bluuebunny/crossref_metadata_2025_split huggingface dataset:
Determinants of acute kidney injury in children with new onset type 1 diabetes: A cohort study of children aged <15 years: Auckland, New Zealand (2006–2016)
Authors: Pittman Fiona , Di Somma Harry , Wong William , Prestidge Chanel , Reed Peter , Gunn Alistair J. , Jefferies Craig 
Published: August 2022

AbstractObjectiveAcute kidney injury (AKI) may contribute to the risk of diabetic kidney disease, however, there have been limited studies of the incidence of AKI in well‐defined populations of children with type 1 diabetes. The aim was to quantify AKI in children presenting with new onset type 1 diabetes from the regional paediatric diabetes service, Auckland, New Zealand.Research Design and MethodsA retrospective analysis of a prospectively identified cohort study of children and adolescents presenting from 2006 to 2016 with type 1 diabetes aged <15 years. AKI was defined using Kidney Disease/Improving Global Outcomes serum creatinine criteria.ResultsThere were 586 subjects: 52% male, with mean (SD) age 8.9 (3.8) years, with 151(25.8%) in diabetic ketoacidosis (DKA). AKI was present in 47%, 278/586, AKI was increased in those with DKA (125/151 (83%) DKA vs. 153/435 (35%) no‐DKA). Univariable analysis showed that increased HbA1c, higher glucose levels, lower BMI SDS, lower bicarbonate and pH levels were all associated with AKI (p < .001). In multivariable analysis, AKI was associated with DKA and higher glucose levels independently. The majority of cases were stage 1 (203/278 [73%]), or stage 2 AKI 62/278 (22%). 13/278 (5%) had severe, Stage 3 AKI, and all presented in DKA (13/151 (8%) vs. 0/435 (0%) without DKA, p < .001).ConclusionIn this regional paediatric, cohort AKI is a common complication of children presenting with new onset type 1 diabetes. AKI is independently associated with higher glucose levels and DKA, and all cases of Stage 3 AKI were associated with DKA.
Removal of heavy metals from industrial wastewater using microbial fuel cell
Authors: Al‐Asheh Sameer , Bagheri Marzieh , Aidan Ahmad 
Published: August 2022

AbstractRemoval efficiency of gold from a solution of pure tetrachloroaurate ions was investigated using microbial fuel cell (MFC) technology. The effects of type of catholyte solution and initial gold concentration on the removal efficiency were considered. Due to its presence at high levels in the gold wastewater, the effect of copper ions on the removal efficiency of the gold ions was also studied. The effects of pH and initial biomass concentration on the gold removal efficiency was also determined. The results showed that after 5 h contact time, 95% of gold removal efficiency from a wastewater containing 250 ppm of initial gold ions at ambient temperature using 80 g/L yeast concentration was achieved. After 48 h of the cell's operation under the same condition, 98.86% of AuCl4– ions were successfully removed from the solution. At initial gold concentration in the waste solution of 250 ppm, pH 2, and initial yeast concentration of 80 g/L, 100% removal efficiency of the gold was achieved. On the other hand, the most suitable condition for copper removal was found at a pH of 5.2, where 53% removal efficiency from the waste solution was accomplished.
Postoperative morphologic changes of the isthmocele and clinical impact in patients treated by channel‐like (360°) hysteroscopic technique
Authors: Casadio Paolo , Raffone Antonio , Alletto Andrea , Filipponi Francesco , Raimondo Diego , Arena Alessandro , La Rosa Mariangela , Virgilio Agnese , Franceschini Camilla , Gubbini Giampietro , Franchini Mario , Paradisi Roberto , Lenzi Jacopo , Travaglino Antonio , Mollo Antonio , Carugno Josè , Seracchioli Renato 
Published: August 2022

