bluuebunny/crossref_metadata_2025_split huggingface dataset:
Case Report: Posterior Uveitis after Divalent Human Papillomavirus Vaccination in an Asian Female
Authors: Ye Hongfei , Feng Huazhang , Zhao Peiquan , Fei Ping 
Published: June 2020

SIGNIFICANCE
Vaccine-associated uveitis has appeared in recent years because of various vaccines, whereas cases for human papillomavirus (HPV) vaccination were rarely reported. With more and more females becoming aware of its importance and choosing HPV vaccination, much more attention should be paid on the adverse effects of it.

PURPOSE
The purpose of this study was to report a rare case of posterior uveitis after divalent HPV vaccination in an Asian female.

CASE REPORT
A 29-year-old woman presented with acute vision loss accompanied by symptoms of headache, tinnitus, and myalgia after the third injection of HPV vaccination. The best-corrected visual acuity dropped to 20/500 for both eyes, and optical coherence tomography revealed bilateral multifocal submacular fluid. A short course of oral prednisone as well as Ozurdex intravitreal injection resulted in the reversal of all signs and symptoms.

CONCLUSIONS
Although this case resembled Harada disease, we diagnosed it as vaccine-induced uveitis rather than coincidental autoimmune disease based on the rapid response to a short course of systemic corticosteroids. Because vaccine-induced uveitis is rare and difficult to distinguish from coincidental autoimmune disease, our case reminds eye care providers to be aware of the possible association between vaccination and a Harada-like reaction and to ask appropriately directed questions when obtaining history from young patients with uveitis. Based on this case, we also suggest Ozurdex intravitreal injection as a potential therapeutic choice, especially for patients with contraindication or personal concern to systemic corticosteroid.
The Mind Cannot Go Blind: Effects of Central Vision Loss on Judging One's Crossing Time
Authors: Graber Madeline , Hassan Shirin E. 
Published: June 2020

SIGNIFICANCE
This study explored whether people with AMD can accurately judge the time they need to cross the street. The results suggest that AMD-related vision loss does not affect a person's ability to estimate his/her own street-crossing time, whereas familiarity with the street does.

PURPOSE
The purpose of this study was to assess whether people with AMD could judge accurately their street-crossing time.

METHODS
Fifty-one AMD subjects and 47 age-matched normally sighted subjects (controls) estimated their time to cross a single-lane, one-way street four times (pre-estimate). Then, subjects actually crossed the street four times and subsequently estimated their crossing time four additional times (post-estimate). A linear mixed model with repeated measures for subject was used to determine if the ratio between subjects' estimated and actual crossing times changed as a function of subject group (AMD vs. control) and whether estimates changed before and after actually crossing the street. Univariate correlations and multiple regression analyses were also performed to determine which of the measured experimental variables were the best predictors of a subject's ability to estimate his/her crossing time.

RESULTS
No significant difference in crossing ratios were found between the AMD (average, 1.05) and control (average, 1.16) subjects (P = .11). This was true for both the pre-crossing (AMD, 1.09; controls, 1.23; P = .11) and post-crossing ratios (AMD, 1.01; controls, 1.09; P = .17). Both subject groups' crossing ratios, however, decreased significantly going from pre to post (P < .0001). Increased age, longer actual crossing time, and experience gained from previously crossing the street resulted in less overestimation of one's crossing time.

CONCLUSIONS
Our data suggest that familiarity with the street as opposed to central vision loss from AMD affects a person's ability to estimate his/her crossing time.
Long-term and Temporal Outcomes of Transcatheter Versus Surgical Aortic-valve Replacement in Severe Aortic Stenosis
Authors: Zhang Xin-Lin , Zhang Xiao-Wen , Lan Rong-Fang , Chen Zheng , Wang Lian , Xu Wei , Xu Biao 
Published: June 2020

Objective:
To determine the 5-year and temporal performance of TAVR versus SAVR.

Background:
TAVR has become a valuable treatment for severe aortic stenosis but the long-term safety and efficacy remain unclear.

Methods:
Databases were searched until October 6, 2019 for randomized trials with ≥5 years’ follow-up. Primary outcome was all-cause mortality. Odds ratios (ORs) with 95% confidence intervals (CIs) were pooled with random-effects models.

