bluuebunny/crossref_metadata_2025_split huggingface dataset:
Electrochemical deposition of lithium coating on titanium implant with enhanced early stage osseointegration
Authors: Huang Tingben , Yu Zhou , Yu Qiong , Chen Yitong , Jiang Zhiwei , Wang Ying , Yang Guoli 
Published: May 2022

AbstractRecently, a large number of studies have reported that lithium (Li) displayed a positive effect on osteogenesis. However, only a few studies have investigated the Li‐incorporated surfaces through electrochemical deposition. In this study, electrochemical deposition was conducted on a CHI600E electrochemical workstation. The characterization of electrochemical deposition (ECD) and ECD‐Li surfaces were detected by field‐emission scanning electron microscopy with energy‐dispersive spectrometer. rBMSCs were cultured on two surfaces for subsequent adhesion, proliferation and live/dead assay. To evaluate the effects of Li‐incorporated implants by electrochemical deposition on osseointegration in vivo, teeth extraction of two premolars and one first molar in bilateral mandible were performed on six male beagle dogs. After 3 months, ZDI and ZDI‐Li implants were inserted into the bilateral mandible of each beagle dog. Micro Computed Tomography (Micro‐CT) and hard tissue sectioning analysis were carried out to evaluate the osseointegration at 4‐ and 8‐weeks post‐implantation. Results showed that ECD‐Li surface promoted adhesion and proliferation of BMSCs in the early stage. More importantly, through micro‐CT analysis, the values of bone volume/total volume (BV/TV) (0.374 ± 0.015), bone‐implant contact (BIC) (0.831 ± 0.025), and Tb.Th (0.412 ± 0.007) in ZDI‐Li group was significantly higher than those of ZDI group (0.302 ± 0.009, 0.700 ± 0.023, 0.353 ± 0.001, p < .01) at 4 weeks. Similarly, ZDI‐Li group manifested more bone contact with the implant surfaces at 4 weeks based on hard tissue sectioning analysis, whereas no significant difference was detected between two groups at 8 weeks. Therefore, incorporating Li into implant surface through ECD could enhance early osseointegration in vivo.
NF‐κB‐upregulated miR‐155‐5p promotes hepatocyte mitochondrial dysfunction to accelerate the development of nonalcoholic fatty liver disease through downregulation of STC1
Authors: Shen Miao , Pan Hanghai , Ke Jinjing , Zhao Fei 
Published: May 2022

AbstractPrevious studies have highlighted the involvement of nuclear factor kappa B (NF‐κB) in the development of nonalcoholic fatty liver disease (NAFLD). The purpose of our investigation is to explore the interaction among NF‐κB, microRNA‐155‐5p (miR‐155‐5p), and Stanniocalcin 1 (STC1), and its effects on NAFLD by establishing a NAFLD model in Sprague Dawley rats. A highly‐expressed miR‐155‐5p and NF‐κB was revealed in the liver tissues of NAFLD rats, and a positive correlation was identified between miR‐155‐5p and NF‐κB. Next, the expression of NF‐κB and STC1 was altered in the modeled rats through lentivirus injection, followed by determination on the levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), total cholesterol, triglycerides, and low‐density lipoprotein cholesterol. Furthermore, the hepatocyte mitochondria were separated to measure the activities of adenosine triphosphate (ATP), reactive oxygen species (ROS), mitochondrial membrane potential (MMP), and mitochondrial respiratory chain complex, and to observe the number, length and ultrastructural length of mitochondrial cristae. The results demonstrated that NF‐κB overexpression induced mitochondrial dysfunction, increased ROS level, decreased ATP and MMP contents, as well as inhibited the number and length of mitochondrial cristae in the hepatocyte mitochondria of NAFLD rats. Besides, miR‐155‐5p was found to negatively regulate STC1 expression based on dual luciferase reporter gene assay, which exert inhibition on mitochondrial activity of hepatocytes in NAFLD rats. These results uncover the possible involvement of NF‐κB/miR‐155‐5p/STC1 axis in NAFLD progression, that NF‐κB could increase miR‐155‐5p expression to inhibit STC1 expression, thus inducing hepatic mitochondrial dysfunction and promoting the occurrence and development of NAFLD.
Synthesis and characterization of boehmite/metal – Organic framework of type AlO(OH)/MOF‐74(Zn) for photocatalytic degradation of Congo red dye
Authors: Sohrabnezhad Shabnam , Kazemi Zahra , Pourahmad Nodehi Arad 
Published: May 2022

