bluuebunny/crossref_metadata_2025_split huggingface dataset:
Clinical significance of serum CXCL9, CXCL10, and CXCL11 in patients with lupus nephritis
Authors: Wang Shuo , Cui Yanhui 
Published: August 2024

AbstractStudy DesignLupus nephritis (LN) is an autoimmune disease as a complication of systemic lupus erythematosus (SLE). LN is typically diagnosed through a combination of clinical evaluation as index scoring, and kidney biopsy as a more accurate but invasive examination. In the current study, we assessed serological markers including IFN‐γ‐inducible chemokines C‐X‐C motif chemokine ligand (CXCL)9, CXCL10, and CXCL11 in diagnosing LN.MethodsA retrospective analysis was conducted on 160 SLE patients with and without LN. Fasting venous blood was collected from the study subjects for measuring serum levels of CXCL9, CXCL10, and CXCL11. The assessment of clinical disease activity in SLE was conducted using the SLE Disease Activity Index (SLEDAI)‐2000 scoring system. LN disease activity was conducted using the Austin scoring system. LN was further confirmed following kidney biopsy, and data were compared by receiver operating characteristic (ROC) analysis.ResultsSLE patients with LN showed longer SLE duration, enhanced SLEDAI scores, lower serum anti‐ds‐DNA antibody levels when compared to SLE patients without LN. Specifically, these patients had significantly higher serum levels of CXCL9, CXCL10 and CXCL11. CXCL9, CXCL10, and CXCL11 showed positive correlation with SLE disease activity in SLE patients with LN. ROC analysis of CXCL9, CXCL10, and CXCL11 showed substantial enhancement of sensitivity and specificity for the diagnosis of LN in the patients with SLE.ConclusionsSerum CXCL9, CXCL10, and CXCL11 levels may improve the sensitivity and specificity for the diagnosis of LN in SLE patients.
Expression of MAF bZIP transcription factor B protects against ulcerative colitis through the inhibition of the NF‐κB pathway
Authors: Li Jingwen , Li Qingmin , Ma Wei , Zhang Yongsheng , Li Xiaonan 
Published: August 2024

AbstractPurposeThe aim of this study was to explore whether MAF bZIP transcription factor B (MAFB) might alleviate ulcerative colitis (UC) in dextran sulfate sodium (DSS)‐induced mice and LPS‐induced IEC‐6 cells.MethodsUC in vivo and in vitro model was established by using DSS and LPS, respectively. The mice body weight and disease activity index (DAI) score were recorded daily, and colon length was measured. Moreover, the permeability was evaluated utilizing a fluorescein isothiocyanate dextran (FITC‐Dextran) probe. Histopathological changes of DSS‐induced colitis mice was assessed utilizing H&E staining. Next, qRT‐PCR was performed to detect IL‐1β, IL‐6, TNF‐α, and IL‐10 level in in vivo and in vitro. Furthermore, the level of MDA, SOD, CAT, and GSH were evaluated in colon tissues. Besides, the expressions of tight junction proteins and NF‐κB pathway relative proteins were examined in colitis mice and IEC‐6 cells using western blot, immunohistochemistry and immunofluorescence.ResultsMAFB level was downregulated in DSS‐induced colitis mice. Moreover, the upregulation of MAFB protected mice from DSS‐induced colitis by suppressing DSS‐induced inflammation, oxidative stress, and intestinal barrier impairment. We also demonstrated that the upregulation of MAFB inactivated NF‐κB pathway in DSS‐caused colitis mice. Subsequently, we observed that MAFB upregulation could inhibit LPS‐caused epithelial barrier impairment and inflammation in IEC‐6 cells. Additionally, MAFB overexpression could suppress the activation of NF‐κB pathway in IEC‐6 cells.ConclusionThe upregulation of MAFB could protect against UC via the suppression of inflammation and the intestinal barrier impairment through inhibiting the NF‐κB pathway.
Vergleichende geobotanische Untersuchungen in der Baschkirischen ASSR
Authors: Klotz Stefan , Köck Uwe‐Volkmar 
Published: August 2024

