bluuebunny/crossref_metadata_2025_split huggingface dataset:
On Death and Examination of the Dead in the Ottoman Empire: A Historical Perspective
Authors: Öner Bedirhan Sezer , Çetin Selçuk 
Published: November 2023

Abstract
The aims of this study were to examine the procedures performed during the death examination by scanning the qadi registry books of the Ottoman Empire in the 16th–18th centuries and to compare them with the procedures performed today. In our study, a total of 12 Konya qadi registry records from the period between 16th and 18th centuries (1563–1731) were examined. In our study, a total of 70 cases that underwent death discovery and examination were found out of 12 Konya qadi registry books. When the causes of death were evaluated in the cases in which the dead were discovered, being trapped in the wreckage was found as the most common cause with a total of 9 cases. This was followed by drowning (n = 8), being found dead in the open area (n = 8), and sharp injuries (n = 7). Because of the developments in all fields of medicine, it is understandable that wound descriptions are much more detailed today. However, descriptions such as “black bruise, battery, wounding” were found in the qadi registers as well. This case study is one of the most historic and comprehensive death series.
From Race to Racism and Disparities to Equity
Authors: Reeder-Hayes Katherine , Roberson Mya L. , Wheeler Stephanie B. , Abdou Yara , Troester Melissa A. 
Published: November 2023

Purpose
Racial disparities in outcomes of breast cancer in the United States have widened over more than 3 decades, driven by complex biologic and social factors. In this review, we summarize the biological and social narratives that have shaped breast cancer disparities research across different scientific disciplines in the past, explore the underappreciated but crucial ways in which these 2 strands of the breast cancer story are interwoven, and present 5 key strategies for creating transformative interdisciplinary research to achieve equity in breast cancer treatment and outcomes.

Design
We first review the key differences in tumor biology in the United States between patients racialized as Black versus White, including the overrepresentation of triple-negative breast cancer and differences in tumor histologic and molecular features by race for hormone-sensitive disease. We then summarize key social factors at the interpersonal, institutional, and social structural levels that drive inequitable treatment. Next, we explore how biologic and social determinants are interwoven and interactive, including historical and contemporary structural factors that shape the overrepresentation of triple-negative breast cancer among Black Americans, racial differences in tumor microenvironment, and the complex interplay of biologic and social drivers of difference in outcomes of hormone receptor positive disease, including utilization and effectiveness of endocrine therapies and the role of obesity. Finally, we present 5 principles to increase the impact and productivity of breast cancer equity research.

Results
We find that social and biologic drivers of breast cancer disparities are often cyclical and are found at all levels of scientific investigation from cells to society. To break the cycle and effect change, we must acknowledge and measure the role of structural racism in breast cancer outcomes; frame biologic, psychosocial, and access factors as interwoven via mechanisms of cumulative stress, inflammation, and immune modulation; take responsibility for the impact of representativeness (or the lack thereof) in genomic and decision modeling on the ability to accurately predict the outcomes of Black patients; create research that incorporates the perspectives of people of color from inception to implementation; and rigorously evaluate innovations in equitable cancer care delivery and health policies.

Conclusions
Innovative, cross-disciplinary research across the biologic and social sciences is crucial to understanding and eliminating disparities in breast cancer outcomes.
A Modified Suture Technique to Improve Scar Appearance in Wounds Under High Tension
Authors: Liu Hui , Lin Mao-Hui , Jiang Ling-Li , Chang Shu-Sen , Chen Wei , Nie Kai-Yu , Huang Guang-Tao , Qi Fang , Zhou Xiao-Fan , Chen Jian-Da , Deng Cheng-Liang , Wei Zai-Rong 
Published: November 2023