AbstractIn the present work, boehmite metal‐organic framework nanocomposite, AlO(OH)/MOF‐74(Zn), was synthesized by a simple, fast, and low‐cost process. The post‐synthetic method was used for preparing new hybrid material. The photocatalytic efficiency of AlO(OH)/MOF‐74(Zn) was investigated by photocatalytic degradation of Congo Red anionic dye. The nanocomposite was characterized by various techniques. The electron microscopy images showed that the spherical MOF‐74 with about 30 nm was located over boehmite. The optical properties indicated the boehmite/MOF‐74 can be used as a visible‐light‐driven photocatalyst. Optimization of significant variables such as adsorbent dosage and initial Congo Red concentration and photodegradation time affecting removal was investigated and the optimized values were found to be 1 g/L, 10 mg/L, and 60 min, respectively. The AlO(OH)/MOF‐74(Zn) photocatalyst exhibited the highest catalytic performance for photodegradation of dye contaminants. Results indicated about 94% of tested dye were removed by a new hybrid photocatalyst under visible light irradiation. The results confirmed that due to some considerable features of AlO(OH)/MOF‐74(Zn) such as high surface area and chemical and thermal resistance, the introduced photocatalyst acts as a high‐performance photocatalyst for degradation of Congo Red dye in aqueous solutions.
Work‐related stress and coping methods of internists and primary care physicians during the COVID‐19 pandemic in Japan: A mixed‐method study
Authors: Shikino Kiyoshi , Kuriyama Akira , Sadohara Michito , Matsuo Takahiro , Nagasaki Kazuya , Nishimura Yoshito , Nonaka Saori , Izumiya Masashi , Moriya Mitsuru , Ohtake Yoichi , Makiishi Tetsuya 
Published: May 2022

AbstractBackgroundThe COVID‐19 pandemic has affected the mental health of health care workers. This study aimed to investigate the stress factors that cause burnout in Japanese physicians and their coping methods during the COVID‐19 pandemic.MethodsWe conducted a sequential explanatory mixed‐method study to investigate the psychological responses of physicians in the early stages of the pandemic. A cross‐sectional, web‐based, anonymous survey was conducted among members of the American College of Physicians Japan Chapter to quantitatively investigate the stress factors and prevalence of burnout. An open‐ended questionnaire with questions about stress factors and coping methods was additionally administered. The qualitative data were analyzed using qualitative content analysis.ResultsAmong the 1173 physicians surveyed, 214 (18.2%) responded. Among the participants, 107 (50.0%) responded “yes” to the question “I feel or have felt very stressed at work during the COVID‐19 pandemic,” and 68 (31.8%) reported burnout symptoms. Those who reported feeling stress (117 respondents) were asked to select 12 items of the stress factors related to COVID‐19. The most significant stress factor related to COVID‐19 was “Perceived risk of spreading COVID‐19 to family members” (n = 47). Content analysis identified 12 categories for the stress factors and 7 for stress‐coping methods corresponding to COVID‐19 (Cohen's kappa = 0.84 and 0.95, respectively).ConclusionSeveral distinct stressors existed during the COVID‐19 pandemic, which might be related to burnout among physicians. Practicing stress‐coping strategies, as identified in the present study, may help reduce work‐related stress and prevent burnout.
Synthesis, antioxidant, and antimicrobial activity of some novel N‐substituted derivatives of 3‐(benzo[b]thiophen‐2‐yl)‐5‐(3‐[trifluoromethyl]styryl)‐4,5‐dihydro‐1H‐pyrazole
Authors: Pandy Karthik Manikandan , Krishnan Radhakrishnan , Paratharaj Senthilkumar 
Published: May 2022

AbstractThe new series of various N‐substituted pyrazoline derivatives containing benzo[b]thiophene and styryl with trifluoromethyl substitution at meta‐ position were synthesized. Compound 1‐(3‐(benzo[b]thiophen‐2‐yl)‐5‐(3‐[trifluoromethyl]styryl)‐4,5‐dihydro‐1H‐pyrazol‐1‐yl)‐2‐chloroethan‐1‐one (3b) was further substituted with various thiols. The structures of newly synthesized compounds were characterized by UV, IR, NMR, and Mass and had been screened for antioxidant and antimicrobial activity. The in vitro antioxidant screening revealed that hydroxyl radical scavenging (HRS) activities of compounds 3a, 3b, 3c, 3f, 3i, 3j, 4a, and 4c are stronger than the other compounds and the in vitro antimicrobial activities of the compounds were tested against Escherichia coli, Klebsiella pneumoniae, Proteus mirabilis, Bacillus subtilis, Staphylococcus aureus, Enterococcus faecalis, Aspergillus flavus, and Aspergillus Niger. The compounds 3d and 3e exhibit good activity against P. mirabilis. Compounds 3a, 3b, 3c, 3 h, 3i, 3j, and 4a showed significant activity against S. aureus. Compounds 3e and 3f showed very good activity against A. flavus. Compounds 3e, 3f, and 4c showed good activity against A. Niger.
IL-7 induces type 2 cytokine response in lung ILC2s and regulates GATA3 and CD25 expression
Authors: Sheikh Abdalla , Lu Julia , Melese Etienne , Seo Jung Hee , Abraham Ninan 
Published: May 2022

