bluuebunny/crossref_metadata_2025_split huggingface dataset:
Predictive value of prognostic nutritional index in patients undergoing gastrectomy for gastric cancer: A systematic review and meta-analysis
Authors: Deng Huachu , He Yiqiang , Huang Gaofei , Huang Yuetong , Wu Jiaheng , Qin Xingan 
Published: October 2024

Background:
The value of prognostic nutritional index (PNI) in gastrectomy remains controversial. This meta-analysis aimed to evaluate the predictive value of PNI in patients undergoing gastrectomy for malignancy.

Methods:
We retrieved studies from medical literature databases to analyze the endpoints of overall survival, cancer-specific survival, recurrence-free survival, and clinicopathologic features. The hazard ratio (HR) and 95% confidence interval (CI) were used to access the survival prognostic value of PNI in patients after gastrectomy. Odds ratio and mean difference were used to evaluate the relationship between the low PNI and clinicopathologic features.

Results:
In total, we included 38 articles (39 trial comparisons) which contained 23,756 gastrectomy patients. The results showed that low PNI was associated with shorter overall survival (HR: 1.82, 95% CI 1.62–2.03), shorter cancer-specific survival (HR: 1.44, 95% CI 1.24–1.67), and shorter recurrence-free survival (HR: 2.52, 95% CI 1.41–4.47). Besides, patients with low PNI had a higher risk of postoperative complications compared with high PNI (HR: 1.65, 95% CI 1.30–2.09). And low PNI group was found to be related to older, lower BMI, larger tumor size, deeper tumor invasion, poorer differentiation, more advanced tumor stage, total gastrectomy, and the presence of lymph node metastasis, lymphatic invasion, and vessel invasion.

Conclusion:
PNI was significantly associated with survival and postoperative complications of gastric cancer patients undergoing gastrectomy. Therefore PNI has the potential to be a prognostic predictor for gastrectomy.
Severe multiple injuries in a 15-year-old boy with pelvic fracture complete anterior dislocation of the sacroiliac joint and rupture of the internal and external iliac arteries: A case report of a rare injury
Authors: Bao Yong-Gang , Li Shu , Liu Bao-Rui , Zhao Yi-Feng , Song Fu-Qiang , Wu Bin 
Published: October 2024

Rationale:
Anterior dislocation of the sacroiliac joint combined with pelvic fractures is relatively rare in clinical practice. It is often associated with hemodynamic instability and severe injuries to other regions, resulting in a complex condition, prolonged treatment duration, and high rates of mortality and disability. However, there are few reports in the literature describing the diagnosis and treatment of anterior dislocation of the sacroiliac joint. In this case, the patient sustained a pelvic fracture with anterior sacroiliac joint dislocation and rupture of both the internal and external iliac arteries following a motor vehicle accident, making it an even rarer and more challenging case to treat. Reporting such cases can enhance the understanding of the diagnosis and treatment of anterior sacroiliac joint dislocation with rupture of the iliac arteries and provide valuable references for similar cases.

Patient Concerns:
The patient was riding an electric bicycle and was hit by a small truck, resulting in a pelvic fracture, anterior dislocation of the sacroiliac joint, and rupture of the internal and external iliac arteries.

Diagnosis:
The patient was diagnosed with open pelvic fracture (type C1.2), left complete anterior dislocation of the sacroiliac joint, left acetabular fracture, left internal and external iliac arteriovenous rupture.

Interventions:
emergency room resuscitation, intensive care unit resuscitation, 6 surgeries and perioperative management.

Results:
He has been discharged from the hospital for more than 1 year and was rechecked every month after discharge, the fracture has healed, there is no obvious pain and discomfort in and around the wound, he has been fitted with a prosthesis, and he is doing the walking function exercise.

Lessons:
Pelvic fracture with anterior sacroiliac dislocation is clinically rare and critical, and is associated with large vessel rupture, severe organ damage, and high mortality and disability rates. Rapid restoration of pelvic stability and hemodynamic stability is the key to treatment. Rapid transfer to a tertiary trauma center, rapid examination through the green channel to clarify the diagnosis, close intensive care, and reasonable multidisciplinary teamwork for surgical intervention are all valuable experiences that we have concluded.
A Chinese CADASIL family with a rare heterozygous mutation in exon 2 of NOTCH3: A case report
Authors: Guo Jingrong , Liu Lulu , Yan Minli 
Published: October 2024

Rationale:
Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is an inherited cerebrovascular disease caused by the neurogenic locus notch homolog protein 3 (NOTCH3) gene mutation. In recent years, most of the newly reported mutations of CADASIL patients mainly occur in exon 3 to 24, while the cases related to exon 2 mutation are rare, and clinical research data are relatively insufficient. In this study, we have reported a case of a rare heterozygous mutation c.128G>A (p.Cys43Tyr) in exon 2 of NOTCH3 in a 41-year-old Chinese man in the light of relevant literatures.

