Correlation of serum Klotho, fetuin-A, and MGP levels with coronary artery calcification in maintenance hemodialysis patients.

OBJECTIVE: This study was to investigate the role of serum Klotho, fetuin-A, and Matrix Gla Protein (MGP) in Coronary Artery Calcification (CAC) in patients with Maintenance Hemodialysis (MHD) and their predictive value for CAC. METHODS: 100 patients receiving MHD were selected. Serum Klotho, fetuin-A, and MGP levels were detected by ELISA. CAC scores were assessed by coronary CT scan. Multifactor analysis was used to evaluate the risk factors affecting CAC. The ability of serum Klotho, fetuin-A, and MGP levels to diagnose CAC was evaluated by receiver operating characteristic curves. RESULTS: Serum Klotho, fetuin-A, and MGP were independent risk factors for CAC. Serum Klotho, fetuin-A, and MGP were valuable in the diagnosis of CAC in MHD patients. CONCLUSION: There is a close relationship between Klotho, fetuin-A, and MGP levels in MHD patients and CAC.

Unveiling the functions of five recently characterized lncRNAs in cancer progression.

Numerous studies over the past few decades have shown that RNAs are multifaceted, multifunctional regulators of most cellular processes, contrary to the initial belief that they only act as mediators for translating DNA into proteins. LncRNAs, which refer to transcripts longer than 200nt and lack the ability to code for proteins, have recently been identified as central regulators of a variety of biochemical and cellular processes, particularly cancer. When they are abnormally expressed, they are closely associated with tumor occurrence, metastasis, and tumor staging. Therefore, through searches on Google Scholar, PubMed, and CNKI, we identified five five recently characterized lncRNAs-Lnc-SLC2A12-10:1, LncRNA BCRT1, lncRNA IGFBP4-1, LncRNA PCNAP1, and LncRNA CDC6-that have been linked to the promotion of cancer cell proliferation, invasion, and metastasis. Consequently, this review encapsulates the existing research and molecular underpinnings of these five newly identified lncRNAs across various types of cancer. It suggests that these novel lncRNAs hold potential as independent biomarkers for clinical diagnosis and prognosis, as well as candidates for therapeutic intervention. In parallel, we discuss the challenges inherent in the research on these five newly discovered lncRNAs and look forward to the avenues for future exploration in this field.

Effects of different anesthesia methods on labor process and postpartum serum estrogen and progesterone levels in primiparas with painless labor.

OBJECTIVE: To look into the effects of different anesthesia methods on the labor process and the expression of serum estrogen and progesterone in primiparas with painless labor. METHODS: 60 primiparas receiving painless labor were selected as the research objects, and they were divided into either a Spinal & Continuous epidural anesthesia group (n = 30) or a continuous epidural anesthesia group (n = 30), anesthesia is administered using the corresponding anesthesia method. The authors compared serum estrogen and progesterone, inflammatory index expression, pain degree and neonatal health status in different periods. RESULTS: At T2 and T3, serum P, LH, FSH and E2 levels in the Spinal & Continuous epidural anesthesia group were signally lower than those in the Spinal & Continuous epidural anesthesia group (p < 0.05). Spinal & Continuous epidural anesthesia group harbored faster onset and longer duration of sensory block and motor block than the Continuous epidural anesthesia group (p < 0.05). SAS and SDS scores of the Spinal & Continuous epidural anesthesia group were clearly lower than those of the Continuous epidural anesthesia group (p < 0.05). VAS score and serum TNF-α, IL-6 levels of pregnant women in the Spinal & Continuous epidural anesthesia group were memorably lower than those in the Continuous epidural anesthesia group at T2 and T3 (p < 0.05). The total incidence of postoperative complications in the Spinal & Continuous epidural anesthesia group was distinctively lower than that in the Continuous epidural anesthesia group (p < 0.05). CONCLUSION: Spinal anesthesia combined with continuous epidural anesthesia has a better anesthesia effect in the painless labor of primiparas, which can effectually ameliorate the labor process and the expression of serum estrogen and progesterone.

Revealing the role of Peg13: A promising therapeutic target for mitigating inflammation in sepsis.

