Near infrared luminescence properties and mechanism of high bismuth-doped SiO2-Al2O3-La2O3 glass.

This research investigated the wideband near-infrared spectroscopy characteristics of 60SiO2-25Al2O3-10La2O3 glass doped with high levels of bismuth up to 5 mol%. The near-infrared radiation range was explored under excitation wavelengths of 488 nm, 532 nm, 808 nm, and 980 nm, resulting in near-infrared radiation spanning from 1000 nm to 1800nm with Full Width at Half Maximum (FWHM) values of 313.0 nm, 336.3 nm, 296.2 nm, and 262.9 nm, respectively. Notably, the sample exhibited a lifetime of 1.473 ms when pumped at 808 nm, corresponding to a stimulated cross-section of σe=3.35 × 10-21 cm2. Through an in-depth investigation of the luminescence properties, the underlying physical mechanism behind the near-infrared luminescence was revealed. The emissions observed at approximately 1150 nm and 1300 nm were attributed to the aluminum-related bismuth active center (BAC-Al) and the silicon-related bismuth active center (BAC-Si), respectively. Furthermore, it is postulated that the emission at the 1150 nm band originates from the 3P1, 3P2 →3P0 transition of Bi+ and the 2D3/2 → 4S3/2 transition of Bi°, while the emission at the 1300 nm band may be linked to mixed valence states of Bi3+. This work will find potential applications in broadband near-infrared optical devices.

Resveratrol Attenuates High-Fat Diet-Induced Hepatic Lipotoxicity by Upregulating Bmi-1 Expression.

Resveratrol (RES), a natural polyphenol phytoalexin, has been reported to attenuate nonalcoholic fatty liver disease (NAFLD). However, its roles on protection of liver from lipotoxicity and underlying mechanism are not fully understood. In this study, we investigated the impacts of RES on alleviating hepatic lipotoxicity and corresponding molecular mechanism. Impacts of RES on oleic acid (OA)-induced lipotoxicity were assessed in L02 cells and C57BL/6J mice, respectively. In L02 cells, lipotoxicity was assessed by detection of apoptosis, mitochondrial function, oxidative stress and ROS-related signaling. In mice, lipotoxicity was evaluated by detecting hepatic function, serum enzyme activity, and reactive oxygen species (ROS) levels. We found that RES reduced OA-induced apoptosis, mitochondrial dysfunction, ROS generation, and DNA damage in L02 cells. RES also decreased expression of cleaved caspase-3 and p53 and increased expression of B-cell lymphoma 2 (Bcl-2). Importantly, RES protected mice from high-fat diet-induced hepatic lipotoxicity, demonstrated by reduced ROS levels and lipid peroxidation. Mechanically, B lymphoma Mo-MLV insertion region 1 (Bmi-1) expression and antioxidative superoxide dismutase were increased after RES treatment. Further mechanistic analysis indicated that protection effects of RES against OA-induced lipotoxicity were abrogated by Bmi-1 small interference RNA (siRNA) in L02 cells. SIGNIFICANCE STATEMENT: Results from clinical studies about the effect of RES on NAFLD are inconsistent and inconclusive. This study confirms the protective role of RES as an anti-ROS agent and its ability to alleviate DNA damage through a pathway involving p53/p21 signaling. Further mechanistic analysis indicated that protection effects of RES were relative with Bmi-1. This is the first study on the role of Bmi-1 in the pathogenesis of NAFLD and the target of resveratrol against NAFLD.

Overexpression of TRIM32 promotes pancreatic ß-cell autophagic cell death through Akt/mTOR pathway under high glucose conditions.

