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Pancreatic β cell failure is a hallmark of diabetes. However, the causes of β cell failure remain incomplete. Here, we report the identification of tetranectin (TN), an adipose tissue–enriched secretory molecule, as a negative regulator of insulin secretion in β cells in diabetes. TN expression is stimulated by high glucose in adipocytes via the p38 MAPK/TXNIP/thioredoxin/OCT4 signaling pathway, and elevated serum TN levels are associated with diabetes. TN treatment greatly exacerbates hyperglycemia in mice and suppresses glucose-stimulated insulin secretion in islets. Conversely, knockout of TN or neutralization of TN function notably improves insulin secretion and glucose tolerance in high-fat diet–fed mice. Mechanistically, TN binds with high selectivity to β cells and inhibits insulin secretion by blocking L-type Ca 2+ channels. Our study uncovers an adipocyte–β cell cross-talk that contributes to β cell dysfunction in diabetes and suggests that neutralization of TN levels may provide a new treatment strategy for type 2 diabetes.

Approximately 90% of tuberculosis (TB) cases among non–US-born persons in the United States are attributable to progression of latent TB infection to TB disease. Using survival analysis, we investigated whether birthplace is associated with time to disease progression among non–US-born persons in whom TB disease developed. We derived a Cox regression model comparing differences in time to TB diagnosis after US entry among 19 birth regions, adjusting for sex, birth year, and age at entry. After adjusting for age at entry and birth year, the median time to TB diagnosis was lowest among persons from Middle Africa, 128 months (95% CI 116–146 months) for male persons and 121 months (95% CI 108–136 months) for female persons. We found time to TB diagnosis among non–US-born persons varied by birth region, which represents a prognostic indicator for progression of latent TB infection to TB disease.

Low molecular weight protein tyrosine phosphatase (LWM-PTP), also known as acid phosphatase, is a highly conserved tyrosine phosphatase in living organisms. However, the function of LWM-PTP homolog has not been reported yet in plants. Here, we revealed a homolog of acid phosphatase, APH, in Arabidopsis plants, is a functional protein tyrosine phosphatase. The aph mutants are hyposensitive to ABA in post-germination growth. We performed an anti-phosphotyrosine antibody-based quantitative phosphoproteomics in wild-type and aph mutant and identified hundreds of putative targets of APH, including multiple splicing factors and other transcriptional regulators. Consistently, RNA-seq analysis revealed that the expression of ABA-highly-responsive genes is suppressed in aph mutants. Thus, APH regulates the ABA-responsive gene expressions by regulating the tyrosine phosphorylation of multiple splicing factors and other post-transcriptional regulators. We also revealed that Tyr383 in RAF9, a member of B2 and B3 RAF kinases that phosphorylate and activate SnRK2s in the ABA signaling pathway, is a direct target site of APH. Phosphorylation of Tyr383 is essential for RAF9 activity. Our results uncovered a crucial function of APH in ABA-induced tyrosine phosphorylation in Arabidopsis.

Background Post marketing safety evaluations of quadrivalent meningococcal diphtheria-toxoid conjugate vaccine (MenACWY-D) have focused on post-vaccination risk of Guillain Barre syndrome (GBS), adverse events (AEs) after maternal vaccination, and comparative studies with the newer quadrivalent meningococcal CRM197 conjugate vaccine (MenACWY-CRM). To provide an updated general safety assessment, we reviewed reports of AEs following MenACWY-D submitted to the Vaccine Adverse Event Reporting System (VAERS). Methods VAERS is a national spontaneous reporting vaccine safety surveillance system co-administered by the Centers for Disease Control and Prevention and the U.S. Food and Drug Administration. We searched the VAERS database for U.S. reports of AEs after administration of MenACWY-D from January 2005 through June 2016. We conducted clinical reviews of serious reports after MenACWY-D administered alone, reports of MenACWY-D use during pregnancy, and reports of selected pre-specified outcomes. We screened for disproportionate reporting of AEs after MenACWY-D using empirical Bayesian data mining. Results VAERS received 13,075 U.S. reports after receipt of MenACWY-D; most (86%) described vaccination in adolescents, were classified as non-serious (94%), and described AEs consistent with pre-licensure studies. We did not find any evidence that reported deaths were related to vaccination. In serious reports, GBS and meningococcal infection were the most commonly reported medical conditions. Many reports of MenACWY-D use during pregnancy described inadvertent vaccination; most (61%) did not report any AE. Conclusions Findings from our comprehensive review of reports to VAERS following MenACWY-D are consistent with data from pre-licensure studies and provide further reassurance on the safety of MenACWY-D.

