bluuebunny/crossref_metadata_2025_split huggingface dataset:
Protein hydrolysates derived from aquaculture and marine byproducts through autolytic hydrolysis
Authors: Nikoo Mehdi , Benjakul Soottawat , Ahmadi Gavlighi Hassan 
Published: November 2022

AbstractAutolysis technology has shown potential for protein hydrolysates production from marine and aquaculture byproducts. Viscera are a source of cheap proteolytic enzymes for producing protein hydrolysates from the whole fish or processing byproducts of the most valuable commercial species by applying autolysis technology. The use of autolysis allows economical production of protein hydrolysate and provides an opportunity to valorize downstream fish and shellfish processing byproducts at a lower cost. As a result, production and application of marine byproduct autolysates is increasing in the global protein hydrolysates market. Nevertheless, several restrictions occur with autolysis, including lipid and protein oxidation mediated by the heterogeneous composition of byproducts. The generally poor storage and handling of byproducts may increase the formation of undesirable metabolites during autolysis, which can be harmful. The formation of nitrogenous compounds (i.e., biogenic amines), loss of freshness, and process of autolysis in the byproducts could increase the rate of quality and safety loss and lead to more significant concern about the use of autolysates for human food applications. The current review focuses on the autolysis process, which is applied for the hydrolysis of aquaculture and marine discards to obtain peptides as functional or nutritive ingredients. It further addresses the latest findings on the mechanisms and factors contributing the deterioration of byproducts and possible ways to control oxidation and other food quality and safety issues in raw materials and protein hydrolysates.
“Fast money” around Federal Statistics Releases
Authors: Huang Joshua , Serra Teresa , Garcia Philip 
Published: November 2022

AbstractMany public statistics are closely followed by the public as they provide valuable information for decision making. Although economic theory suggests that low‐latency traders (LLTs) can earn excess arbitrage profits from trading on public statistics releases due to their speed advantage, the empirical literature fails to find meaningful LLTs' stock market profits when trading on macroeconomic statistical releases. Here we confirm previous findings with improved techniques, but also show that excess profits can be earned quickly in agricultural commodity futures markets around United States Department of Agriculture (USDA) statistical releases. We attribute differences in the magnitude of the profits to the straightforward nature of the information and to the direct relevance of the reports to traders for the markets considered. Motivated by market concerns, USDA and the United States Department of Labor recently changed their news media prerelease lockup policy to mitigate LLTs' speed advantage. However, we find the policy change had little effect on the speed advantage as no significant reduction in LLTs' profits occurred. Implications of the research are relevant for government agencies concerned with mitigating LLT speed advantages particularly during the release of public statistical information.
Diagnostic accuracy of vaccine and vaccine excipient testing in the setting of allergic reactions to COVID‐19 vaccines: A systematic review and meta‐analysis
Authors: Greenhawt Matthew , Shaker Marcus , Golden David B. K. , Abrams Elissa M. , Blumenthal Kimberly G. , Wolfson Anna R. , Stone Cosby A. , Krantz Matthew S. , Chu Derek K. , Dwamena Ben A. 
Published: November 2022

AbstractFor persons with immediate allergic reactions to mRNA COVID‐19 vaccines, skin testing (ST) to the vaccine/excipients (polyethylene glycol[PEG] and polysorbate 80 [PS]) has been recommended, but has unknown accuracy. To assess vaccine/excipient ST accuracy in predicting all‐severity immediate allergic reactions upon re‐vaccination, systematic review was performed searching Medline, EMBASE, Web of Science, and the WHO global coronavirus database (inception‐Oct 4, 2021) for studies addressing immediate (≤4 h post‐vaccination) all‐severity allergic reactions to 2nd mRNA COVID‐19 vaccination in persons with 1st dose immediate allergic reactions. Cases evaluating delayed reactions, change of vaccine platform, or revaccination without vaccine/excipient ST were excluded. Meta‐analysis of diagnostic testing accuracy was performed using Bayesian methods. The GRADE approach evaluated certainty of the evidence, and QUADAS‐2 assessed risk of bias. Among 20 studies of mRNA COVID‐19 first dose vaccine reactions, 317 individuals underwent 578 ST to any one or combination of vaccine, PEG, or PS, and were re‐vaccinated with the same vaccine. Test sensitivity for either mRNA vaccine was 0.2 (95%CrI 0.01–0.52) and specificity 0.97 (95%CrI 0.9–1). PEG test sensitivity was 0.02 (95%CrI 0.00–0.07) and specificity 0.99 (95%CrI 0.96–1). PS test sensitivity was 0.03 (95%CrI 0.00–0.0.11) and specificity 0.97 (95%CrI 0.91–1). Combined for use of any of the 3 testing agents, sensitivity was 0.03 (95%CrI 0.00–0.08) and specificity was 0.98 (95%CrI 0.95–1.00). Certainty of evidence was moderate. ST has low sensitivity but high specificity in predicting all‐severity repeat immediate allergic reactions to the same agent, among persons with 1st dose immediate allergic reactions to mRNA COVID‐19 vaccines. mRNA COVID‐19 vaccine or excipient ST has limited risk assessment utility.
Intestinal ultrasound detects an increased diameter and submucosal layer thickness in the appendix of patients with ulcerative colitis compared to healthy controls – a prospective cohort study
Authors: Reijntjes Maud A. , de Voogd Floris A. E. , Bemelman Willem A. , Hompes Roel , d'Haens Geert , Buskens Christianne J. , Gecse Krisztina B. 
Published: November 2022