AbstractInterleukin-7 is a cytokine with well-established roles in lymphocyte development and more recently, an expanded role in immune function. IL-7Rα is highly expressed by innate lymphoid cells (ILCs), but how IL-7 directs the development or function of ILCs is not well studied. Using mice with inducible deletion of IL-7Rα, we showed that loss of IL-7 signaling led to impaired production of IL-5, IL-13 and amphiregulin in lung ST2+ group 2 innate lymphoid cells (ILC2s) following influenza/A infection. Conversely, mice treated with IL-7 increased production of IL-5 and IL-13 by lung ILC2s. Moreover, we showed that IL-7 enhanced GATA3 and CD25 expression in ILC2s and loss of IL-7 signaling led to their reduced expression. Altogether, this study demonstrates that IL-7 regulates the function of ILC2s during airway viral infection and induces GATA3 and CD25 expression.
Untargeted metabolomic profiling in a patient with glycogen storage disease Ib receiving empagliflozin treatment
Authors: Tallis Eran , Karsenty Cecile L. , Grimes Amanda B. , Karam Lina B. , Elsea Sarah H. , Sutton Vernon Reed , Rawls‐Castillo Brandy L. , Liu Ning , Soler‐Alfonso Claudia 
Published: May 2022

AbstractGlycogen storage disease type Ib (GSD‐Ib) is a rare inborn error of glycogen metabolism uniquely associated with neutropenia and neutrophil dysfunction, causing severe infections, inflammatory bowel disease (IBD), and impaired wound healing. Recently, kidney sodium‐glucose co‐transporter‐2 (SGLT2) inhibitors such as empagliflozin known to reduce plasma levels of 1,5‐anhydroglucitol (1,5‐AG) and its toxic derivatives in neutrophils, have been described as a new treatment option in case reports of patients with GSD‐Ib from Europe and Asia. We report our experience with an 11‐year‐old girl with GSD‐Ib presenting with short fasting hypoglycemia, neutropenia with neutrophil dysfunction, recurrent infections, suboptimal growth, iron‐deficiency anemia, and IBD. Treatment with daily empagliflozin improved neutrophil counts and function with a significant reduction in G‐CSF needs. Significant improvement in IBD has led to weight gain with improved nutritional markers and improved fasting tolerance. Reduction of maximum empagliflozin dose was needed due to arthralgia. No other significant side effects of empagliflozin were observed. This report uniquely highlights the novel use of untargeted metabolomics profiling for monitoring plasma levels of 1,5‐AG to assess empagliflozin dose responsiveness and guide dietary management and G‐CSF therapy. Clinical improvement correlated to rapid normalization of 1,5‐AG levels in plasma sustained after dose reduction. In conclusion, empagliflozin appeared to be a safe treatment option for GSD‐Ib‐associated neutropenia and neutrophil dysfunction. Global untargeted metabolomics is an efficient method to assess biochemical responsiveness to treatment.
The role of nurses in the management of atopic dermatitis: Results of an international survey
Authors: Aubert Hélène , Thormann Kathrin , Barbarot Sebastien , Chernyshov Pavel , Deleuran Meete , El‐Hachem Maya , de Groot Jette , Marcoux Danielle , Simon Dagmar , Raymakers Florine , Stalder Jean‐François 
Published: May 2022