To investigate the role of Peg13 in modulating the inflammatory response in sepsis, we established Lipopolysaccharide (LPS)-induced 293T cells and mouse models. Peg13 expression was assessed at various time points after infection using RT-qPCR. The levels of high mobility group box 1 (HMGB1) and interleukin-6 (IL-6) were quantified through ELISA. A total of 44 septic patients and 36 healthy participants were recruited to measure Peg13 and HMGB1 levels in the blood. Peg13 demonstrated significant down-regulation in the supernatant of LPS-induced 293T cells and in the blood of LPS-induced mice. Moreover, the levels of proinflammatory cytokines HMGB1 and IL-6 were elevated in both the supernatant of LPS-induced cell models and blood specimens from LPS-induced murine models, and this elevation could be notably reduced by Peg13 suppression. In a clinical context, Peg13 and HMGB1 levels were higher in septic patients compared to healthy subjects. Peg13 exhibited a negative correlation with HMGB1, C-reactive protein (CRP), and erythrocyte sedimentation rate (ESR) among septic patients. Peg13 mitigates the inflammatory response by reducing the release of proinflammatory cytokines HMGB1 and IL-6 in sepsis, presenting a potential therapeutic target for alleviating inflammation in sepsis treatment.

Abnormal Insula Network Characteristics in Panic Disorder.

BACKGROUND: Panic disorder (PD) is a common disabling condition characterized by recurrent panic attacks. Emotional and behavioral impairments are associated with functional connectivity (FC) and network abnormalities. We used the whole brain FC, modular networks, and graph-theory analysis to investigate extensive network profiles in PD. METHOD: The functional MRI data from 82 PD and 97 controls were included. Intrinsic FC between each pair of 160 regions, 6 intra-networks, and 15 inter-networks were analyzed. The topological properties were explored. RESULTS: PD patients showed altered FCs within the right insula, between frontal cortex-posterior cingulate cortex (PCC), frontal cortex-cerebellum, and PCC-occipital cortex (corrected P values < 0.001). Lower connections within the Sensorimotor Network (SMN) and SMN-Occipital Network (OCN) were detected (P values < 0.05). Various decreased global and local network features were found in PD (P values < 0.05). In addition, significant correlations were found between PD symptoms and nodal efficiency (Ne) in the insula (r = -0.273, P = 0.016), and the FC of the intra-insula (r = -0.226, P = 0.041). CONCLUSIONS: PD patients present with abnormal functional brain networks, especially the decreased FC and Ne within insula, suggesting that dysfunction of information integration plays an important role in PD.

Upregulation of PGC-1α expression by pioglitazone mediates prevention of sepsis-induced acute lung injury.

The imbalance between pro-inflammatory M1 and anti-inflammatory M2 macrophages plays a critical role in the pathogenesis of sepsis-induced acute lung injury (ALI). Peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α) may modulate macrophage polarization toward the M2 phenotype by altering mitochondrial activity. This study aimed to investigate the role of the PGC-1α agonist pioglitazone (PGZ) in modulating sepsis-induced ALI. A mouse model of sepsis-induced ALI was established using cecal ligation and puncture (CLP). An in vitro model was created by stimulating MH-S cells with lipopolysaccharide (LPS). qRT-PCR was used to measure mRNA levels of M1 markers iNOS and MHC-II and M2 markers Arg1 and CD206 to evaluate macrophage polarization. Western blotting detected expression of peroxisome proliferator-activated receptor gamma (PPARγ) PGC-1α, and mitochondrial biogenesis proteins NRF1, NRF2, and mtTFA. To assess mitochondrial content and function, reactive oxygen species levels were detected by dihydroethidium staining, and mitochondrial DNA copy number was measured by qRT-PCR. In the CLP-induced ALI mouse model, lung tissues exhibited reduced PGC-1α expression. PGZ treatment rescued PGC-1α expression and alleviated lung injury, as evidenced by decreased lung wet-to-dry weight ratio, pro-inflammatory cytokine secretion (tumor necrosis factor-α, interleukin-1ß, interleukin-6), and enhanced M2 macrophage polarization. Mechanistic investigations revealed that PGZ activated the PPARγ/PGC-1α/mitochondrial protection pathway to prevent sepsis-induced ALI by inhibiting M1 macrophage polarization. These results may provide new insights and evidence for developing PGZ as a potential ALI therapy.

