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Background A distinctive metabolic phenotype provides the opportunity to discover noninvasive biomarkers for the diagnosis of Crohn’s disease (CD) and for differentiating it from other intestinal inflammatory diseases. The study sought to identify new biomarkers for CD diagnosis. Methods Serum metabolites from 68 newly diagnosed and treatment-naïve patients with CD and 56 healthy control (HC) subjects were profiled using targeted liquid chromatography-mass spectrometry. Five metabolic biomarkers were identified to distinguish patients with CD from the HC subjects and validated in a separate cohort consisting of 110 patients with CD and 90 HC subjects using a combination of univariate analysis, orthogonal partial least-squares discriminant analysis, and receiver-operating characteristic curve analysis. Differences in the 5 metabolites were evaluated among patients with CD and patients with ulcerative colitis (n = 62), intestinal tuberculosis (n = 48), and Behçet’s disease (n = 31). Results Among the 185 quantified metabolites, a panel of 5 (pyruvate, phenylacetylglutamine, isolithocholic acid, taurodeoxycholic acid, and glycolithocholic acid) were found to distinguish patients with CD with high accuracy from HC subjects, with an area under the curve of 0.861 (P Conclusions The combination of 5 serum metabolite biomarkers for the diagnosis of CD has the potential to provide an accurate, noninvasive, and inexpensive alternative to conventional tests and might be valuable for the differentiation from other diagnostically challenging intestinal inflammatory diseases.

The intestinal epithelial barrier facilitates homeostatic host-microbiota interactions and immunological tolerance. However, mechanistic dissections of barrier dynamics following luminal stimulation pose a substantial challenge. Here, we describe anex-vivointestinal permeability assay, X-IPA, for quantitative analysis of gut permeability dynamics at the whole-tissue level. We demonstrate that specific gut microbes and metabolites induce rapid, dose-dependent increases to gut permeability, thus providing a powerful approach for precise investigation of barrier functions.

Background: Previous studies indicated that excessive engagement in digital devices could lead to negative psychological impacts in general population. The present study aimed to determine the effects of electronic screen exposure on depression among women in early pregnancy. Methods:A cross-sectional study was conducted from June 2021 to June 2022. A total of 665 women in early pregnancy were recruited and the information included socio-demographic characteristics, screen exposure and Patient Health Questionnaire -9 depression scale. Results: Among the women in early pregnancy, the total daily smartphone viewing time was the longest (median [P25-P75], 5 [3-6] hours/day) in the three types of electronic screen exposure. The total daily smartphone viewing time (Z=-2.239, P=0.025), smartphone (Z=-2.494, P=0.013) and television viewing time (Z=-2.640, P=0.008) before nocturnal sleep were significantly associated with depression among women in early pregnancy. The thresholds calculated by receiver operator characteristic curves were 7.5 hours/day, 1.5 hours/day and 1.5 hours/day, respectively. In addition, women with higher scores of smartphone addiction were more susceptible to depression (Z=-6.201, P＜0.001). The top three smartphone usages in women with depression were watching videos (22.0%), listening to music (20.9%) and playing games (16.7%). Conclusions:In conclusion, electronic screen exposure, including screen viewing time, smartphone addiction and problematic smartphone use was associated with depression among women in early pregnancy. Further studies are warranted to verify the conclusions.

In this review, we summarize recent understandings on the assembly, activation and regulation patterns of the NLRP6 inflammasome, as well as its diverse impacts on tissue homeostasis and disease in multiple organs., Summary The NOD‐like receptor family pyrin domain containing 6 (NLRP6), a member of the NOD‐like receptor (NLR) family, acts as a cytosolic innate immune sensor that recognizes microbe‐associated molecular patterns. In some circumstances upon activation, NLRP6 recruits the adaptor apoptosis‐associated speck‐like protein (ASC) and the inflammatory caspase‐1 or caspase‐11 to form an inflammasome, which mediates the maturation and secretion of the pro‐inflammatory cytokines IL‐18 and IL‐1β. In other contexts, NLRP6 can exert its function in an inflammasome‐independent manner. Tight regulation of the NLRP6 inflammasome is critical in maintaining tissue homeostasis, while improper inflammasome activation may contribute to the development of multiple diseases. In intestinal epithelial cells, the NLRP6 inflammasome is suggested to play a role in regulating gut microbiome composition, goblet cell function and related susceptibility to gastrointestinal inflammatory, infectious and neoplastic diseases. Additionally, NLRP6 may regulate extra‐intestinal diseases. In this review, we summarize current knowledge on the NLRP6 inflammasome and its activation and regulation patterns, as well as its effector functions contributing to disease modulation. We discuss current challenges in NLRP6 research and future prospects in harnessing its function into potential human interventions.