SummaryBackgroundIncreasing evidence suggests that appendicectomy as alternative treatment for ulcerative colitis (UC), especially in patients with histopathological appendiceal inflammation. Intestinal ultrasound (IUS) is a non‐invasive diagnostic modality to characterise appendiceal inflammation.AimsTo assess appendiceal IUS characteristics in UC patients and compare findings to healthy controls (HC).MethodsIn this prospective study, appendiceal IUS was performed in consecutive UC patients with active (A; n = 35) or quiescent (Q; n = 30) disease and in HC (n = 30). Transverse appendiceal diameter (TAD) and additional IUS parameters (bowel wall thickness, submucosal layer thickness and colour Doppler signal) were assessed.ResultsThe appendix was visualised in 41/65 UC patients (63.1%; A vs. Q: 23/35 vs. 18/30, p = 0.67) and 18/30 (60%) HC. UC patients had a higher TAD (A: 5.5 mm, Q: 5.0 mm, HC: 4.3 mm; A‐HC p < 0.01; Q‐HC p = 0.01, A‐Q p = ns) and submucosal layer thickness (A: 1.0 mm, Q: 1.0 mm, HC: 0.7 mm; A‐HC p < 0.01, Q‐HC: p = 0.01, A‐Q: p = ns) when compared to HC. A TAD ≥6 mm corresponding to an ultrasonographic suspicion of acute appendicitis was mainly reported in A‐UC patients (A: 43%; Q: 6%; HC: 0%, p = 0.01) and occurred irrespective of disease extent. However, none of the patients had a clinical suspicion of acute appendicitis.ConclusionA TAD ≥6 mm was predominantly seen in A‐UC. TAD was higher in UC patients compared to HC irrespective of disease activity and was characterised by an increased submucosal layer thickness. IUS therefore has the potential to identify UC patients with appendiceal inflammation.
Potential cerebrovascular accident signal for risankizumab: A disproportionality analysis of the FDA Adverse Event Reporting System (FAERS)
Authors: Woods Richard H. 
Published: November 2022

AimsThe interleukin‐23 (IL‐23) inhibitor risankizumab was recently approved for the treatment of moderate‐to‐severe plaque psoriasis in the United States. Low rates of cerebrovascular accident (CVA) were observed in risankizumab‐treated patients during clinical trials. The aim of this study was to determine whether risankizumab may be associated with CVA in a real‐world setting.MethodsA retrospective disproportionality analysis was conducted utilizing postmarketing adverse event reports submitted to the US Food and Drug Administration Adverse Event Reporting System (FAERS) through the fourth quarter of 2021. A custom query consisting of 22 CVA‐related Medical Dictionary for Regulatory Activities (MedDRA) preferred terms previously reported in clinical trials of plaque psoriasis medications was used to identify cases. Disproportionality was measured by calculating reporting odds ratios (ROR) and 95% confidence intervals (CI), whereby the lower limit of a 95% CI >1.0 and ≥ three cases was considered a signal.ResultsRisankizumab was associated with significantly disproportionate CVA reporting compared to all other drugs in FAERS (ROR 2.48; 95% CI 2.14–2.88) as well as 11 alternative plaque psoriasis therapeutics across five pharmacologic classes. The largest disproportionality signals for risankizumab were identified relative to apremilast (ROR 9.07; 95% CI 7.56–10.89), ixekizumab (ROR 6.75; 95% CI 5.14–8.86), guselkumab (ROR 6.74; 95% CI 4.68–9.71), certolizumab (ROR 5.70; 95% CI 4.74–6.85) and etanercept (ROR 4.91; 95% CI 4.21–5.73).ConclusionThis study detected a previously unreported signal of disproportionate CVA reporting with the real‐world use of risankizumab. Further long‐term observational data will be necessary to better characterize this unconfirmed potential safety signal.
Isoflurane impairs GluN2B‐containing NMDA receptors trafficking and cognition via decreasing histone acetylation and EphB2 expression in aged hippocampal neurons
Authors: Hao Jing‐Ru , Hu Qiu‐Mei , Yang Xiu , Wei Pan , Wang Hu‐Yi , Sun Nan , Gao Can 
Published: November 2022