ZusammenfassungDer dritte Teil der „Vergleichenden geobotanischen Untersuchungen in der Baschkirischen ASSR“ enthält die Ergebnisse pflanzensoziologischer Untersuchungen der Wasserpflanzen‐, Flußufer‐ und Halophytenvegetation. Auf der Grundlage der nach den Methoden von Braun‐Blanquet gewonnenen Vegetationsaufnahmen wird der floristisch‐soziologische Aufbau der ausgeschiedenen Vegetationseinheiten dargestellt; sie werden synökologisch charakterisiert; und es werden pflanzengeographisch‐synchorologische Aspekte beim Vergleich mit entsprechenden mitteleuropäischen Pflanzengesellschaften diskutiert. Folgende Vegetationseinheiten werden besprochen: Lemno‐Spirodeletum Koch 54, Stratiotetum aloidis (Now. 30) Milj. 33, Potamogetonetum lucentis Hueck 31, P. perfoliati W. Koch 26 cm. Pass. 64, Potamogeton pectinatus‐, P. pusillus Gesell., Elodeetum canadensis Pign. 53, Myriophyllo‐Nupharetum W. Koch 26, Sparganium emersum‐Potamogeton perfoliatus‐Gesell., Phragmitetum communis (Gams 27) Schmale 39, Typhetum angustifoliae Pign. 53, Scirpetum lacustris (Eggl. 33) Schmale 39 S. tabernaemontani Pass. 64, S. maritimi (Br.‐Bl. 31) Tx. 37, Glycerietum maximae Hueck 41, Sparganietum erecti Roll 38, Equisetetum fluviatilis Steff. 31, Sagittario‐Sparganietum Tx. 53, Eleocharis palustris‐, Alisma graminea Gesell., Phalaridetum Libb. 31, Eleocharidetum acicularis Koch 26 cm. Oberd. 57, Xanthium strumarium‐Chenopodium glaucum‐, Petasites spurius‐Gesell., Junco‐Glaucetum Mahn et Schub. 62, Junco gerardii‐Agrostietum (D. R. 25) Tx. 50.
Lonicerin alleviates intestinal myenteric neuron injury induced by hypoxia/reoxygenation treated macrophages by downregulating EZH2
Authors: Yao Zhiguang , Liang Yuan , Pan Chunyan , Zeng Kun , Qu Zhibo 
Published: August 2024

AbstractIntestinal ischemia‐reperfusion (IR) injury is a common gastrointestinal disease that induces severe intestinal dysfunction. Intestinal myenteric neurons participate in maintaining the intestinal function, which will be severely injured by IR. Macrophages are widely reported to be involved in the pathogenesis of organ IR injury, including intestine, which is activated by NLRP3 signaling. Lonicerin (LCR) is a natural extracted monomer with inhibitory efficacy against the NLRP3 pathway in macrophages. The present study aims to explore the potential protective function of LCR in intestinal IR injury. Myenteric neurons were extracted from mice. RAW 264.7 cells were stimulated by H/R with or without 10 μM and 30 μM LCR. Remarkable increased release of IL‐6, MCP‐1, and TNF‐α were observed in H/R treated RAW 264.7 cells, along with an upregulation of NLRP3, cleaved‐caspase‐1, IL‐1β, and EZH2, which were sharply repressed by LCR. Myenteric neurons were cultured with the supernatant collected from each group. Markedly decreased neuron number and shortened length of neuron axon were observed in the H/R group, which were signally reversed by LCR. RAW 264.7 cells were stimulated by H/R, followed by incubated with 30 μM LCR with or without pcDNA3.1‐EZH2. The inhibition of LCR on NLRP3 signaling in H/R treated RAW 264.7 cells was abolished by EZH2 overexpression. Furthermore, the impact of LCR on neuron number and neuron axon length in myenteric neurons in the H/R group was abated by EZH2 overexpression. Collectively, LCR alleviated intestinal myenteric neuron injury induced by H/R treated macrophages via downregulating EZH2.
Inflammation alters the expression pattern of drug transporters during Caco‐2 cell stimulation and azoxymethane‐induced colon tumorigenesis
Authors: El‐Daly Sherien M. , Gouhar Shaimaa A. , Abdelrahman Sahar S. 
Published: August 2024

