bluuebunny/crossref_metadata_2025_split huggingface dataset:
Accelerated tibia fracture healing in traumatic brain injury in accordance with increased hematoma formation
Authors: Shim Dong Woo , Hong Hyunjoo , Cho Kwang-Chun , Kim Se Hwa , Lee Jin Woo , Sung Seung-Yong 
Published: December 2022

Abstract
Background
Traumatic brain injury (TBI) has been known to accelerate bone healing. Many cells and molecules have been investigated but the exact mechanism is still unknown. The neuroinflammatory state of TBI has been reported recently. We aimed to investigate the effect of TBI on fracture healing in patients with tibia fractures and assess whether the factors associated with hematoma formation changed more significantly in the laboratory tests in the fractures accompanied with TBI.

Methods
We retrospectively investigated patients who were surgically treated for tibia fractures and who showed secondary bone healing. Patients with and without TBI were divided for comparative analyses. Radiological parameters were time to callus formation and the largest callus ratio during follow-up. Preoperative levels of complete blood count and chemical battery on admission were measured in all patients. Subgroup division regarding age, gender, open fracture, concomitant fracture and severity of TBI were compared.

Results
We included 48 patients with a mean age of 44.9 (range, 17–78), of whom 35 patients (72.9%) were male. There were 12 patients with TBI (Group 1) and 36 patients without TBI (Group 2). Group 1 showed shorter time to callus formation (P <  0.001), thicker callus ratio (P = 0.015), leukocytosis and lymphocytosis (P ≤ 0.028), and lower red blood cell counts (RBCs), hemoglobin, and hematocrit (P <  0.001). Aging and severity of TBI were correlated with time to callus formation and callus ratio (P ≤ 0.003) while gender, open fracture, and concomitant fracture were unremarkable.

Conclusion
Tibia fractures with TBI showed accelerated bone healing and superior measurements associated with hematoma formation (lymphocytes, RBCs, hemoglobin, hematocrit). Promoted fracture healing in TBI was correlated with the enhanced proinflammatory state.

Level of evidence
III, case control study.
Walking speed is associated with postoperative pain catastrophizing in patients with lumbar spinal stenosis: a prospective observational study
Authors: Wada Takashi , Tanishima Shinji , Kitsuda Yuki , Osaki Mari , Nagashima Hideki , Noma Hisashi , Hagino Hiroshi 
Published: December 2022

Abstract
Background
The purpose of this study was to investigate whether walking speed is associated with postoperative pain catastrophizing in patients with lumbar spinal stenosis.

Methods
In this prospective observational study, consecutive patients with clinically and radiologically defined lumbar spinal stenosis underwent surgical treatment (decompression, or posterolateral or transforaminal lumbar interbody fusion) at Tottori University Hospital, between October 2015 and April 2018. The pain catastrophizing scale, walking speed, leg and back pain (numerical rating scale), and Japanese Orthopaedic Association score were evaluated preoperatively and at 3, 6, and 12 months postoperatively. Correlations between the pain catastrophizing scale and each variable were analyzed at each evaluation time point. The effect of walking speed on the pain catastrophizing scale was analyzed using mixed-effect models for repeated measurements.

Results
Ninety-four patients were included at baseline, and 83, 88, and 82 patients were analyzed at 3, 6, and 12 months postoperatively, respectively. The pain catastrophizing scale was significantly correlated with walking speed, leg pain, back pain, and the Japanese Orthopaedic Association score at all evaluation time points. The pain catastrophizing scale was associated with walking speed at all evaluation time points.

Conclusions
Our results suggest that changes in postoperative pain catastrophizing after lumbar spine surgery are associated with walking speed. Thus, walking speed is a necessary assessment for the management of pain catastrophizing and associated pain and disability in patients after lumbar spine surgery.
Diagnostic errors in Dentistry, opinions of egyptian dental teaching staff, a cross-sectional study
Authors: El-Wakeel Naglaa , Ezzeldin Naglaa 
Published: December 2022

Abstract
Background
Diagnostic errors is a known problem in healthcare practice. Data on diagnostic errors in the dental field are extremely lacking. The objective of the study is to explore the perception of dental teaching staff about the prevalence of dental diagnostic errors in Egypt, identify the most commonly misdiagnosed dental conditions and point out the contributing factors and levels of patient harm.

Methods
A cross-sectional questionnaire-based study was conducted on 151 dental teaching staff of Egyptian governmental and private universities. The questionnaire was distributed electronically via social media and messaging apps to dental staff members with at least five years of clinical experience to assess their opinion regarding the study objectives. Results were collected and statistically analyzed.