Upregulation of PGC-1α expression by pioglitazone mediates prevention of sepsis-induced acute lung injury

Abstract The imbalance between pro-inflammatory M1 and anti-inflammatory M2 macrophages plays a critical role in the pathogenesis of sepsis-induced acute lung injury (ALI). Peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α) may modulate macrophage polarization toward the M2 phenotype by altering mitochondrial activity. This study aimed to investigate the role of the PGC-1α agonist pioglitazone (PGZ) in modulating sepsis-induced ALI. A mouse model of sepsis-induced ALI was established using cecal ligation and puncture (CLP). An in vitro model was created by stimulating MH-S cells with lipopolysaccharide (LPS). qRT-PCR was used to measure mRNA levels of M1 markers iNOS and MHC-II and M2 markers Arg1 and CD206 to evaluate macrophage polarization. Western blotting detected expression of peroxisome proliferator-activated receptor gamma (PPARγ) PGC-1α, and mitochondrial biogenesis proteins NRF1, NRF2, and mtTFA. To assess mitochondrial content and function, reactive oxygen species levels were detected by dihydroethidium staining, and mitochondrial DNA copy number was measured by qRT-PCR. In the CLP-induced ALI mouse model, lung tissues exhibited reduced PGC-1α expression. PGZ treatment rescued PGC-1α expression and alleviated lung injury, as evidenced by decreased lung wet-to-dry weight ratio, pro-inflammatory cytokine secretion (tumor necrosis factor-α, interleukin-1β, interleukin-6), and enhanced M2 macrophage polarization. Mechanistic investigations revealed that PGZ activated the PPARγ/PGC-1α/mitochondrial protection pathway to prevent sepsis-induced ALI by inhibiting M1 macrophage polarization. These results may provide new insights and evidence for developing PGZ as a potential ALI therapy.

Genomic sequencing revealed recombination event between clade 1 and clade 2 occurs in circulating varicella-zoster virus in China.

Varicella-zoster virus (VZV), a member of the Alphaherpesvirinae subfamily, causes varicella in primary infections and establishing a latent stage in sensory ganglia. Upon reactivation, VZV causes herpes zoster with severe neuralgia, especially in elderly patients. The mutation rate for VZV is comparatively lower than the other members of other alpha herpesviruses. Due to geographic isolation, different genotypes of VZV are circulating on separate continents. Here, we successfully isolated a VZV from the vesicular fluid of a youth zoster patient. Based on the single-nucleotide polymorphism profiles of different open reading frames that define the genotype, this newly isolated VZV primarily represents genotype clade 2 but also has characteristics of genotype clade 1. The next-generation sequencing provided a nearly full-length sequence, and further phylogenetic analysis revealed that this VZV isolate is distinct from clades 1 and 2. The Recombination Detection Program indicates that a possible recombinant event may occur between the VZV isolate and clade 1. In summary, we found that there is a circulating VZV isolate in China that may represent a recombinant between clade 1 and clade 2, providing new concerns that need to be considered in the future VZV vaccination program.

Puerarin alleviated oxidative stress and ferroptosis during renal fibrosis induced by ischemia/reperfusion injury via TLR4/Nox4 pathway in rats.

PURPOSE: To investigate the role of puerarin on renal fibrosis and the underlying mechanism in renal ischemia and reperfusion (I/R) model. METHODS: Rats were intraperitoneally injected with puerarin (50 or 100 mg/kg) per day for one week before renal I/R. The level of renal collagen deposition and interstitial fibrosis were observed by hematoxylin and eosin and Sirius Red staining, and the expression of α-smooth muscle actin (α-SMA) was examined by immunohistochemical staining. The ferroptosis related factors and TLR4/Nox4-pathway-associated proteins were detected by Western blotting. RESULTS: Puerarin was observed to alleviate renal collagen deposition, interstitial fibrosis and the α-SMA expression induced by I/R. Superoxide dismutase (SOD) activities and glutathione (GSH) level were decreased in I/R and hypoxia/reoxygenation (H/R), whereas malondialdehyde (MDA) and Fe2+ level increased. However, puerarin reversed SOD, MDA, GSH and Fe2+ level changes induced by I/R and H/R. Besides, Western blot indicated that puerarin inhibited the expression of ferroptosis related factors in a dose-dependent manner, which further demonstrated that puerarin had the effect to attenuate ferroptosis. Moreover, the increased expression of TLR/Nox4-pathway-associated proteins were observed in I/R and H/R group, but puerarin alleviated the elevated TLR/Nox4 expression. CONCLUSIONS: Our results suggested that puerarin inhibited oxidative stress and ferroptosis induced by I/R and, thus, delayed the progression of renal fibrosis, providing a new target for the treatment of renal fibrosis.