Patient concerns:
A 41-year-old man who suffered slurred speech for 5 days and right lower limb weakness for 4 days was admitted to our hospital.

Diagnoses:
Magnetic resonance imaging of the head revealed diffuse white matter lesions involving the outer capsular area and bilateral temporal poles. The rare heterozygous mutation c.128G>A (p.Cys43Tyr) in exon 2 of NOTCH3 was identified through molecular genetic testing. The proband was diagnosed as having CADASIL. Meanwhile, the same mutation was detected in 2 other family members III5 and IV9.

Interventions:
Atorvastatin calcium tablet (20 mg qd) and aspirin enteric-coated tablet (100 mg qd).

Outcomes:
The patient was hospitalized for 3 weeks and discharged after his symptoms improved.

Lessons:
The heterozygous Cys43Tyr mutation in exon 2 of NOTCH3 is rare. Thus, our case report complements the rare mutation of exon 2 and offers additional clinical data for CADASIL patients.
Comparative diagnostic utility of Rockall and Glasgow-Blatchford scores in non-variceal upper gastrointestinal bleeding: a systematic review and meta-analysis
Authors: Kozai Landon , Tan Arvin , Nebrejas Kevin , Nishimura Yoshito 
Published: October 2024

Introduction
The Rockall score and Glasgow-Blatchford score (GBS) are two scoring systems validated in the evaluation of upper gastrointestinal bleeding (UGIB). However, no meta-analysis exists to summarize the current data and clarify the use of Rockall score and GBS focusing on non-variceal UGIB. We aimed to evaluate and compare the utility of the Rockall score and GBS in predicting clinical outcomes in non-variceal UGIB.

Methods
We conducted a systematic review and meta-analysis, searching the MEDLINE and EMBASE databases for all peer-reviewed articles using the terms including ‘Glasgow-Blatchford’, ‘Rockall’, and ‘gastrointestinal bleed’ from their inception to 22 March 2023. Outcomes included mortality, rebleeding, need for blood transfusion, and need for surgical intervention.

Results
Seven studies with 755 participants with non-variceal bleeding were included in the analysis. Pooled analysis demonstrated no difference in the area under the receiver operating characteristic (AUROC) between GBS and Rockall score to predict mortality [weighted mean difference (WMD) = 0.01, 95% CI: −0.06 to 0.08] or rebleeding (WMD = 0.04, 95% CI: −0.03 to 0.11). GBS had a higher AUROC to predict the outcomes compared to Rockall score for the needs for transfusion (WMD = 0.09, 95% CI: 0.01–0.16) and surgical intervention (WMD = 0.21, 95% CI: 0.14–0.29).

Conclusion
The GBS could be superior to the Rockall score in predicting the needs for transfusion and surgical intervention in non-variceal UGIB. However, both scores demonstrate low performance for predicting mortality or rebleeding.
Comparative Assessment of Outcomes
Authors: Ahmed Aleena , Fatima Maurish , Khan Muhammad Hammad , Faisal Muhammad Hashim , Sehar Ayesha , Khan Muhammad Jahanzaib , Aziz Hassan 
Published: October 2024

Objective:
This systematic review and meta-analysis aimed to compare outcomes between abdominal drain placement and no drain placement post-pancreatectomy

Background:
Left pancreatectomy (LP) is a surgical procedure commonly employed for various pancreatic conditions, often associated with postoperative complications like post-operative pancreatic fistula (POPF). While routine abdominal drainage following LP has been standard practice, recent evidence suggests potential benefits of omitting this approach.

Methods:
A comprehensive search was conducted on PubMed, Cochrane, and Embase from inception up to 15 March 2024, yielding nine studies comprising 15,817 patients. Data were extracted from randomized and non-randomized studies reporting primary and secondary outcomes. The analysis was performed in Revman. Risk ratios were calculated with 95% confidence intervals, and a P-value of <0.05 was considered statistically significant.