Results:
We included 4 trials with 3,758 patients. TAVR was associated with a significantly higher 5-year all-cause mortality than SAVR (OR, 1.19; 95% CI, 1.03–1.37; P = 0.02). Landmark analysis showed no significant difference within 2 years (OR, 0.92; 95% CI, 0.79–1.08; P = 0.33) but a statistically higher mortality in TAVR between 2 and 5 years (OR, 1.32; 95% CI, 1.14–1.52; P = 0.0002), with significant difference between these 2 temporal phases (P for interaction = 0.001). Similar interaction was found for cardiovascular mortality and several other outcomes. Rates of all-cause mortality or disabling stroke, permanent pacemaker implantation, aortic-valve rehospitalization, and reintervention were higher, but rates of major bleeding and new-onset fibrillation were lower in TAVR at 5 years. The incidences of myocardial infarction, stroke, and transient ischemic attack were not statistically different between TAVR and SAVR.

Conclusions:
TAVR was associated with a significantly higher all-cause mortality at 5 years compared with SAVR. Of note, all-cause mortality presented a characteristic temporal pattern showing increased risk between 2 and 5 years but not within 2 years. Longer-term follow-up data are warranted.
The Effect of Beta-lactam Allergy Status on the Rate of Surgical Site Infections: A Retrospective Cohort Study
Authors: Wilhelm Nathaniel B. , Bonsall Thomas J. , Miller Clayton L. 
Published: June 2020

Objective:
To determine if patients with reported BL allergies have increased odds of developing SSI compared to reported NBL allergic patients.

Summary of Background Data:
SSI represent a significant risk of morbidity and mortality for patients. Cefazolin-based perioperative antibiotic prophylaxis is the guideline-recommended drug-of-choice for most procedures. Due to over-reporting of BL allergies, many patients may not receive guideline-directed cephalosporin-based prophylaxis, which may result in an increased SSI rate.

Methods:
A single-center retrospective cohort design study was performed. Data was collected on all targeted surgical procedures: cesarean section, vaginal, and abdominal hysterectomy, colon, laminectomy, and spinal fusion surgeries.

Results:
During the study period, 2676 procedures were analyzed with 454 (17%) and 2222 (83%) in reported BL and NBL allergic cohorts, respectively. Significantly more SSI developed in the BL cohort versus NBL cohort (3.1% vs 1.5%, odds ratio 2.015; 95% confidence interval, 1.090–3.724; P = 0.023). Through a multivariate logistic regression, receipt of a NBL antibiotic regimen was the only variable to have a significant effect on SSI rate (adjusted odds ratio, 3.815; 95% confidence interval, 1.142–12.749; P = 0.030).

Conclusion:
Reported BL allergic patients have an increased odds of developing SSI in comparison to NBL allergic patients. The increased risk is likely related to administration of NBL antibiotic regimens in comparison to BL-based regimens. Thorough antibiotic allergy history collection can be a valuable SSI prevention tool to safely increase the proportion of patients receiving BL regimen.
Diagnostic Model of in-Hospital Mortality in Patients with Acute ST-Segment Elevation Myocardial Infarction Used Artificial Intelligence Methods
Authors: Li Yong 
Published: June 2020

AbstractBackgroundPreventing in-hospital mortality in Patients with ST-segment elevation myocardial infarction (STEMI) is a crucial step.ObjectivesThe objective of our research was to to develop and externally validate the diagnostic model of in-hospital mortality in acute STEMI patients used artificial intelligence methods.MethodsWe divide non-randomly the American population with acute STEMI into a training set, a test set,and a validation set. We converted the unbalanced data into balanc ed data. We used artificial intelligence methods to develop and externally validate the dia gnostic model of in-hospital mortality in acute STEMI patients. We used confusion matrix combined with the area under the receiver operating characteristic curve (AUC) to evaluat e the pros and cons of the above models.ResultsThe strongest predictors of in-hospital mortality were age, gender, cardiogenic shock, atrial fibrillation(AF), ventricular fibrillation(VF),third degree atrioventricular block,in-hospital bleeding, underwent percutaneous coronary intervention(PCI) during hospitalization, underwent coronary artery bypass grafting (CABG) during hospitalization, hypertension history, diabetes history, and myocardial infarction history.The F2 score of logistic regression in the training set, the test set, and the validation data set were 0.81, 0.6, and 0.59 respectively.The AUC of logistic regression in the training set, the test set, and the validation data set were 0.77, 0.78, and 0.8 respectively. The diagnostic model built by logistic regression was the best.ConclusionWe had used artificial intelligence methods developed and externally validated the diagnostic model of in-hospital mortality in acute STEMI patients.We registered this study with WHO International Clinical Trials Registry Platform (ICTRP) (registration number: ChiCTR1900027129; registered date: 1 November 2019).
Dopamine Release Neuroenergetics in Mouse Striatal Slices
Authors: Msackyi Msema , Chen Yuanxin , Tsering Wangchen , Wang Ninghan , Zhao Jingyu , Zhang Hui 
Published: June 2020

