bluuebunny/crossref_metadata_2025_split huggingface dataset:
Saikosaponin D mitigate pilocarpine‐induced astrocyte injury by regulating the NLRP3/caspase‐1 signaling pathway
Authors: Liu Jun‐yan , Shen Yu‐ling , Zhu Jing‐yi , Yang Dong‐dong 
Published: March 2024

AbstractStudies have shown that saikosaponin D (SSD) has favorable neurotherapeutic effects. Therefore, the objective of this study was to explore the efficacy and possible molecular mechanisms of SSD on pilocarpine (PP)‐induced astrocyte injury. Primary astrocytes were isolated from juvenile rats and identified using immunofluorescence. The cells were treated with PP and/or SSD for 6 h and 12 h, respectively, followed by measurement of their viability through 3‐(4,5‐dimethylthiazol)‐2,5‐diphenyl‐tetrazolium bromide (MTT) assay. Next, quantitative real‐time polymerase chain reaction (qRT‐PCR) was used to measure the expression levels of Glial fibrillary acidic protein (GFAP), C3, S100 calcium binding protein A10 (S100a10), pentraxin 3 (Ptx3), toll‐like receptor 4 (TLR4), and RAG in astrocytes after different treatments. Enzyme‐linked immunosorbent assay and biochemical tests were utilized to evaluate the level of inflammatory factors [interleukin (IL)‐1β, IL‐6, and tumor necrosis factor alpha (TNF‐α)] secreted by cells and the content of oxidative stress‐related factors (malondialdehyde [MDA] and glutathione [GSH]) or enzyme activity (catalase [CAT] and glutathione peroxidase [GPX]) in cells. The JC‐1 mitochondrial membrane potential (MMP) fluorescence probe was used to measure the MMP in astrocytes. Additionally, western blot was applied to test the expression of proteins related to the nod‐like receptor protein 3 (NLRP3)/caspase‐1 signaling pathway. PP treatment (1 mM) induced cell injury by significantly reducing the viability of astrocytes and expression of cellular markers. SSD treatment (4 μM) had no toxicity to astrocytes. Besides, SSD (4 μM) treatment could significantly up‐regulate the cell viability and marker expression of PP‐induced astrocytes. Furthermore, SSD could be employed to inhibit inflammation (reduce IL‐1β, IL‐6, and TNF‐α levels) and oxidative stress (decrease MDA level, elevate GSH level, the activity of CAT and GPX), and ameliorate mitochondrial dysfunction (upregulate JC‐1 ratio) in PP‐induced astrocytes. Moreover, further mechanism exploration revealed that SSD treatment significantly reduced the activity of the NLRP3/caspase‐1 signaling pathway activated by PP induction. SSD increased cell viability, inhibited inflammation and oxidative stress response, and ameliorated mitochondrial dysfunction in PP‐induced astrocyte injury model, thus playing a neuroprotective role. The mechanism of SSD may be related to the inhibition of the NLRP3/caspase‐1 inflammasome.
Fingolimod improves diffuse brain injury by promoting AQP4 polarization and functional recovery of the glymphatic system
Authors: Feng Dongyi , Liu Tao , Zhang Xinjie , Xiang Tangtang , Su Wanqiang , Quan Wei , Jiang Rongcai 
Published: March 2024