AbstractObjectiveTo evaluate the changes in (1) residual myometrial thickness (RMT), (2) cesarean scar defect (CSD) size, and (3) clinical symptoms, before and after channel‐like (360°) hysteroscopic resection for the treatment of CSD.MethodsA single‐center, observational, prospective, cohort study was carried out enrolling all symptomatic patients of childbearing age, diagnosed with CSD and routinely scheduled for channel‐like (360°) hysteroscopic resection from July 2020 to July 2021 at the Division of Gynecology and Human Reproduction Physiopathology, Department of Medical and Surgical Sciences, IRCCS Azienda Ospedaliero‐Univeristaria di Bologna. University of Bologna, Italy. The primary outcome was the difference in mean RMT before and after the procedure. Secondary outcomes were the differences before and 4 months after the surgery in: (1) CSD size measured by transvaginal ultrasound, (2) visual analog scale (VAS) scores for the symptoms, and (3) abnormal uterine bleeding (AUB) rate. Lastly, patients' satisfaction was assessed by the global impression of improvement (PGI‐I) score.ResultsWe found a significant difference before and after the procedure in: (1) mean RMT (+2.0 mm; P < 0.001); mean size of the CSD (base: +1.6 mm; height: −2.5 mm; transverse diameter: −3.2 mm; volume: −263.7 mm3; P < 0.001); (2) mean VAS score for dyspareunia (−5.84; P < 0.001), dysmenorrhea (−8.94; P < 0.001), pelvic pain (−2.94; P < 0.001); (3) AUB rate (91% vs. 3%; P < 0.001). Lastly, the mean PGI‐I score ± SD was 1.7 ± 0.9.ConclusionChannel‐like (360°) hysteroscopic resection for the treatment of patients with symptomatic CSD may lead to an increase in RMT, decrease in CSD, and improvement of symptoms after the procedure, with high patient satisfaction.
Succinate dehydrogenase‐deficient malignant paraganglioma complicated by succinate dehydrogenase‐deficient renal cell carcinoma
Authors: Yamaguchi Yoshitomo , Yokoyama Minato , Takemoto Akira , Nakamura Yuki , Fukuda Shohei , Uehara Sho , Tanaka Hajime , Yoshida Soichiro , Matsuoka Yoh , Fujii Yasuhisa 
Published: August 2022

IntroductionSDH Gene mutation is known to be a common cause of pheochromocytoma/paraganglioma and renal cell carcinoma. Here, we report a case of succinate dehydrogenase B‐deficient paraganglioma, which has a high risk of metastasis and recurrence, complicated by succinate dehydrogenase‐deficient renal cell carcinoma, which is rare and accounts for approximately 0.1% of all renal cell carcinomas.Case presentationA 50‐year‐old man underwent en bloc resection of a retroperitoneal tumor and the right kidney for retroperitoneal paraganglioma and right renal tumor. Both tumors showed negative expressions of succinate dehydrogenase B in immunostaining. The patient was diagnosed with succinate dehydrogenase‐deficient paraganglioma and succinate dehydrogenase‐deficient renal cell carcinoma. Seventeen months later, retroperitoneal lymphadenectomy revealed lymph node metastasis of the paraganglioma. Deletion of the SDHB gene was revealed by genome sequencing of the lymph node.ConclusionThis is the first reported case of synchronously diagnosed succinate dehydrogenase‐deficient paraganglioma and succinate dehydrogenase‐deficient renal cell carcinoma.
Dentoalveolar Defects of Hypophosphatasia are Recapitulated in a Sheep Knock-In Model
Authors: Mohamed Fatma F. , Chavez Michael B. , Huggins Shannon , Bertels Joshua , Falck Alyssa , Suva Larry J. , Foster Brian L. , Gaddy Dana 
Published: August 2022

