The study included four RCTs with a total of 417 patients successfully resuscitated from CA. Compared to standard post-resuscitation care with normothermia, patients in the hypothermia group were more likely to have good neurologic outcome (RR=1.43, 95% CI 1.14-1.80, P=0.002) and were more likely to survive to hospital discharge (RR=1.32, 95% CI 1.08-1.63, P=0.008). There was no significant difference in adverse events between the normothermia and hypothermia groups (P>0.05), nor heterogeneity and publication bias. CONCLUSION: Therapeutic mild hypothermia improves neurologic outcome and survival in patients successfully resuscitated from CA.