Type 2 diabetes mellitus (T2DM) is a growing worldwide epidemic and is characterized by progressive pancreatic ß-cell dysfunction and insulin resistance. Tripartite motif protein 32 (TRIM32) belongs to the TRIM family protein and has been shown to be involve in insulin resistance in skeletal muscle and the liver. However, the effect of TRIM32 on pancreatic ß-cell dysfunction and its mechanism remains unknown. In the current study, we found that serum TRIM32 concentrations of T2DM in patients were significantly elevated compared to those in healthy controls, which indicated that TRIM32 might be used as a diagnostic biomarker in T2DM patients. In INS-1 cells, exposure to high glucose (HG) conditions caused a significant elevation in TRIM32 expression and TRIM32 was located in the nucleus. Overexpression of TRIM32 in INS-1 cells exacerbated the effects of HG-induced autophagy and impaired insulin secretion. In contrast, the silencing of TRIM32 produced the opposite effect. Furthermore, TRIM32 overexpression decreased the phosphorylation levels of Akt and mTOR under HG conditions. However, the activation of Akt/mTOR by MHY1485 reversed the effects of TRIM32 on HG-treated INS-1 cells. Collectively, the present results suggested that TRIM32 participates in the development of T2DM by modulating autophagic cell death and insulin secretion, which might occur through the Akt/mTOR pathway. Thus, TRIM32 might be a promising target in T2DM therapy.

Could a Growth Mindset Attenuate the Link Between Family Socioeconomic Status and Depressive Symptoms? Evidence from Chinese Adolescents.

Purpose: The alleviating effects of a growth mindset on depression are promising. However, whether a growth mindset can attenuate the effect of low family socioeconomic status (SES) on depressive symptoms among adolescents remains unknown. Based on the Family Stress Model, the current study explores whether a growth mindset could moderate the associations between family SES, interparental conflict, and adolescent depressive symptoms. Methods: The participants were 1572 Chinese adolescents (Mage = 13.35 years, SD = 1.16, 51.84% female). They completed the family SES questionnaire, Children's Perceptions of Interparental Conflict scale, Growth Mindset scale, and Center for Epidemiologic Studies Depression scale. We tested the moderation, mediation, and moderated mediation models using the SPSS macro program PROCESS. Results: A growth mindset moderated the association between family SES and depressive symptoms. Family SES was significantly related to depressive symptoms in adolescents with a lower growth mindset, but not in those with a higher growth mindset. After incorporating the mediating effect of interparental conflict, the growth mindset did not exert a significant moderating influence on the direct path; however, it significantly moderated the mediating effect of interparental conflict on depressive symptoms. Specifically, while a lower growth mindset in adolescents was associated with an increased risk of depressive symptoms due to interparental conflict, those with a higher growth mindset showed a less pronounced effect. Conclusion: A growth mindset attenuates the link between family SES and depressive symptoms among adolescents. These findings highlight the benefits of a growth mindset on mental health, especially for low-SES adolescents.

Effects of Co on Mechanical Properties and Precipitates in a Novel Secondary-Hardening Steel with Duplex Strengthening of M2C and ß-NiAl.

Synergistic strengthening of nano-scaled M2C and ß-NiAl has become a new route to develop ultra-high secondary-hardening steel. At present, the effect of Co on the synergistic precipitation behavior of duplex phases of M2C and ß-NiAl has been rarely reported. This paper revealed the effects of Co on the mechanical properties and duplex precipitates of M2C and ß-NiAl in a novel 2.5 GPa ultra-high strength secondary-hardening steel. The tensile tests indicated that a 10% Co-alloy steel achieved a much stronger secondary-hardening effects compared to a Co-free steel during aging process, especially in the early-aging state. Needle-shaped M2C and spherical ß-NiAl particles were observed in both Co-alloy and Co-free steels. However, the number density, and volume fraction of M2C were significantly enhanced in the 10% Co-alloy steel. The Mo contents in M2C carbide and α-Fe after aging treatment were both analyzed through experimental determination and thermodynamic calculation, and the results indicated that Co decreased the solubility of Mo in α-Fe, thus promoting the precipitation of Mo-rich carbides.