AbstractDrug transporters play a pivotal role in modulating drug disposition and are subject to alterations under inflammatory conditions. This study aimed to elucidate the intricate expression patterns of drug transporters during both acute and chronic inflammation, which are closely linked to malignant transformation. To investigate acute inflammation, we employed an in vitro model by subjecting Caco‐2 cells to various inflammatory stimuli (IL‐1β, TNF‐α, or LPS) individually or in combination. The successful induction of inflammation was confirmed by robust increases in IL‐6 and NO production. Notably, inflamed Caco‐2 cells exhibited significantly diminished levels of ABCB1 and ABCG2, while the expression of ABCC2 was upregulated. For chronic inflammation induction in vivo, we employed the well‐established AOM/DSS mouse model known for its association with colitis‐driven tumorigenesis. Persistent inflammation was effectively monitored throughout the experiment via elevated IL‐6 and NO levels. The sequential stages of tumorigenesis were confirmed through Ki‐67 immunohistochemistry. Intriguingly, we observed gradual alterations in the expression patterns of the studied drug transporters during stepwise induction, with ABCB1, ABCG2, and ABCC1 showing downregulation and ABCC2 exhibiting upregulation. Immunohistochemistry further revealed dynamic changes in the expression of ABCB1 and ABCC2 during the induction cycles, closely paralleling the gradual increase in Ki‐67 expression observed during the development of precancerous lesions. Collectively, our findings underscore the significant impact of inflammation on drug transporter expression, potentially influencing the process of malignant transformation of the colon.
Reduced myotube diameter induced by combined inhibition of transforming growth factor‐β type I receptors Acvr1b and Tgfbr1 is associated with enhanced β1‐syntrophin expression
Authors: Shi Andi , He Chuqi , Otten Kirsten , Wu Gang , Forouzanfar Tymour , Wüst Rob C. I. , Jaspers Richard T. 
Published: August 2024

AbstractSimultaneous inhibition of transforming growth factor‐β (TGF‐β) type I receptors Acvr1b and Tgfbr1 signalling has been associated with excessive skeletal muscle hypertrophy in vivo. However, it remains unclear whether the increased muscle mass in vivo is a direct result of inhibition of intracellular TGF‐β signalling or whether this is an indirect effect of an altered extracellular anabolic environment. Here, we tested whether individual or simultaneous knockdown of TGF‐β type I receptors in C2C12 myotubes was sufficient to induce muscle hypertrophy. The expression levels of TGF‐β type I receptors Acvr1b and Tgfbr1 in myotubes were knocked down individually or in combination in the absence or presence of TGF‐β1 and myostatin. Knocking down either Acvr1b or Tgfbr1 did not significantly change cell phenotype. Unexpectedly, simultaneous knockdown of both receptors reduced C2C12 myotube diameter, mRNA expression levels of Hgf, Ccn2 and Mymx with or without TGF‐β1 and myostatin administration. In spite of decreased phosphorylation of Smad2/3, phosphorylation of P70S6K was reduced. In addition, the gene expression level of β1‐syntrophin (Sntb1), which encodes a protein associated with the dystrophin−glycoprotein complex, was increased. Parallel experiments where Sntb1 gene expression was reduced showed an increase in myotube diameter and fusion of C2C12 myoblasts. Together, these results indicate that the knockdown of both TGF‐β type I receptors reduced myotube diameter. This atrophic effect was attributed to reduced protein synthesis signalling and an increased expression of β1‐syntrophin. These results have implications for our fundamental understanding of how TGF‐β signalling regulates skeletal muscle size.
Adsorption of vanadium using a new anionic Schiff Base adsorbent and its application to vanadium separation from boiler ash
Authors: Abdalla Mohamed 
Published: August 2024

AbstractBackgroundThis study reports the preparation of 2‐hydroxy‐3‐(4‐(((2‐((2‐(((E)‐4‐(2‐hydroxy‐3‐(trimethylammonio)propoxy)‐3‐methoxybenzylidene)amino)ethyl)amino)ethyl)imino)methyl)‐2‐methoxyphenoxy)‐N,N,N‐trimethylpropan‐1‐aminium (HYM/QA). The adsorbent was employed to extract and concentrate vanadium from its solutions and boiler ash samples.ResultsThe impact of initial dosage, pH, reaction time and temperature on the sorption behavior of V(V) was examined. Under optimal conditions (pH 5, 0.08 g dose, 45 min at room temperature), a sorption capacity of 392.25 mg g−1 was achieved. The uptake of V(V) on HYM/QA was effectively reversed using 1 mol L−1 NaOH, regenerating the material. After six cycles of sorption and elution, the sorption capability remained at 91.4% of its initial value. The efficiency and selectivity of HYM/QA toward V5+ ions were assessed using the separation factor parameter, revealing limited interference from heavy metals such as Mn2+, Cr3+, Pb2+, Si4+, Al3+, NO32−, HCO3− and Zn2+. The uptake process of HYM/QA for V(V) conformed to the Langmuir and Dubinin–Radushkevich isotherm models and the pseudo‐second‐order kinetic model. HYM/QA was characterized by infrared, Brunauer–Emmett–Teller surface area, 1H NMR, 13C NMR and gas chromatography–mass spectrometry analyses, confirming successful preparation. Thermodynamic assessments suggested that the sorption process is endothermic, spontaneous and becoming more favorable with rising temperature.ConclusionThe optimized conditions were used to adsorb vanadium from boiler ash samples, and the obtained vanadium pentaoxide was analyzed and confirmed using various tools, demonstrating the material's effectiveness for vanadium extraction. © 2024 Society of Chemical Industry (SCI).
The experiences of podiatrists prescribing custom foot orthoses and patients using custom foot orthoses for foot pain management in the United Kingdom: A focus group study
Authors: Leach Emily , Cowley Emma , Bowen Catherine 
Published: August 2024