AbstractBackgroundDiffuse brain injury (DBI) models are characterized by intense global brain inflammation and edema, which characterize the most severe form of TBI. In a previous experiment, we found that fingolimod promoted recovery after controlled cortical impact injury (CCI) by modulating inflammation around brain lesions. However, it remains unclear whether fingolimod can also attenuate DBI because of its different injury mechanisms. Furthermore, whether fingolimod has additional underlying effects on repairing DBI is unknown.MethodsThe impact acceleration model of DBI was established in adult Sprague–Dawley rats. Fingolimod (0.5 mg/kg) was administered 0.5, 24, and 48 h after injury for 3 consecutive days. Immunohistochemistry, immunofluorescence analysis, cytokine array, and western blotting were used to evaluate inflammatory cells, inflammatory factors, AQP4 polarization, apoptosis in brain cells, and the accumulation of APP after DBI in rats. To evaluate the function of the glymphatic system (GS), a fluorescent tracer was injected into the cistern. The neural function of rats with DBI was evaluated using various tests, including the modified neurological severity score (mNSS), horizontal ladder‐crossing test, beam walking test, and tape sensing and removal test. Brain water content was also measured.ResultsFingolimod administration for 3 consecutive days could reduce the levels of inflammatory cytokines, neutrophil recruitment, microglia, and astrocyte activation in the brain following DBI. Moreover, fingolimod reduced apoptotic protein expression, brain cell apoptosis, brain edema, and APP accumulation. Additionally, fingolimod inhibited the loss of AQP4 polarization, improved lymphatic system function, and reduced damage to nervous system function. Notably, inhibiting the GS weakened the therapeutic effect of fingolimod on the neurological function of rats with DBI and increased the accumulation of APP in the brain.ConclusionsIn brief, these findings suggest that fingolimod alleviates whole‐brain inflammation and GS system damage after DBI and that inhibiting the GS could weaken the positive effect of fingolimod on nerve function in rats with DBI. Thus, inhibiting inflammation and regulating the GS may be critical for the therapeutic effect of fingolimod on DBI.
The cytosolic DNA‐sensing cGAS–STING pathway in neurodegenerative diseases
Authors: Guo Xiaofeng , Yang Lin , Wang Jiawei , Wu You , Li Yi , Du Lixia , Li Ling , Fang Zongping , Zhang Xijing 
Published: March 2024

AbstractBackgroundWith the widespread prevalence of neurodegenerative diseases (NDs) and high rates of mortality and disability, it is imminent to find accurate targets for intervention. There is growing evidence that neuroimmunity is pivotal in the pathology of NDs and that interventions targeting neuroimmunity hold great promise. Exogenous or dislocated nucleic acids activate the cytosolic DNA sensor cyclic GMP‐AMP synthase (cGAS), activating the stimulator of interferon genes (STING). The activated STING triggers innate immune responses and then the cGAS‐STING signaling pathway links abnormal nucleic acid sensing to the immune response. Recently, numerous studies have shown that neuroinflammation regulated by cGAS‐STING signaling plays an essential role in NDs.AimsIn this review, we summarized the mechanism of cGAS‐STING signaling in NDs and focused on inhibitors targeting cGAS‐STING.ConclusionThe cGAS‐STING signaling plays an important role in the pathogenesis of NDs. Inhibiting the cGAS‐STING signaling may provide new measures in the treatment of NDs.
Could robotic‐assisted surgery reduce mesh‐related complications after ventral mesh rectopexy? Experience of a tertiary centre and systematic review of the literature
Authors: Yasar Necdet F. , Waked Weam , Sturiale Alessandro , Fabiani Bernardina , Naldini Gabriele 
Published: March 2024

AbstractAimThe development of robotic assistance has made dissection and suturing in the deep pelvis much easier. The augmented quality of the images and the articulation of the robotic arms have also enabled a more precise dissection. The aim of this study is to present the data on robotic‐assisted ventral mesh rectopexy procedures in a university hospital and examine the literature in terms of mesh erosion.MethodThe electronic databases Pubmed, Embase and Cochrane were searched. Studies from January 2004 until January 2023 in the English language were included. Studies which included fewer than 10 patients were excluded. Laparoscopic or robotic‐assisted ventral mesh rectopexies were included. Mesh erosion rates following laparoscopic or robotic‐assisted ventral mesh rectopexies were measured.ResultsOverall, the systematic review presents 5911 patients from 43 studies who underwent laparoscopic ventral mesh rectopexy compared with 746 patients treated with robotic‐assisted ventral mesh rectopexy from six studies and our centre. Mesh erosion was rare in both groups; however, the prevalence was greater in the laparoscopy group (0.90% vs. 0.27%).ConclusionThe mesh erosion rates are very low with robotic‐assisted ventral mesh rectopexy. For precise results, more studies and experience in robotic surgery are required.
Factors influencing traumatic brain injuries in maxillofacial fractures: A 12‐year retrospective analysis of 2841 patients
Authors: Mao Jingjing , Xue Jiawen , Li Yunlong , Zhou Qi , Zhou Shuo , Zhou Zhongwei 
Published: March 2024