Influence of Cyclic Heat Treatment Temperature on Microstructure and Mechanical Properties of 18Ni(C250) Maraging Steel.

Cyclic heat treatment is an effective approach for enhancing the mechanical properties of 18Ni(C250) maraging steel, and the selection of cyclic heat treatment temperature is a key factor. In this study, a cyclic heat treatment process with a two-step solution treatment is employed to investigate the influence of cyclic heat treatment temperature, specifically the first solution treatment temperature (920 °C, 950 °C, and 980 °C), on the microstructure and mechanical properties of 18Ni(C250) maraging steel. The results indicate that with an increase in the cyclic heat treatment temperature, the average grain size of the 18Ni(C250) maraging steel decreases initially and then increases. When the cyclic heat treatment temperature reaches 950 °C, the grain size is at its minimum, exhibiting optimal grain uniformity. Additionally, the increase in cyclic heat treatment temperature results in a reduction in the size of martensitic lath with the same orientation inside the grains, along with an increase in the relative quantity of low-angle grain boundaries. Furthermore, the volume fraction and size of retained austenite show a monotonous increase with the rise in the temperature of the cyclic heat treatment, and the rate of increase becomes notably larger when the temperature is raised from 950 °C to 980 °C. Based on the observed microstructural changes, the variation in the mechanical properties of the 18Ni(C250) maraging steel was analyzed. Specifically, as the cyclic heat treatment temperature increases, the tensile strength of the 18Ni(C250) maraging steel initially increases and then stabilizes, while the elongation and fracture toughness exhibit a monotonic increase.

Unveiling the Stacking Fault-Driven Phase Transition Delaying Cryogenic Fracture in Fe-Co-Cr-Ni-Mo-C-Based Medium-Entropy Alloy.

In this work, the tensile deformation mechanisms of the Fe55Co17.5Cr12.5Ni10Mo5-xCx-based medium-entropy alloy at room temperature (R.T.), 77 K, and 4.2 K are studied. The formation of micro-defects and martensitic transformation to delay the cryogenic fracture are observed. The results show that FeCoCrNiMo5-xCx-based alloys exhibit outstanding mechanical properties under cryogenic conditions. Under an R.T. condition, the primary contributing mechanism of strain hardening is twinning-induced plasticity (TWIP), whereas at 77 K and 4.2 K, the activation of martensitic transformation-induced plasticity (TRIP) becomes the main strengthening mechanism during cryogenic tensile deformation. Additionally, the carbide precipitation along with increased dislocation density can significantly improve yield and tensile strength. Furthermore, the marked reduction in stacking fault energy (SFE) at cryogenic temperatures can promote mechanisms such as twinning and martensitic transformations, which are pivotal for enhancing ductility under extreme conditions. The Mo4C1 alloy obtains the optimal strength-ductility combination at cryogenic-to-room temperatures. The tensile strength and elongation of the Mo4C1 alloy are 776 MPa and 50.5% at R.T., 1418 MPa and 71.2% in liquid nitrogen 77 K, 1670 MPa and 80.0% in liquid helium 4.2 K, respectively.

Effect of Cerium on Inclusion Modification in a Secondary-Hardening Steel.

Owing to the continuous increasing of steel strength, mechanical properties including toughness and fatigue performance are becoming increasingly sensitive to inclusions in ultra-high strength steel. Rare-earth treatment is considered as an effective method to reduce the harmful effects of inclusions, but is rarely applied in secondary-hardening steel. In the present study, different amounts of cerium were added in a secondary-hardening steel to investigate the modification effect of Ce on non-metallic inclusions in steel. The characteristics of inclusions were observed experimentally using SEM-EDS and the modification mechanism was analyzed based on thermodynamic calculations. The results indicated that the main inclusions in Ce-free steel are Mg-Al-O + MgS. Thermodynamic calculation indicated that MgAl2O4 is firstly formed in liquid steel and then successively transformed into MgO and MgS during cooling process. When the Ce content is 0.0030%, the typical inclusions in steel were individual Ce2O2S and MgO + Ce2O2S complex inclusions. When the Ce content was increased to 0.0071%, the typical inclusions in steel were individual Ce2O2S- and Mg-containing inclusions. Ce treatment modifies the angular magnesium aluminum spinel inclusions into spherical and ellipsoidal Ce-containing inclusions, thus reducing the harmful effect of inclusion on steel properties.