AbstractIntroductionFoot pain can be a significant burden for patients. Custom foot orthoses (CFOs) have been a mainstay in podiatry treatment for foot pain management and improving foot function. However, little is known about podiatrists' experience of prescribing CFOs or patient experience of using foot orthoses (FOs), including CFOs, for foot pain.MethodsA focus group (FG) discussion with three FOs users (Female = 2 and Male = 1) was conducted in November 2022 within a private podiatry practice. This group represented non‐experts from the general local population of individuals with existing or previous foot pain who have personally experienced using either over‐the‐counter FOs or CFOs. An online FG discussion with five musculoskeletal (MSK) specialist podiatrists (Female = 2 and Male = 3) was also conducted in December 2022. This group represented podiatrists with specialist knowledge in foot biomechanics and clinical experience in CFO provision. The FG discussions were recorded and lasted 49 and 57 min respectively. Transcribed data was manually coded, and a thematic analysis was undertaken to identify patterns within the collected data.ResultsThe participants in the patient FG detailed mixed experiences of the prescription process and CFOs received, with reports of limited involvement/input in their prescription, the need for frequent adjustments and high costs. The impact on footwear choices, replicability and transferability of CFOs into different types of shoes and technologies to aid design were also highlighted. In the podiatrist FG, lack of confidence in design and manufacture processes, prescription form language, relationship and communication building with manufacturers, variability in the CFOs issued and the need for better student education in CFO provision emerged as key themes.ConclusionPatients and podiatrists shared similar views on CFO provision, namely poor communication with manufacturers leading to dissatisfaction with the CFOs prescribed causing negative impacts on patient experiences. Podiatrists called for greater education at registration level to increase new graduate podiatrist knowledge in CFO design and manufacture and better collaboration with manufacturing companies.
Patterns of dermal denticle loss in sharks
Authors: Fath Michael A. , Wong Greta , Colombero Chloé‐Rose , Gabler‐Smith Molly K. , Lauder George V. , Wainwright Dylan K. 
Published: August 2024

AbstractAs they grow, sharks both replace lost denticles and proliferate the number of denticles by developing new (de novo) denticles without prior denticle shedding. The loss and replacement of denticles has potential impacts on the energetic cost of maintaining the skin surface, the biomechanical functions of shark skin, as well as our ability to predict shark abundance from fossil denticle occurrence in sediment cores. Here, we seek to better understand patterns of denticle loss and to show how denticles are being replaced in mature sharks. We illustrate shark skin surfaces with missing denticles and quantify both within‐species and between‐species patterns of missing denticles using images from across regions of the body for two species and images at similar body regions for 16 species of sharks. Generally, sharks are missing similar numbers of denticles (0%–6%) between species and regions. However, there are exceptions: in the smooth dogfish, the nose region is missing significantly more denticles than most posterior‐body and fin regions, and the common thresher shark is missing significantly more denticles than the smooth dogfish, leopard shark, angel shark, bonnethead, and gulper shark. Denticle regrowth starts with crown development and mineralization beneath the epidermis, followed by eruption of the crown, and finally the mineralization of the root. The pulp cavity of replacement denticles is initially large and surrounded by a thin shell of enameloid upon eruption of the denticle. After eruption of the denticle, the deposition of dentine continues internally after the denticle reaches its final position. Replacement of missing denticles, representing less than 6% of the skin surface at any one time, may not compromise hydrodynamic function, but by constantly updating the skin surface throughout life, sharks may reduce surface fouling and maintain a functional complex skin surface by repairing local damage to individual denticles.
A novel model based on serum N‐glycan markers for evaluating stage of liver necroinflammation in treatment‐naïve chronic hepatitis B patients
Authors: Su Rui , Yan Lihua , Jiang Bei , Li Jia , Li Ping , Liu Yonggang , Miao Jing , Chen Cuiying , Xu Liang , Ren Li , Mi Yuqiang 
Published: August 2024

