Three-dimensional sealing and disinfecting is a very difficult challenge in the canals affected by internal resorption. Hybrid irrigation is a method that takes advantage of both ultrasonic / sonic activations, which has previously proven effective in cleaning the root canals. Also, modern biological materials are suitable to seal these canals.

In this work, the new VIKOR methods are established using the generalized Pythagorean fuzzy soft sets (GPFSSs). For GPFSSs, the distance measures such as Hamming, Euclidean, and generalized are given. Further, the basic characteristics of these distance measures are examined. Fuzzy and soft sets are strong instruments for uncertainty. This strongness has been demonstrated by the GPFSS combining Pythagorean fuzzy sets and soft sets and applied to imprecise and ambiguous information. In this context, new remoteness index-based methods have been proposed, which are dissimilar from available VIKOR methods. The displaced and fixed ideals positive and negative Pythagorean fuzzy values (PFV) were defined. Thus, based on this definition, displaced positive ideal remoteness indices, negative ideal remoteness indices, and fixed positive ideal, negative ideal remoteness indices were discussed. Two different weights are used here: weights based on OF preference information and precise weights calculated with the expectation score function. The VIKOR method given here provides a different way from canonical VIKOR methods: rank candidate alternatives and determining a compromise solution based on different preference structures. The processes principles of the newly defined GPFSSs VIKOR methods are given by four algorithms. An example of these algorithms is given with the behavioral development and cognitive development of the children of Early Childhood children in the COVID-19 quarantine.

Derek R. Lovley1,2* Pier-Luc Tremblay3 Xinying Liu2,41Electrobiomaterials Institute, Key Laboratory for Anisotropy and Texture of Materials(Ministry of Education), Northeastern University, Shenyang 110819, China.2Department of Microbiology and Institute for Applied Life Sciences (IALS)University of Massachusetts, Amherst, MA, USA.3School of Chemistry, Chemical Engineering, and Life ScienceWuhan University of Technology, Wuhan 430070, China4College of Environmental Science and Engineering, Beijing Forestry University,Beijing 100083, China*Corresponding author: dlovley@umass.edu

Abstract Objective: To summarize the risk prediction models of chronic disease in Chinese medicine, describe their performance, and assess suitability of clinical or administrative use. Methods: The China National Knowledge Infrastructure and Wanfang Data were searched through February 2021, and hand searches were performed of the retrieved reference lists. Dual review was conducted to identify studies of prediction models of chronic disease in Chinese medicine. Results: From 399 citations reviewed, 17 studies were included in the analysis. Most of the studies were from single-centers (50%) or did not external validated (81.25%). The sample sizes were smaller and the models’ discrimination were larger compared with studies in fully western medicine. All the models used both laboratory findings and subjective judgements from doctors or patients. 9 models concentrated on diabetes mellitus or cardiovascular disease, and showed better performance and clinical application. Conclusions: The prediction models of chronic disease in Chinese medicine have unique advantages due to their considerations of doctors’ and patients’ subjective judgement. Diabetes mellitus and cardiovascular disease prediction models were in higher quality and clinical usability. Efforts to improve their quality are needed as use becomes more widespread.

A 72-year-old female used the oral phosphate binder lanthanum carbonate for 6 years, before discontinuing it after receiving a pancreas and kidney transplant. Now, 7 years after discontinuation, the patient developed bilious emesis. An upper gastrointestinal endoscopy showed an unspecific gastritis. Biopsies showed subepithelial crystalline deposits consistent with gastric lanthanosis.