ABSTRACTHypophosphatasia (HPP) is the inherited error-of-metabolism caused by mutations in ALPL, reducing the function of tissue-nonspecific alkaline phosphatase (TNAP/TNALP/TNSALP). HPP is characterized by defective skeletal and dental mineralization and is categorized into several clinical subtypes based on age of onset and severity of manifestations, though premature tooth loss from acellular cementum defects is common across most HPP subtypes. Genotype–phenotype associations and mechanisms underlying musculoskeletal, dental, and other defects remain poorly characterized. Murine models that have provided significant insights into HPP pathophysiology also carry limitations including monophyodont dentition, lack of osteonal remodeling of cortical bone, and differing patterns of skeletal growth. To address this, we generated the first gene-edited large-animal model of HPP in sheep via CRISPR/Cas9-mediated knock-in of a missense mutation (c.1077C&gt;G; p.I359M) associated with skeletal and dental manifestations in humans. We hypothesized that this HPP sheep model would recapitulate the human dentoalveolar manifestations of HPP. Compared to wild-type (WT), compound heterozygous (cHet) sheep with one null allele and the other with the targeted mutant allele exhibited the most severe alveolar bone, acellular cementum, and dentin hypomineralization defects. Sheep homozygous for the mutant allele (Hom) showed alveolar bone and hypomineralization effects and trends in dentin and cementum, whereas sheep heterozygous (Het) for the mutation did not exhibit significant effects. Important insights gained include existence of early alveolar bone defects that may contribute to tooth loss in HPP, observation of severe mantle dentin hypomineralization in an HPP animal model, association of cementum hypoplasia with genotype, and correlation of dentoalveolar defects with alkaline phosphatase (ALP) levels. The sheep model of HPP faithfully recapitulated dentoalveolar defects reported in individuals with HPP, providing a new translational model for studies into etiopathology and novel therapies of this disorder, as well as proof-of-principle that genetically engineered large sheep models can replicate human dentoalveolar disorders. © 2022 The Authors. Journal of Bone and Mineral Research published by Wiley Periodicals LLC on behalf of American Society for Bone and Mineral Research (ASBMR).
Genetic polymorphisms in the mismatch repair pathway (MMR) genes contribute to hematological and gastrointestinal toxicity in North Indian lung cancer patients treated with platinum‐based chemotherapy
Authors: Singh Sidhartha , Singh Navneet , Sharma Siddharth 
Published: August 2022

AbstractThe present study investigated the relationship between MLH1, MSH2, MSH3, and MSH6 polymorphisms and toxicity due to platinum‐based doublet chemotherapy for North Indian lung cancer patients. Polymerase chain reaction‐restriction fragment length polymorphism technique was used to assess the polymorphism. For MSH2 IVS1 + 9G > C polymorphism variant type genotype reported a 1.4‐fold increased risk of anemia (AOR = 1.4; 95% CI = 0.98–1.99; p = 0.04) and decreased risk of developing gastrointestinal toxicity (diarrhea) (AOR = 0.53; 95% CI = 0.28–1.01; p = 0.04). Further, we also reported a 10‐fold increased risk of developing severe grade anorexia in combined genotype (GC + CC) (AOR = 9.18; 95% CI = 0.98–86.1; p = 0.05). For MSH2 T > C/‐6 polymorphism, variant type reported a 3‐fold and 2‐fold increased risk of developing severe grade leukopenia (AOR = 3.37; 95% CI = 1.44–7.88; p = 0.005) and neutropenia respectively (AOR = 2.23; 95% CI = 1.07–4.66; p = 0.03). For MSH3 G > A polymorphism, heterozygous (GA) and combined genotype (GA + AA) reported a 7‐fold and 6‐fold increased risk of developing anemia (AOR = 7.23; 95% CI = 1.51–34.6; p = 0.01, AOR = 6.39; 95% CI = 1.53–26.6; p = 0.01). Our results suggest that polymorphisms in DNA mismatch repair genes are associated with hematological, and gastrointestinal toxicities and might be considered a predictor for pretreatment evaluation in lung cancer patients.
Investigation of the effect of boron on thyroid functions and biochemical parameters in hypothyroid induced‐rats
Authors: Kan Fahriye , Kucukkurt Ismail 
Published: August 2022