Puerarin alleviated oxidative stress and ferroptosis during renal fibrosis induced by ischemia/reperfusion injury via TLR4/Nox4 pathway in rats

Purpose: To investigate the role of puerarin on renal fibrosis and the underlying mechanism in renal ischemia and reperfusion (I/R) model. Methods: Rats were intraperitoneally injected with puerarin (50 or 100 mg/kg) per day for one week before renal I/R. The level of renal collagen deposition and interstitial fibrosis were observed by hematoxylin and eosin and Sirius Red staining, and the expression of α-smooth muscle actin (α-SMA) was examined by immunohistochemical staining. The ferroptosis related factors and TLR4/Nox4-pathway-associated proteins were detected by Western blotting. Results: Puerarin was observed to alleviate renal collagen deposition, interstitial fibrosis and the α-SMA expression induced by I/R. Superoxide dismutase (SOD) activities and glutathione (GSH) level were decreased in I/R and hypoxia/reoxygenation (H/R), whereas malondialdehyde (MDA) and Fe2+ level increased. However, puerarin reversed SOD, MDA, GSH and Fe2+ level changes induced by I/R and H/R. Besides, Western blot indicated that puerarin inhibited the expression of ferroptosis related factors in a dose-dependent manner, which further demonstrated that puerarin had the effect to attenuate ferroptosis. Moreover, the increased expression of TLR/Nox4-pathway-associated proteins were observed in I/R and H/R group, but puerarin alleviated the elevated TLR/Nox4 expression. Conclusions: Our results suggested that puerarin inhibited oxidative stress and ferroptosis induced by I/R and, thus, delayed the progression of renal fibrosis, providing a new target for the treatment of renal fibrosis.

Combined training and explosive strength in basketball players' lower limbs / Treinamento combinado e força explosiva nos membros inferiores dos jogadores de basquete / Entrenamiento combinado y fuerza explosiva en los miembros inferiores de los jugadores de baloncesto

ABSTRACT Introduction: Basketball presents unique competitive characteristics, requiring athletes a high level of strength, especially explosive strength. Objective: Study the effect of combined training on the explosive power of lower limbs in basketball players. Methods: The author selected 18 basketball players, equally distributed with the random method into a unipodal combined training group (S group), a two-legged combined training group (D group), and a conventional strength training group (W group), for the three-test data. Statistical analysis was performed on the data collected from the experiment. Results: There was a significant difference in approach height and three-quarter sprint in group S (p<0.05). The difference was not evident in the height of touch in situ (p>0.05). In group D, there was a significant difference in situ touch height p<0.01. There was no significant difference in the results of the three test indicators in group W (p>0.05). Conclusion: Compared to conventional strength training, unipodal combined training is more effective for the development of explosive strength in the lower limbs of basketball students. Level of evidence II; Therapeutic studies - investigation of treatment outcomes.

RESUMO Introdução: O basquetebol tem suas características competitivas singulares, exigindo que os atletas tenham um alto nível de força, sobretudo a força explosiva. Objetivo: Estudar o efeito do treinamento combinado sobre o poder explosivo dos membros inferiores em jogadores de basquetebol. Métodos: O autor selecionou 18 jogadores de basquetebol, distribuídos igualmente com o método aleatório em grupo de treinamento combinado unipodal (grupo S), grupo de treinamento combinado de duas pernas (grupo D) e grupo de treinamento convencional de força (grupo W), para os três dados de teste. Foi realizada uma análise estatística com os dados coletados do experimento. Resultados: Houve uma diferença significativa na altura de aproximação e no sprint de três quartos no grupo S (p<0,05). Na altura de toque in situ (p>0,05), a diferença não foi evidenciada. No grupo D, houve uma diferença significativa entre a altura de toque in situ p<0,01. Não houve diferença significativa nos resultados dos três indicadores de teste no grupo W (p>0,05). Conclusão: Comparativamente ao treinamento convencional de força, o treinamento combinado unipodal é mais eficaz para o desenvolvimento de força explosiva nos membros inferiores dos estudantes de basquetebol. Nível de evidência II; Estudos terapêuticos - investigação dos resultados do tratamento.