IL-36 has been implicated in the pathogenesis of spondyloarthropathies (SpA) like psoriasis and inflammatory bowel disease. Enthesitis related arthritis (ERA) category of juvenile idiopathic arthritis is a form of juvenile SpA, however no data is available on the role of IL-36 in this disease. IL-36α, β, γ and IL-36R mRNA expression in blood and synovial fluid mononuclear cells and IL-36α, γ, IL-36Ra, IL-6 and IL-17 levels were measured in serum and synovial fluid (SF). IL-36γ production by fibroblast like synoviocytes (FLS) by pro-inflammatory cytokines and its effect on FLS was also studied.mRNA levels of IL-36α, IL-36γ and IL-36R were increased in PBMCs of ERA patients as compared to healthy controls however only IL-36γ was measurable in serum of one third of patients. In SFMCs, all 4 mRNA were detectable but were lower than RA patients. SF IL-36γ levels correlated with disease activity score (r=0.51, p< 0.0001), SF IL-6 (r=0.4,p= 0.0063) and IL-17 levels (r=0.57,p=0.0018). Pro-inflammatory cytokines increased expression of IL-36γ and IL-6 in FLS cultures. SFs from 5 ERA patients also increased expressions of IL-36γ and IL-6 in FLS which could be blocked by using IL-36Ra.This suggests that pro-inflammatory cytokines aid in upregulation of IL-36γ which in turn upregulates expression of IL-6. This might lead to a positive feedback loop of inflammation in ERA. Association of SF levels of IL-36γ with disease activity further supports this possibility. IL-36Ra based therapy may have a role in ERA.

We previously showed increased steroid resistant CD28null CD8+ senescent lymphocyte subsets in peripheral blood from COPD patients. These cells expressed decreased levels of the glucocorticoid receptor (GCR), suggesting their contribution to the steroid resistant property of these cells. COPD is a disease of the small airways. We therefore hypothesized that there would be a further increase in these steroid resistant lymphocytes in the lung, particularly in the small airways. We further hypothesized that the pro-inflammatory/cytotoxic potential of these cells could be negated using prednisolone with low-dose cyclosporin A.Blood, bronchoalveolar lavage, large proximal and small distal airway brushings were collected from 11 COPD patients and 10 healthy aged-matched controls. The cytotoxic mediator granzyme b, pro-inflammatory cytokines IFNγ/TNFα, and GCR were determined in lymphocytes subsets before and after their exposure to 1µM prednisolone and/or 2.5ng/mL cyclosporin A.Particularly in the small airways, COPD subjects showed an increased percentage of CD28null CD8 T-cells and NKT-like cells, with increased expression of granzyme b, IFNγ and TNFα and a loss of GCR, compared with controls. Significant negative correlations between small airway GCR expression and IFNγ/TNFα production by T and NKT-like cells (eg, T-cell IFNγ R= -.834, p=.031) and with FEV1 (R= -890) were shown. Cyclosporine A and prednisolone synergistically increased GCR expression and inhibited pro-inflammatory cytokine production by CD28null CD8- T and NKT-like cells.COPD is associated with increased pro-inflammatory CD28null CD8+ T and NKT-like cells in the small airways. Treatments that increase GCR in these lymphocyte subsets may improve morbidity in COPD patients.