AbstractThis study aimed to establish a novel noninvasive model based on the serum N‐glycan spectrum for providing an objective value for determining the stage of liver necroinflammation related to chronic hepatitis B (CHB) patients. N‐glycan profiles of the sera of 295 treatment‐naïve CHB patients were analyzed. N‐glycan profiles were tested for different liver necroinflammation stages using DNA sequence‐assisted fluorophore‐assisted carbohydrate electrophoresis. A serum N‐glycan model named N‐glycan‐LI (NGLI) using support vector machine was selected to evaluate the classification of liver necroinflammation (G < 2 and G ≥ 2). The area under the receiver operating characteristic curves (AUROCs) was 0.898 (training set, n = 236) and 0.911 (validation set, n = 59) regardless of the stage of liver fibrosis (AUROC = 0.886 and 0.926, respectively, in S < 2 and S ≥ 2 group). The NGLI correspondingly had the highest specificity (SP) of 90.79% and negative predictive value of 92.00% in an inactive stage (including immune‐tolerant [IT] and inactive‐carrier [IC] stage), had the highest positive predictive value of 95.18% in stage immune‐active, and had the highest SP of 93.94% in grey zone IT + IC. N‐glycan profiles appear to correlate well with hepatic necroinflammation in CHB when compared with liver biopsy. The newly developed model appears to reliably predict liver damage in naïve‐treatment patients with CHB.
Understanding the landscape of the SARS‐CoV‐2‐specific T cells post‐omicron surge
Authors: Binayke Akshay , Zaheer Aymaan , Vishwakarma Siddhesh , Sharma Priyanka , Dandotiya Jyotsna , Raghavan Sreevatsan , Gosain Mudita , Singh Savita , Chattopadhyay Souvick , Kaushal Jyotsana , Madan Upasna , Kshetrapal Pallavi , Batra Gaurav , Wadhwa Nitya , Pandey Anil Kumar , Bhatnagar Shinjini , Garg Pramod Kumar , Awasthi Amit 
Published: August 2024

AbstractEmerging evidence shows increased humoral response post‐omicron surge, but research on T cell responses is limited. This study investigated the durability, magnitude, and breadth of SARS‐CoV‐2‐spike‐specific T cell responses in 216 two‐dose vaccinated individuals pre‐ and post‐omicron surge. Post‐surge samples showed enhanced T cell responses, indicating widespread asymptomatic exposure to omicron. Further analysis of 105 individuals with multiple exposures to SARS‐CoV‐2 through boosters or infections showed that post‐omicron, two‐dose vaccinated individuals had T cell responses comparable to those of COVID‐19 convalescents or boosted individuals. Additionally, we report cross‐reactive T cell responses against omicron sub‐variants, including BA2.86, remained strong, with preserved frequencies of spike‐specific stem‐cell‐like memory T cells. In silico prediction indicates that mutated epitopes of JN.1 and KP.2 retain over 95.6% of their HLA binding capability. Overall, our data suggests that T cell responses are sustained, enhanced, and cross‐reactive against emerging SARS‐CoV‐2 variants following symptomatic or asymptomatic omicron infection.
The primate‐specific presence of interferon regulatory factor‐5 pseudogene 1
Authors: Marquis Avery , Hubing Vanessa , Ziemann Chanasei , Moriyama Etsuko N. , Zhang Luwen 
Published: August 2024

AbstractInterferon regulatory factor 5 (IRF5) is a key transcription factor in inflammatory and immune responses, with its dysregulation linked to autoimmune diseases. Using bioinformatic approaches, including Basic Local Alignment Search Tool (BLAST) for sequence similarity searches, BLAST‐Like Alignment Tool (BLAT) for genome‐wide alignments, and several phylogenetics software, such as Multiple Alignment using Fast Fourier Transform (MAFFT), for phylogenetic analyses, we characterized the structure, origin, and evolutionary history of the human IRF5 pseudogene 1 (IRF5P1). Our analyses reveal that IRF5P1 is a chimeric processed pseudogene containing sequences derived from multiple sources, including IRF5‐like sequences from disparate organisms. We find that IRF5P1 is specific to higher primates, likely originating through an ancient retroviral integration event approximately 60 million years ago. Interestingly, IRF5P1 resides within the triple QxxK/R motif‐containing (TRIQK) gene, and its antisense strand is predominantly expressed as part of the TRIQK pre‐messenger RNA (mRNA). Analysis of publicly available RNA‐seq data suggests potential expression of antisense IRF5P1 RNA. We hypothesize that this antisense RNA may regulate IRF5 expression through complementary binding to IRF5 mRNA, with human genetic variants potentially modulating this interaction. The conservation of IRF5P1 in the primate lineage suggests its positive effects on primate evolution and innate immunity. This study highlights the importance of investigating pseudogenes and their potential regulatory roles in shaping lineage‐specific immune adaptations.