Effect of Aging Treatment on the Microstructure and Properties of 2.2 GPa Tungsten-Containing Maraging Steel.

Maraging steel is a prominent category of ultrahigh-strength steel (UHSS) characterized by excellent comprehensive properties, and it finds wide applications in manufacturing load-bearing structural components. In this study, a novel tungsten-containing maraging steel, C-250W, was designed. The effects of aging treatments on the mechanical properties, microstructure, precipitations, and reverted austenite of C-250W steel were investigated. The results revealed that the optimal combination of strength and toughness could be achieved through an aging treatment of C-250W steel carried out for 5 h at 480 °C after solution treatment at 1000 °C for 1 h. As the aging temperature increased, the proportion of dimples in the impact fracture gradually decreased while that of quasi-cleavage increased, leading to a reduction in Charpy impact energy. The boundary of martensitic lath decomposed gradually as the aging temperature increased, and it disappeared entirely at temperatures higher than 550 °C. Moreover, the aging process resulted in the formation of phases, including spherical Fe2M (M represents Mo, W) and thin strip-shaped Ni3N (N represents Mo, Ti) precipitates. These precipitates coarsened from 5 nm to 50-200 nm with increasing aging temperature. Additionally, the content of reverted austenite increased with the aging temperature. Within the temperature range of 400 °C to 500 °C for aging treatment, the content of film-shaped reverted austenite was approximately 3%, primarily distributed at the boundary of martensite lath. When the aging temperature exceeded 550 °C, the content of reverted austenite reached 20.2%, and its morphology changed from film-shaped to block-shaped, resulting in a decline in strength and toughness.

Targeting SLP2-mediated lipid metabolism reprograming restricts proliferation and metastasis of hepatocellular carcinoma and promotes sensitivity to Lenvatinib.

SLP2, a protein located on mitochondrial, has been shown to be associated with mitochondrial biosynthesis. Here we explored the potential mechanisms by which SLP2 regulates the development of hepatocellular carcinoma. SLP2 could bind to the c-terminal of JNK2 to affect the ubiquitinated proteasomal degradation pathway of JNK2 and maintain the protein stability of JNK2. The increase of JNK2 markedly increases SREBP1 activity, promoting SREBP1 translocation into the nucleus to promote de novo lipogenesis. Alteration of the JNK2 C-terminal disables SLP2 from mediating SLP2-enhanced de novo lipogenesis. YTHDF1 interacts with SLP2 mRNA in a METTL3/m6A-dependent manner. In a spontaneous HCC animal model, SLP2/c-Myc/sgP53 increases the incidence rate of spontaneous HCC, tumor volume, and tumor number. Importantly, statistical analyses show that levels of SLP2 correlate with tumor sizes, tumor metastasis, overall survival, and disease-free survival of the patients. Targeting the SLP2/SREBP1 pathway effectively inhibits proliferation and metastasis of HCC tumors with high SLP2 expression in vivo combined with lenvatinib. These results illustrate a direct lipogenesis-promoting role of the pro-oncogenic SLP2, providing a mechanistic link between de novo lipogenesis and HCC.

Adatom Defect Induced Spin Polarization of Asymmetric Structures.