Abstract
The purpose of this study was to introduce a modified suture technique and to compare its effects on skin scar formation with 2 traditional suture methods: simple interrupted suture (SIS) and vertical mattress suture (VMS). Three groups of healthy adult female Sprague-Dawley rats were selected (6 replicates in each group), and the full-thickness skin of 5 cm × 0.2 cm was cut off on the back of the rats after anesthesia. The wounds were then sutured using 1 of the 3 methods for each group: SIS, VMS, and a newly introduced modified vertical mattress suture (M-VMS) technique with the needle reinsertion at the exit point. A traction device was installed on the back of the rats to achieve high tension wounds. The tensile distance was increased by 1 mm every day for 20 days. After 20 days of healing, the hematoxylin-eosin staining method was used for observation of scar morphology. The collagen production rate was measured by Masson staining, and the type I collagen and type III collagen were detected by the immunofluorescence method. Immunohistochemical staining was used to detect the expression of myofibroblast marker α-smooth muscle actin, and real-time quantitative polymerase chain reaction and Western blot techniques were used to detect the expressions of transforming growth factors TGFβ1, TGFβ2, and TGFβ3 to understand the mechanisms of scar formation. Results showed that the quantity and density of collagen fibers were both lower in the M-VMS group than in the other 2 groups. Immunofluorescence results showed that type I collagen was significantly lower, whereas type III collagen was significantly higher in the M-VMS group than in the other 2 groups. The expressions of α-smooth muscle actin and TGFβ1 both were lower in the M-VMS group than in the other 2 groups. The expression of TGFβ2 and TGFβ3 had no obvious difference among the 3 groups. For wounds under high tension, compared with SIS and VMS methods, the M-VMS technique we proposed can reduce scar formation due to the reduction of collagen formation, myofibroblast expression, and TGFβ1 expression.
RESTRICTIVE FLUID RESUSCITATION IN SEPTIC SHOCK PATIENTS HAS LOWER MORTALITY AND ORGAN DYSFUNCTION RATES THAN STANDARD THERAPY
Authors: Jiang Zhizhao , Luo Fenbin , Liu Yuqi , Sun Xuri , Tan Guoliang , Chen Zhiliang , Chen Yongqiang 
Published: November 2023

ABSTRACTBackground: The influence of restrictive fluid resuscitation and the early administration of vasopressors on the clinical outcomes in patients with septic shock are not fully understood. The purpose of this study was to evaluate the effects of restrictive fluid management on mortality and organ dysfunction in patients with septic shock.Methods: This study included consecutive patients with septic shock in need of fluid resuscitation. Based on the fluid management provided in the initial resuscitation phase, a comparison was made between a restrictive group and a standard fluid management group. The primary outcome was in-hospital death, whereas secondary outcomes included organ dysfunction and other adverse events.Results: A total of 238 patients were included in this study. Restrictive fluid management was administered to 59.2% of patients, whereas 40.8% received standard fluid management. Restrictive resuscitation was associated with a lower in-hospital mortality rate (24.8% vs. 52.6%), as well as a shorter median intensive care unit stay (8.0 vs. 11.0 days). The restrictive strategy was associated with a significantly lower prevalence of new-onset acute kidney injury (25.5% vs. 51.5%) and a decrease in the incidence of renal replacement therapy (20.6% vs. 40.2%). The standard group had a higher risk of the need for mechanical ventilation and a significantly lower median number of days without a ventilator than the restrictive group. The median duration of vasopressor-free days in the restrictive group was significantly longer than that in the standard group (25.0 vs. 18.0). The administration rate of inotropes in the restrictive group was significantly lower than that in the standard group. A multivariate logistic regression model showed that restrictive fluid management (odds ratio [OR], 0.312; 95% confidence interval [CI], 0.098–0.994) and vasopressor-free days (OR, 0.807; 95% CI, 0.765–0.851) protect against in-hospital death, whereas Acute Physiology and Chronic Health Evaluation II scores (OR, 1.121; 95% CI, 1.018–1.234) were independent risk factors for in-hospital death.Conclusions: Restrictive fluid resuscitation and early vasopressor protocol in patients with septic shock are associated with better outcomes, indicating that this regimen is feasible and safe.
Astragaloside IV modulates gut macrophages M1/M2 polarization by reshaping gut microbiota and SCFA in sepsis
Authors: Yang Tao , Xie Shuhua , Cao Lei , Li Man , Ding Ling , Wang Lei , Pang Shenyue , Wang Zhifen , Geng Licheng 
Published: November 2023