Results
94.7% of participants believed that diagnostic errors represent an urgent problem, lecturers believed by 2.703 folds more than professors that diagnostic errors are an urgent problem The percentage of diagnostic errors was estimated to be < 20% and 20–40% by more than 90% of participants. The most commonly misdiagnosed conditions were oral mucosal lesions (83.4%), followed by temporomandibular joint and periodontal conditions (58.9%) for each. More than half of the participants (60.9%) believe that medical education methodology is one of the factors that lead to dental diagnosis errors. For the impact of errors on patients, 53% of participants reported moderate impacts followed by minor impact (37.7%) while 4.6% reported no impact and the same percentage reported major impact.

Conclusion
This study with statistically significant results reported that dental diagnostic errors are frequent and need to be approached. Oral mucosal lesions, periodontal and temporomandibular joint diseases represent areas that include the most commonly seen errors. Further, besides the lack of resources, the dental education system and lack of proper training are the main causes of this problem.
The analysis of National Health Accounts and financial communications network in Iran health insurance ecosystem
Authors: Rahimisadegh Rohaneh , Mehrolhassani Mohammad Hossein , Jafari Sirizi Mohammad , Noori Hekmat Somayeh 
Published: December 2022

Abstract
Background
One of the major reforms in the health system of any country is the financing reform. Network analysis as a practical method for investigating complex systems allows distinguishing prominent actors in the relation networks. Leading to the identification of the effective actors and key links between them, the analysis of financial networks helps policymakers to implement reformations by providing appropriate evidence. This study aimed to design and analyze the network of National Health Accounts (NHA) and the cost network in the Iran health insurance ecosystem.

Methods
The present study is a network analysis study based on the data from NHA, and both cost and referral rates that was conducted in 2021. Data, which was for the years 2014 to 2018 and related to NHA, was collected from the Statistical Center of Iran, and cost data and referral rates, which were both related to Basic Insurance Organizations (BIOs), were collected from statistical yearbooks. To analyze the network and identify the key actors, macro indicators, such as network size and density, and micro indicators, such as centrality indicators and the combined importance index, were used.

Results
In the financing of the health system in Iran, insurance organizations, as agents and sources of financing, do not have a very good position, so direct payments have become a key element in the network of NHA. Providing treatment-oriented services is quite prior. Regarded to health services, hospitals and outpatient services, such as pharmacies and physicians are the key elements of cost and referral rates respectively.

Conclusion
Consisting of several organizations with different insurance policies and being supervised under different ministries, Iran's health financing system lacks a coherent structure. It is suggested to create a coherent insurance system by creating a single governance system and paying more attention to health-oriented instead of treatment-oriented services. The health insurance ecosystem has become a health-oriented system to reduce the direct payments as well as cost management.
Polyglutamine-expanded ATXN7 alters a specific epigenetic signature underlying photoreceptor identity gene expression in SCA7 mouse retinopathy
Authors: Niewiadomska-Cimicka Anna , Hache Antoine , Le Gras Stéphanie , Keime Céline , Ye Tao , Eisenmann Aurelie , Harichane Imen , Roux Michel J. , Messaddeq Nadia , Clérin Emmanuelle , Léveillard Thierry , Trottier Yvon 
Published: December 2022