With rapid development of computing technology, Bayesian statistics have increasingly gained more attention in various areas of public health. However, the full potential of Bayesian sequential methods applied to vaccine safety surveillance has not yet been realized, despite acknowledged practical benefits and philosophical advantages of Bayesian statistics. In this paper, we describe how sequential analysis can be performed in a Bayesian paradigm in the field of vaccine safety. We compared the performance of the frequentist sequential method, specifically, Maximized Sequential Probability Ratio Test (MaxSPRT), and a Bayesian sequential method using simulations and a real world vaccine safety example. The performance is evaluated using three metrics: false positive rate, false negative rate, and average earliest time to signal. Depending on the background rate of adverse events, the Bayesian sequential method could significantly improve the false negative rate and decrease the earliest time to signal. We consider the proposed Bayesian sequential approach to be a promising alternative for vaccine safety surveillance.

Clade A PP2C phosphatases are central components of the ABA-receptor coupled core signaling pathway, and are involved in multiple stress responses and developmental processes. However, the direct targets or partner proteins of A clade PP2Cs that participate in these biological processes are largely unknown. Here, we used a TurboID-based proximity labeling method to identify putative associated proteins of one A clade PP2C phosphatase, ABI1. By combining the results from affinity purification or proximity labeling of biotinylated proteins, we identified more than four hundred putative ABI1-associated proteins, including dozens of known ABI1-intreacting proteins, as well as proteins involved in TOR signaling, phospho-regulation, and other biological processes. We found that RAFs, a group of protein kinases that phosphorylate and activate SnRK2s in ABA and osmotic stress signaling, are direct substrates of ABI1. A conserved serine residue located in the P-loop of the kinase domain, corresponding to Ser619 in RAF3, is a major functional ABI1 target site. ABI1-mediated dephosphorylation on this site strongly promotes the kinase activity of most B2 and B3 RAFs. Thus, ABI1 has dual functions in ABA signaling by dephosphorylating and inhibiting SnRK2 to prevent SnRK2 activation in unstressed conditions, while dephosphorylating B2 and B3 subgroup RAFs to maintain their basal kinase activity. PP2C-mediated dephosphorylation at the conserved serine residue may be a mechanism for RAF activation in both plants and animals, with potential implications for tumorigenesis in humans.

Introduction: Atherosclerosis is a chronic disease characterized by the inflammatory process and lipid depositions. We previously reported that microRNA-216a (miR-216a) can accelerate the progression of atherosclerosis by promoting the polarization of M1 pro-inflammatory phenotype. Ginsenoside Rb2 (Rb2), the major pharmacologically active compound extracted from ginseng, has a high affinity to miR-216a. In this study, we aimed to investigate whether Rb2 can counteract the effect of miR-216a in macrophages to ameliorate atherosclerosis.Methods: The apolipoprotein E deficiency (ApoE−/−) mice model was chronically infected with miR-216a adenovirus via the tail vein and then intraperitoneally injected with Rb2. The plaque lesion area and stability of thoracic aorta were examined. The human myeloid leukemia mononuclear cells (THP-1) or human peripheral blood mononuclear cells (PBMCs) were cultured in vitro, transfected with miR-216a mimics, and treated with Rb2 to explore the mechanisms of Rb2 on the polarization of M1 macrophages, inflammatory process, and lipid accumulation.Results: In the atherosclerotic ApoE−/− mice model, miR-216a greatly increased en face aortic lesion area of the thoracic aorta, lipid accumulation, and M1 macrophages infiltration in plaques, whereas these effects of miR-216a on atherosclerosis burden were significantly alleviated by Rb2 treatment. In the in vitro THP-1 model, the flow cytometry experiment showed that Rb2 treatment inhibited miR-216a–mediated polarization of M1 macrophages characterized by the surface marker CD86 expression but had no effects on M2 polarization characterized by the surface marker CD206 expression. Mechanistically, Rb2 suppressed the miR-216a–mediated inflammatory response through the Smad3/nuclear factor kappa B inhibitor alpha pathway. Moreover, Rb2 reduced the lipid uptake and promoted cholesterol efflux by counteracting the effects of miR-216a in the THP-1–derived foam cells and in the PBMC-derived foam cells under the oxidized low-density lipoproteins.Conclusion: Our findings indicated that Rb2 might be a potential therapeutic molecule for atherosclerosis by attenuating the atherosclerosis plaque lesion, lipid accumulation, and M1 macrophages polarization by targeting miR-216a. Given that accumulation of foam cells in the intima takes place chronically, the role of Rb2 in atherosclerosis progression needs further investigation.