AbstractBackground/AimResults of studies investigating the association between traumatic brain injury (TBI) and maxillofacial fractures (MFs) have varied considerably. The present study aimed to evaluate the correlation between TBIs and MFs, as well as the impact of age, sex, trauma mechanism, and season on TBIs.Materials and MethodsThis 12‐year retrospective study of 2841 patients used univariate and multivariate logistic regression to assess the association between MFs and other factors impacting TBIs.ResultsAmong 2841 patients, 1978 TBIs occurred in 829 (29.2%), with intracranial injuries (n = 828) is the most common. Of 829 patients with TBIs, 688 were male and 141 were female, corresponding to a male‐to‐female ratio of 4.9:1.0. The most common age group was 40–49 years (24.6%). Vehicles (including motor vehicles and electric vehicles) accidents were the primary causes of injuries. Multivariate regression analyses revealed an increased risk for TBIs among males (odds ratio [OR] 0.632, p < 0.001). Patients >40 years of age were at higher risk for TBIs, especially those ≥70 years (OR 3.966, p = 0.001). Vehicle accidents were a high‐risk factor for TBIs (OR 6.894, p < 0.001), and winter was the most prevalent season for such injuries (OR 1.559, p = 0.002). Risk for TBI increased by 136.4% in combined midfacial and mandibular fractures (p = 0.016) and by 101.6% in multiple midfacial fractures (p = 0.045). TBIs were less common in single mandibular fractures, notably in single‐angle fractures, with a risk of only 0.204‐fold.ConclusionTBIs in MFs were significantly correlated with sex, age, aetiology, season and fracture location. Maxillofacial surgeons and emergency physicians must be aware of the possible association between TBIs and MFs to assess and manage this complicated relationship in a timely manner.
A cross‐sectional study of the impact of the COVID‐19 lockdown on domestic violence‐related oral and maxillofacial injuries
Authors: Naran‐Ochir Ochbayar , Narantsetseg Tsetsegkhen , Bayartsogt Batzorig , Batbileg Batzorig , Gan‐Ochir Batbold , Altannamar Munkhdul , Batbayar Enkh‐Orchlon 
Published: March 2024

AbstractBackgroundDuring the COVID‐19 lockdown, more domestic violence‐related traumas were reported. In this study, we investigated and compared the incidence of domestic violence‐related injuries—in particular oral and maxillofacial injuries—in Ulaanbaatar, Mongolia, before and during the COVID‐19 lockdown.Materials and MethodsWe conducted a cross‐sectional study based on 3974 domestic violence cases registered at the Public Health Department, National Traumatology and Orthopedics Research Center of Mongolia between 2018 and 2022. Descriptive and binary logistic regression analyses were conducted. The victims were categorized according to their age (child, adult, and elderly).ResultsThe mean age of the victims was children 9.7 ± 5.4 years, adults 34.8 ± 8.3 years, and elderly 64.3 ± 8.7 years. Binary logistic regression analysis (no/yes) showed that oral and maxillofacial injuries during the lockdown increased 1.3 times (OR = 1.3; CI 95% = 1.0–1.6; p = .003) in adults and 2.5 times in children (OR = 2.5; CI 95% = 1.7–3.9; p = .001). Additionally, injuries to upper limbs increased 4.6 times (OR = 4.6; CI 95% = 3.5–6.1; p = .001) in adults and 5.2 times in elderly patients (OR = 5.2; CI 95% = 1.8–16.2; p = .01). Additionally, thorax injury in children increased 3.1 times (OR = 3.1; CI 95% = 1.7–5.7; p = .001).ConclusionsDuring the lockdown, injury to oral and maxillofacial regions increased in adult and child victims of domestic violence.
Munchausen syndrome by proxy: A narrative review and update for the dentist and other healthcare professionals
Authors: Yee Ruixiang , Sim Sarah Ying , Chow Wen Hann , Rajasegaran Kumudhini , Hong Catherine Hsu Ling 
Published: March 2024