AbstractPerioperative neurocognitive disorders (PND) is a common complication that occurs among elderly patients in the perioperative course. Current clinical evidence has shown that isoflurane exposure could cause cognitive decline, but the exact molecular mechanisms remain unclear. As both NMDARs‐dependent synaptic plasticity and histone acetylation play vital roles in processing learning and memory, we postulated that these alternations might occur in the isoflurane‐associated PND. Here, we found that isoflurane impaired fear memory in aged mice, decreased GluN2B‐containing NMDA receptors phosphorylation and trafficking, as well as the expression of EphB2, a key regulator of synaptic localization of NMDA receptors. We also identified that isoflurane could increase the expression of HDAC2, which was significantly enriched at the ephb2 gene promoter and regulated the transcription of ephb2. Furthermore, we showed that suberoylanilide hydroxamic acid (SAHA), a nonselective HDAC inhibitor or knocking‐down HDAC2 rescued the cognitive dysfunction in isoflurane‐treated aged mice via increasing acetylation of H3Ac, expression of EphB2 and promoting NMDA receptor trafficking. Collectively, our study highlighted the crucial role of histone posttranslational modifications for EphB2‐GluN2B signals in isoflurane‐associated PND, and modulating HDAC2 might be a new therapeutic strategy for isoflurane‐associated PND.
Latent Multinomial Models for Extended Batch-Mark Data
Authors: Zhang Wei , Bonner Simon J. , McCrea Rachel S. 
Published: November 2022

Abstract
Batch marking is common and useful for many capture–recapture studies where individual marks cannot be applied due to various constraints such as timing, cost, or marking difficulty. When batch marks are used, observed data are not individual capture histories but a set of counts including the numbers of individuals first marked, marked individuals that are recaptured, and individuals captured but released without being marked (applicable to some studies) on each capture occasion. Fitting traditional capture–recapture models to such data requires one to identify all possible sets of capture–recapture histories that may lead to the observed data, which is computationally infeasible even for a small number of capture occasions. In this paper, we propose a latent multinomial model to deal with such data, where the observed vector of counts is a non-invertible linear transformation of a latent vector that follows a multinomial distribution depending on model parameters. The latent multinomial model can be fitted efficiently through a saddlepoint approximation based maximum likelihood approach. The model framework is very flexible and can be applied to data collected with different study designs. Simulation studies indicate that reliable estimation results are obtained for all parameters of the proposed model. We apply the model to analysis of golden mantella data collected using batch marks in Central Madagascar.
CHCHD2 p.Thr61Ile knock‐in mice exhibit motor defects and neuropathological features of Parkinson's disease
Authors: Fan Liyuan , Zhang Shuo , Li Xinwei , Hu Zhengwei , Yang Jing , Zhang Shuyu , Zheng Huimin , Su Yun , Luo Haiyang , Liu Xinjing , Fan Yu , Sun Huifang , Zhang Zhongxian , Miao Jinxin , Song Bo , Xia Zongping , Shi Changhe , Mao Chengyuan , Xu Yuming 
Published: November 2022