ABSTRACT
M1 macrophage-mediated inflammation is critical in sepsis. We previously found protective role of Astragaloside IV (AS-IV) in sepsis-associated gut impairment, whose specific mechanism remains unknown. Gut microbiota modulates gut homeostatic balance to avoid excessive inflammation. Here, we aimed to investigate effects of AS-IV on gut macrophages polarization and potential roles of gut microbiota and short chain fatty acids (SCFA) in septic gut damage. Mice were pre-treated by AS-IV gavage for 7 days before cecal ligation and puncture (CLP). M1 polarization of gut lamina propria macrophages (LpMs) was promoted by CLP, accompanied by abnormal cytokines release and intestinal barrier dysfunction. NLRP3 inflammasome was activated in M1 LpMs. 16S rRNA sequencing demonstrated gut microbiota imbalance. The levels of acetate, propionate and butyrate in fecal samples decreased. Notably, AS-IV reversed LpMs M1/M2 polarization, lightened gut inflammation and barrier injury, reduced NLRP3 inflammasome expression in LpMs, restored the diversity of gut microbiome and increased butyrate levels. Similarly, these benefits were mimicked by fecal microbiota transplantation (FMT) or exogenous butyrate supplementation. In Caco-2 and THP-1 co-cultured model, lipopolysaccharide (LPS) and interferon-γ (IFN-γ) caused THP-1 M1 polarization, Caco-2 barrier impairment, abnormal cytokines release and high NLRP3 inflammasome expression in THP-1 cells, all of which were mitigated by butyrate administration. However, these protective effects of butyrate were abrogated by NLRP3 gene overexpression in THP-1. In conclusion, AS-IV can ameliorate sepsis-induced gut inflammation and barrier dysfunction by modulating M1/M2 polarization of gut macrophages, whose underlying mechanism may be restoring gut microbiome and SCFA to restrain NLRP3 inflammasome activation.
Comparison Between Cz-C3/C4 and C3-C4 Montages to Protect Against Peripheral Stimulation in Transcranial Facial Motor-Evoked Potential Monitoring
Authors: Matsuoka Ryuta , Hamada Naoya , Nishimura Nobuyuki , Mitsui Takaaki , Shiraishi Yuki , Hayami Hiromichi , Fukutome Kenji , Tei Rinsei , Shin Yasushi , Aketa Shuta , Kato Daizo , Kita Takashi , Motoyama Yasushi 
Published: November 2023

Introduction:
In facial motor-evoked potential monitoring, efforts to reduce peripheral stimulation are necessary because it can cause false-negatives. The effects of peripheral stimulation on Cz-C3/C4 and C3-C4 montages were compared.

Methods:
Facial motor-evoked potentials were recorded from bilateral orbicularis oculi (Oculi) and oris (Oris) muscles. The double-train approach combining single-pulse and five-train pulse stimulation was used to determine the effect of peripheral stimulation. If the five-train pulse produced a significant waveform, it was defined as “total success.” In total success cases, “true success” was defined as a case in which no waveform appeared after the single pulse at the threshold level of the five-train pulse. The total and true success rates and the threshold value of Oculi and Oris were compared between Cz-C3/C4 and C3-C4 montages.

Results:
Thirty-six muscles each of Oculi and Oris of 18 patients were used for the analysis. True success was more likely to be obtained by the Cz-C3/C4 montage than the C3-C4 montage in Oculi (42% vs. 22%, p = 0.039). Both Oculi and Oris had higher thresholds to elicit facial motor-evoked potentials with the Cz-C3/C4 montage (Oculi: 101.7 vs. 71.4 mA, p = 0.038; Oris: 94.8 vs. 73.1 mA, p = 0.016).

Conclusions:
Cz-C3/4 montage is more effective at reducing peripheral stimulation compared with the C3-4 montage. This effect was primarily seen in the orbicularis oculi muscle. It should be noted that the Cz-C3/C4 montage has a higher threshold than the C3-C4 montage in facial muscles. In facial motor-evoked potential monitoring, the Cz-C3/C4 montage may be more suitable to eliminate peripheral stimulation.
Providing a scaffold for considering theoretical frameworks in evidence implementation projects: the JBI approach to evidence implementation
Authors: Munn Zachary , McArthur Alexa , Klugar Miloslav , Stannard Daphne , Cooper Adam S. , Enuameh Yeetey , Porritt Kylie 
Published: November 2023