The spin polarization of carbon nanomaterials is crucial to design spintronic devices. In this paper, the first-principles is used to study the electronic properties of two defect asymmetric structures, Cap-(9, 0)-Def [6, 6] and Cap-(9, 0)-Def [5, 6]. We found that the ground state of Cap-(9, 0)-Def [6, 6] is sextet and the ground state of Cap-(9, 0)-Def [5, 6] is quartet, and the former has a lower energy. In addition, compared with Cap-(9, 0) CNTs, the C adatom on C30 causes spin polarization phenomenon and Cap-(9, 0)-Def [6, 6] has more spin electrons than Cap-(9, 0)-Def [5, 6] structure. Moreover, different adsorb defects reveal different electron accumulation. This finding shows that spin polarization of the asymmetric structure can be adjusted by introducing adatom defects.

Magnetic coupling induced by the interaction between endohedral metal borofullerenes.

Superatom-assembled materials have highly tunable magnetic and electronic properties and parameters of clusters. Here, eight superatom dimers composed of two U@B40 motifs have been studied by the density functional theory. Calculation results show that U@B40 dimers exhibit spin antiferromagnetic coupling, spin ferromagnetic coupling and nonmagnetic, that is, the magnetic coupling is induced by the interaction between the U@B40 superatoms. In addition, the monomers in U@B40 dimers still retain the superatomic orbitals, and some of the super atomic orbitals disappear due to the interaction between monomers. The assembly based on U@B40 induced a decrease in the energy gap. This study provides a basis for a deep understanding of controlling the cluster-assembled materials for tailoring their functionalities.

CD44-fibrinogen binding promotes bleeding in acute promyelocytic leukemia by in situ fibrin(ogen) deposition.

Early hemorrhagic death is still the main obstacle for the successful treatment of acute promyelocytic leukemia (APL). However, the mechanisms underlying hemostatic perturbations in APL have not been fully elucidated. Here, we report that CD44 on the membrane of APL blasts and NB4 cells ligated bound fibrinogen, resulting in in situ deposition of fibrin and abnormal fibrin distribution. Clots formed by leukemic cells in response to CD44 and fibrinogen interaction exhibited low permeability and resistance to fibrinolysis. Using flow cytometry and confocal microscopy, we found that CD44 was also involved in platelet and leukemic cell adhesion. CD44 bound activated platelets but not resting platelets through interaction with P-selectin. APL cell-coated fibrinogen-activated platelets directly induce enhanced procoagulant activity of platelets. In vivo studies revealed that CD44 knockdown shortened bleeding time, increased the level of fibrinogen, and elevated the number of platelets by approximately twofold in an APL mouse model. Moreover, CD44 expression on leukemic cells in an APL mouse model was not only associated with bleeding complications but was also related to the wound-healing process and the survival time of APL mice. Collectively, our results suggest that CD44 may be a potential intervention target for preventing bleeding complications in APL.

A Salt-Tolerant Streptomyces paradoxus D2-8 from Rhizosphere Soil of Phragmites communis Augments Soybean Tolerance to Soda Saline-Alkali Stress.

Soil salinity and alkalization limit plant growth and agricultural productivity worldwide. The application of salt-tolerant plant growth-promoting rhizobacteria (PGPR) effectively improved plant tolerance to saline-alkali stress. To obtain the beneficial actinomyces resources with salt tolerance, thirteen isolates were isolated from rhizosphere saline and alkaline soil of Phragmites communis. Among these isolates, D2-8 was moderately halophilic to NaCl and showed 120 mmol soda saline-alkali solution tolerance. Moreover, the plant growth-promoting test demonstrated that D2-8 produced siderophore, IAA, 1-aminocyclopropane-1-carboxylate deaminase (ACCD), and organic acids. D2-8 showed 99.4% homology with the type strain Streptomyces paradoxus NBRC 14887T and shared the same branch, and, therefore, it was designated S. paradoxus D2-8. Its genome was sequenced to gain insight into the mechanism of growth-promoting and saline-alkali tolerance of D2-8. IAA and siderophore biosynthesis pathway, genes encoding ACC deaminase, together with six antibiotics biosynthesis gene clusters with antifungal or antibacterial activity, were identified. The compatible solute ectoine biosynthesis gene cluster, production, and uptake of choline and glycine betaine cluster in the D2-8 genome may contribute to the saline-alkali tolerance of the strain. Furthermore, D2-8 significantly promoted the seedling growth even under soda saline-alkali stress, and seed coating with D2-8 isolate increased by 5.88% of the soybean yield in the field. These results imply its significant potential to improve soybean soda saline-alkali tolerance and promote crop health in alkaline soil.