IntroductionDyslipidemia is one of the main modifiable risk factors for the development of cardiovascular diseases (CVD), being the ischemic heart disease the leading cause of mortality in the world. Every year, more people die from CVD than from any other reason, according to data from the World Health Organization, it is estimated that 17.9 million people died from this cause in 2019, which represents 32% of all registered deaths in the world . In addition to high blood pressure, diabetes, obesity, and smoking, dyslipidemia is one of the main cardiovascular risk factors. The latter it is defined as disorders in blood lipids characterized by an increase in cholesterol and/or triglyceride levels called hypercholesterolemia and triglyceridemia, respectively .While most of the triglyceride and cholesterol content is obtained from dietary sources, de novo lipogenesis contributes significantly to serum lipid content in people who have a high-carbohydrate diet. The metabolic pathways by which the macromolecules obtained through the diet are processed, such as glycolysis, Krebs cycle, oxidative phosphorylation, beta oxidation, among others, have as their main function the generation of energy, and an imbalance in these can promote pathological processes, such as dyslipidemia . These metabolic pathways not only provide energy for cellular homeostasis, but also control immune cell functions. Immune cells at rest, use processes such as Krebs cycle and oxidative phosphorylation for ATP generation, but cells with pro-inflammatory phenotype such as M1 macrophages and activated T lymphocytes tend to change to aerobic glycolysis, while M2 macrophages and regulatory T lymphocytes induced in the periphery continue with oxidative phosphorylation. Reprogramming of the metabolic state of immune cells influences the generation of epigenetic changes which lead to functional changes. This cellular metabolic state is affected by systemic metabolism, either by nutrients availability or by signalling pathways induced by each metabolite . These concepts are the basis of innate immunological memory, this phenomenon, also called immune training, is defined by metabolic changes originated after priming with pathogens or sterile stimuli that lead to sustained functional changes orchestrated mainly by epigenetic reprogramming, which are sustained changes in gene expression and cellular physiology, which does not imply permanent changes .An immune cell type that attracts more attention in the immunometabolism area is the macrophages population. Macrophages are phagocytic cells of innate immunity with a broad functional spectrum, from pro-inflammatory to anti-inflammatory phenotypes representing the extremes. Monocytes, cells that develop from bone marrow precursors, travel in bloodstream for a few days, then they migrate to tissue and become macrophages with different phenotypes . Tissue-resident macrophages are long-lived cells derived mostly from erythro-myeloid progenitors that emerge from the yolk sac . The first to emerge are the primitive macrophages, which are not derived from monocytes and seed every tissue. When erythro-myeloid progenitors seed the fetal liver, they generate fetal monocytes that differentiate into macrophages, and represent the most abundant tissue-resident macrophage population . Furthermore, monocytes derived from hematopoietic stem cells emerge from the fetal liver and differentiate into long-lived macrophages, while adult hematopoiesis begins in the bone marrow. Bone marrow -derived monocytes contribute to the different populations of postnatal tissue resident macrophages .Monocytes/ macrophages are recognized because their important roles in regulating homeostasis and immune defense through their inflammatory or tissue repair properties . The importance of metabolism in immune cells for the programming of macrophages with their different functional spectra suggests that metabolic pathways may play a role for long-term functional changes in monocytes and macrophages during immune training . The role of these cells is widely described in obesity, being the main population present in the adipose tissue stromal vascular fraction, where there is an increase in the proliferation of macrophages coupled with the recruitment of circulating monocytes to this tissue. Due to the production of cytokines such as IL-1β, IL-6 and TNF-α, M1 macrophages participate in the low-grade chronic inflammation that characterizes obesity .In past years, it has been shown that when treating monocyte derived macrophages with high concentrations of insulin, glucose and palmitate, characteristic of metabolic syndrome, a different pro-inflammatory phenotype is induced. These cells present surface markers and transcription factors different from classical macrophages and were called metabolically activated macrophages (MMe) . MMe present surface molecules such as CD36, which binds to long chain fatty acids and facilitates their transport in the cell, participating in the use of lipids in muscle, storage of adipose energy and absorption of intestinal fat ; ABCA1 is a cholesterol efflux pump in the elimination pathway of cellular lipids that are then collected by apoA-I, forming high-density lipoproteins (HDL) ; and PLIN2, which is a protein expressed on the lipid droplet membrane . These MMe have been described in metabolic syndrome and have been found in adipose tissue during obesity, performing beneficial and detrimental functions during diet-induced obesity in mice , and in mammary adipose tissue promoting tumorigenesis during obesity . MMe produce pro-inflammatory cytokines, although in a lesser extent than classic M1 macrophages. The expression of their characteristic surface markers, as well as the attenuated inflammatory response, is mainly mediated by the transcription factor PPAR-γ , that could be contributing to the chronic low-grade inflammatory state present in metabolic syndrome and obesity.Due to dietary overload, the metabolites produced by the different metabolic pathways can be used for alternative pathways in organs and tissues, such as adipose tissue, modifying and defining systemic metabolic responses It is not completely clear whether the change from a healthy systemic metabolic state to a pathological one, such as the dyslipidemic state, lead to changes causing immune training influencing polarization to different cell types.The aim of this study was to evaluate if high cholesterol and triglycerides levels, main feature of dyslipidemia, are promoting immune training in peripheral blood cells, functioning as a first stimulus, conditioning monocytes to present a metabolic phenotype and leading them to polarization into metabolically activated macrophages. We found that monocytes with metabolic phenotype expressing CD36, ABCA1 and PLIN2, are present in systemic circulation. In vitro stimulation showed that MMe from patients with dyslipidemia, play a dynamic role with production of pro- and anti-inflammatory cytokines.