AbstractBackgroundSpinocerebellar ataxia type 7 (SCA7) is a neurodegenerative disorder that primarily affects the cerebellum and retina. SCA7 is caused by a polyglutamine expansion in the ATXN7 protein, a subunit of the transcriptional coactivator SAGA that acetylates histone H3 to deposit narrow H3K9ac mark at DNA regulatory elements of active genes. Defective histone acetylation has been presented as a possible cause for gene deregulation in SCA7 mouse models. However, the topography of acetylation defects at the whole genome level and its relationship to changes in gene expression remain to be determined.MethodsWe performed deep RNA-sequencing and chromatin immunoprecipitation coupled to high-throughput sequencing to examine the genome-wide correlation between gene deregulation and alteration of the active transcription marks,e.g.SAGA-related H3K9ac, CBP-related H3K27ac and RNA polymerase II (RNAPII), in a SCA7 mouse retinopathy model.ResultsOur analyses revealed that active transcription marks are reduced at most gene promoters in SCA7 retina, while a limited number of genes show changes in expression. We found that SCA7 retinopathy is caused by preferential downregulation of hundreds of highly expressed genes that define morphological and physiological identities of mature photoreceptors. We further uncovered that these photoreceptor genes harbor unusually broad H3K9ac profiles spanning the entire gene bodies and have a low RNAPII pausing. This broad H3K9ac signature co-occurs with other features that delineate superenhancers, including broad H3K27ac, binding sites for photoreceptor specific transcription factors and expression of enhancer-related non-coding RNAs (eRNAs). In SCA7 retina, downregulated photoreceptor genes show decreased H3K9 and H3K27 acetylation and eRNA expression as well as increased RNAPII pausing, suggesting that superenhancer-related features are altered.ConclusionsOur study thus provides evidence that distinctive epigenetic configurations underlying high expression of cell-type specific genes are preferentially impaired in SCA7, resulting in a defect in the maintenance of identity features of mature photoreceptors. Our results also suggest that continuous SAGA-driven acetylation plays a role in preserving post-mitotic neuronal identity.
Pro-resolving and pro-inflammatory fatty acid-derived mediators in sputum of stable state bronchiectasis patients
Authors: Terranova Leonardo , Risé Patrizia , Gramegna Andrea , Pinna Christian , Agostoni Carlo , Syrén Marie-Louise , Turolo Stefano , Marchisio Paola , Amati Francesco , Aliberti Stefano , Sala Angelo , Blasi Francesco 
Published: December 2022

Abstract
Background
Bronchiectasis is characterized by neutrophilic inflammation and frequent exacerbations often associated with infections. Lipid mediators play critical roles in the inflammatory response, and the balance between anti-inflammatory and pro-inflammatory mediators could drive to chronic inflammation. The aim of this study was to evaluate the metabolites of docosahexaenoic acid and arachidonic acid in sputum of adults with bronchiectasis defining their associations with clinical data, bacterial load and neutrophil elastase.

Methods
An observational, cross-sectional study was conducted at the bronchiectasis program of the Policlinico Hospital in Milan, Italy, where patients were enrolled. Active neutrophil elastase was measured by enzyme-linked immunosorbent assay, pro-resolving and pro-inflammatory fatty acid-derived mediators were evaluated by mass spectrometry and respiratory pathogens were assessed by real-time PCR. Analysis were performed on sputum collected during stable state and clinical data were also collected.

Results
Levels of pro-inflammatory mediators derived from arachidonic acid metabolism showed association with neutrophil elastase, were proportional to Pseudomonas aeruginosa identifications and were linked with radiological gravity index, while the concentrations of pro-resolution mediators derived from docosahexaenoic acid were associated with a better health status, highlighted by the inverse correlation with radiological gravity index, bacterial infections and sputum volume production.

Conclusion
Pro-inflammatory mediators derived from FA metabolisms are associated with severity of bronchiectasis while DHA-derived metabolites are inversely associated with severity of the disease, which may be used for personized treatment of bronchiectasis.
Elevated circulating level of β-aminoisobutyric acid (BAIBA) in heart failure patients with type 2 diabetes receiving sodium-glucose cotransporter 2 inhibitors
Authors: Katano Satoshi , Yano Toshiyuki , Kouzu Hidemichi , Nagaoka Ryohei , Numazawa Ryo , Yamano Kotaro , Fujisawa Yusuke , Ohori Katsuhiko , Nagano Nobutaka , Fujito Takefumi , Nishikawa Ryo , Ohwada Wataru , Katayose Masaki , Sato Tatsuya , Kuno Atsushi , Furuhashi Masato 
Published: December 2022

Abstract
Aims
The mechanism by which a sodium-glucose cotransporter inhibitor (SGLT2i) induces favorable effects on diabetes and cardiovascular diseases including heart failure (HF) remains poorly understood. Metabolomics including amino acid profiling enables detection of alterations in whole body metabolism. The aim of this study was to determine whether plasma amino acid profiles are modulated by SGLT2i use in HF patients with type 2 diabetes mellitus (T2DM).

Methods
We retrospectively examined 81 HF patients with T2DM (68 ± 11 years old; 78% male). Plasma amino acid concentrations in a fasting state after stabilization of HF were determined using ultraperformance liquid chromatography. To minimize potential selection bias in the retrospective analyses, the differences in baseline characteristics between patients receiving an SGLT2i and patients not receiving an SGLT2i were controlled by using an inverse probability of treatment weighting (IPTW)-adjusted analysis.