Results:
A total of 13,081 patients underwent drain placement after left pancreatectomy, and 2,736 patients were included in the no-drain group. Out of the total, 45.1% (n=7140) patients were male, with 45.9% (n=6012) males in the drain group and 41.2% (n=1128) males in the no-drain group. Major morbidity, defined as Clavien-Dindo grade ≥III complications, was significantly lower in the no-drain group (relative risk [RR]: 0.77, 95% confidence interval [CI]: 0.64–0.93, P=0.006). Similarly, lower rates of postoperative pancreatic fistula (POPF) (RR: 0.51, 95% CI: 0.38–0.67, P<0.00001), readmission (RR: 0.75, 95% CI: 0.59–0.96, P=0.02), and surgical site infections (RR: 0.82, 95% CI: 0.70–0.95, P=0.009) were observed in the no-drain group. Additionally, a shorter length of hospital stay was noted in this group (mean difference MD: –1.65, 95% CI: –2.50 to –0.81, P=0.0001).

Conclusions:
Omitting routine drainage after left pancreatectomy is associated with reduced complications and shorter hospital stays, supporting its potential benefits in improving postoperative outcomes.
Bacterial sensing via Neuronal Receptor Initiates Gut Mitochondrial Surveillance for Host Adaptation
Authors: Liu Huimin , Chen Panpan , Yang Xubo , Hao FanRui , Tian Guojing , Shan Zhao , Qi Bin 
Published: October 2024

AbstractAnimals exist within a microbial world and are constantly challenged by pathogen infections. Microbe-mediated protection for against infection is the survival strategy for host. However, elucidating specific microbial molecules and understanding how they interact with the host’s intracellular surveillance system for protection is difficult but highly desirable. Here, by establishing “pathogen-like-bacteria” screening system, we identifiedE. colimutants, including ΔymcB, that act as “pathogen-like-bacteria” to defend animals againstPseudomonas aeruginosaPA14 infection by activating UPRmt. Additionally, through genetic screening, we identified neuronal transmembrane protein, MDSS-1, that is crucial for sensing ΔymcBand activating intestinal UPRmt. Moreover, we demonstrated that MDSS-1 functions as a receptor in ASE neurons, responsible for detecting ΔymcB. It then communicates microbial signals through neuropeptides, GPCR, Wnt signaling and endopeptidase inhibitors to trigger intestinal UPRmt, that defends the host animals against infections. Furthermore, Constitutionally activation of MDSS-1 in ASE neurons is sufficient to trigger intestinal UPRmtin animals, resulting in protection against infection. Our study uncovers an intriguing mechanism involving intracellular mitochondrial surveillance, where neuron-intestine crosstalk originates from ASE neurons to detect bacteria and combat pathogens. This study identifies a bacteria-sensing mechanism in neurons that regulates intestinal mitochondrial surveillance pathway for host adaptation.HighlightsEstablishment of “pathogen-like-bacteria” screening system inC. elegansΔymcBpromotes animal defend against infections via triggering UPRmtNeuronal MDSS-1, a single transmembrane protein, detects “pathogen-like-bacteria”Activated-MDSS-1 induces distant UPRmtvia inter-tissue communication factors
Insights into the Molecular Mechanism of Pulmonary Vein Stenosis in Pediatric Patients
Authors: Kalustian Alyssa B , Ji Pengfei , Wadhwa Lalita , Caldarone Christopher A. , Bansal Manish , Qureshi Athar M. , Heinle Jeffrey S. , Birla Ravi K. 
Published: October 2024

AbstractBackgroundPediatric pulmonary vein stenosis (PVS) is associated with substantial morbidity and mortality for the subset of patients with recurrent or progressive disease. The molecular mechanisms underlying the development and trajectory of PVS remain unclear. This study characterizes the transcriptome of clinical and phenotypic subtypes of PVS.MethodsBulk RNA sequencing analysis was performed on human pulmonary vein tissue samples obtained from surgical interventions for pediatric patients with PVS. Transcriptomic profiles were compared for primary versus post-repair PVS as well as aggressive versus non-aggressive clinical phenotypes. Principal component analysis was performed, the differential gene expression quantified, and pathway analysis conducted based on gene ontology, KEGG and Reactome.ResultsWhen comparing AggPPVS vs NonAggPPVS, differences were noted in the genes associated in extracellular matrix regulation and PIEZO1, a mechanosensitive receptor present in endothelial cells. In addition, there were notable changes in cardiac muscle contractility, calcium handling, respiratory and energy metabolism. These results point to a potential mechanism for aggressive PPVS phenotype, due to an overexpression of PIEOZ1 in response to elevated shear stress, subsequent activation of intracellular signaling pathways and leading to reduced contractility and intracellular calcium transients with cardiomyocytes.ConclusionsThe result of this study suggests that aggressive PPVS phenotype is caused by an increase in PIEZO1 expression and subsequent changes in extracellular matrix production, heart muscle contractility and changes in calcium transients within cardiomyocytes. These results provide a potential target for therapeutic invention for primary PPVS by inhibiting the activity of PIEZO1. This could potentially reduce morbidity in this patient population.
Granulocyte colony-stimulating factor protects against arthritogenic alphavirus pathogenesis in a type I IFN-dependent manner
Authors: Hameed Muddassar , Hossain Md Shakhawat , Daamen Andrea R. , Lipsky Peter E. , Weger-Lucarelli James 
Published: October 2024