AbstractMunchausen syndrome by proxy (MSbP) is a form of abuse in which a caregiver with Factitious Disorder Imposed on Another (FDIA) fabricates or induces signs or symptoms in a person under their care to satisfy a self‐serving psychological need. Unnecessary clinical evaluations, procedures, and treatments that are initiated based on falsification by the abuser inadvertently add to the trauma experienced by the victim. It is a form of abuse and the impact on victims can be severe, sometimes fatal, and far‐reaching such as prolonged neglect and extension to affected siblings. The long‐term exposure to MSbP may predispose the victim to eventually developing factitious disorder imposed on self (FDIS). While MSbP often involves child victims, elderly, adults, and pets have also been reported as victims. MSbP can be a diagnostic challenge, and the important keys to timely identification of MSbP include the ability to detect deception by caregivers through awareness, clinical suspicion, and careful review of available health records; it also involves collecting collaborative information from other relevant healthcare providers including dentists, schoolteachers, and social workers. To date, there are limited published cases of MSbP with oral findings. This paper provides a narrative review of the current understanding of MSbP with a section on cases with oral findings. This paper aims to increase awareness about the clinical presentations and management considerations for MSbP among dentists and other healthcare professionals.
Clinical benefits of autologous platelet concentrate in periodontal intrabony defects: A network meta‐analysis of randomized controlled trials
Authors: Cui Yue , Mai Yuhe , Liu Xuewei , Mu Hong 
Published: March 2024

AbstractThis study aimed to compare clinical benefits of autologous platelet concentrate with other periodontal regenerative approaches in intrabony defects. An electronic and hand search of studies up to December 2022 was conducted. Randomized controlled trials with at least 6 months of follow‐up were identified to compare autologous platelet concentrates with enamel matrix derivative, bone graft, guided tissue regeneration, and open‐flap debridement. All approaches involved papilla preservation flap surgery. The outcomes included probing depth reduction, clinical attachment level gain, linear bone fill, and safety. A network meta‐analysis and meta‐regression were performed. Fifty‐seven studies were included in five network meta‐analyses. Autologous platelets concentrate and its adjunct treatments achieved significantly greater clinical and radiographic parameters than did open‐flap debridement, and had comparable or better performance than other regenerative treatments. Platelet‐rich fibrin showed superiority over platelet‐rich plasma in probing depth reduction at 6‐month follow‐up. Minimal pain and improved wound healing were observed in the treatments with autologous platelet concentrate. Meta‐regression showed that deeper baseline intrabony defects resulted in larger probing depth reductions, while smoking impaired the effectiveness of regenerative surgeries. Minimal invasive flap designs led to less effect of regenerative materials. Autologous platelet concentrate is a promising biomaterial in periodontal regeneration due to its convenience, safety, and biocompatibility characteristics.
Eradication of skin microbiota restores cytokine production and release in polymorphic light eruption
Authors: Zarfl Maximilian , Patra Vijaykumar , Bordag Natalie , Quehenberger Franz , Golob‐Schwarzl Nicole , Gruber‐Wackernagel Alexandra , Wolf Peter 
Published: March 2024

AbstractPolymorphic light eruption (PLE) has been mechanistically linked to cytokine abnormalities. Emerging preclinical evidence posits the skin microbiome as a critical modulator of ultraviolet (UV)‐induced cytokine expression, thereby influencing subsequent immune responses. This intricate relationship remains underexplored in the context of PLE. Hence, we investigated the differential responses between disinfected and non‐disinfected skin following both single and repetitive exposures to solar‐simulated UV radiation in patients with PLE. An experimental, half‐body pilot study was conducted involving six PLE patients and 15 healthy controls. Participants' skin was exposed to single and multiple doses of solar‐simulated UV radiation, both in disinfected and in non‐disinfected skin areas. The co‐primary outcomes were PLE score and cytokine expression in blister fluid analysed through OLINK proteomic profiling. Secondary outcomes were erythema, pigmentation, induction of apoptotic cells in vacuum‐generated suction blisters, and density of infiltrate in skin biopsies of PLE patients. Among the 71 cytokines analysed, baseline expression levels of 20 specific cytokines—integral to processes such as apoptosis, inflammation, immune cell recruitment, cellular growth, and differentiation—were significantly impaired in PLE patients compared with healthy controls. Notably, skin disinfection reversed the observed cytokine imbalances following a single UV exposure at the minimal erythema dose (MED) level and exhibited even more pronounced effects after multiple UV exposures. However, no significant differences were evident in PLE score, erythema, pigmentation, or rates of apoptotic cell induction upon UV radiation. These findings provide evidence for UV‐driven cytokine regulation by the skin microbiota and imply microbiome involvement in the PLE immune response.
Global patterns of tree wood density
Authors: Yang Hui , Wang Siyuan , Son Rackhun , Lee Hoontaek , Benson Vitus , Zhang Weijie , Zhang Yahai , Zhang Yuzhen , Kattge Jens , Boenisch Gerhard , Schepaschenko Dmitry , Karaszewski Zbigniew , Stereńczak Krzysztof , Moreno‐Martínez Álvaro , Nabais Cristina , Birnbaum Philippe , Vieilledent Ghislain , Weber Ulrich , Carvalhais Nuno 
Published: March 2024