AbstractBackgroundAtopic dermatitis (AD) is a chronic inflammatory skin condition that has a major impact on the quality of life of patients and their families. Therapeutic patient education (TPE) is recommended for all patients with this condition to improve disease management, adherence to therapy, and quality of life. Nurse‐led consultation, when performed by expert nurses, can be as effective as consultation by dermatologists in this field.ObjectiveThis study aimed to examine the role of nurses in the management of patients with atopic dermatitis.MethodsA global survey was carried out to determine the current role of nurses in TPE for patients with AD. A 24‐item online questionnaire was sent to all members of the ISAD‐OPENED network.ResultsIn total, 85 health care professionals from 20 countries answered the questionnaire. About 75% of the responding physicians and nurses reported effective interprofessional collaboration. The collaboration between nurse and physician was deemed to be excellent by 51% of the respondents. According to caregivers, a trained nurse could be helpful in many other fields, such as nurse consultations, patient care demonstrations, telephone follow‐ups between consultations, and patient workshops. The main obstacles preventing nurse involvement in TPE are insufficient training of nurses, lack of recognition, and lack of specific funding.ConclusionThis study emphasises the potential of the help provided by trained nurses throughout the TPE process. Doctor/nurse teams are very promising for TPE in the field of AD because of their potential to improve patient care.
A patient‐friendly 16‐channel transmit/64‐channel receive coil array for combined head–neck MRI at 7 Tesla
Authors: May Markus W. , Hansen Sam‐Luca J. D. , Mahmutovic Mirsad , Scholz Alina , Kutscha Nicolas , Guerin Bastien , Stockmann Jason P. , Barry Robert L. , Kazemivalipour Ehsan , Gumbrecht Rene , Kimmlingen Ralph , Adriany Markus , Chang Yulin , Triantafyllou Christina , Knake Susanne , Wald Lawrence L. , Keil Boris 
Published: May 2022

PurposeTo extend the coverage of brain coil arrays to the neck and cervical–spine region to enable combined head and neck imaging at 7 Tesla (T) ultra‐high field MRI.MethodsThe coil array structures of a 64‐channel receive coil and a 16‐channel transmit coil were merged into one anatomically shaped close‐fitting housing. Transmit characteristics were evaluated in a B1+‐field mapping study and an electromagnetic model. Receive SNR and the encoding capability for accelerated imaging were evaluated and compared with a commercially available 7 T brain array coil. The performance of the head–neck array coil was demonstrated in human volunteers using high‐resolution accelerated imaging.ResultsIn the brain, the SNR matches the commercially available 32‐channel brain array and showed improvements in accelerated imaging capabilities. More importantly, the constructed coil array improved the SNR in the face area, neck area, and cervical spine by a factor of 1.5, 3.4, and 5.2, respectively, in regions not covered by 32‐channel brain arrays at 7 T. The interelement coupling of the 16‐channel transmit coil ranged from −14 to −44 dB (mean = −19 dB, adjacent elements <−18 dB). The parallel 16‐channel transmit coil greatly facilitates B1+ field shaping required for large FOV neuroimaging at 7 T.ConclusionThis new head–neck array coil is the first demonstration of a device of this nature used for combined full‐brain, head–neck, and cervical‐spine imaging at 7 T. The array coil is well suited to provide large FOV images, which potentially improves ultrahigh field neuroimaging applications for clinical settings.
Decreasing integration within face network and segregation beyond the face network in the aging brain
Authors: Qing Tianying , Chen Jing , Xue Licheng , Tan Yufei , Huang Zehao , Yang Shimeng , Chen Yuqiu , Wang Jinhui , Zou Qihong , Lv Yating , Zhao Jing 
Published: May 2022

AbstractFace processing is known to decline in older adults; however, a clear understanding of the brain networks behind this cognitive decline is still lacking. In this study, we investigated the neural correlates of the declined face processing with aging from a resting‐state brain network perspective. Nineteen healthy old adults and 22 young adults were recruited and underwent two functional magnetic resonance imaging (fMRI) scanning sessions (i.e., resting‐state and localizer task) and two behavioral tests (face matching and symbol‐form matching). We examined age‐related alterations in resting‐state functional connectivity (FC) within face network as well as between face network and other networks, and tested their associations with behavioral performance of face and symbol‐form processing. We found that (a) compared with young adults, old adults exhibited decreased FC between face‐selective regions (fusiform face area and occipital face area), but increased FC between face‐selective regions and non‐face‐selective regions; (b) these age‐related FC alterations were correlated with individuals’ behavioral performance of face and symbol‐form processing. Collectively, these findings suggest the declines of face processing are associated with a mixture of decreased integration within the face network and segregation beyond the face network in the aging brain, and provide evidence for a neural basis of cognitive aging in face processing from an intrinsic brain network perspective.
In vitro evaluation of fenfluramine and norfenfluramine as victims of drug interactions
Authors: Martin Parthena , Czerwiński Maciej , Limaye Pallavi B. , Muranjan Seema , Ogilvie Brian W. , Smith Steven , Boyd Brooks 
Published: May 2022