AbstractArthritogenic alphaviruses cause disease characterized by fever, rash, and incapacitating joint pain. Alphavirus infection stimulates robust inflammatory responses in infected hosts, leading to the upregulation of several cytokines, including granulocyte colony-stimulating factor (G-CSF). G-CSF is secreted by endothelial cells, fibroblasts, macrophages, and monocytes and binds to colony stimulating factor 3 receptor (CSF3R, also known as G-CSFR) on the surface of myeloid cells. G-CSFR signaling initiates proliferation, differentiation, and maturation of myeloid cells, especially neutrophils. Importantly, G-CSF has been found at high levels in both the acute and chronic phases of chikungunya disease; however, the role of G-CSF in arthritogenic alphavirus disease remains unexplored. Here, we sought to test the effect of G-CSF on chikungunya virus (CHIKV) and Mayaro virus (MAYV) infection using G-CSFR-deficient mice (G-CSFR−/−). We observed sustained weight loss in G-CSFR−/−mice following viand MAYV infection compared to wild-type mice. Furthermore, G-CSFR−/−mice had a significantly higher percentage of inflammatory monocytes and reduction in neutrophils throughout infection. The difference in weight loss in G-CSFR−/−mice induced by alphavirus infection was corrected by blocking type I IFN signaling. In summary, these studies show that type I IFN signaling contributes to G-CSFR mediated control of arthritogenic alphavirus disease.
CandyCollect: An Open-Microfluidic Device for the Direct Capture and Enumeration of Salivary-Extracellular Vesicles
Authors: Pierce Corinne , Suryoraharjo Kezia , Robertson Ingrid H. , Su Xiaojing , Hatchett Daniel B. , Shin Albert , Adams Karen N. , Berthier Erwin , Thongpang Sanitta , Ogata Alana , Theberge Ashleigh B. , Sohn Lydia L. 
Published: October 2024

AbstractExtracellular Vesicles (EVs) are membrane-derived vesicles shed by cells into the extracellular space that play key roles in intercellular communication and other biological processes. As membrane-bound cargos of nucleic acids and other proteins that are abundantly found in virtually every biofluid including blood, urine, and saliva, EVs are widely regarded as promising biomarkers for disease detection. While it is an increasingly promising biofluid from which to isolate EVs, saliva poses challenges due its complexity and heterogeneity—cells, debris, and other proteins can inhibit the isolation of EVs by traditional platforms. Here, we employ the CandyCollect, a lollipop-inspired sampling device with open microfluidic channels, as a non-invasive and patient-friendly alternative for the capture of salivary EVs. The CandyCollect simplifies sample preparation by effectively pre-concentrating EVs on the device surface before EVs are eluted off of the CandyCollect, labeled with cholesterol-tagged oligonucleotides, and subsequently detected by qPCR with primers specific for the tagged oligos to enumerate the relative number of EVs. We demonstrate that downstream EV cargo analysis can be performed using Simoa. Overall, the CandyCollect ushers a new method to capture, enumerate, and analyze salivary EVs.
Lack of evidence for the contribution of cone photoreceptors to human melatonin suppression and alerting response to light at night
Authors: Fazlali Fatemeh , Lazar Rafael , Yahya Faady , Epple Christian , Spitschan Manuel , Stefani Oliver , Cajochen Christian 
Published: October 2024