Background The NOD-like receptors (NLR) are important family members of the intracellular pathogen recognition receptors, which recognise pathogen- or danger-associated molecular patterns in the cell. The NLR signalling pathways are increasingly recognised to play critical roles in the pathogenesis of inflammatory bowel diseases. We have identified an NLR member, Nlrp9b, whose expression is restricted to the epithelium of the gastrointestinal tract. However, the role of Nlrp9b in regulating intestinal inflammation and the underlying mechanism remains to be clarified. Methods We generated constitutive Nlrp9b-deficient (Nlrp9b−/−) mice to study the function of Nlrp9b. We induced experimental colonic inflammation by using dextran sulphate sodium (DSS). Bone marrow transfer experiments were conducted to clarify the cell type in which Nlrp9b exerts its function. We then performed RNA-sequencing of intestinal tissues from Nlrp9b−/− mice and WT controls to investigate the potential mechanisms. Results Nlrp9b−/− mice were more susceptible to DSS-induced colitis compared with cohousing wild-type (WT) mice, manifesting as exacerbated weight loss, more severe inflammation in colonoscopy and histopathology. Non-haematopoietic expression of Nlrp9b was responsible for protection against intestinal inflammation. Inflammasome activation was not impaired in Nlrp9b−/− mice, as we detected no defects in both cleavage of caspase 1 and secretion of IL18 in Nlrp9b−/− mice. Through RNA sequencing, we identified 300 differentially expressed genes in the intestinal tissue between Nlrp9b−/− and the co-housed WT controls, which primarily belongs to pathways involved in intestinal IgA production, as well as antigen processing and presentation. Indeed, IgA levels were globally reduced in Nlrp9b−/− mice, on the levels of mRNA expression, secreted antibodies measured in the intestinal lumen, and serum IgA. Furthermore, the total numbers of immune cells in the Peyer's patches were significantly reduced in Nlrp9b−/− mice, including leukocytes, B cells and B cells in the germinal centres, where they class switch to IgA producing cells. Conclusions Nlrp9b functions in the non-haematopoietic compartments of intestine and is protective against experimental intestinal inflammation, through potential mechanisms involving intestinal IgA production.

Conceptual scientific and medical advances have led to a recent realization that there may be no single, one-size-fits-all diet and that differential human responses to dietary inputs may rather be driven by unique and quantifiable host and microbiome features. Integration of these person-specific host and microbiome readouts into actionable modules may complement traditional food measurement approaches in devising diets that are of benefit to the individual. Although many host-derived factors are hardwired and difficult to modulate, the microbiome may be more readily reshaped by environmental factors such as dietary exposures and is increasingly recognized to potentially impact human physiology by participating in digestion, the absorption of nutrients, shaping of the mucosal immune response and the synthesis or modulation of a plethora of potentially bioactive compounds. Thus, diet-induced microbiota alterations may be harnessed in order to induce changes in host physiology, including disease development and progression. However, major limitations in ‘big-data’ processing and analysis still limit our interpretive and translational capabilities concerning these person-specific host, microbiome and diet interactions. In this Review, we describe the latest advances in understanding diet–microbiota interactions, the individuality of gut microbiota composition and how this knowledge could be harnessed for personalized nutrition strategies to improve human health. In this Review, Kolodziejczyk, Zheng and Elinav describe the latest advances in understanding diet–microbiota interactions, the individuality of gut microbiota composition and how this knowledge could be harnessed for personalized nutrition strategies to improve human health.

Human gut commensals are increasingly suggested to impact non-communicable diseases, such as inflammatory bowel diseases (IBD), yet their targeted suppression remains a daunting unmet challenge. In four geographically distinct IBD cohorts (n = 537), we identify a clade of Klebsiella pneumoniae (Kp) strains, featuring a unique antibiotics resistance and mobilome signature, to be strongly associated with disease exacerbation and severity. Transfer of clinical IBD-associated Kp strains into colitis-prone, germ-free, and colonized mice enhances intestinal inflammation. Stepwise generation of a lytic five-phage combination, targeting sensitive and resistant IBD-associated Kp clade members through distinct mechanisms, enables effective Kp suppression in colitis-prone mice, driving an attenuated inflammation and disease severity. Proof-of-concept assessment of Kp-targeting phages in an artificial human gut and in healthy volunteers demonstrates gastric acid-dependent phage resilience, safety, and viability in the lower gut. Collectively, we demonstrate the feasibility of orally administered combination phage therapy in avoiding resistance, while effectively inhibiting non-communicable disease-contributing pathobionts.

