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Approximately 50% of the patients with ulcerative colitis (UC) are primarily nonresponsive to anti‐tumor necrosis factor (TNF) therapy or lose their responsiveness over time. The gut microbiota plays an important role in the resistance of UC to anti‐TNF therapy; however, the underlying mechanism remains unknown. Here, it is found that the transplantation of gut fecal microbiota from patients with UC alters the diversity of the gut microbiota in dextran sulfate sodium‐induced colitis mice and may affect the therapeutic responsiveness of mice to infliximab. Furthermore, the abundances of Romboutsia and Fusobacterium increase in the tissues of patients with UC who do not respond to anti‐TNF therapy. Differentially abundant metabolites are mainly enriched in nicotinate and nicotinamide metabolism in NCM460 cells after Fusobacterium nucleatum infection. Mechanistically, F. nucleatum promotes the nicotinamide adenine dinucleotide (NAD+) salvage pathway by upregulating NAMPT expression, which subsequently leads to the activation of the p38 mitogen‐activated protein kinase (MAPK) signaling pathway and promotes the secretion of inflammatory factors, ultimately inhibiting the therapeutic response to anti‐TNF drugs. These findings demonstrate that the gut microbiota can influence the response to anti‐TNF therapy in patients with UC and highlight the therapeutic potential of targeting F. nucleatum and its associated pathways for preventing and treating drug resistance in UC. The gut microbiota affects the response to anti‐TNF therapy in UC patients. F. nucleatum activates the p38 MAPK signaling pathway by regulating the NAD+ salvage pathway to inhibit anti‐TNF therapy responsiveness. Interfering with the NAD+ salvage pathway or inhibiting the growth of F. nucleatum may alleviate the resistance of UC to anti‐TNF therapy.

This study aimed to assess and compare the healing outcome associated with different aqueous-based calcium hydroxide intracanal medicaments in patients with pulpal necrosis and symptomatic apical periodontitis. Seventy five patients with pulpal necrosis and symptomatic apical periodontitis in permanent mandibular molar teeth were selected as the part of this study. The participants were randomly allocated to three groups, each comprising 25 patients, based on the type of intracanal medicament used during the treatment procedure. Group 1 consisted of calcium hydroxide (CH) mixed with 0.9% saline (NS), Group 2 contained CH combined with 2% lidocaine, and Group 3 included CH with 2% chlorhexidine (CHX). The Periapical Index Score was utilized to assess the healing of periapical lesions in preoperative and post-operative periapical radiographs at 3 month intervals for 12 months. The Kruskal-Wallis test was used to determine the significance, with Post Hoc Dunn tests for multiple comparisons. At the 12-month follow-up, the CH+CHX group demonstrated significantly improved periapical healing, with a mean PAI score of 1.57 +- 0.66, compared to CH+LA (2.27+-0.63) and CH+NS (2.48+-0.79), with Kruskal-Wallis p<0.05. The mean time to achieve a healthy periapical status (PAI ≤2) was shortest in the CH+CHX group (8.10+-3.28 months), followed by CH+NS (8.23+-3.28 months) and CH+LA (8.25+-3.31 months), with the multivariate Log-Rank test indicating a statistically significant difference among the groups (p<0.05). The findings of this study indicate that CH when combined with 2% CHX as an aqueous vehicle demonstrated superior healing of periapical lesions in patients with pulpal necrosis and symptomatic apical periodontitis compared to saline or lidocaine.

In this Opinion article, the authors discuss how the induction of regulated cell death and inflammatory pathways may lead to an auto-amplification loop that causes tissue damage and organ failure. They propose that targeting both processes could be useful for treating a broad range of clinical conditions with an inflammatory basis. Regulated cell death (RCD) is either immunologically silent or immunogenic. RCD in parenchymal cells may lead to the release of damage- associated molecular patterns that drive both tissue inflammation and the activation of further pathways of RCD. Following an initial event of regulated necrosis, RCD and inflammation can induce each other and drive a local auto-amplification loop that leads to exaggerated cell death and inflammation. In this Opinion article, we propose that such crosstalk between pro-inflammatory and RCD pathways has pathophysiological relevance in solid organ failure, transplantation and cancer. In our opinion, clinicians should not only prescribe immunosuppressive treatments to disrupt this circuit, but also implement the neglected therapeutic option of adding compounds that interfere with RCD.

PurposeRadiation necrosis (RN) represents a serious post-radiotherapy complication in patients with brain metastases. Bevacizumab and laser interstitial thermal therapy (LITT) are viable treatment options, but direct comparative data is scarce. We reviewed the literature to compare the two treatment strategies.MethodsPubMed, EMBASE, Scopus, and Cochrane databases were searched. All studies of patients with RN from brain metastases treated with bevacizumab or LITT were included. Treatment outcomes were analyzed using indirect meta-analysis with random-effect modeling.ResultsAmong the 18 studies included, 143 patients received bevacizumab and 148 underwent LITT. Both strategies were equally effective in providing post-treatment symptomatic improvement (P = 0.187, I2 = 54.8%), weaning off steroids (P = 0.614, I2 = 25.5%), and local lesion control (P = 0.5, I2 = 0%). Mean number of lesions per patient was not statistically significant among groups (P = 0.624). Similarly, mean T1-contrast-enhancing pre-treatment volumes were not statistically different (P = 0.582). Patterns of radiological responses differed at 6-month follow-ups, with rates of partial regression significantly higher in the bevacizumab group (P = 0.001, I2 = 88.9%), and stable disease significantly higher in the LITT group (P = 0.002, I2 = 81.9%). Survival rates were superior in the LITT cohort, and statistical significance was reached at 18 months (P = 0.038, I2 = 73.7%). Low rates of adverse events were reported in both groups (14.7% for bevacizumab and 12.2% for LITT).ConclusionBevacizumab and LITT can be safe and effective treatments for RN from brain metastases. Clinical and radiological outcomes are mostly comparable, but LITT may relate with superior survival benefits in select patients. Further studies are required to identify the best patient candidates for each treatment group.