SummaryLight exposure at night can suppress melatonin production and increase alertness, primarily through the action of melanopsin-containing intrinsically photosensitive retinal ganglion cells (ipRGCs). This study investigated whether cone photoreceptors also influence melatonin suppression and subjective alertness using non-visual metameric light emitted from a display. Forty-eight participants with normal trichromatic vision were exposed to three lighting conditions: a baseline (9 lxmEDI), constant background (149 lxmEDI), and cone-modulated flickering light targeting different cone combinations and post-receptoral channels (149 lxmEDI) for 2 hours after their habitual bedtime. Salivary melatonin levels and subjective alertness were measured throughout a 9-h protocol. Bayesian analysis showed that cone-modulated flickering light did not significantly affect melatonin suppression or alertness, providing evidence against the hypothesis that cone photoreceptors contribute to these non-visual effects of light. In conclusion, our results suggest cone photoreceptors do not play a measurable role in light’s effects on melatonin suppression and subjective alertness at night.
Comparative single-cell analyses reveal evolutionary repurposing of a conserved gene program in bat wing development
Authors: Schindler Magdalena , Feregrino Christian , Aldrovandi Silvia , Lo Bai-Wei , Monaco Anna A. , Ringel Alessa R. , Morales Ariadna , Zehnder Tobias , Behncke Rose Yinghan , Glaser Juliane , Barclay Alexander , Andrey Guillaume , Kragesteen Bjørt K. , Hägerling René , Haas Stefan , Vingron Martin , Ulitsky Igor , Marti-Renom Marc , Hechavarria Julio , Fasel Nicolas , Hiller Michael , Lupiáñez Darío , Mundlos Stefan , Real Francisca M. 
Published: October 2024

AbstractBats are the only mammals capable of self-powered flight, an evolutionary innovation based on the transformation of forelimbs into wings. The bat wing is characterized by an extreme elongation of the second to fifth digits and a wing membrane calledchiropatagiumconnecting them. Here we investigated the developmental and cellular origin of this structure by comparing bat and mouse limbs using omics tools and single-cell analyses. Despite the substantial morphological differences between the species, we observed an overall conservation of cell populations and gene expression patterns including interdigital apoptosis. Single-cell analyses of micro-dissected embryonic chiropatagium identified a specific fibroblast population, independent of apoptosis-associated interdigital cells, as the origin of this tissue. These distal cells express a conserved gene program including the transcription factorsMEIS2andTBX3, which are commonly known to specify and pattern the early proximal limb. Transgenic ectopic expression ofMEIS2andTBX3in mouse distal limb cells resulted in the activation of genes expressed during wing development and phenotypic changes related to wing morphology, such as the fusion of digits. Our results elucidate fundamental molecular mechanisms of bat wing development and illustrate how drastic morphological changes can be achieved through repurposing of existing developmental programs during evolution.
Inhibition of the transcription factor PU.1 suppresses tumor growth in mice by promoting the recruitment of cytotoxic lymphocytes through the CXCL9-CXCR3 axis
Authors: Sleapnicov Nichita , Ha Soon-Duck , Zhong Shanshan Jenny , Duchscher Jackie , Ezra Sally , Li Shawn Shun-Cheng , Kim Sung O. 
Published: October 2024

AbstractTumor-associated macrophages (TAMs) are among the most abundant immune cells associated with tumors, which often exhibit immune regulatory phenotypes that promote tumor growth and confer resistance to anti-tumor immune therapies. Despite extensive efforts in developing immunotherapeutic strategies aimed at controlling the recruitment or reprogramming of TAMs, success has been limited due to strategic caveats, underscoring the need for a novel approach targeting the TAMs. PU.1, a lineage-dependent transcription factor, is highly expressed throughout the lifespan of macrophages. We have found that inhibition of PU.1 by the small molecule DB2313 suppresses melanoma tumor growth in mice through enhanced tumor recruitment of CD4+ T helper cells and cytotoxic T/NK cells mediated by TAMs. Whole transcriptome and targeted gene expression analyses revealed that DB2313 upregulates CXCL9 expression in bone marrow-derived macrophages (BMDMs) and TAMs. The anti-tumor effects of DB2313 were abolished by depleting macrophages with clodronate or inhibiting the CXCL9-CXCR3 chemokine axis using neutralizing antibodies against CXCL9 or CXCR3. Collectively, these results suggest that pharmacological inhibition of PU.1 suppresses tumor growth by promoting tumor infiltrating lymphocytes through the CXCL9-CXCR3 chemokine axis. Our study establishes a framework for developing TAM-modulating immunotherapies by targeting the transcriptional factor PU.1.