RESUMEN Introducción: El baloncesto tiene unas características competitivas únicas, que exigen que los deportistas tengan un alto nivel de fuerza, especialmente la fuerza explosiva. Objetivo: Estudiar el efecto del entrenamiento combinado sobre la potencia explosiva de los miembros inferiores en jugadores de baloncesto. Métodos: El autor seleccionó a 18 jugadores de baloncesto, distribuidos equitativamente con el método aleatorio en grupo de entrenamiento combinado unipodal (grupo S), grupo de entrenamiento combinado bipodal (grupo D) y grupo de entrenamiento de fuerza convencional (grupo W), para los tres datos de la prueba. Se realizó un análisis estadístico con los datos recogidos en el experimento. Resultados: Hubo una diferencia significativa en la altura de aproximación y en el sprint de tres cuartos en el grupo S (p<0,05). En la altura de toque in situ (p>0,05), no se evidenció la diferencia. En el grupo D, hubo una diferencia significativa entre la altura del tacto in situ p<0,01. No hubo diferencias significativas en los resultados de los tres indicadores de prueba en el grupo W (p>0,05). Conclusión: En comparación con el entrenamiento de fuerza convencional, el entrenamiento combinado unipodal es más eficaz para el desarrollo de la fuerza explosiva en las extremidades inferiores de los estudiantes de baloncesto. Nivel de evidencia II; Estudios terapéuticos - investigación de los resultados del tratamiento.

miR-146b suppresses LPS-induced M1 macrophage polarization via inhibiting the FGL2-activated NF-κB/MAPK signaling pathway in inflammatory bowel disease.

OBJECTIVES: M1 macrophage polarization and phenotype in Inflammatory Bowel Disease (IBD) are common biological responses. METHOD: Herein, IBD mice models were constructed and macrophages were derived. RESULTS: It was discovered that microRNA-146b (miR-146b) was downregulated in IBD mice and Lipopolysaccharide (LPS)-induced macrophages. Moreover, the inhibitory role of overexpressed miR-146b in reducing the inflammation level and blocking M1 macrophage polarization was confirmed. Further investigation indicated that Fibrinogen Like 2 (FGL2) acted as the target gene of miR-146b, and FGL2 mediated activation of NLRP3, NF-κB-p65, and p38-MAPK. More importantly, it was validated that miR-146b could ameliorate inflammatory phenotype and prevent M1 macrophage polarization via inhibiting FGL2 in vitro, and miR-146b overexpression alleviated the intestinal injury of IBD mice in vivo. CONCLUSIONS: Overall, it is potential to use miR-146b for the amelioration of IBD.

miR-146b suppresses LPS-induced M1 macrophage polarization via inhibiting the FGL2-activated NF-κB/MAPK signaling pathway in inflammatory bowel disease

Abstract Objectives: M1 macrophage polarization and phenotype in Inflammatory Bowel Disease (IBD) are common biological responses. Method: Herein, IBD mice models were constructed and macrophages were derived. Results: It was discovered that microRNA-146b (miR-146b) was downregulated in IBD mice and Lipopolysaccharide (LPS)-induced macrophages. Moreover, the inhibitory role of overexpressed miR-146b in reducing the inflammation level and blocking M1 macrophage polarization was confirmed. Further investigation indicated that Fibrinogen Like 2 (FGL2) acted as the target gene of miR-146b, and FGL2 mediated activation of NLRP3, NF-κB-p65, and p38-MAPK. More importantly, it was validated that miR-146b could ameliorate inflammatory pheno-type and prevent M1 macrophage polarization via inhibiting FGL2 in vitro, and miR-146b overexpression alleviated the intestinal injury of IBD mice in vivo. Conclusions: Overall, it is potential to use miR-146b for the amelioration of IBD. HIGHLIGHTS miR-146b was downregulated in Inflammatory Bowel Disease (IBD) mice and LPS-induced macrophages. Fibrinogen Like 2 (FGL2) was identified as the target gene of miR-146b. miR-146b ameliorated the inflammation and blocked M1 macrophage polarization via inhibiting FGL2. miR-146b ameliorated the symptoms and pathological injury of IBD via inhibiting FGL2.