AbstractIn the study investigating the effects of boron on thyroid hormones and some biochemical parameters in hypothyroid rats, 49 Wistar Albino male rats were divided into seven groups; (Control (C), Hypothyroidism (H), boron groups (B10, and B20), hypothyroid + boron groups (HB10 and HB20), and Treatment (T). Four groups (H, HB10, HB20, and T) were administered 10 mg/kg (B10 and HB10), 20 mg/kg (B20 and HB20) boron for 3 weeks, respectively after hypothyroidism was induced using Propycil® containing propylthiouracil (PTU). Thyroid hormone analyses and biochemical measurements were made from the serum and thyroid gland tissue was examined histopathologically. According to the findings, the fT3 level increased in the B10 group compared to the control group (p < 0.05). While AST, ALT, and ALP activities were found to be higher in the hypothyroid group than in the control group, AST and ALP activities in the HB10 and HB20 groups decreased to values close to the control group. Total cholesterol levels were found to be lower in boron‐given groups compared to control and hypothyroid groups (p < 0.05). Sodium iodide symporter (NIS) immunoreactivity was found to be high in hypothyroid rat groups. As a result, it was observed that the increased AST and ALP activities in rats decreased with boron administration. The serum hormone levels measured in the study are not sufficient to understand the effect of boron on the thyroid gland, and it was concluded that further studies at the molecular level are needed to understand the effects of boron on the thyroid gland.
Hepcidin regulates neuronal ferroptosis: A mechanism for postoperative cognitive dysfunction
Authors: Shen Heping , Zhai Liping , Wang Genghuan 
Published: August 2022

AbstractToll‐like receptor 4 (TLR4) is a signaling molecule responsible for the expression of hepcidin (Hepc), while myeloid differentiation protein 2 (MD2) is one major accessory protein of TLR4. This study focuses on exploring the neurocyte ferroptosis mediated through the regulation of Hepc expression by MD2, which is also one of the mechanisms for postoperative cognitive dysfunction (POCD). An experimental study was carried out using aged wild‐type (Wt) and MD2 transgenic (Tg) mice. The neurocyte ferroptosis and POCD in the mice were assessed following splenectomy. Morris water maze was utilized to assess the neurocognitive abilities, hematoxylin and eosin (H&E) assay was performed to examine histopathology, and Nissl staining was used to evaluate the neurocyte damage. The Fe2+, superoxide dismutase(SOD), malondialdehyde (MDA), glutathione(GSH), and glutathione peroxidase 4 (GPX4) levels were determined with kits. The expressions of transferrin receptor (TFR), Hepc, and MD2 were measured by Western blotting, while the expressions of TFR and GPX4 were measured by immunohistochemical staining. In Tg mice, we observed neurocyte ferroptosis and POCD following treatment with an MD2 inhibitor. PC12 cells were used as a neurocyte model. Ferroptosis was induced after treatment with an MD2 inhibitor, and the cell viability was assayed by Cell Counting Kit‐8. Immunofluorescent staining was used to measure the TFR and GPX4 expressions. Meanwhile, the intracellular levels of Fe2+, SOD, MDA, GSH, GPX4, and Hepc were also measured. POCD occurred among aged Wt and Tg mice. The Tg‐POCD mice had more apparent POCD than the Wt‐POCD mice. Nissl and H&E staining revealed neurocyte damage in brain tissues. Besides this, the Fe2+ and MDA expressions were upregulated, while the SOD, GSH, and GPX4 expressions were downregulated. Elevations in tissue levels of TFR, Hepc, and MD2 were observed, which were higher than those of Wt‐POCD mice. After treatment with an MD2 inhibitor, the POCD could be prominently ameliorated in Tg‐POCD mice, the Fe2+ and MDA levels could be reduced, while the SOD, GSH, and GPX4 levels could be elevated. In the PC12 model, ferroptosis could be suppressed by inhibiting the expression of MD2. MD2 is capable of regulating neurocyte ferroptosis by promoting Hepc expression, which has great potential as a novel target for POCD therapy.
White to brown adipocyte transition mediated by Apigenin via VEGF‐PRDM16 signaling
Authors: Sreekumar Sreelekshmi , Vijayan Vinu , Singh Fathe , Sudhakar Manu , Lakra Rachita , Korrapati Purna Sai , Kiran Manikantan Syamala 
Published: August 2022