AbstractParkinson’s disease (PD) is the second most common neurodegenerative disease. Dopamine (DA) neurons in the substantia nigra par compacta with axonal projections to the dorsal striatum (dSTR) degenerate in PD while in contrast, DA neurons in the ventral tegmental area with axonal projections to the ventral striatum including the nucleus accumbens (NAcc) shell, are largely spared. To understand the pathogenesis of PD, it is important to study the neuroenergetics of DA neurons. This study aims to uncover the relative contribution of glycolysis and oxidative phosphorylation (OxPhos) to evoked DA release in the striatum. We measured evoked DA release in mouse striatal brain slices by fast-scan cyclic voltammetry every 2 minutes. Blocking OxPhos caused a greater reduction in evoked DA release in the dSTR compared to the NAcc shell, and blocking glycolysis caused a greater reduction in evoked DA release in the NAcc shell than in the dSTR. Furthermore, when glycolysis was bypassed in favor of direct OxPhos, evoked DA release in the NAcc shell was decreased by ∼50% over 40 minutes whereas evoked DA release in the dSTR was largely unaffected. These results demonstrated that the dSTR relies primarily on OxPhos for energy production to maintain evoked DA release whereas the NAcc shell relies more on glycolysis. Using two-photon imaging, we consistently found that the oxidation level of the DA terminals was higher in the dSTR than in the NAcc shell. Together, these findings partially explain the specific vulnerability of DA terminals in the dSTR to degeneration in PD.Significant statementThe neuroenergetics of dopaminergic neuron is important to understand Parkinson’s disease (PD), a neurodegenerative disorder associated with mitochondrial dysfunctions. However, the relative contributions of glycolysis and oxidative phosphorylation (OxPhos) to presynaptic energy demands in DA terminals are unclear. We addressed this question by measuring DA release in the dorsal striatum and nucleus accumbens (NAcc) shell of mouse brain using FSCV under reagents blocking different energy systems. We found that the NAcc shell relies on both glycolysis and OxPhos to maintain DA release while the dSTR relies heavily on OxPhos. We demonstrate the different neuroenergetics of DA terminals in these two brain areas, providing new fundamentally important insight into the specific vulnerability of DA terminals in the dSTR to degeneration in PD.
Therapy-induced transdifferentiation promotes glioma growth independent of EGFR signaling
Authors: Oh Hwanhee , Hwang Inah , Wu Lingxiang , Cao Dongqing , Yao Jun , Ying Haoqiang , Li Jian Yi , Yao Yu , Hu Baoli , Wang Qianghu , Zheng Hongwu , Paik Jihye 
Published: June 2020