Objective Previously, the protective effect of microRNA (miR)-145-5p has been discovered in acute lung injury (ALI). Thus, this study attempts to further discuss the mechanism of miR-145-5p in ALI through the downstream E26 transformation-specific proto-oncogene 2 (ETS2)/transforming growth factor β1 (TGF-β1)/Smad pathway. Methods A lipopolysaccharide (LPS)-induced rat ALI model was established. Recombinant adenovirus miR-145-5p and/or ETS2 overexpression plasmid was administrated into rats. Afterwards, pathological damage in the lung tissue, wet/dry (W/D) ratio, apoptosis and contents of serum inflammatory factors were observed. miR-145-5p, ETS2, TGF-β1, Smad2/3, phosphorylated Smad2/3 levels were measured in rats. Results miR-145-5p was down-regulated, ETS2 was up-regulated and TGF-β1/Smad pathway was activated in LPS-suffered rats. Overexpression of miR-145-5p inactivated the TGF-β1/Smad pathway and attenuated ALI, as reflected by relived pathological damage, and decreased W/D ratio, apoptosis and inflammatory response. Oppositely, loss of miR-145-5p or enhancement of ETS2 worsened ALI and activated the TGF-β1/Smad pathway. Moreover, elevation of ETS2 decreased miR-145-5p-mediated protection against ALI. Conclusion Evidently, miR-145-5p negatively regulates ETS2 expression and inactivates TGF-β1/Smad pathway to ameliorate ALI in rats.

Multicellular organisms such as plants contain different types of cells with specialized functions. Analyzing the characteristics of each type of cells will reveal specific cell functions and enhance understanding of how an organism organizes and works. Due to the lack of a method to enrich the particular type of cells and the limited sensitivity and capability of mass spectrometry-based technologies, comprehensive analyses of the proteome in a single plant cell are still impossible. Here we report a high-sensitive and efficient cell-type-specific proteomic pipeline, combining simplified flow cytometry-based fluorescent cell-sorting for fluorescent protoplasts and an optimized nano-scale proteomics method, which allows us to identify more than 1,000 unique proteins from 500 guard cell protoplasts. By this method, we performed an in-depth, quantitative comparison between the proteomics of guard cells and mesophyll cells, and revealed that the enrichment of signal transduction-related proteins enables guard cells to respond to various environmental stimuli quickly. This method was also applied to profile the proteome of different cells in root tips of Arabidopsis and rice seedlings. Thus, this pipeline is applicable to various types of cells in plant or non-plant systems to acquire systemic knowledge of how cells work specifically and in highly organized multiple cell organisms.

Background Nucleic acid amplification (NAA) tests rapidly detect Mycobacterium tuberculosis complex directly from clinical specimens, providing valuable results for those evaluated for tuberculosis. Methods We analyzed characteristics of cases with NAA testing performed, compared cases with positive and negative NAA test results, and calculated turnaround time and time-to-treatment for all verified cases reported to the National Tuberculosis Surveillance System in the United States during 2011–2017. Results Among 67,082 verified tuberculosis cases with NAA testing information, 30,820 (45.9%) were reported as not having a NAA test performed; the proportion without NAA testing declined annually, from 60.5% in 2011 to 33.6% in 2017. Of 67,082 verified cases, 27,912 (41.6%) had positive, 8,215 (12.2%) had negative, and 135 (0.2%) had indeterminate NAA test results. Among the 33,937 cases with an acid-fast-bacilli–smear-positive result, 70.9% (24,093) had a NAA test performed; 38.0% (11,490) of the 30,244 with an acid-fast-bacilli–smear-negative result had a NAA test performed. Although sputum was the most common specimen type tested, 79.8% (7,023 of 8,804) of non-sputum specimen types had a positive NAA test result. Overall, 63.7% of cases with laboratory testing had NAA test results reported Conclusions Our analyses demonstrate increased NAA test utilization between 2011 and 2017. However, a large proportion of cases did not have a NAA test performed, reflecting challenges in broader uptake, suggesting an opportunity to expand use of this diagnostic methodology.