Extracellular Traps Increase Burden of Bleeding by Damaging Endothelial Cell in Acute Promyelocytic Leukaemia.

The rate of complete remission of acute promyelocytic leukemia (APL) is currently over 90% because of the use of all-trans retinoic acid (ATRA) with arsenic trioxide (ATO). However, hemorrhagic mortality has emerged as the most significant barrier to APL-induced remission. Neutrophils extracellular traps (NETs/ETs) cause vascular leakage by damaging the integrity of endothelial cells. We have previously demonstrated that APL cells treated with ATRA/ATO undergo a cell death process, releasing extracellular chromatin, termed ETosis/NETosis. However, the mechanism underlying the involvement of ETs in endothelial injury in APL remain largely unknown. Here, we analysed the ability of mature and immature neutrophils to release ETs, and their interaction with platelets (PLTs) in APL. Importantly, the effect of ETs on vascular endothelium in APL was discussed. Our results showed that the ability of immature neutrophils to release ETs was impaired in APL, whereas mature neutrophils produced ETs, which were associated with activated PLTs. Moreover, ATRA+ATO induced immature neutrophil differentiation, as well as increased the release of ETs from mature neutrophils. The excessive ETs damaged endothelial cells, causing blood cell leakage. Removing ETs using DNase 1 alleviated endothelial damage and improved blood cells leakage. Our results indicate that vascular endothelial injury is at least partially associated with ETs in APL, and that targeting ETs production may be an effective approach for relieving vascular leakage and reducing the burden of bleeding in APL.

Facile fabrication of PS/Cu2S/Ag sandwich structure as SERS substrate for ultra-sensitive detection.

In this work, a serials of PS(polystyrene)/Cu2S/Ag sandwich substrates were successfully constructed using the magnetic sputtering method by adjusting the Ag sputtering time (0 min, 2 min, 4 min, 6 min, 8 min and 10 min) and used as the surface-enhanced Raman scattering (SERS) substrates. When the Ag sputtering time was 6 min, the strongest SERS signal was observed. The optimized SERS substrate has strong SERS activity on 4-mercaptobenzoic acid (4-MBA), the minimum detection limit was 10-13 M and the enhancement factor was as high as 4.7 × 107. In addition, the SERS signals were highly reproducible with small standard deviation. The SERS enhancement mechanism of the PS/Cu2S/Ag system was attributed to the synergistic effect of the chemical mechanism and the electromagnetic enhancement mechanism. This strategy has find a new way for manufacturing SERS activity sensor with high sensitivity and reproducibility.

The impact of platelets on pulmonary microcirculation throughout COVID-19 and its persistent activating factors.

Patients with COVID-19 often have hypoxemia, impaired lung function, and abnormal imaging manifestations in acute and convalescent stages. Alveolar inflammation, pulmonary vasculitis, and thromboembolism synergistically damage the blood-air barrier, resulting in increased pulmonary permeability and gas exchange disorders. The incidence of low platelet counts correlates with disease severity. Platelets are also involved in the impairment of pulmonary microcirculation leading to abnormal lung function at different phases of COVID-19. Activated platelets lose the ability to protect the integrity of blood vessel walls, increasing the permeability of pulmonary microvasculature. High levels of platelet activation markers are observed in both mild and severe cases, short and long term. Therefore, the risk of thrombotic events may always be present. Vascular endothelial injury, immune cells, inflammatory mediators, and hypoxia participate in the high reactivity and aggregation of platelets in various ways. Microvesicles, phosphatidylserine (PS), platelets, and coagulation factors are closely related. The release of various cell-derived microvesicles can be detected in COVID-19 patients. In addition to providing a phospholipid surface for the synthesis of intrinsic factor Xase complex and prothrombinase complex, exposed PS also promotes the decryption of tissue factor (TF) which then promotes coagulant activity by complexing with factor VIIa to activate factor X. The treatment of COVID-19 hypercoagulability and thrombosis still focuses on early intervention. Antiplatelet therapy plays a role in relieving the disease, inhibiting the formation of the hypercoagulable state, reducing thrombotic events and mortality, and improving sequelae. PS can be another potential target for the inhibition of hypercoagulable states.