Worldwide tendency and perspectives in traumatic dental injuries: A bibliometric analysis over two decades (1999-2018).

BACKGROUND/AIMS: Traumatic dental injuries (TDIs) are considered to be a public dental health problem worldwide. The aim of the current study was to provide the worldwide tendency and perspectives in TDIs in the last two decades via bibliometric analysis. METHODS: ''Tooth injuries'' was searched as the Medical Subject Headings term within PubMed with the date range from 1999 to 2018. Two investigators perused information in the articles according to the inclusion and exclusion criteria. The articles were independently categorized according to the following aspects: (a) annual scholarly output; (b) leading countries or regions; (c) leading journals; (d) productive authors; (e) citations; (f) study design; (f) distribution of topics; and (g) the type of dentition and TDIs. VOSviewer 1.6.7 and Citespace 5.2 were used for analyzing and visualizing bibliometric networks. RESULTS: A total of 2627 articles about traumatic dental injuries were published and indexed in PubMed during the two decades, and the number of publications on traumatic dental injuries was rising in general. The research outputs were mainly concentrated in developed countries and affiliated hospitals of universities. Brazil was the most productive country. The journal Dental Traumatology had the most contributions to the scientific research of traumatic dental injuries. "Case report" was the most frequent type of article (36.50%), followed by cross-sectional studies (19.57%) and case-control studies (13.67%). Most studies focused on the treatment of TDIs (38.94%), especially for avulsion (21.01%), crown fracture (9.71%), and intrusion (5.25%). Permanent teeth (66%) were the dominant dentition. CONCLUSION: There is a lack of high-quality well-designed studies such as cohort studies. The number of publications on prevention and the primary dentition is disproportionate in relation to their significance.

Distribution of serotypes, antimicrobial resistance and virulence genes among Streptococcus agalactiae isolated from bovine in China

Background: Bovine mastitis, a global disease that is responsible for large economic losses each year due to lower milkyield and reduced milk quality. In some countries, especially in China, Streptococcus agalactiae has become one of themost frequently detected pathogen. Antibiotic treatment and vaccine immunization are important strategies for the controlof infectious diseases. The main objective of the present study was to evaluate distribution of bovine mastitis pathogensand antimicrobial resistance of S. agalactiae, and contribute to the treatment of bovine mastitis.Materials, Methods & Results: Clinical mastitis samples (n= 1,122) were collected from 27 dairy farms located in 15different provinces of China during 2012-2018. The pathogens were identified by 16S rDNA method. Antimicrobial susceptibility was assessed by disc diffusion method. Molecular characteristics was distinguished based on PCR. The resultsshowed that the main pathogens were Streptococcus agalactiae (n= 324, 26.2%), Escherichia coli (n= 287, 23.2%), andStaphylococcus aureus (n= 131, 10.6%). The serotypes of Streptococcus agalactiae were serotype II (53.6%), Ia (44 %)and VII (1.2%), respectively. Streptococcus agalactiae were resistant to kanamycin (93.8%), gentamicin (49.4%), vancomycin (49.4%), tetracycline (35.8%), clindamycin (34.6%) and erythromycin (32.1%). The main resistance genes wereermA (53.1%) and ermB (85.2%). Resistance to erythromycin was attributed to the genes ermA (P < 0.05) and resistanceto tetracycline was attributed to the genes tetK, tetM, tetO (P < 0.01). The virulence genes scpB (81.4%), cyl (100%), glnA(76.6%), cfb (98.8%), hylB (98.8%), scaA (69.1%) were detected in almost all isolates.Discussion: In the present study, Streptococcus agalactiae, Escherichia coli and Staphylococcus aureus were the pathogens isolated most frequently from clinical mastitis. In the case of S. agalactiae, we performed capsular serotyping ofisolates...(AU)

Comparative Proteomic Analysis of the Hevea brasiliensis Latex under Ethylene and Calcium Stimulation.