AbstractEpidermal growth factor receptor (EGFR) is frequently amplified, mutated and overexpressed in malignant gliomas. Yet the EGFR-targeted therapies have thus far produced only marginal clinical response, and the underlying mechanism remains poorly understood. Through analyses of an inducible oncogenic EGFR-driven glioma mouse model system, our current study reveals a small population of glioma cells that can evade therapy-initiated apoptosis and potentiate relapse development by adopting a mesenchymal-like phenotypic state that no longer depends on oncogenic EGFR signaling. Transcriptome analyses of proximal and distal treatment responses further identify TGFβ/YAP/Slug signaling cascade activation as major regulatory mechanism that promotes therapy-induced glioma mesenchymal lineage transdifferentiation. Following anti-EGFR treatment, the TGFβ secreted from the stressed glioma cells acts to promote YAP nuclear translocation and activation, which subsequently stimulates upregulation of the pro-mesenchymal transcriptional factor Slug and then glioma lineage transdifferentiation towards a stable therapy-refractory state. Blockade of this adaptive response through enforced dominant negative YAP expression significantly delayed anti-EGFR relapse and significantly prolonged animal survival. Together, our findings shed new insight into EGFR-targeted therapy resistance and suggest that combinatorial therapies of targeting both EGFR and mechanisms underlying glioma lineage transdifferentiation could ultimately lead to deeper and more durable responses.SignificanceThis study demonstrates that molecular reprogramming and lineage transdifferentiation underlie anti-EGFR therapy resistance and is clinically relevant to the development of new combinatorial targeting strategies against malignant gliomas carrying aberrant EGFR signaling.
Highly multiplexed oligonucleotide probe-ligation testing enables efficient extraction-free SARS-CoV-2 detection and viral genotyping
Authors: Credle Joel J. , Robinson Matthew L , Gunn Jonathan , Monaco Daniel , Sie Brandon , Tchir Alexandra , Hardick Justin , Zheng Xuwen , Shaw-Saliba Kathryn , Rothman Richard E. , Eshleman Susan H. , Pekosz Andrew , Hansen Kasper , Mostafa Heba , Steinegger Martin , Larman H. Benjamin 
Published: June 2020

AbstractThe emergence of SARS-CoV-2 has caused the current COVID-19 pandemic with catastrophic societal impact. Because many individuals shed virus for days before symptom onset, and many show mild or no symptoms, an emergent and unprecedented need exists for development and deployment of sensitive and high throughput molecular diagnostic tests. RNA-mediated oligonucleotide Annealing Selection and Ligation with next generation DNA sequencing (RASL-seq) is a highly multiplexed technology for targeted analysis of polyadenylated mRNA, which incorporates sample barcoding for massively parallel analyses. Here we present a more generalized method, capture RASL-seq (“cRASL-seq”), which enables analysis of any targeted pathogen-(and/or host-) associated RNA molecules. cRASL-seq enables highly sensitive (down to ∼1-100 pfu/ml or cfu/ml) and highly multiplexed (up to ∼10,000 target sequences) detection of pathogens. Importantly, cRASL-seq analysis of COVID-19 patient nasopharyngeal (NP) swab specimens does not involve nucleic acid extraction or reverse transcription, steps that have caused testing bottlenecks associated with other assays. Our simplified workflow additionally enables the direct and efficient genotyping of selected, informative SARS-CoV-2 polymorphisms across the entire genome, which can be used for enhanced characterization of transmission chains at population scale and detection of viral clades with higher or lower virulence. Given its extremely low per-sample cost, simple and automatable protocol and analytics, probe panel modularity, and massive scalability, we propose that cRASL-seq testing is a powerful new surveillance technology with the potential to help mitigate the current pandemic and prevent similar public health crises.
Egr1loss-of-function promotes beige adipocyte differentiation and activation specifically in inguinal subcutaneous white adipose tissue
Authors: Bléher Marianne , Meshko Berbang , Gergondey Rachel , Kovacs Yoann , Duprez Delphine , L’Honoré Aurore , Havis Emmanuelle 
Published: June 2020

AbstractExercise, cold exposure and fasting lead to the differentiation of inducible-brown adipocytes, called beige adipocytes, within white adipose tissue and have beneficial effects on fat burning and metabolism, through heat production. This browning process is associated with an increased expression of the key thermogenic mitochondrial uncoupling protein 1, Ucp1. Egr1 transcription factor has been described as a regulator of white and beige differentiation programs, and Egr1 depletion is associated with a spontaneous increase of subcutaneous white adipose tissue browning, in absence of external stimulation. Here, we demonstrate thatEgr1mutant mice exhibit a restrainedUcp1expression specifically increased in subcutaneous fat, resulting in a metabolic shift to a more brown-like, oxidative metabolism, which was not observed in other fat depots. In addition,Egr1is necessary and sufficient to promote white and alter beige adipocyte differentiation of mouse stem cells. These results suggest that modulation ofEgr1expression could represent a promising therapeutic strategy to increase energy expenditure and to restrain obesity-associated metabolic disorders.
ATP dependent DNA transport within cohesin: Scc2 clamps DNA on top of engaged heads while Scc3 promotes entrapment within the SMC-kleisin ring
Authors: Collier James E , Lee Byung-Gil , Roig Maurici B , Yatskevich Stanislav , Petela Naomi J , Metson Jean , Voulgaris Menelaos , Llamazares Andres Gonzalez , Löwe Jan , Nasmyth Kim A 
Published: June 2020