Background: The occupancy of healthcare resources by the COVID-19 outbreak had led to the unmet health needs of non-COVID-19 diseases. We aimed to explore whether the social media information could help surveil and understand the characteristics of unmet non-COVID-19 health needs during the COVID-19 outbreak in Wuhan city. Methods: This was an observational study based on social media data. The study period was set during the 3 months of the COVID-19 outbreak. Non-COVID-19 urgent and emergent health needs in Wuhan city were derived from Sina Weibo-one of China's largest social media platforms. Lag Spearman correlation was used to investigate the epidemiological relationship between the COVID-19 outbreak and non-COVID-19 health needs. Patient's primary diseases and needed care were annotated and categorized according to the International Classification of Diseases 11th Revision. The delay time in seeking help was calculated and compared. Results: After screening 114,795 Weibo posts, a total of 229 patients with non-COVID-19 health needs were included in our study. There were significant correlations between the daily number of COVID-19 cases at a 10-day lag, deaths at a 5-day lag, and non-COVID-19 Weibo. The actual number of non-COVID-19 patients with urgent and emergent health needs was estimated to be about 6,966. Patients with non-COVID-19 health needs were skewed to those aged 50 to 70 years. The non-COVID-19 diseases were diverse, with 46.3% as non-neoplastic diseases and 53.7% as neoplasms. The most needed cares were palliative cancer care (22.7%), chemotherapy (18.8%), and critical care (17.0%). The median delay in seeking help was 3 days [interquartile range (IQR), 1 to 15 days] for acute care, and 18.5 days (IQR, 6 to 30 days) for cancer care. Conclusions: Our preliminary findings in Wuhan city indicated that the social media data might provide a viable option to surveil and understand the unmet health needs during an outbreak. Those heterogeneous health needs derived from the social media data might inspire a more resilient healthcare system to address the unmet needs promptly.

Inflammasomes are cytoplasmic multiprotein complexes comprising a sensor protein, inflammatory caspases, and in some but not all cases an adapter protein connecting the two. They can be activated by a repertoire of endogenous and exogenous stimuli, leading to enzymatic activation of canonical caspase-1, noncanonical caspase-11 (or the equivalent caspase-4 and caspase-5 in humans) or caspase-8, resulting in secretion of IL-1β and IL-18, as well as apoptotic and pyroptotic cell death. Appropriate inflammasome activation is vital for the host to cope with foreign pathogens or tissue damage, while aberrant inflammasome activation can cause uncontrolled tissue responses that may contribute to various diseases, including autoinflammatory disorders, cardiometabolic diseases, cancer and neurodegenerative diseases. Therefore, it is imperative to maintain a fine balance between inflammasome activation and inhibition, which requires a fine-tuned regulation of inflammasome assembly and effector function. Recently, a growing body of studies have been focusing on delineating the structural and molecular mechanisms underlying the regulation of inflammasome signaling. In the present review, we summarize the most recent advances and remaining challenges in understanding the ordered inflammasome assembly and activation upon sensing of diverse stimuli, as well as the tight regulations of these processes. Furthermore, we review recent progress and challenges in translating inflammasome research into therapeutic tools, aimed at modifying inflammasome-regulated human diseases.