The role of angiotensin II (Ang II) in hypertension has been clarified, but recent studies show that aging-associated arterial changes and those with hypertension as well as atherosclerosis may have some common pathogenesis. This study aimed to clarify the effects of Ang II on endothelial senescence by establishing a replicative senescence model of human umbilical vein endothelial cells (HUVECs) in vitro. The population-doubling level (PDL) was calculated, PDL5 and PDL25 respectively referred to cells cultured for 2 days and 30 days. Compared with Ang II-treated young PDL5 cells, chronic stimulation of Ang II significantly promoted the senescence-associated β-galactosidase activity and expression of senescence-related genes p16 and p21, slowed down cell growth rate, and decreased expression of longevity-related genes sirtuin1 as well as telomerase activity in senescent PDL25 cells (all P 0.05). Moreover, expression of pro-inflammatory cytokines and adhesion molecules were up-regulated in Ang II-treated PDL25 cells (all P 0.05). Ang II-induced senescent progression and inflammation were attenuated by angiotensin receptor blocker valsartan. In young PDL5 cells, Ang II promoted the endothelial viability including cell proliferation, migration, angiogenesis and cell adhesion to monocytes; however, chronic stimulation of Ang II suppressed the cell viability, promoted cell adhesion and apoptosis in senescent PDL25 cells, which could be ameliorated by short-term valsartan, but long-term valsartan had no effects. In addition, Ang II-induced senescent features could be partly recovered if Ang II was stopped at PDL20. These findings suggested that chronic stimulation of Ang II can accelerate the endothelial senescence process which is implicated in aging-related atherosclerosis.

Background: Endothelial dysfunction contributes to the initiation of atherosclerosis, which has been associated with the long noncoding RNAs (lncRNAs). However, the role of lncRNAs in endothelial function remains largely unknown. This study aimed to investigate whether the differentiation antagonizing non-protein coding RNA 201 (DANCR201) regulated the endothelial function. Methods and Results: The whole transcriptome sequencing was conducted to identify differentially expressed lncRNAs in the peripheral blood from patients with coronary artery diseases who had coronary calcified plaques (n=10), vulnerable plaques (n=5), and control subjects without coronary plaques (n=10). The characteristics of plaques were determined by the coronary computed tomography angiography. The results showed that DANCR201 was significantly downregulated in patients with vulnerable plaques compared to those with calcified plaques and control subjects. The RNA fluorescence in situ hybridization showed that DANCR201 was localized in both cytoplasm and nuclei. Next, we assessed the role of DANCR201 in endothelial function. In the replicative aging model of human umbilical vein endothelial cells (HUVECs), DANCR201 was found to decrease in senescent passage 20 cells compared with young passage 3 cells. Furthermore, DANCR201 overexpression in HUVECs significantly repressed monocytes adhesion to endothelium, inhibited the expression of pro-inflammatory cytokines interleukin 1β, intercellular cell adhesion molecule 1, tumor necrosis factor α, and promoted the abilities of endothelial proliferation and migration, indicating that DANCR201 was a protective factor for endothelial function. Bioinformatics analysis of miRNA-lncRNA interactions indicated that DANCR201 contained a candidate binding sequence of miR-216a which had been reported to promote the endothelial dysfunction through NF-κB pathway. The luciferase assay further showed that DANCR201 specifically combined with miR-216a. Conclusions: Our data indicated that DANCR201 can improve endothelial function via sponging miR-216a, ultimately maintaining vascular normalization. DANCR201 maybe a potential therapeutic target for atherosclerotic plaque progression and instability.

N-terminal (Nt) acetylation (NTA) is an ample and irreversible cotranslational protein modification catalyzed by ribosome-associated Nt-acetyltransferases. NTA on specific proteins can act as a degradation signal (called an Ac/N-degron) for proteolysis in yeast and mammals. However, in plants, the biological relevance of NTA remains largely unexplored. In this study, we reveal that Arabidopsis (Arabidopsis thaliana) SIGMA FACTOR-BINDING PROTEIN1 (SIB1), a transcription coregulator and a positive regulator of salicylic acid-primed cell death, undergoes an absolute NTA on the initiator Met; Nt-acetyltransferase B (NatB) partly contributes to this modification. While NTA results in destabilization of certain target proteins, our genetic and biochemical analyses revealed that plant NatB-involved NTA instead renders SIB1 more stable. Given that the ubiquitin/proteasome system stimulates SIB1 degradation, it seems that the NTA-conferred stability ensures the timely expression of SIB1-dependent genes, mostly related to immune responses. Taking our findings together, here we report a noncanonical NTA-driven protein stabilization in land plants.