ABSTRACTThere are many theories, models, and frameworks that have been proposed in the field of implementation science. Despite this, many evidence implementation or practice improvement projects do not consider these theories, models, or frameworks in their improvement efforts. The JBI approach is one example of an implementation theory, model, or framework. This approach has been developed particularly with health care professionals in mind and is designed to clearly guide pragmatic evidence implementation efforts based on the best available evidence. In this paper, we discuss how the JBI approach to evidence implementation can interact with and support theory-informed, pragmatic evidence implementation projects.
AlzGenPred: A CatBoost based method using network features to classify the Alzheimer’s Disease associated genes from the high throughput sequencing data
Authors: Shukla Rohit , Singh Tiratha Raj 
Published: November 2023

AbstractBackground and ObjectiveAD is a progressive neurodegenerative disorder characterized by memory loss. Due to the advancement in next-generation sequencing technologies, an enormous amount of AD-associated genomics data is available. However, the information about the involvement of these genes in AD association is still a research topic because all these algorithms are based on statistical techniques. Therefore, AlzGenPred is developed to identify the AD-associated genes from a large set of data.MethodsTo develop the AlzGenPred, we have compiled a benchmark dataset consisting of 1086 AD and non-AD genes and used them as positive and negative datasets. We have generated several features including the fused features and evaluated them through machine learning methods. Then hyperparameter tuning approach was also applied and the final model was selected. The proposed method was validated by using the AlzGene and transcriptomics datasets and proposed as a standalone tool.ResultsTotal 13504 features belonging to eight different encoding schemes of these sequences were generated and evaluated by using 16 ML algorithms. It reveals that network-based features can classify AD genes while sequence-based features are not able to classify them. Then we generated 24 different fused features (6020 D) using sequence-based features and fed them into a two-step lightGBM-based recursive feature selection method. It increased up to 5-7% accuracy. After that selected eight fused features with CKSAAP were used for the hyperparameter tuning. They showed <70% accuracy. Therefore, network-based features were used to generate the CatBoost-based ML method called AlzGenPred with 96.55% accuracy and 98.99% AUROC. The developed method is tested on the AlzGene dataset where it showed 96.43% accuracy. Then the model is validated using the transcriptomics dataset also.ConclusionThe validation of AlzGenPred using the AlzGene dataset and transcriptomics dataset obtained from Human, mouse, and ES-derived neural cells revealed that it can classify the omics data and can sort the AD-associated genes. These predicted genes can be directly used in the wet lab for further testing which will reduce labor cost and time expenses. The AlzGenPred is developed as a standalone package and is available for users athttps://www.bioinfoindia.org/alzgenpred/andhttps://github.com/shuklarohit815/AlzGenPred.
Clinical Utility of Ultrasonography BI-RADS in the Evaluation of Breast Cancer in Patients with Palpable Breast Masses: A Diagnostic Test Accuracy Original Article
Authors: Gami Vismit , Desai Dev , Shah Sahil , Rana Devang 
Published: November 2023

AbstractIntroductionDiagnosing and staging breast cancer with an easy and widely useable method that can be employed worldwide in the poorest and wealthiest settings is important.Mammography is a technique that might not be available in faraway clinics and it is technically challenging whereas USG can be available in most remote areas and small hospitals far from tertiary care hospitals. Even a trainee Radiology resident can use USG BIRADS and can be used diagnostically for that, it is important to define its, diagnostic accuracy with Sensitivity, Specificity, and other diagnostic parameters.AimsTo determine the Diagnostic accuracy of USG BIRADS compared to the gold standard Histopathology reportMethodologyA Retrospective cohort study was conducted at a tertiary care hospital. a total of 84 female patients presenting to Surgical OPD with complaints of a breast lump or pain were enrolled from their records. Their Breast USG results were analyzed to identify their BIRADS stage correctly and then their corresponding Histopathology report was considered the gold standard to compare the USG results against. Excel, SPSS, and Revman were used to conduct analysis and create results.Results36 of these 84 patients belonged to BIRADS 1, 2, and 5 where Sensitivity, Specificity, and PPV were calculated at 100%. No one was diagnosed with BIRADS III from USG reports. For USG BIRADS 4, in total 48 patients Sensitivity was 0.667, specificity was 0.883, and PPV was 0.364.ConclusionPatients whose USG shows Benign growth or can be diagnosed in BIRADS 1, 2, 3, and 5 can be counted as accurate and precise. When the USG diagnosis describes the patient to be in BIRADS 4, the sensitivity and PPV show poor results showing a very low probability of the patient being truly positive when the diagnosis gives a positive result.
Subregion and sex differences in ethanol activation of cholinergic and glutamatergic cells in the mesopontine tegmentum
Authors: Mulloy SM , Aback EM , Gao R , Engel S , Pawaskar K , Win C , Moua A , Hillukka L , Lee AM 
Published: November 2023