The discovery of innate immune sensors (pattern recognition receptors, PRRs) has profoundly transformed the notion of innate immunity, in providing a mechanistic basis for host immune interactions with a wealth of environmental signals, leading to a variety of immune-mediated outcomes including instruction and activation of the adaptive immune arm. As part of this growing understanding of host-environmental cross talk, an intimate connection has been unveiled between innate immune sensors and signals perceived from the commensal microbiota, which may be regarded as a hub integrating a variety of environmental cues. Among cytosolic PRRs impacting on host homeostasis by interacting with the commensal microbiota are nucleotide-binding domain, leucine-rich repeat-containing protein receptors (NLRs), together with a number of cytosolic DNA sensors and the family of absent in melanoma (AIM)-like receptors (ALRs). NLR sensors have been a particular focus of research, and some NLRs have emerged as key orchestrators of inflammatory responses and host homeostasis. Some NLRs achieve this through the formation of cytoplasmic multiprotein complexes termed inflammasomes. More recently discovered PRRs include retinoic acid-inducible gene-I (RIG-I)-like receptors (RLRs), cyclic GMP-AMP synthase (cGAS), and STING. In the present review, they summarize recent advancements in knowledge on structure and function of cytosolic PRRs and their roles in host-microbiota cross talk and immune surveillance. In addition, we discuss their relevance for human health and disease and future therapeutic applications involving modulation of their activation and signaling.

The interplay between the commensal microbiota and the mammalian immune system development and function includes multifold interactions in homeostasis and disease. The microbiome plays critical roles in the training and development of major components of the host’s innate and adaptive immune system, while the immune system orchestrates the maintenance of key features of host-microbe symbiosis. In a genetically susceptible host, imbalances in microbiota-immunity interactions under defined environmental contexts are believed to contribute to the pathogenesis of a multitude of immune-mediated disorders. Here, we review features of microbiome-immunity crosstalk and their roles in health and disease, while providing examples of molecular mechanisms orchestrating these interactions in the intestine and extra-intestinal organs. We highlight aspects of the current knowledge, challenges and limitations in achieving causal understanding of host immune-microbiome interactions, as well as their impact on immune-mediated diseases, and discuss how these insights may translate towards future development of microbiome-targeted therapeutic interventions.

Host circadian rhythmicity and the timing of feeding are increasingly recognized to cross-regulate and entrain each other, and may play crucial roles in regulating multiple physiological functions including host immunity and metabolic health. Of relevance, these circadian diet–immune interactions may be modulated by the gut microbiota. We review current knowledge linking the circadian clock and dietary timing to host immune–microbiota interactions, exemplifying how this axis may impact on host immunity in health and in a variety of immune-mediated diseases. We also discuss current challenges in reaching mechanistic insights regarding the functions of the diurnally shifting diet–microbiome–host immune axis. We highlight the possible implications of circadian reprogramming by dietary timing patterns as a future intervention to modulate a variety of immune-related diseases.

Background & Aims The intestinal barrier protects intestinal cells from microbes and antigens in the lumen—breaches can alter the composition of the intestinal microbiota, the enteric immune system, and metabolism. We performed a screen to identify molecules that disrupt and support the intestinal epithelial barrier and tested their effects in mice. Methods We performed an imaging-based, quantitative, high-throughput screen (using CaCo-2 and T84 cells incubated with lipopolysaccharide; tumor necrosis factor; histamine; receptor antagonists; and libraries of secreted proteins, microbial metabolites, and drugs) to identify molecules that altered epithelial tight junction (TJ) and focal adhesion morphology. We then tested the effects of TJ stabilizers on these changes. Molecules we found to disrupt or stabilize TJs were administered mice with dextran sodium sulfate-induced colitis or Citrobacter rodentium-induced intestinal inflammation. Colon tissues were collected and analyzed by histology, fluorescence microscopy, and RNA sequencing. Results The screen identified numerous compounds that disrupted or stabilized (after disruption) TJs and monolayers of epithelial cells. We associated distinct morphologic alterations with changes in barrier function, and identified a variety of cytokines, metabolites, and drugs (including inhibitors of actomyosin contractility) that prevent disruption of TJs and restore TJ integrity. One of these disruptors (putrescine) disrupted TJ integrity in ex vivo mouse colon tissues; administration to mice exacerbated colon inflammation, increased gut permeability, reduced colon transepithelial electrical resistance, increased pattern recognition receptor ligands in mesenteric lymph nodes, and decreased colon length and survival times. Putrescine also increased intestine levels and fecal shedding of viable C rodentium, increased bacterial attachment to the colonic epithelium, and increased levels of inflammatory cytokines in colon tissues. Colonic epithelial cells from mice given putrescine increased expression of genes that regulate metal binding, oxidative stress, and cytoskeletal organization and contractility. Co-administration of taurine with putrescine blocked disruption of TJs and the exacerbated inflammation. Conclusions We identified molecules that disrupt and stabilize intestinal epithelial TJs and barrier function and affect development of colon inflammation in mice. These agents might be developed for treatment of barrier intestinal impairment-associated and inflammatory disorders in patients, or avoided to prevent inflammation.