IntroductionKawasaki disease (KD) , also known as Kawasaki syndrome, is an acute, self-limited febrile vasculitis that predominantly affects infants and children under 5 years of age [1]. KD is characterized by high spiking fever persisting for more than 5 days, erythematous rash, bilateral conjunctivitis, congestive oral mucosa, swelling lymph node, and edematous extremity [2]. Furthermore, KD is the most common cause of acquired cardiac disease, especially coronary artery aneurysms in children [3]. Although KD has been studied for almost half a century, the pathogenic mechanism of KD remains unclear. Furthermore, while most patients respond well to intravenous immunoglobulin (IVIG), roughly one-quarter of the children meeting clinical criteria will go on to have coronary artery inflammation, including aneurysms [4]. Hence, further illustration of the mechanism of KD is a crying need to find a therapeutic for KD treatment clinically.Both innate and adaptive immune systems are involved in the pathogenesis of KD [5]. The early event of visualized immunological abnormality is the activation of innate immune system represented as the elevated numbers of activated monocytes and increased expression of circulating cytokines, such as interleukin (IL)-6 and tumor necrosis factor (TNF) -α [6]. Subsequently, it is generally believed that autoreactive T cell and their inflammatory cytokines play a major role in the development of KD [7]. T helper (Th) 17 cells, a recently identified lineage of CD4+ Th cells, predominantly produce IL-17A. Th17 cell and IL-17A have been shown to participate in host defense responses and inflammatory diseases, such as systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), Graves’ disease (GD), and Crohn’s disease (CD) [8-11]. A recent study has shown that a high frequency of Th17 cells and high levels of IL-17 were demonstrated in the acute stage of KD, and that elevated Th17 cells might be associated with tissue damage and coronary artery aneurysm formation [7, 12]. However, there is little information about whether higher frequency of Th17 and higher concentrations of IL-17A also exist in Chinese patients with KD and how Th17 responses are associated with the development of coronary artery aneurysm in KD patients.More notably, a newly identified T-cell subset, termed Th22 cells, has been described as expressing their key cytokines interleukin (IL)-22, which can activate signal transduction and transcription 3 (STAT3) [13]. IL-22, originally termed as an IL-10-related T-cell-derived-inducible factor, enhance innate immunity and promote epithelial cell proliferation and tissue. In contrast, IL-22 also act as regulator in the pathogenesis of RA and SLE [14-15]. Furthermore, recent studies have reported that IL-22 may function as a biphasic cytokine: protective and regenerative in steady state while amplifying proinflammatory signals given by TNF-α [16], which is necessary for exacerbation of vascular injury in KD. However, little is known about the role of Th22 cells in the pathogenesis of KD. We believe that Th22 cells may partially contribute to the formation of coronary aneurysms.Here, in the current study, we sought to further clarify the mechanism underlying hyperactivation of Th22 and Th17 during acute KD. We characterized the numbers of circulating Th22 and Th17 cells by flow cytometry, and measured the concentration of serum inflammatory cytokines by enzymelinked immunosorbent assay (ELISA) in 43 Chinese patients with new onset KD. Furthermore, we analyzed the potential association of the numbers of Th22 and Th17 cells with the clinical measures in these KD patients. Our findings indicated that increased numbers of Th22 and Th17 cells might be contributed to the pathogenesis of KD in Chinese patients.

Xiaoling Zhou1, Xiaoyuan Wang1, Yanzheng Gu2, Lan Chen3 , Yueping Shen4, Jingluan Tian1, Mingyuan Wang5, Shujun Chen1, Xiaoyu Duan1, Hanqing Gao1, Xiaopei Ji1, Qi Fang1,2, Xueguang Zhang2,3, Qun Xue*1,21. Department of Neurology, First Affiliated Hospital of Soochow University, Suzhou, Jiangsu, 215006, China.2. Institute of Clinical Immunology, Jiangsu Key Laboratory of Clinical Immunology, First Affiliated Hospital of Soochow University, Suzhou, Jiangsu, 215006, China.3. Department of Neurology, Nantong First People’s Hospital, Nantong, Jiangsu, 226000, China.4. Department of Epidemiology and Health Statistics, Soochow University, Suzhou, Jiangsu, 215006, China.5. Suzhou Red Cross Central Blood Station, Suzhou, Jiangsu, 215006, China.*Correspondence Author: Qun Xue (email: qxue_sz@163. com)