AbstractThe dysregulated energy metabolism in white adipose tissues results in derangement of biological signaling resulting in obesity. Lack of vascularization in these white adipose tissues is one of the major reasons for dysregulated energy metabolism. Not much work has been done in this direction to understand the role of angiogenesis in white adipose tissue metabolism. In the present study, we evaluated the effect of angiogenic modulator in the metabolism of white adipocyte (WAC). Bioactive Apigenin was selected and its angiogenic ability was studied. Apigenin was shown to be highly proangiogenic hence the effect of Apigenin on de novo and trans‐differentiation of WAT was studied. Apigenin showed enhanced de novo differentiation and trans‐differentiation of mouse WAC into brown‐like phenotype. To understand the effect of Apigenin on adipose tissue vasculature, coculture studies were conducted. Cross talk between endothelial cell and adipocytes were observed in coculture studies. Gene expression studies of cocultured cells revealed that browning of WAC occurred by triggering the expression of Vascular endothelial growth factor A. The study provides a new insight for inducing metabolic shift in WACs by modulation of angiogenesis in WAC microenvironment by the upregulation of PRDM16 cascade to trigger browning for the treatment of obesity.
Altered muscle oxidative phenotype impairs exercise tolerance but does not improve after exercise training in multiple sclerosis
Authors: Spaas Jan , Goulding Richie P. , Keytsman Charly , Fonteyn Lena , van Horssen Jack , Jaspers Richard T. , Eijnde Bert O. , Wüst Rob C.I. 
Published: August 2022

AbstractBackgroundPatients with multiple sclerosis (MS) experience reduced exercise tolerance that substantially reduces quality of life. The mechanisms underpinning exercise intolerance in MS are not fully clear. This study aimed to determine the contributions of the cardiopulmonary system and peripheral muscle in MS‐induced exercise intolerance before and after exercise training.MethodsTwenty‐three patients with MS (13 women) and 20 age‐matched and sex‐matched healthy controls (13 women) performed a cardiopulmonary exercise test. Muscle fibre type composition, size, succinate dehydrogenase (SDH) activity, capillarity, and gene expression and proteins related to mitochondrial density were determined in vastus lateralis muscle biopsies. Nine MS patients (five women) were re‐examined following a 12 week exercise training programme consisting of high‐intensity cycling interval and resistance training.ResultsPatients with MS had lower maximal oxygen uptake compared with healthy controls (V̇O2peak, 25.0 ± 8.5 vs. 35.7 ± 6.4 mL/kg/min, P < 0.001). The lower gas exchange threshold (MS: 14.5 ± 5.5 vs. controls: 19.7 ± 2.9 mL/kg/min, P = 0.01) and slope of V̇O2 versus work rate (MS: 9.5 ± 1.7 vs. controls: 10.8 ± 1.1 mL/min/W, P = 0.01) suggested an intramuscular contribution to exercise intolerance in patients with MS. Muscle SDH activity was 22% lower in MS (P = 0.004), and strongly correlated with several indices of whole‐body exercise capacity in MS patients (e.g. V̇O2peak, Spearman's ρ = 0.81, P = 0.002), but not healthy controls (ρ = 0.24, P = 0.38). In addition, protein levels of mitochondrial OXPHOS complexes I (−40%, P = 0.047) and II (−45%, P = 0.026) were lower in MS patients versus controls. Muscle capillary/fibre ratio correlated with V̇O2peak in healthy controls (ρ = 0.86, P < 0.001) but not in MS (ρ = 0.35, P = 0.22), and did not differ between groups (1.41 ± 0.30 vs. 1.47 ± 0.38, P = 0.65). Expression of genes involved in mitochondrial function, such as PPARA, PPARG, and TFAM, was markedly reduced in muscle tissue samples of MS patients (all P < 0.05). No differences in muscle fibre type composition or size were observed between groups (all P > 0.05). V̇O2peak increased by 23% following exercise training in MS (P < 0.001); however, no changes in muscle capillarity, SDH activity, gene or protein expression were observed (all P > 0.05).ConclusionsSkeletal muscle oxidative phenotype (mitochondrial complex I and II content, SDH activity) is lower in patients with MS, contributing to reduced exercise tolerance. However, skeletal muscle mitochondria appeared resistant to the beneficial effects of exercise training, suggesting that other physiological systems, at least in part, drive the improvements in exercise capacity following exercise training in MS.
Quartic graphs with minimum spectral gap
Authors: Abdi Maryam , Ghorbani Ebrahim 
Published: August 2022