AbstractWood density is a fundamental property related to tree biomechanics and hydraulic function while playing a crucial role in assessing vegetation carbon stocks by linking volumetric retrieval and a mass estimate. This study provides a high‐resolution map of the global distribution of tree wood density at the 0.01° (~1 km) spatial resolution, derived from four decision trees machine learning models using a global database of 28,822 tree‐level wood density measurements. An ensemble of four top‐performing models combined with eight cross‐validation strategies shows great consistency, providing wood density patterns with pronounced spatial heterogeneity. The global pattern shows lower wood density values in northern and northwestern Europe, Canadian forest regions and slightly higher values in Siberia forests, western United States, and southern China. In contrast, tropical regions, especially wet tropical areas, exhibit high wood density. Climatic predictors explain 49%–63% of spatial variations, followed by vegetation characteristics (25%–31%) and edaphic properties (11%–16%). Notably, leaf type (evergreen vs. deciduous) and leaf habit type (broadleaved vs. needleleaved) are the most dominant individual features among all selected predictive covariates. Wood density tends to be higher for angiosperm broadleaf trees compared to gymnosperm needleleaf trees, particularly for evergreen species. The distributions of wood density categorized by leaf types and leaf habit types have good agreement with the features observed in wood density measurements. This global map quantifying wood density distribution can help improve accurate predictions of forest carbon stocks, providing deeper insights into ecosystem functioning and carbon cycling such as forest vulnerability to hydraulic and thermal stresses in the context of future climate change.
Impact of mixed‐infection rate of clarithromycin‐susceptible and clarithromycin‐resistant Helicobacter pylori strains on the success rate of clarithromycin‐based eradication treatment
Authors: Tsuda Momoko , Watanabe Yoshiyuki , Oikawa Ritsuko , Watanabe Ryosuke , Higashino Masayuki , Kubo Kimitoshi , Yamamoto Hiroyuki , Itoh Fumio , Kato Mototsugu 
Published: March 2024

AbstractBackgroundClarithromycin (CAM) resistance is a major contributor to the failure to eradicate Helicobacter pylori (H. pylori). The mixed‐infection ratio of CAM‐susceptible and CAM‐resistant H. pylori strains differs among individuals. Pyrosequencing analysis can be used to quantify gene mutations at position each 2142 and 2143 of the H. pylori 23S rRNA gene in intragastric fluid samples. Herein, we aimed to clarify the impact of the rate of mixed infection with CAM‐susceptible and CAM‐resistant H. pylori strains on the success rate of CAM‐containing eradication therapy.Materials and MethodsSixty‐four H. pylori‐positive participants who received CAM‐based eradication therapy, also comprising vonoprazan and amoxicillin, were enrolled in this prospective cohort study. Biopsy and intragastric fluid samples were collected during esophagogastroduodenoscopy. H. pylori culture and CAM‐susceptibility tests were performed on the biopsy samples, and real‐time PCR and pyrosequencing analyses were performed on the intragastric fluid samples. The mutation rates and eradication success rates were compared.ResultsThe overall CAM‐based eradication success rate was 84% (54/64): 62% (13/21) for CAM‐resistant strains, and 95% (39/41) for CAM‐sensitive strains. When the mutation rate of the 23S rRNA gene was 20% or lower for both positions (2142 and 2143), the eradication success rate was 90% or more. However, when the mutation rate was 20% or higher, the eradication success rate was lower (60%).ConclusionsThe mutation rate of the CAM‐resistance gene was related to the success of eradication therapy, as determined via pyrosequencing analysis.