BACKGROUND: Calcium ions usually act as a second messenger in the signal transmission process and a major element required by plants. In Hevea, calcium ion could alleviate the negative effects of long-term ethylene application to a certain extent. However, the molecular mechanisms remain unclear. METHODS: Two-dimensional electrophoresis was used to determine the pattern of protein changes in latex after treatments with calcium and/or ethylene. Quantitative real-time polymerase chain reaction and Western blotting were used to determine the expression levels of some proteins and genes. STRING software was used to determine the protein-protein interaction network of the identified proteins. RESULTS: Comparative proteomics identified 145 differentially expressed proteins, which represented 103 unique proteins. The abundance change patterns of some proteins involved in signal transduction, rubber particle aggregation, and natural rubber biosynthesis were altered upon calcium stimulation. Quantitative real-time polymerase chain reaction analysis of 29 proteins showed that gene expression did not always maintain the same trend as protein expression. The increased enzyme activities of superoxide dismutase, ascorbate peroxidase, and glutathione reductase suggested that calcium can enhance the antistress ability of plants by increasing the activity of their antioxidant enzyme systems. CONCLUSION: These results supplement the rubber latex proteome, and provide evidence for investigating the molecular mechanisms by which calcium alleviates the negative effects of ethylene stimulation.

Distribution of serotypes, antimicrobial resistance and virulence genes among Streptococcus agalactiae isolated from bovine in China

Background: Bovine mastitis, a global disease that is responsible for large economic losses each year due to lower milkyield and reduced milk quality. In some countries, especially in China, Streptococcus agalactiae has become one of themost frequently detected pathogen. Antibiotic treatment and vaccine immunization are important strategies for the controlof infectious diseases. The main objective of the present study was to evaluate distribution of bovine mastitis pathogensand antimicrobial resistance of S. agalactiae, and contribute to the treatment of bovine mastitis.Materials, Methods & Results: Clinical mastitis samples (n= 1,122) were collected from 27 dairy farms located in 15different provinces of China during 2012-2018. The pathogens were identified by 16S rDNA method. Antimicrobial susceptibility was assessed by disc diffusion method. Molecular characteristics was distinguished based on PCR. The resultsshowed that the main pathogens were Streptococcus agalactiae (n= 324, 26.2%), Escherichia coli (n= 287, 23.2%), andStaphylococcus aureus (n= 131, 10.6%). The serotypes of Streptococcus agalactiae were serotype II (53.6%), Ia (44 %)and VII (1.2%), respectively. Streptococcus agalactiae were resistant to kanamycin (93.8%), gentamicin (49.4%), vancomycin (49.4%), tetracycline (35.8%), clindamycin (34.6%) and erythromycin (32.1%). The main resistance genes wereermA (53.1%) and ermB (85.2%). Resistance to erythromycin was attributed to the genes ermA (P < 0.05) and resistanceto tetracycline was attributed to the genes tetK, tetM, tetO (P < 0.01). The virulence genes scpB (81.4%), cyl (100%), glnA(76.6%), cfb (98.8%), hylB (98.8%), scaA (69.1%) were detected in almost all isolates.Discussion: In the present study, Streptococcus agalactiae, Escherichia coli and Staphylococcus aureus were the pathogens isolated most frequently from clinical mastitis. In the case of S. agalactiae, we performed capsular serotyping ofisolates...

Expression Profiling of Mitogen-Activated Protein Kinase Genes Reveals Their Evolutionary and Functional Diversity in Different Rubber Tree (Hevea brasiliensis) Cultivars.