A micro-grid system based on a source dual active bridge (DAB) converter connected with load buck-boost DC/DC converter and DC/AC converter by the common DC-link is studied in this paper, which is widely investigated in the yield of intelligent distribution microgrid. As the power transmission hub, the stability of the DC-link voltage plays a key role in the normal operation of the whole system, which affects the stable operation of the back-stage inverters as well as the normal power supply of connected loads. The stability problem in DC-link may occur at the low frequency, if the impedance characteristic of DAB as a source is incompatible with the impedance characteristic of back-stage converters, which will be investigated in this paper. Seen from common DC-link, the impedance of DAB, DC/DC and DC/AC converters on this side are modeled. Based on the model, the mechanism and main contributor of low-frequency oscillation in DC-link are presented. The derived impedance model in the frequency domain and the result of stability analysis are verified by the simulation.

Diet is increasingly appreciated to have a tremendous impact on many aspects of the host’s biology in health and disease. Dietary content and timing are also central in shaping the gut microbiome, and contribute to its taxonomic and functional diversity. Regardless, current dietary recommendations remain largely non-personalized, and feature disappointing long-term efficacy in treating obesity and its complications. Personalized nutrition aims to utilize inter-individual host and microbiome variations in generating data-driven personalized dietary recommendations. While personalized nutrition has yielded encouraging and potentially clinically applicable results across several cohorts, host–microbiome interaction networks driving such crosstalk and the mechanisms mediating their metabolic impact remain elusive and merit further studies. Herein, we summarize the latest advances in utilizing diet-microbiota interactions towards the development of personalized nutrition, while focusing on the prospects, challenges and unknowns in integrating this promising new data-driven approach into human precision health.

Background and study aims For bowel preparation, using a reduced volume of polyethylene glycol (PEG) solution without influencing its effectiveness would be preferable. While simethicone shows great potential as an adjunctive agent, data on its use are limited. We aimed to clarify whether simethicone added to low-volume PEG solution improved bowel cleansing. Patients and methods Consecutive adult patients registered for colonoscopy were recruited from seven medical centers in South China between 15 April and 15 July 2015 and prospectively randomized into two groups: 2 L PEG (conventional group) and 2 L PEG plus simethicone (simethicone group). The primary endpoint was the effectiveness of bowel cleansing according to the Boston Bowel Preparation Scale (BBPS). Secondary endpoints included cecal intubation time, adenoma detection rate (ADR), patient safety and compliance, and adverse events. Results We included 290 and 289 patients in the conventional and simethicone groups, respectively, for analysis. The proportion with acceptable bowel cleansing (BBPS ≥ 6) was significantly higher in the simethicone group than in the conventional group (88.2 % vs. 76.6 %; P Conclusions Simethicone added to low-volume PEG solution improves bowel-cleansing efficacy, with similar safety and compliance, shorter cecal intubation time, and higher ADR.

The activation of EphA2 receptor by its natural ligand EphrinA1 causes blood brain barrier dysfunction, and inactivation of EphA2 reduces BBB damage in ischemic stroke. Thus, EphA2 targeted antagonists may serve as neuroprotective agents. We engineered four mutants of EphrinA1, EM1, EM2, EM3 and EM4, respectively. The computational analysis showed that these four mutants were capable of interacting with EphA2. Their potential neuroprotective effects were examined in mouse focal ischemia/reperfusion (I/R) model. EM2 exhibited strong neuroprotective effects, including reduced brain infarct volume, neuronal apoptosis, cerebral edema, and improved neurological scores. The EM2-mediated protection was associated with a comparative decrease in BBB leakage, inflammatory infiltration, and higher expression levels of tight junction proteins, such as zonula occludens-1 and Occludin. I/R-induced high expression of Rho-associated protein kinase 2 (ROCK2) was down-regulated after EM2 treatment. Moreover, EM2 reduced agonist doxazosin-induced EphA2 phosphorylation and cells rounding in PC3 cells, indicating EphA2-antagonizing activity of EM2. These finding provided evidences of the neuroprotection of EphA2 antagonist and a novel approach for ischemic stroke treatment. These results also suggested that a receptor agonist can be switched to an antagonist by substituting one or more relevant residues.