To date, the mechanism of systemic lupus erythematosus (SLE) has not been thoroughly deciphered. Recent research demonstrated that CD138+ T cells accumulate in an SLE murine model, indicating that they are autoreactive T cells that significantly promote autoantibody production. Double negative (DN) T cells have been demonstrated to participate in the progression of SLE, but their detailed mechanism and the role in SLE remain unclear. Importantly, the expression of CD138 in CD3+ T cells plays a key role in the progression of lupus; it causes the accumulation of autoreactive T cells, including DN T cells, by significantly preventing their apoptosis. T helper 1 cells and interferon gamma both prevail in SLE; they may play essential roles in building the inflammatory condition of SLE. Defects occur in regulatory B (Breg) cells during their expansion in SLE, resulting in more differentiation of activated B cells into plasma cells; this subsequently increases antibody production. Myeloid-derived suppressor cells (MDSCs) enhance the expansion of Breg cells. However, the sustained increase of cytokine levels in SLE promotes the differentiation of more MDSCs into macrophage and dendritic cells, resulting in the defective expansion of MDSCs. The defective expansion of Breg cells and MDSCs breaks the immune-tolerance milieu in SLE, resulting in increased autoantibody secretion from those abnormal plasma cells. This review discusses recent advances regarding the detailed roles and mechanisms of these immunocytes in SLE.

ACE-2 receptor plays a vital role not only in the SARS-CoV-induced epidemic but also in some diseases. Studies have been carried out on the interactions of ACE-2- SARS-CoV proteins. However, comprehensive research has not been conducted on ACE2 protein by using bioinformatic tools. The present study especially two places, G104 and L108 points, which are effective in protecting the structure of the ACE-2 protein, play a critical role in the biological functioning of this protein, and play an essential role in determining the chemical-physical properties of this protein, and play a crucial role for ACE-2 protein-SARS CoV surface glycoprotein, were determined. It was also found that the G104 and L108 regions were more prone to possible mutations or deletions than the other ACE-2 protein regions. Moreover, it was determined that all possible mutations or deletions in these regions affect the chemical-physical properties, biological functions, and structure of the ACE-2 protein. Having a negative GRAVY value, one transmembrane helix, a significant molecular weight, a long-estimated half-life as well as most having unstable are results of G104 and L108 points mutations or deletions. Finally, it was determined that LQQNGSSVLS, which belong to the ACE-2 protein, may play an active role in binding the spike protein of SARS-CoV. All possible docking score results were estimated. It is thought that this study will bring a different perspective to ACE-2 _SARS-CoV interaction and other diseases in which ACE-2 plays an important role and will also be an essential resource for studies on ACE-2 protein.

Tumor-infiltrating lymphocyte (TIL) therapy has been clinically proved as a promising therapeutic approach for patients with solid tumor. TIL therapy could effectively control tumor growth in cervical cancer as indicated by a phase 2 pivotal trial with an objective response rate of 44.4%. Vulvar cancer is believed to share a similar biological and immunological phenotype with cervical cancer. However, the therapeutic potential of TIL in vulvar cancer remains to be explored. In this study, we described a manufacturing procedure that can expand clinical-scale TILs from both vulvar cancer and cervical cancer with a high success rate. Characterization of the phenotype of TIL populations showed that TILs from vulvar cancer are prone to maintaining a higher percentage of progenitor-like phenotype and have stronger tumor-killing capacity compared to TILs from cervical cancer. TCR clonality analysis indicated that all TIL samples have more enriched TCR clones than PBMC, which might be expanded during anti-tumor responses and tend to be patient specific. Thus, our study provides a feasible method of TIL preparation from and a potential new therapeutic strategy for vulvar cancer patients.

Thyroid function tests (TFTs’) are one of the most common tests requested. Interpretation of most TFTs’ are straight forward. TFTs’ can be confusing in an important subgroup of patients. We present such a case in a previously healthy individual.