AbstractFenfluramine (FFA) has potent antiseizure activity in severe, pharmacoresistant childhood‐onset developmental and epileptic encephalopathies (e.g., Dravet syndrome). To assess risk of drug interaction affecting pharmacokinetics of FFA and its major metabolite, norfenfluramine (nFFA), we conducted in vitro metabolite characterization, reaction phenotyping, and drug transporter−mediated cellular uptake studies. FFA showed low in vitro clearance in human liver S9 fractions and in intestinal S9 fractions in all three species tested (t1/2 > 120 min). Two metabolites (nFFA and an N‐oxide or a hydroxylamine) were detected in human liver microsomes versus six in dog and seven in rat liver microsomes; no metabolite was unique to humans. Selective CYP inhibitor studies showed FFA metabolism partially inhibited by quinidine (CYP2D6, 48%), phencyclidine (CYP2B6, 42%), and furafylline (CYP1A2, 32%) and, to a lesser extent (<15%), by tienilic acid (CYP2C9), esomeprazole (CYP2C19), and troleandomycin (CYP3A4/5). Incubation of nFFA with rCYP1A2, rCYP2B6, rCYP2C19, and rCYP2D6 resulted in 10%−20% metabolism and no clear inhibition of nFFA metabolism by any CYP‐selective inhibitor. Reaction phenotyping showed metabolism of FFA by recombinant human cytochrome P450 (rCYP) enzymes rCYP2B6 (10%–21% disappearance for 1 and 10 µM FFA, respectively), rCYP1A2 (22%−23%), rCYP2C19 (49%−50%), and rCYP2D6 (59%−97%). Neither FFA nor nFFA was a drug transporter substrate. Results show FFA metabolism to nFFA occurs through multiple pathways of elimination. FFA dose adjustments may be needed when administered with strong inhibitors or inducers of multiple enzymes involved in FFA metabolism (e.g., stiripentol).
Association of income and educational levels with adherence to direct oral anticoagulant therapy in patients with incident atrial fibrillation: A Finnish nationwide cohort study
Authors: Teppo Konsta , Jaakkola Jussi , Biancari Fausto , Halminen Olli , Linna Miika , Haukka Jari , Putaala Jukka , Tiili Paula , Lehtonen Ossi , Niemi Mikko , Mustonen Pirjo , Kinnunen Janne , Hartikainen Juha , Airaksinen K. E. Juhani , Lehto Mika 
Published: May 2022

AbstractLow socioeconomic status has been associated with poor outcomes in patients with atrial fibrillation (AF). However, little is known about socioeconomic disparities in adherence to stroke prevention with direct oral anticoagulants (DOACs). We assessed the hypothesis that AF patients with higher income or educational levels have better adherence to DOACs in terms of treatment implementation and persistence. The used nationwide registry‐based FinACAF cohort covers all patients with incident AF starting DOACs in Finland during 2011–2018. The implementation analyses included 74 222 (mean age 72.7 ± 10.5 years, 50.8% female) patients, and persistence analyses included 67 503 (mean age 75.3 ± 8.9 years, 53.6% female) patients with indication for permanent anticoagulation (CHA2DS2‐VASc score >1 in men and >2 in women). Patients were divided into income quartiles and into three categories based on their educational attainment. Therapy implementation was measured using the medication possession ratio (MPR), and patients with MPR ≥0.90 were defined adherent. Persistence was measured as the incidence of therapy discontinuation, defined as the first 135‐day period without DOAC purchases after drug initiation. Patients with higher income or education were consistently more likely adherent to DOACs in the implementation phase (comparing the highest income or educational category to the lowest: adjusted odds ratios 1.18 (1.12–1.25) and 1.21 (1.15–1.27), respectively). No association with income or educational levels was observed on the incidence of therapy discontinuation. In conclusion, we observed that income and educational levels both have independent positive association on the implementation of DOAC therapy but no association on therapy persistence in patients with AF.
Hearing loss: The final frontier of pharmacology
Authors: Foster Alan C. , Jacques Bonnie E. , Piu Fabrice 
Published: May 2022

AbstractDespite a prevalence greater than cancer or diabetes, there are no currently approved drugs for the treatment of hearing loss. Research over the past two decades has led to a vastly improved understanding of the cellular and molecular mechanisms in the cochlea that lead to hearing deficits and the advent of novel strategies to combat them. Combined with innovative methods that enable local drug delivery to the inner ear, these insights have paved the way for promising therapies that are now under clinical investigation. In this review, we will outline this renaissance of cochlear biology and drug development, focusing on noise, age‐related, and chemotherapy‐induced hearing dysfunction.