AbstractAldous and Fill conjectured that the maximum relaxation time for the random walk on a connected regular graph with vertices is . This conjecture can be rephrased in terms of the spectral gap as follows: the spectral gap (algebraic connectivity) of a connected ‐regular graph on vertices is at least , and the bound is attained for at least one value of . We determine the structure of connected quartic graphs on vertices with a minimum spectral gap which enables us to show that the minimum spectral gap of connected quartic graphs on vertices is . From this result, the Aldous–Fill conjecture follows for .
Effects of boosted mRNA and adenoviral‐vectored vaccines on immune responses to omicron BA.1 and BA.2 following the heterologous CoronaVac/AZD1222 vaccination
Authors: Suntronwong Nungruthai , Kanokudom Sitthichai , Auphimai Chompoonut , Assawakosri Suvichada , Thongmee Thanunrat , Vichaiwattana Preeyaporn , Duangchinda Thaneeya , Chantima Warangkana , Pakchotanon Pattarakul , Chansaenroj Jira , Puenpa Jiratchaya , Nilyanimit Pornjarim , Srimuan Donchida , Thatsanatorn Thaksaporn , Sudhinaraset Natthinee , Wanlapakorn Nasamon , Mongkolsapaya Juthathip , Poovorawan Yong 
Published: August 2022

AbstractThe coronavirus 2019 omicron variant has surged rapidly and raises concerns about immune evasion even in individuals with complete vaccination, because it harbors mutations. Here we examine the capability of booster vaccination following CoronaVac/AZD1222 prime to induce neutralizing antibodies (NAbs) against omicron (BA.1 and BA.2) and T‐cell responses. A total of 167 participants primed with heterologous CoronaVac/AZD1222 for 4–5 months were enrolled, to receive AZD1222, BNT162b2, or mRNA‐1273 as a third dose. Reactogenicity was recorded. Immunogenicity analyses of severe acute respiratory syndrome coronavirus 2‐binding antibodies were measured using enzyme‐linked immunosorbent assay. The NAb titers against omicron BA.1 and BA.2 were determined using the focus reduction neutralization test (FRNT50) and total interferon‐γ responses were measured to observe the T‐cell activation. A substantial loss in neutralizing potency to omicron variant was found at 4–5 months after receiving the heterologous CoronaVac/AZD1222. Following booster vaccination, a significant increase in binding antibodies and neutralizing activities toward delta and omicron variants was observed. Neutralization to omicron BA.1 and BA.2 were comparable, showing the highest titers after boosted mRNA‐1273 followed by BNT162b2 and AZD1222. In addition, individuals boosted with messenger RNA (mRNA) vaccines develop a T‐cell response to spike protein, whereas those boosted with AZD1222 did not. Reactogenicity was mild to moderate without serious adverse events. Our findings demonstrated that mRNA booster vaccination is able to overcome waning immunity to provide antibodies that neutralize omicron BA.1 and BA.2, as well as a T‐cell response.