High sensitivity of biosensor is one of the most important factor to realize the accurate detection of biomarkers. To achieve this purpose, enhancing initial signal and amplifying the value of signal change are two main approaches. In this study, a novel signal-off photoelectrochemical (PEC) immunosensor for highly sensitive determination of insulin was developed upon dual inhibition effect of CuS-SiO 2 composites toward CdS sensitized carbon doped titanium dioxide (C-TiO 2 /CdS). Due to the doping of carbon and sensitization of CdS, C-TiO 2 /CdS sensitized structure was employed as ideal photoactive matrix, which provided stable and enhanced basal signal. To achieve the amplification of signal change value, CuS-SiO 2 composites were prepared and used as labels. On account of the competitively light harvesting and electron donors consuming by p-type semiconductor CuS, less light energy and electron donors arrived at the C-TiO 2 /CdS sensitized structure. Besides, the remarkable steric hindrance effect of CuS-SiO 2 labeled secondary antibodies (CuS-SiO 2 -Ab 2 ) conjugates obstructed the transfer of electrons and diffusion of the electron donors to the photoelectrode surface, leading to further decrease of photocurrent compared with the pure CuS nanoparticles. Greatly enhanced sensitivity is achieved due to the dual inhibition effect of CuS-SiO 2 composites on C-TiO 2 /CdS. Taking advantage of the synergy effect of C-TiO 2 /CdS sensitized structure and dual inhibition effect of CuS-SiO 2 -Ab 2 bioconjugates, the as-prepared immunosensor for insulin exhibited high sensitivity and good stability with a low detection limit of 0.03 pg mL −1 . Additionally, the strategy provided an efficient and simple approach for signal amplification and held great promise for other PEC immunoassay development.

BACKGROUND AND OBJECTIVES: Metabolomics is instrumental in identifying novel biomarkers of kidney function to aid in the prevention and management of CKD. However, data linking the metabolome to incident eGFR are sparse, particularly in Asian populations with different genetic backgrounds and environmental exposures. Therefore, we aimed to investigate the associations of amino acid and acylcarnitine profiles with change in eGFR in a Chinese cohort. DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS: This study included 1765 community-living Chinese adults aged 50–70 years with baseline eGFR≥60 ml/min per 1.73 m(2). At baseline, 22 amino acids and 34 acylcarnitines in plasma were quantified by gas or liquid chromatography coupled with mass spectrometry. Annual rate of change in eGFR was calculated, and incident eGFR decline was defined as eGFR

PURPOSE The objective of our study was to conduct a data mining analysis to identify potential adverse events (AEs) following MENACWY-D using the tree-temporal scan statistic in the Vaccine Safety Datalink population and demonstrate the feasibility of this method in a large distributed safety data setting. METHODS Traditional pharmacovigilance techniques used in vaccine safety are generally geared to detecting AEs based on pre-defined sets of conditions or diagnoses. Using a newly developed tree-temporal scan statistic data mining method, we performed a pilot study to evaluate the safety profile of the meningococcal conjugate vaccine Menactra® (MenACWY-D), screening thousands of potential AE diagnoses and diagnosis groupings. The study cohort included enrolled participants in the Vaccine Safety Datalink aged 11 to 18 years who had received MenACWY-D vaccination(s) between 2005 and 2014. The tree-temporal scan statistic was employed to identify statistical associations (signals) of AEs following MENACWY-D at a 0.05 level of significance, adjusted for multiple testing. RESULTS We detected signals for 2 groups of outcomes: diseases of the skin and subcutaneous tissue, fever, and urticaria. Both groups are known AEs following MENACWY-D vaccination. We also identified a statistical signal for pleurisy, but further examination suggested it was likely a false signal. No new MENACWY-D safety concerns were raised. CONCLUSIONS As a pilot study, we demonstrated that the tree-temporal scan statistic data mining method can be successfully applied to screen broadly for a wide range of vaccine-AE associations within a large health care data network.