Conceptual scientific and medical advances have led to a recent realization that there may be no single, one-size-fits-all diet and that differential human responses to dietary inputs may rather be driven by unique and quantifiable host and microbiome features. Integration of these person-specific host and microbiome readouts into actionable modules may complement traditional food measurement approaches in devising diets that are of benefit to the individual. Although many host-derived factors are hardwired and difficult to modulate, the microbiome may be more readily reshaped by environmental factors such as dietary exposures and is increasingly recognized to potentially impact human physiology by participating in digestion, the absorption of nutrients, shaping of the mucosal immune response and the synthesis or modulation of a plethora of potentially bioactive compounds. Thus, diet-induced microbiota alterations may be harnessed in order to induce changes in host physiology, including disease development and progression. However, major limitations in 'big-data' processing and analysis still limit our interpretive and translational capabilities concerning these person-specific host, microbiome and diet interactions. In this Review, we describe the latest advances in understanding diet-microbiota interactions, the individuality of gut microbiota composition and how this knowledge could be harnessed for personalized nutrition strategies to improve human health.

Multiport dc-dc converter has attracted increasing research interest in ac/dc hybrid grid and vehicle systems due to the advantages of flexibility, low-cost and high-efficiency. However, under the conventional phase-shifting control strategy, mismatching of dc-port voltages may increase the current in transformer and switching devices, which reduce efficiency of multiport dc-dc converter. To solve the problem, a phase-shifting PWM strategy to control the power flow and minimize the losses of the isolated three port triple active bridge(TAB) dc-dc converter is proposed in this paper, in which phase-shifting control is used for managing the power flow between triple ports, duty cycle control is utilized for optimizing the system losses and ZVS conditions are checked. Finally, the simulation is conducted to validate the feasibility of the strategy.

Background To date, it is not clarified whether patients with gastric polyps without any alarming symptoms for colorectal neoplasia need colonoscopy screening. The objective of this study is to prospectively determine the association between gastric polyps and colorectal neoplasia. Methods A multicenter prospective cross-sectional study was performed from July 2012 to December 2014. We compared patients with and without gastric polyps for prevalence of colorectal adenomas. The odds ratios (OR) were computed by logistic regression analysis after multivariable adjustments. Results Totally 1546 patients were included, with 770 patients in the gastric polyp group and 776 in the age- and sex- matched control group. Patients with gastric polyps had greater odds of having any colorectal adenoma (adjusted OR=2.34, 95% confidence interval [CI]: 1.79 to 3.06, p

Nonalcoholic fatty liver disease (NAFLD) is the hepatic manifestation of cardiometabolic syndrome, which often also includes obesity, diabetes, and dyslipidemia. It is rapidly becoming the most prevalent liver disease worldwide. A sizable minority of NAFLD patients develop nonalcoholic steatohepatitis (NASH), which is characterized by inflammatory changes that can lead to progressive liver damage, cirrhosis, and hepatocellular carcinoma. Recent studies have shown that in addition to genetic predisposition and diet, the gut microbiota affects hepatic carbohydrate and lipid metabolism as well as influences the balance between pro‐inflammatory and anti‐inflammatory effectors in the liver, thereby impacting NAFLD and its progression to NASH. In this review, we will explore the impact of gut microbiota and microbiota‐derived compounds on the development and progression of NAFLD and NASH, and the unexplored factors related to potential microbiome contributions to this common liver disease.

Background: A suitable disease classification is essential for individualized therapy in patients with Crohn’s disease (CD). Although a potential mechanistic classification of colon-involving and non-colon-involving disease was suggested by recent genetic and microbiota studies, the clinical implication has seldom been investigated. We aimed to explore the association of this colonic-based classification with clinical outcomes in patients with CD compared with the Montreal classification. Methods: This was a retrospective study of CD patients from a tertiary referral center. Patients were categorized into colon-involving and non-colon-involving disease, and according to the Montreal classification. Clinico-demographic data, medications, and surgeries were compared between the two classifications. The primary outcome was the need for major abdominal surgery. Results: Of 934 patients, those with colonic involvement had an earlier median (interquartile range) age of onset [23.0 (17.0–30.0) versus 26.0 (19.0–35.0) years, p = 0.001], higher frequency of perianal lesions (31.2% versus 14.5%, p Conclusion: This study supports the rationale for disease classification based on the involvement of colon. This new classification of CD is a better predictor of clinical outcomes than the Montreal classification.