Necrotizing pneumonia induced by Panton-Valentine leukocidin-secreting Staphylococcus aureus is a rare but life-threatening infection that has been described in patients after they had influenza. We report a fatal case of this superinfection in a young adult who had coronavirus disease.

Necrotic enteritis (NE) is a severe intestinal disease, which can change gut microbiota and result in a high cost for the poultry industry worldwide. However, little is known regarding how the gut microbiota of NE chicken ileum are changed by Bacillus licheniformis . This study was conducted to investigate how ileum microbiota structure was changed by B. licheniformis in broiler chickens challenged with Clostridium perfringens -induced NE through Illumina MiSeq sequencing. The broilers were randomly separated into four groups: the negative control group (NC), the positive control group (PC), the fishmeal and coccidia group (FC), and the PC group supplied with feed containing B. licheniformis (BL). Compared to the PC and FC, alpha diversity, beta diversity, and the bacterial taxa of the ileum microbiota were more similar in BL and NC. Some genera, which were related to the NE control, became insignificant in BL with NC, such as Lactobacillus , Lactococcus , Bacteroides , Ruminococcus and Helicobacter . The PICRUSt analysis revealed that a tumour suppressor gene, p53, which was negatively correlated with Helicobacter , was enriched in the BL group. Our findings showed that the ileum microbiota disorder caused by NE in chickens was normalized by dietary B. licheniformis supplementation.

Regenerative endodontic procedures (REPs) is a biologic-based treatment modality for immature permanent teeth diagnosed with pulp necrosis. The ultimate objective of REPs is to regenerate the pulp-dentin complex, extend the tooth longevity and restore the normal function. Scientific evidence has demonstrated the efficacy of REPs in promotion of root development through case reports, case series, cohort studies, and randomized controlled studies. However, variations in clinical protocols for REPs exist due to the empirical nature of the original protocols and rapid advancements in the research field of regenerative endodontics. The heterogeneity in protocols may cause confusion among dental practitioners, thus guidelines and considerations of REPs should be explicated. This expert consensus mainly discusses the biological foundation, the available clinical protocols and current status of REPs in treating immature teeth with pulp necrosis, as well as the main complications of this treatment, aiming at refining the clinical management of REPs in accordance with the progress of basic researches and clinical studies, suggesting REPs may become a more consistently evidence-based option in dental treatment.

Histones are positively charged nuclear proteins that facilitate packaging of DNA into nucleosomes common to all eukaryotic cells. Upon cell injury or cell signalling processes, histones are released passively through cell necrosis or actively from immune cells as part of extracellular traps. Extracellular histones function as microbicidal proteins and are pro‐thrombotic, limiting spread of infection or isolating areas of injury to allow for immune cell infiltration, clearance of infection and initiation of tissue regeneration and repair. Histone toxicity, however, is not specific to microbes and contributes to tissue and end‐organ injury, which in cases of systemic inflammation may lead to organ failure and death. This review details the processes of histones release in acute inflammation, the mechanisms of histone‐related tissue toxicity and current and future strategies for therapy targeting histones in acute inflammatory diseases.

Purpose To evaluate and assess the current knowledge about apexification and regenerative techniques as a meaningful treatment modality and to map the scientific evidence for the efficacy of both methods for the management of traumatised immature teeth with pulp necrosis and apical periodontitis. Methods This systematic review searched five databases: PubMed, Web of Science, Cochrane Library, Ovid (Medline), and Embase. Published articles written in English were considered for inclusion. The following keywords were used: Regenerative endodontic treatment OR regenerat* OR revital* OR endodontic regeneration OR regenerative endodontics OR pulp revascularization OR revasculari* OR ‘traumatized immature teeth’. Only peer-reviewed studies with a study size of at least 20 cases followed up for 24 months were included. Eligibility assessment was performed independently in a blinded manner by three reviewers and disagreements were resolved by consensus. Subgroup analyses were performed on three clinical outcomes: survival, success, and continued root development. Results Seven full texts out of 1359 citations were included and conventional content analysis was performed. Most of the identified citations were case reports and case series. Conclusions In the present systematic review, the qualitative analysis revealed that both regenerative and apexification techniques had equal rates of success and survival and proved to be effective in the treatment of immature necrotic permanent teeth. Endodontic regenerative techniques appear to be superior to apexification techniques in terms of stimulation of root maturation, i.e. root wall thickening and root lengthening. Knowledge gaps were identified regarding the treatment and follow-up protocols for both techniques.