[Epidermal growth factor receptor gene mutations and clinicopathologic correlation in 309 patients with non-small cell lung cancer].

OBJECTIVE: To investigate the epidermal growth factor receptor (EGFR) gene mutation profile and related clinicopathological features in Chinese patients with non-small cell lung carcinoma (NSCLC). METHODS: Optimized oligonucleotide probe method was applied to detect EGFR mutations involving exons 18 - 21 using formalin fixed paraffin embedded tissue specimens of 309 NSCLC patients. The relationship between EGFR mutations and clinicopathological features were analyzed. RESULTS: The overall EGFR mutation rate was 34% (105/309) in this study cohort. Mutation rates in male and female were 30.4% (56/184) and 39.2% (49/125), respectively. The mutation rate was higher in patients less than 60 years of age, non-smokers and adenocarcinoma subtype than in their counterparts (P<0.05), with the percentage of 40.5% (87/215), 40.2% (51/127), 38.8% (78/201), respectively. The EGFR mutation types included exon 18 G719X mutation (5.7%, 6/105), exon 19 deletion (39.0%, 41/105) and exon 21 L858R mutation (55.2%, 58/105). In large cell undifferentiated carcinomas and squamous cell carcinomas, EGFR mutation rates were 22.2% (58/105) and 3/14, respectively. The overall mutation rate of exon 18 was low, but the proportion of its mutation was higher in squamous and adenosquamous carcinomas than in adenocarcinomas. CONCLUSIONS: There is a higher EGFR mutation rate in female, age of less than 60 years, non-smoker and adenocarcinoma among Chinese patients with NSCLC. Optimized oligonucleotide probe method is a sensitive and convenient method for the detection of EGFR mutations.

Complete Genome Sequences of Two Shiga Toxin-Producing Escherichia coli O146:H10 Strains Recovered from a Foodborne Outbreak in China.

Shiga toxin-producing Escherichia coli (STEC) is one of the primary pathogenic contaminants of foods, contributing to several foodborne outbreaks in recent years. Here, we report the complete genome sequences of two non-O157 STEC strains isolated from an outbreak of diarrhea in the city of Guilin, Guangxi Zhuang Autonomous Region, China.

COVID­19 and ischemic stroke: Mechanisms of hypercoagulability (Review).

During the coronavirus disease 2019 (COVID­19) pandemic, some patients with severe COVID­19 exhibited complications such as acute ischemic stroke (AIS), which was closely associated with a poor prognosis. These patients often had an abnormal coagulation, namely, elevated levels of D­dimer and fibrinogen, and a low platelet count. Certain studies have suggested that COVID­19 induces AIS by promoting hypercoagulability. Nevertheless, the exact mechanisms through which COVID­19 leads to a hypercoagulable state in infected patients remain unclear. Understanding the underlying mechanisms of hypercoagulability is of utmost importance for the effective treatment of these patients. The present review aims to summarize the current status of research on COVID­19, hypercoagulability and ischemic stroke. The present review also aimed to shed light into the underlying mechanisms through which COVID­19 induces hypercoagulability, and to provide therapies for different mechanisms for the more effective treatment of patients with COVID­19 with ischemic stroke and prevent AIS during the COVID­19 pandemic.