Objective The aim of this project was to identify gaps and research waste in the dissemination of fertility evidence in the Cochrane database of systematic reviews (CDSR). Design A research article. Setting The Cochrane Gynaecology and Fertility (CGF) Group’s specialised register of random controlled trials (RCTs). Sample Infertility trials contained in the CGF specialised register, published between the years 2010-2011. Methods Infertility trials from the CGF specialised register were matched, by the specific fertility issue and treatment, to existing Cochrane reviews. Unmatched trials were categorised to develop and prioritise new review topics. Main outcome measures Proportions Results 564 trials, published from 2010 to 2011, were exported from the specialised register and after removing duplicates, 318 trials were found to be already included in a Cochrane review. 187 (37%) of trials were found to be unused, however 115 (23%) of these could be included in an existing CGF SR, if it were updated. 72 trials (14%) were not matched to any review topic and from these, eight new Cochrane review titles were developed. The topic with the largest number of associated ‘unused’ trials, was ‘Traditional Chinese Medicine for women undergoing assisted reproductive techniques’. Conclusions This project was used to consider unused trials, prioritise new review topics and identify those reviews that need to be updated, thereby identifying the gaps in evidence for couples with fertility problems. Keywords research waste, gaps, fertility, infertility, randomized controlled trials, systematic reviews, prioritisation.

G protein-coupled receptors modulate a plethora of physiological processes and mediate the effects of one-third of FDA-approved drugs. Notably, depending on which ligand has activated a particular receptor, it can engage different intracellular transducers. This paradigm of ligand-dependent ‘biased signaling’ dictates a need to advance beyond the level of receptors to consider the combined ligand-receptor pair in order to understand physiological signaling. Bias signaling also has the potential to improve medicines by reducing adverse effects. However, this is challenged by inconsistent interpretation of results and lack of commonly agreed guidelines. Here, we present recommended terminology and guidelines to conduct, report and quantify bias in a comparable and reproducible fashion. We expect these recommendations will facilitate a common understanding of experiments and findings across basic receptor research and drug discovery, while the area and the analytical methods to measure bias are still evolving, especially in complex cellular, tissue and organismal systems.

A document by sumit saurabh, written on Authorea.

Structural variations (SVs) have been associated with genetic diversity and adaptation in diverse taxa. Despite these observations, it is not yet clear what their relative importance is for microevolution, especially with respect to known drivers of diversity, e.g., nucleotide substitutions, in rapidly adapting species. Here we examine the significance of SVs in pesticide resistance evolution of the agricultural super-pest, the Colorado potato beetle, Leptinotarsa decemlineata. By employing a trio-binning procedure, we develop near chromosomal reference genomes to characterize structural variation within this species. These updated assemblies represent >100-fold improvement of contiguity and include derived pest and ancestral non-pest individuals. We identify >200,000 SVs, which appear to be non-randomly distributed across the genome as they co-occur with transposable elements. SVs intersect exons for genes associated with insecticide resistance, development, and transcription, most notably cytochrome P450 (CYP) genes. To understand the role that SVs might play in adaptation, we incorporate an additional 66 genomes among pest and non-pest populations of North America into the SV graph. Single nucleotide polymorphisms (SNPs) and SVs have a similar proportion in coding and non-coding regions of the genome, but there is a deficit of SNPs in SVs, suggesting SVs may be under selection. Using multiple lines of evidence, we identify 28 positively selected genes that include 337 SVs and 442 outlier SNPs. Among these, there are four associated with insecticide resistance. Two of these genes (CYP4g15 and glycosyltransferase-13) are physically linked by a structural variant and have previously been shown to be co-induced during insecticide exposure.

Stent migration due to haemodynamic drag remains the primary cause of type I endoleak, potentially leading to aneurysm rupture. The prevalence of migration and endoleak can be partially attributed to deficiencies in stent-graft radial spring design and a lack in understanding of the mechanical properties of endovascular stents. A converged finite element model of a custom radial extensometer was developed, fit, and validated using experimental results for bare stent wire (”uncovered”) with outer diameter of 12 mm stent. During stent constriction to 50 % of the original cross- sectional area, a comparison of experimental and modeled results produced an r2 value of 0.946, a standard error of 0.099 N, and a mean percent error of 1.69 %. This validated finite element model can be used to analyze the mechanisms responsible for radial force generation in 316L stainless steel self-expanding endovascular stents, as well as to evaluate new stent designs.