Roux-en-Y Gastric bypass surgery (RYGB) is emerging as a powerful tool for treatment of obesity and may also cause remission of type 2 diabetes. However, the molecular mechanism of RYGB leading to diabetes remission independent of weight loss remains elusive. In this study, we profiled plasma metabolites and proteins of 10 normal glucose-tolerant obese (NO) and 9 diabetic obese (DO) patients before and 1-week, 3-months, 1-year after RYGB. 146 proteins and 128 metabolites from both NO and DO groups at all four stages were selected for further analysis. By analyzing a set of bi-molecular associations among the corresponding network of the subjects with our newly developed computational method, we defined the represented physiological states (called the edge-states that reflect the interactions among the bio-molecules), and the related molecular networks of NO and DO patients, respectively. The principal component analyses (PCA) revealed that the edge states of the post-RYGB NO subjects were significantly different from those of the post-RYGB DO patients. Particularly, the time-dependent changes of the molecular hub-networks differed between DO and NO groups after RYGB. In conclusion, by developing molecular network-based systems signatures, we for the first time reveal that RYGB generates a unique path for diabetes remission independent of weight loss., Highlights • Plasma proteomic and metabolomic datasets were collected with time-series mode in patients treated with RYGB. • Workflow to define the physiological states based on associations between biomolecules • Systems signatures reveal unique path for diabetes remission independent of weight loss.

A series of K 3 B 6 O 10 Br (KBB) polar crystals have been grown along , and seed directions by top seeded solution growth (TSSG) method. By optimizing the growth condition, transparent KBB crystal with the sizes of 52×29×25 mm 3 was successfully grown by using seed -orientation from KF–PbO flux. The full-width at half-maximum (FWHM) and optical homogeneity were measured as 0.0038° and 3.3×10 −5 from the rocking curve and optical interferometry measurements, respectively, indicating high optical quality of the as-grown crystals. The Verdet coefficient of KBB crystal was obtained as 5.3 rad T −1 m −1 at 635 nm by comparative method.

Lineage conversion by expression of lineage-specific transcription factors is a process of epigenetic remodeling that has low efficiency. The mechanism by which a cell resists lineage conversion is largely unknown. Using hepatic-specific transcription factors Foxa3, Hnf1α and Gata4 (3TF) to induce hepatic conversion in mouse fibroblasts, we showed that 3TF induced strong activation of the ATM-p53 pathway, which led to proliferation arrest and cell death, and it further prevented hepatic conversion. Notably, ATM activation, independent of DNA damage, responded to chromatin opening during hepatic conversion. By characterizing the early molecular events during hepatic conversion, we found that Baf60b, a member of the SWI/SNF chromatin remodeling complex, links chromatin opening to ATM activation by facilitating ATM recruitment to the open chromatin regions of a panel of hepatic gene loci. These findings shed light on cellular responses to lineage conversion by revealing a function of the ATM-p53 pathway in sensing chromatin opening.

Background Limited data are available describing the post-licensure safety of meningococcal vaccines, including Menveo®. We reviewed reports of adverse events (AEs) to the Vaccine Adverse Event Reporting System (VAERS) to assess safety in all age groups. Methods VAERS is a national spontaneous vaccine safety surveillance system co-administered by the Centers for Disease Control and Prevention and the US Food and Drug Administration. We searched the VAERS database for US reports of adverse events in persons who received Menveo from 1 January 2010 through 31 December 2015. We clinically reviewed reports and available medical records for serious AEs, selected pre-specified outcomes, and vaccination during pregnancy. We used empirical Bayesian data mining to identify AEs that were disproportionately reported after receipt of Menveo. Results During the study period, VAERS received 2614 US reports after receipt of Menveo. Of these, 67 were classified as serious, including 1 report of death. Adolescents (aged 11–18 years) accounted for 74% of reports. Most of the reported AEs were non-serious and described AEs consistent with data from pre-licensure studies. Anaphylaxis and syncope were the two most common events in the serious reports. We did not identify any new safety concerns after review of AEs that exceeded the data mining threshold, although we did observe disproportionate reporting for terms that were not associated with an adverse event (e.g., “incorrect drug dosage form administered”, “wrong technique in drug usage process”). Although reports were limited, we did not find any evidence for concern regarding the use of Menveo during pregnancy. Conclusions In our review of VAERS reports, findings of AEs were consistent with the data from pre-licensure studies. Vaccine providers should continue to emphasize and adhere to proper administration of the vaccine.

Ni-W/diamond composite coatings were prepared by electrodeposition from a Ni-W plating bath with diamond particles suspended into the bath. The effect of the plating parameters on microstructure and mechanical properties was investigated. The deposits reported a maximum hardness of 1207 ± 32 Hv. The film hardness is depended on the concentration of diamond particles in the plating bath and also on the size of the co-deposited diamond particles. The sample with diamond concentration of 10 g/L in the bath and co-deposited at current density of 0.15 A/cm2 reported the optimized wear resistance and diamond content in the deposit. In this paper the effect of the incorporation of diamond particles into the Ni-W matrix has been discussed in terms of the aforesaid operating conditions and particle size.