Results
Of amino acids measurable in the present assay, plasma β﻿﻿-aminoisobutyric acid (BAIBA), an exercise-induced myokine-like molecule also known as 3-aminoisobutyric acid or 3-amino-2-methyproponic acid, was detected in 77% of all patients and the proportion of patients in whom plasma BAIBA was detected was significantly higher in patients receiving an SGLT2i than in patients not receiving an SGLT2i (93% vs. 67%, p = 0.01). Analyses in patients in whom plasma BAIBA was detected showed that plasma BAIBA concentration was significantly higher in patients receiving an SGLT2i than in patients not receiving an SGLT2i (6.76 ± 4.72 vs. 4.56 ± 2.93 nmol/ml, p = 0.03). In multivariate logistic regression analyses that were adjusted for age and sex, SGLT2i use was independently associated with BAIBA detection. The independent association between BAIBA and SGLT2i use remained after inclusion of body mass index, HF with reduced ejection fraction, ischemic etiology, renal function, NT-proBNP, albumin, hemoglobin, and HbA1c into the Cox proportional hazards model. When the differences in baseline characteristics between patients receiving an SGLT2i and patients not receiving an SGLT2i were controlled by using an IPTW-adjusted analysis, least squares mean of plasma BAIBA concentration was significantly higher in patients receiving an SGLT2i than in patients not receiving an SGLT2i.

Conclusion
SGLT2i use is closely associated with increased circulating BAIBA concentration in HF patients with T2DM.
Constitutive glucose dehydrogenase elevates intracellular NADPH levels and luciferase luminescence in Bacillus subtilis
Authors: Wu Yuzheng , Kawabata Honami , Kita Kyosuke , Ishikawa Shu , Tanaka Kan , Yoshida Ken-ichi 
Published: December 2022

Abstract
Background
Genetic modifications in Bacillus subtilis have allowed the conversion of myo-inositol into scyllo-inositol, which is proposed as a therapeutic agent for Alzheimer’s disease. This conversion comprises two reactions catalyzed by two distinct inositol dehydrogenases, IolG and IolW. The IolW-mediated reaction requires the intracellular regeneration of NADPH, and there appears to be a limit to the endogenous supply of NADPH, which may be one of the rate-determining factors for the conversion of inositol. The primary mechanism of NADPH regeneration in this bacterium remains unclear.

Results
The gdh gene of B. subtilis encodes a sporulation-specific glucose dehydrogenase that can use NADP+ as a cofactor. When gdh was modified to be constitutively expressed, the intracellular NADPH level was elevated, increasing the conversion of inositol. In addition, the bacterial luciferase derived from Photorhabdus luminescens became more luminescent in cells in liquid culture and colonies on culture plates.

Conclusion
The results indicated that the luminescence of luciferase was representative of intracellular NADPH levels. Luciferase can therefore be employed to screen for mutations in genes involved in NADPH regeneration in B. subtilis, and artificial manipulation to enhance NADPH regeneration can promote the production of substances such as scyllo-inositol.
Sarcopenia is associated with worse surgical complications but not relapse-free survival and overall survival in patients with retroperitoneal liposarcoma
Authors: Zhao Mingkun , Lv Minzhi , Fang Yuan , Zhuang Aobo , Wu Qian , Tong Hanxing , Lu Weiqi , Zhang Yong 
Published: December 2022

Abstract

Objective
This investigation aimed to explore the relationship between sarcopenia and severe postoperative complications, relapse-free survival (RFS), and overall survival (OS) in patients with retroperitoneal liposarcoma (RLPS).

Material and methods
This retrospective study included 72 RLPS patients (47 men, 25 women; mean age, 57.49 years, SD 10.92) who had abdominal CT exams. Clinical information was recorded, including RLPS characteristics (histologic subtypes, grade, size), laboratory assessment (ALB, PALB, A/G, Hb, SCr), relapse-free survival, overall survival, and postoperative complications. The relationships between those variables and RFS and OS were analyzed using Cox proportional hazard models.

Results
There were 8 severe postoperative complications (Clavien-Dindo grade > 2). The chi-square test showed sarcopenia was associated with severe postoperative complications (P = 0.011). In multivariate analysis, sarcopenia was not associated with relapse-free survival (P = 0.574) and overall survival (P = 0.578).