AbstractThe p.Thr61Ile (p.T61I) mutation in coiled‐coil‐helix–coiled‐coil‐helix domain containing 2 (CHCHD2) was deemed a causative factor in Parkinson's disease (PD). However, the pathomechanism of the CHCHD2 p.T61I mutation in PD remains unclear. Few existing mouse models of CHCHD2‐related PD completely reproduce the features of PD, and no transgenic or knock‐in (KI) mouse models of CHCHD2 mutations have been reported. In the present study, we generated a novel CHCHD2 p.T61I KI mouse model, which exhibited accelerated mortality, progressive motor deficits, and dopaminergic (DA) neurons loss with age, accompanied by the accumulation and aggregation of α‐synuclein and p‐α‐synuclein in the brains of the mutant mice. The mitochondria of mouse brains and induced pluripotent stem cells (iPSCs)‐derived DA neurons carrying the CHCHD2 p.T61I mutation exhibited aberrant morphology and impaired function. Mechanistically, proteomic and RNA sequencing analysis revealed that p.T61I mutation induced mitochondrial dysfunction in aged mice likely through repressed insulin‐degrading enzyme (IDE) expression, resulting in the degeneration of the nervous system. Overall, this CHCHD2 p.T61I KI mouse model recapitulated the crucial clinical and neuropathological aspects of patients with PD and provided a novel tool for understanding the pathogenic mechanism and therapeutic interventions of CHCHD2‐related PD.
Selective neurodegeneration generated by intravenous α‐synuclein pre‐formed fibril administration is not associated with endogenous α‐synuclein levels in the rat brain
Authors: Kuan Wei‐Li , Alfaidi Maha , Horne Catherine B. , Vallin Benjamin , Fox Sarah , Fazal Shaline V. , Williams‐Gray Caroline H. , Barker Roger A. 
Published: November 2022

AbstractSelective loss of discrete neuronal populations is a prominent feature of many neurodegenerative conditions, but the molecular basis of this is poorly understood. A central role of α‐synuclein in the selective neurodegeneration of Parkinson's disease has been speculated, as its level of expression critically determines the propensity of this protein to misfold. To investigate whether the propensity of neuronal cell loss is associated with the level of endogenous α‐synuclein expression, non‐transgenic rats were given a single intravenous administration of α‐synuclein pre‐formed fibrils (PFFs) reversibly complexed with the rabies virus glycoprotein peptide (RVG9R). The number of surviving cells in different neuronal populations was systematically quantified using unbiased stereology. Our data demonstrated that a non‐selective, transvascular delivery of α‐synuclein PFFs led to a time‐dependent loss of specific populations of midbrain (but not olfactory) dopaminergic neurons, medullary (but not pontine) cholinergic neurons, and brainstem serotonergic neurons. Contrary to the central role of endogenous α‐synuclein expression in determining the seeding and aggregation propensity of pathological α‐synuclein, we did not observe an association between the levels of α‐synuclein expression in different regions of the rodent brain (although did not ascertain this at the individual cell level) and neurodegenerative propensity. The results from our study highlight the complexity of the neurodegenerative process generated by α‐synuclein seeding. Further investigations are therefore required to elucidate the molecular basis of neurodegeneration driven by exogenous pathogenic α‐synuclein spread.
STAT1‐ and NFAT‐independent amplification of purinoceptor function integrates cellular senescence with interleukin‐6 production in preadipocytes
Authors: Majeed Yasser , Madani Aisha Y. , Altamimi Ahmed I. , Courjaret Raphael , Vakayil Muneera , Fountain Samuel J. , Machaca Khaled , Mazloum Nayef A. 
Published: November 2022

AbstractBackground and PurposeSenescent preadipocytes promote adipose tissue dysfunction by secreting pro‐inflammatory factors, although little is known about the mechanisms regulating their production. We investigated if up‐regulated purinoceptor function sensitizes senescent preadipocytes to cognate agonists and how such sensitization regulates inflammation.Experimental ApproachEtoposide was used to trigger senescence in 3T3‐L1 preadipocytes. CRISPR/Cas9 technology or pharmacology allowed studies of transcription factor function. Fura‐2 imaging was used for calcium measurements. Interleukin‐6 levels were quantified using quantitative PCR and ELISA. Specific agonists and antagonists supported studies of purinoceptor coupling to interleukin‐6 production. Experiments in MS1 VEGF angiosarcoma cells and adipose tissue samples from obese mice complemented preadipocyte experiments.Key ResultsDNA damage‐induced senescence up‐regulated purinoceptor expression levels in preadipocytes and MS1 VEGF angiosarcoma cells. ATP‐evoked Ca2+ release was potentiated in senescent preadipocytes. ATP enhanced interleukin‐6 production, an effect mimicked by ADP but not UTP, in a calcium‐independent manner. Senescence‐associated up‐regulation and activation of the adenosine A3 receptor also enhanced interleukin‐6 production. However, nucleotide hydrolysis was not essential because exposure to ATPγS also enhanced interleukin‐6 secretion. Pharmacological experiments suggested coupling of P2X ion channels and P2Y12–P2Y13 receptors to downstream interleukin‐6 production. Interleukin‐6 signalling exacerbated inflammation during senescence and compromised adipogenesis.Conclusions and ImplicationsWe report a previously uncharacterized link between cellular senescence and purinergic signalling in preadipocytes and endothelial cancer cells, raising the possibility that up‐regulated purinoceptors play key modulatory roles in senescence‐associated conditions like obesity and cancer. There is potential for exploitation of specific purinoceptor antagonists as therapeutics in inflammatory disorders.
Gut microbiota‐derived nicotinamide mononucleotide alleviates acute pancreatitis by activating pancreatic SIRT3 signalling
Authors: Liu Li‐Wei , Xie Yu , Li Guan‐Qun , Zhang Tao , Sui Yu‐Hang , Zhao Zhong‐Jie , Zhang Yang‐Yang , Yang Wen‐Bo , Geng Xing‐Long , Xue Dong‐Bo , Chen Hua , Wang Yong‐Wei , Lu Tian‐Qi , Shang Li‐Ren , Li Zhi‐Bo , Li Le , Sun Bei 
Published: November 2022