This paper introduces an improved control strategy for triple-port power electronic transformer (PET) which includes two DC ports with different voltage levels and an AC power supply port. When three-phase unbalanced loads connect with the AC port, both the power and intermediate DC bus voltage will contain ripples of twice fundamental frequency, which will deteriorate the output voltage quality of the AC port. To restrain the ripples of the DC bus voltage and achieve flexible allocation of the power fluctuation among three ports, as well as to keep the AC port voltage balanced, an improved control strategy of PET based on proportional integral resonance (PIR) control is proposed according to the power decoupling control method. Finally, simulation results validate the effectiveness of the proposed strategy.

Metabolic syndrome, leaky guts, and infection Metabolic syndrome often accompanies obesity and hyperglycemia and is associated with a breakdown in the integrity of the intestinal barrier and increased risk of systemic infection. Thaiss et al. found that mice with systemic infection of a Salmonella analog, Citrobacter rodentium , also exhibited hyperglycemia. Deletion of the glucose transporter GLUT2 altered sensitivity to chemically induced epithelial permeability and protected mice from pathogen invasion. The authors also found a correlation in humans between glycated hemoglobin (an indicator of hyperglycemia) and serum levels of pathogen recognition receptor ligands. Science , this issue p. 1376

Background Today, it is not clarified whether patients with gastric polyps without any alarming symptoms for colorectal neoplasia need colonoscopy screening. The objective of this study is to prospectively determine the association between gastric polyps and colorectal neoplasia. Methods A multicenter prospective cross-sectional study was performed from July 2012 to December 2014. We compared patients with and without gastric polyps for the prevalence of colorectal adenomas. The odds ratios (OR) were computed by logistic regression analysis after multivariable adjustments. Results Totally 1546 patients were included, with 770 patients in the gastric polyp group and 776 in the age- and sex-matched control group. Patients with gastric polyps had greater odds of having any colorectal adenoma (adjusted OR=2.36, 95% confidence interval [CI]: 1.81 to 3.09, p Conclusions The presence of gastric polyps is significantly associated with a higher prevalence of colorectal adenomas, especially advanced colorectal adenomas. Colonoscopy might be considered in patients with gastric polyps, of any gender, and over the age of 40.

A new cool-tip radiofrequency (RF) ablation therapeutic instrument based on impedance control algorithm is introduced in this paper. The equipment is composed of hardware system and software system. The RF power output and real time data acquisition are completed by the hardware system, while the software is used mainly to finish the control of the ablation range, the core of which is impedance control algorithm, and it also used to complete the display of the real time data in the course of the experiment. The impedance algorithm has solved the problem of impedance increased rapidly during the RF ablation, which has also expanded the scope of ablation. The pig liver experiments showed that the impedance control algorithm had strong adaptability. It also obtained a result of ablation range up to 3.5-4.5 cm single needle. It has the high clinical practical value of one-time inactivation of 3-5 cm tumor.

Background The accuracy of computed tomography (CT) for detecting donor hepatic steatosis (HS) before liver transplantation is not well established. Methods A meta-analysis was performed to determine the accuracy of CT for HS detection in liver donor candidates. Pooled sensitivity, specificity, positive and negative likelihood ratios, hierarchical summary receiver operating characteristic (HSROC) curves, and the area under the curve (AUC) were estimated using HSROC and bivariate random-effects models. Results Twelve studies involving 1782 subjects were eligible for this meta-analysis. For detecting significant HS (>10% to 30% steatosis in liver pathology) with CT in liver donors, the pooled sensitivity, specificity, positive likelihood ratio, and negative likelihood ratio were 0.81 (95% confidence interval [CI]: 0.70-0.89), 0.94 (95%CI: 0.90-0.96), 13.7 (95%CI: 8.1-23.1), and 0.20 (95%CI: 0.12-0.33). The AUC was 0.95 (95%CI: 0.92-0.96). For detecting the presence of HS, these corresponding diagnostic estimates were 0.50 (95%CI: 0.36-0.64), 0.90 (95%CI: 0.83-0.95), 5.2 (95%CI: 3.1-8.9), 0.55 (95%CI: 0.42-0.72) and 0.80 (95%CI: 0.76-0.83). Moderate to high heterogeneity was detected. Conclusion CT shows high accuracy in detecting significant HS while poor accuracy in detecting the presence of HS in liver donors. Donors estimated to have significant HS by CT may avoid unnecessary liver biopsy. This article is protected by copyright. All rights reserved.