Conclusions
Sarcopenia predicts worse surgical complications but does not affect relapse-free survival and overall survival.
Insufficient HtrA2 causes meiotic defects in aging germinal vesicle oocytes
Authors: Gao Min , Qiu Yanling , Cao Tianqi , Li Dungao , Wang Jingwen , Jiao Yiren , Chen Zhiyun , Huang Junjiu 
Published: December 2022

AbstractBackgroundHigh-temperature requirement protease A2 (HtrA2/Omi) is a mitochondrial chaperone that is highly conserved from bacteria to humans. It plays an important role in mitochondrial homeostasis and apoptosis. In this study, we investigated the role of HtrA2 in mouse oocyte maturation.MethodsThe role of HtrA2 in mouse oocyte maturation was investigated by employing knockdown (KD) or overexpression (OE) of HtrA2 in young or old germinal vesicle (GV) oocytes. We employed immunoblotting, immunostaining, fluorescent intensity quantification to test the HtrA2 knockdown on the GV oocyte maturation progression, spindle assembly checkpoint, mitochondrial distribution, spindle organization, chromosome alignment, actin polymerization, DNA damage and chromosome numbers and acetylated tubulin levels.ResultsWe observed a significant reduction in HtrA2 protein levels in aging germinal vesicle (GV) oocytes. Young oocytes with low levels of HtrA2 due to siRNA knockdown were unable to complete meiosis and were partially blocked at metaphase I (MI). They also displayed significantly more BubR1 on kinetochores, indicating that the spindle assembly checkpoint was triggered at MI. Extrusion of the first polar body (Pb1) was significantly less frequent and oocytes with large polar bodies were observed when HtrA2 was depleted. In addition, HtrA2 knockdown induced meiotic spindle/chromosome disorganization, leading to aneuploidy at metaphase II (MII), possibly due to the elevated level of acetylated tubulin. Importantly, overexpression of HtrA2 partially rescued spindle/chromosome disorganization and reduced the rate of aneuploidy in aging GV oocytes.ConclusionsCollectively, our data suggest that HtrA2 is a key regulator of oocyte maturation, and its deficiency with age appears to contribute to reproduction failure in females.
NLRP3 deficiency decreases alcohol intake controlling anxiety-like behavior via modification of glutamatergic transmission in corticostriatal circuits
Authors: Li Ziyi , Vidjro Olivia Ewi , Guo Gengni , Du Yanfeng , Zhou Yao , Xie Qian , Li Jiaxin , Gao Keqiang , Zhou Li , Ma Tengfei 
Published: December 2022

Abstract
Background
Alcohol use disorders result from repeated binge and chronic alcohol consumption followed by negative effects, such as anxiety, upon cessation. This process is associated with the activation of NLRP3 inflammasome-mediated responses. However, whether and how inhibition of the NLRP3 inflammasome alters alcohol intake and anxiety behavior remains unclear.

Methods
A combination of drinking-in-the-dark and gavage was established in NLRP3-knockout and control mice. Behavior was assessed by open-field and elevated plus maze tests. Binge alcohol drinking was measured at 2 h and 4 h. A 2 h/4 h/24 h voluntary drinking was determined by a two-bottle choice paradigm. Western blotting and ELISA were applied to examine the levels of the NLRP3 inflammasome and- inflammatory factors, such as IL-1β and TNF-α. Nissl staining was used to measure neuronal injury. The electrophysiological method was used to determine glutamatergic transmission in corticostriatal circuits. In vivo optogenetic LTP and LTD were applied to control the function of corticostriatal circuits on the behavior of mice. MCC950 was used to antagonize the NLRP3 inflammasome.

Results
The binge alcohol intake was decreased in NLRP3 KO mice compared to the control mice. During alcohol withdrawal, NLRP3 deficiency attenuated anxiety-like behavior and neuronal injury in the mPFC and striatum. Moreover, we discovered that glutamatergic transmission to striatal neurons was reduced in NLRP3 KO mice. Importantly, in vivo optogenetic induction of long-term potentiation (LTP) of corticostriatal circuits reversed the effects of NLRP3 deficiency on glutamatergic transmission and anxiety behavior. We also demonstrated that optogenetic induction of LTD decreased anxiety-like behavior and caused a reduction in glutamatergic transmission. Interestingly, NLRP3 deficiency or inhibition (MCC950 injection) attenuated the anxiety-like behavior, but it did not prevent DID + gavage paradigm-induced a persistent enhancement of drinking in a two-bottle choice at 2 and 4 days into withdrawal.

Conclusion
Our results demonstrate that NLRP3 deficiency decreases binge alcohol intake and anxiety-like behavior through downregulation of glutamatergic transmission in corticostriatal circuits, which may provide an anti-inflammatory target for treating alcohol use disorders.