Rubber tree (Heveabrasiliensis) is the only commercially cultivated plant for producing natural rubber, one of the most essential industrial raw materials. Knowledge of the evolutionary and functional characteristics of kinases in H. brasiliensis is limited because of the long growth period and lack of well annotated genome information. Here, we reported mitogen-activated protein kinases in H.brasiliensis (HbMPKs) by manually checking and correcting the rubber tree genome. Of the 20 identified HbMPKs, four members were validated by proteomic data. Protein motif and phylogenetic analyses classified these members into four known groups comprising Thr-Glu-Tyr (TEY) and Thr-Asp-Tyr (TDY) domains, respectively. Evolutionary and syntenic analyses suggested four duplication events: HbMPK3/HbMPK6, HbMPK8/HbMPK9/HbMPK15, HbMPK10/HbMPK12 and HbMPK11/HbMPK16/HbMPK19. Expression profiling of the identified HbMPKs in roots, stems, leaves and latex obtained from three cultivars with different latex yield ability revealed tissue- and variety-expression specificity of HbMPK paralogues. Gene expression patterns under osmotic, oxidative, salt and cold stresses, combined with cis-element distribution analyses, indicated different regulation patterns of HbMPK paralogues. Further, Ka/Ks and Tajima analyses suggested an accelerated evolutionary rate in paralogues HbMPK10/12. These results revealed HbMPKs have diverse functions in natural rubber biosynthesis, and highlighted the potential possibility of using MPKs to improve stress tolerance in future rubber tree breeding.

miR-22 suppresses tumorigenesis and improves radiosensitivity of breast cancer cells by targeting Sirt1.

BACKGROUND: miR-22 has been shown to be frequently downregulated and act as a tumor suppressor in multiple cancers including breast cancers. However, the role of miR-22 in regulating the radioresistance of breast cancer cells, as well as its underlying mechanism is still not well understood. METHODS: The expressions of miR-22 and sirt1 at mRNA and protein levels were examined by qRT-PCR and Western Blot. The effects of miR-22 overexpression and sirt1 knockdown on cell viability, apoptosis, radiosensitivity, γ-H2AX foci formation were evaluated by CCK-8 assay, flow cytometry, colony formation assay, and γ-H2AX foci formation assay, respectively. Luciferase reporter assay and qRT-PCR analysis were performed to confirm the interaction between miR-22 and sirt1. RESULTS: miR-22 was downregulated and sirt1 was upregulated at both mRNA and protein levels in breast cancer cells. miR-22 overexpression or sirt1 knockdown significantly suppressed viability, induced apoptosis, reduced survival fraction, and increased the number of γ-H2AX foci in breast cancer cells. Sirt1 was identified as a target of miR-22 and miR-22 negatively regulated sirt1 expression. Ectopic expression of sirt1 dramatically reversed the inhibitory effect of miR-22 on cell viability and promotive effect on apoptotic rates and radiosensitivity in breast cancer cells. CONCLUSIONS: miR-22 suppresses tumorigenesis and improves radiosensitivity of breast cancer cells by targeting sirt1, providing a promising therapeutic target for breast cancer.

miR-22 suppresses tumorigenesis and improves radiosensitivity of breast cancer cells by targeting Sirt1

BACKGROUND: miR-22 has been shown to be frequently downregulated and act as a tumor suppressor in multiple cancers including breast cancers. However, the role of miR-22 in regulating the radioresistance of breast cancer cells, as well as its underlying mechanism is still not well understood. METHODS: The expressions of miR-22 and sirt1 at mRNA and protein levels were examined by qRT-PCR and Western Blot. The effects of miR-22 overexpression and sirt1 knockdown on cell viability, apoptosis, radiosensitivity, γ-H2AX foci formation were evaluated by CCK-8 assay, flow cytometry, colony formation assay, and γ-H2AX foci formation assay, respectively. Luciferase reporter assay and qRT-PCR analysis were performed to confirm the interaction between miR-22 and sirt1. RESULTS: miR-22 was downregulated and sirt1 was upregulated at both mRNA and protein levels in breast cancer cells. miR-22 overexpression or sirt1 knockdown significantly suppressed viability, induced apoptosis, reduced survival fraction, and increased the number of γ-H2AX foci in breast cancer cells. Sirt1 was identified as a target of miR-22 and miR-22 negatively regulated sirt1 expression. Ectopic expression of sirt1 dramatically reversed the inhibitory effect of miR-22 on cell viability and promotive effect on apoptotic rates and radiosensitivity in breast cancer cells. CONCLUSIONS: miR-22 suppresses tumorigenesis and improves radiosensitivity of breast cancer cells by targeting sirt1, providing a promising therapeutic target for breast cancer.