Background and PurposeGut microbiota dysbiosis induced by acute pancreatitis (AP) exacerbates pancreatic injury and systemic inflammatory responses. The alleviation of gut microbiota dysbiosis through faecal microbiota transplantation (FMT) is considered a potential strategy to reduce tissue damage and inflammation in many clinical disorders. Here, we aim to investigate the effect of gut microbiota and microbiota‐derived metabolites on AP and further clarify the mechanisms associated with pancreatic damage and inflammation.Experimental ApproachAP rat and mouse models were established by administration of caerulein or sodium taurocholate in vivo. Pancreatic acinar cells were exposed to caerulein and lipopolysaccharide in vitro to simulate AP.Key ResultsNormobiotic FMT alleviated AP‐induced gut microbiota dysbiosis and ameliorated the severity of AP, including mitochondrial dysfunction, oxidative damage and inflammation. Normobiotic FMT induced higher levels of NAD+ (nicotinamide adenine dinucleotide)‐associated metabolites, particularly nicotinamide mononucleotide (NMN). NMN administration mitigated AP‐mediated mitochondrial dysfunction, oxidative damage and inflammation by increasing pancreatic NAD+ levels. Similarly, overexpression of the NAD+‐dependent mitochondrial deacetylase sirtuin 3 (SIRT3) alleviated the severity of AP. Furthermore, SIRT3 deacetylated peroxiredoxin 5 (PRDX5) and enhanced PRDX5 protein expression, thereby promoting its antioxidant and anti‐inflammatory activities in AP. Importantly, normobiotic FMT‐mediated NMN metabolism induced SIRT3–PRDX5 pathway activation during AP.Conclusion and ImplicationsGut microbiota‐derived NMN alleviates the severity of AP by activating the SIRT3–PRDX5 pathway. Normobiotic FMT could be served as a potential strategy for AP treatment.
Identification of 5‐(3‐(methylsulfonyl)phenyl)‐3‐(4‐(methylsulfonyl)phenyl)‐3H‐imidazo[4,5‐b]pyridine as novel orally bioavailable and metabolically stable antimalarial compound for further exploration
Authors: Kundu Mrinalkanti , Dutta Aditi , Roy Kuldeep K. , Mal Sajal K. , Karmakar Shouvik , Mandal Aritra , Mondal Susanta K. , Kumar Sanjay , Saha Soumya , Pradhan Subhankar , Sarkar Ratul , Chakrabarti Monali , Malik Pradip K. , Banerjee Manish 
Published: November 2022

AbstractMalaria continues to be a significant public health problem threatened by the emergence and spread of resistance to artemisinin‐based combination therapies and marked half a million deaths in 2016. A new imidazopyridine chemotype has been envisaged through scaffold‐hopping approach combined with docking studies for putative‐binding interactions with Plasmodium falciparum phosphatidylinositol‐4‐kinase (PfPI4K) target. The docking results steered to the synthesis of compound 1 [5‐(3‐(methylsulfonyl)phenyl)‐3‐(4‐(methylsulfonyl)phenyl)‐3H‐imidazo[4,5‐b]pyridine] followed by the in vitro screening for antiplasmodial activity and ADME‐PK studies. Combined with potent antimalarial activity of compound 1 (Pf3D7 IC50 = 29 nM) with meager in vitro intrinsic clearance, moderate plasma‐protein binding, and acceptable permeability, compound 1 displayed sustained exposure and high oral bioavailability in mice and can thus have the potential as next generation PI4K inhibitor for in vivo studies.