AbstractEthanol engages cholinergic signaling and elicits endogenous acetylcholine release. Acetylcholine input to the midbrain originates from the mesopontine tegmentum (MPT), which is composed of the laterodorsal tegmentum (LDT) and the pedunculopontine tegmental nucleus (PPN). We investigated the effect of acute and chronic ethanol administration on cholinergic and glutamatergic neuron activation in the PPN and LDT in male and female mice. We show that ethanol selectively activates neurons of the PPN and not the LDT in male mice. Acute 4.0 g/kg and chronic 15 daily injections of 2.0 g/kgi.p.ethanol inducedFosexpression in cholinergic and glutamatergic PPN neurons in male mice, whereas cholinergic and glutamatergic neurons of the LDT were unresponsive. In contrast, acute or chronic ethanol at either dose or duration had no effect on the activation of cholinergic or glutamatergic neurons in the MPT of female mice. Female mice had higher level of baseline activation in cholinergic neurons compared with males. We also found a population of co-labeled cholinergic and glutamatergic neurons in the PPN and LDT which were highly active in the saline- and ethanol-treated groups in both sexes. These findings illustrate the complex differential effects of ethanol across dose, time point, MPT subregion and sex.
KSR1 knockout mouse model demonstrates MAPK pathway’s key role in cisplatin- and noise-induced hearing loss
Authors: Ingersoll Matthew A. , Lutze Richard D. , Kelmann Regina G. , Kresock Daniel F. , Marsh Jordan D. , Quevedo Rene V. , Zuo Jian , Teitz Tal 
Published: November 2023

AbstractHearing loss is a major disability in everyday life and therapeutic interventions to protect hearing would benefit a large portion of the world population. Here we found that mice devoid of the protein kinase suppressor of RAS 1 (KSR1) in their tissues (germline KO mice) exhibit resistance to both cisplatin- and noise- induced permanent hearing loss compared to their wild-type KSR1 littermates. KSR1 is expressed in the cochlea and is a scaffold protein that brings in proximity the mitogen-activated protein kinase (MAPK) proteins BRAF, MEK and ERK and assists in their activation through a phosphorylation cascade induced by both cisplatin and noise insults in the cochlear cells. Deleting the KSR1 protein tempered down the MAPK phosphorylation cascade in the cochlear cells following both cisplatin and noise insults and conferred hearing protection of up to 30 dB SPL in three tested frequencies in mice. Treatment with dabrafenib, an FDA- approved oral BRAF inhibitor, downregulated the MAPK kinase cascade and protected the KSR1 wild-type mice from both cisplatin- and noise-induced hearing loss. Dabrafenib treatment did not enhance the protection of KO KSR1 mice, as excepted, providing evidence dabrafenib works primarily through the MAPK pathway. Thus, either elimination of the KSR1 gene expression or drug inhibition of the MAPK cellular pathway in mice resulted in profound protection from both cisplatin- and noise-induce hearing loss. Inhibition of the MAPK pathway, a cellular pathway that responds to damage in the cochlear cells, can prove a valuable strategy to protect and treat hearing loss.Significance StatementTen percent of the world population suffers from hearing loss but this impairment may be preventable. We show that mice devoid of the KSR1 protein (KO) exhibit resistance to cisplatin- and noise-induced permanent hearing loss compared to wild-type littermates that harbor the protein. Removing KSR1 tempers down the MAPK phosphorylation cascade of BRAF-MEK-ERK induced in the cochlea following cisplatin and noise insults. Treatment of KSR1 wild-type mice following cisplatin or noise with an FDA-approved BRAF inhibitor, dabrafenib, protected the hearing and, importantly, did not confer additional protection to the KO KSR1 mice. Hence, the MAPK pathway has a unique role in responding to cochlear damage, and removing KSR1 gene expression or drug inhibition of the pathway results in hearing protection.