INTRODUCTIONPreoperative administration of dual antiplatelet therapy (DAPT) in patients undergoing urgent coronary artery bypass grafting (CABG) surgery remains controversial. DAPT including aspirin and a P2Y12-inhibitor is most administered before urgent CABG in the setting of acute coronary syndrome (ACS) in accordance with the current guidelines [1]. Although preoperative P2Y12-inhibitor treatment is associated with reduced occurrence of ischemic events, there is a clear evidence that it can increase the risk of surgery-related bleeding, especially in the case of the third-generation thienopyridines such as prasugrel [2]. Current guidelines recommend a discontinuation of prasugrel a minimum of 7 days before non-emergent cardiac surgery to allow the recovery of platelet function and attenuate the risk of perioperative bleeding [1].However, these recommendations do not account for highly variable recovery of platelet reactivity following discontinuation of P2Y12-inhibitor [3]. Prasugrel is an inactive prodrug that is transformed into its active metabolite with a half-life of 7 hours and results in a faster, more consistent platelet inhibition, when compared to clopidogrel [1,2,4]. Preoperative point-of-care (POC) platelet function testing (PFT) in patients receiving prasugrel could be helpful to measure platelet reactivity and predict the risk of perioperative bleeding and transfusion requirements [5-8]. We presented a rare case of unexpected complete platelet function recovery in a patient with ACS treated with prasugrel and revealed by preoperative platelet function monitoring with thromboelastography (TEG) platelet mapping before urgent surgical coronary revascularization.

Diversity-stability relationships in grasslands depend on the environment. Climate change and soil degradation potentially alter soil pH and community stability within grassland environments, although it remains unclear how soil acidity and alkalinity affect diversity-stability relationships. We conducted a three-year experiment of acidification and alkalization treatments in an arid grassland in northern China, and found that increasing and decreasing soil pH reduced community species richness, community diversity, community and dominant species asynchrony, and biomass stability. Soil acidification reduced community stability by reducing dominant species stability. Soil alkalization reduced community stability by reducing species asynchrony and dominant species stability. Acidification significantly enhanced the availabilities of soil NO3—N, P, and K, but did not affect the concentrations of soil total C, N, and P. By contrast, alkalization significantly reduced soil total C and N, but did not affect the availabilities of soil N, P, and K. Structural equation model analysis revealed that altered soil pH affected soil nutrients associated with species asynchrony and community stability, which indicated the importance of soil nutrients in driving community stability. Our results suggest that soil pH–mediated community stability is mainly driven by dominant species stability rather than diversity. This study provides novel insights indicating that arid grassland stability would be weakened under changing soil pH, subsequently leading to land degradation and reducing long‐term productivity and sustainability.

Zeinab Mohseni Afshar1, Mohammad Barary2, Babak Sayad1, Soheil Ebrahimpour3, Terence T. Sio4, Mark J. M. Sullman5,6, Kristin Carson-Chahhoud7, Arefeh Babazadeh3, *1- Clinical Research Development Center, Imam Reza Hospital, Kermanshah University of Medical Sciences, Kermanshah, Iran.2- Student Research Committee, Babol University of Medical Sciences, Babol, Iran3- Infectious Diseases and Tropical Medicine Research Center, Health Research Institute, Babol University of Medical Sciences, Babol, Iran.4- Department of Radiation Oncology, Mayo Clinic, Phoenix, Arizona, USA5- Department of Social Sciences, University of Nicosia, Nicosia, Cyprus6- Department of Life and Health Sciences, University of Nicosia, Nicosia, Cyprus7- Australian Centre for Precision Health, University of South Australia, Adelaide, AustraliaCorrespondence: Arefeh Babazadeh, Infectious Diseases and Tropical Medicine Research Center, Health Research Institute, Babol University of Medical Sciences, Babol, Iran. Tel: +989113133397, Fax: +98-1132207918, Email: drbabazadeh.a@yahoo.com

Recently, only two splice-site mutations of the UBE2A gene have been observed in patients with X-linked ID type Nascimento (XLID). We found a novel splice site mutation in UBE2A (c.241+1 G>A) and novel clinical appearances, including a typical four-finger line and erected head unstable.

Cutis Vertcis gyrata is an uncommon neurocutaneous syndrome characterized by excessive growth of the skin of the scalp or the face, forming folds of similar aspect to cerebral cortex gyri. Three categories have been individualized: the primary form, essential or non-essential, and the secondary form.