SUMMARYIn addition to extruding DNA loops, cohesin entraps within its SMC-kleisin ring (S-K) individual DNAs during G1 and sister DNAs during S-phase. All three activities require related hook-shaped proteins called Scc2 and Scc3. Using thiol-specific crosslinking we provide rigorous proof of entrapment activity in vitro. Scc2 alone promotes entrapment of DNAs in the E-S and E-K compartments, between ATP-bound engaged heads and the SMC hinge and associated kleisin, respectively. This does not require ATP hydrolysis nor is it accompanied by entrapment within S-K rings, which is a slower process requiring Scc3. Cryo-EM reveals that DNAs transported into E-S/E-K compartments are “clamped” in a sub-compartment created by Scc2’s association with engaged heads whose coiled coils are folded around their elbow. We suggest that clamping may be a recurrent feature of cohesin complexes active in loop extrusion and that this conformation precedes the S-K entrapment required for sister chromatid cohesion.
Ozone therapy for patients with COVID-19 pneumonia: a Quasi-Randomized Controlled Trial
Authors: Hernández Alberto , Viñals Montserrat , Pablos Asunción , Vilás Francisco , Papadakos Peter J , Wijeysundera Duminda , Bergese Sergio D. , Vives Marc 
Published: June 2020

AbstractBackgroundThere is still no specific treatment strategies for COVID-19 other than supportive management. The potential biological benefits of ozonated autohemotherapy include reduced tissue hypoxia, decreased hypercoagulability, modulated immune function with inhibition of inflammatory mediators, improved phagocytic function, and impaired viral replication.ObjectiveTo determine the impact of the use of ozonated blood on time to clinical improvement in patients with severe COVID-19 pneumonia.DesignA Quasi-Randomized Controlled Trial determined by admittance to the hospital based on bed availability.SettingInternal Medicine ward at Policlinica Ibiza Hospital, Spain.ParticipantsEighteen patients with COVID-19 infection (laboratory confirmed) severe pneumonia admitted to hospital between 20th March and 19th April 2020. The mean age of the cohort was 68 years-old and 72% (n=13) were male.InterventionPatients admitted to the hospital during the study period were pre-randomized to different beds based on bed availability. Depending on the bed the patient was admitted, the treatment was ozone autohemotherapy or standard treatment. Patients in the therapy arm received ozonated blood twice daily starting on the day of admission for a median of four days. Each treatment involved administration of 200 mL autologous whole blood enriched with 200 mL of oxygen-ozone mixture with a 40 μg/mL ozone concentration.Main OutcomesThe primary outcome was time from hospital admission to clinical improvement, which was defined as either hospital discharge or a two-point improvement in clinical status measured on a six-point ordinal scale. Secondary outcomes were clinical improvement measured on the 7th, 14th and 28th day after admission, as well as time to a two-fold reduction in concentrations of C-reactive protein, ferritin, D-dimer and lactate dehydrogenase.ResultsNine patients (50%) received ozonated autohemotherapy beginning on the day of admission. Ozonated autohemotherapy was associated with shorter time to clinical improvement (median [IQR]), 7 days [6-10] vs 28 days [8-31], p=0.04) and better outcomes at 14-days (88.8% vs 33.3%, p=0.01). In risk-adjusted analyses, ozonated autohemotherapy was associated with a shorter mean time to clinical improvement (−11.3 days, p=0.04, 95% CI −22.25 to −0.42).ConclusionOzonated autohemotherapy was associated with a significantly shorter time to clinical improvement in this quasi-randomized controlled trial. Given the small sample size and study design, these results require evaluation in larger randomized controlled trials.
Vimentin is Required for Tumor Progression and Metastasis in a Mouse Model of Non-Small Cell Lung Cancer
Authors: Berr Alexandra L. , Wiese Kristin , dos Santos Gimena , Davis Jennifer M. , Koch Clarissa M. , Anekalla Kishore R. , Kidd Martha , Cheng Yuan , Hu Yuan-Shih , Ridge Karen M. 
Published: June 2020

AbstractVimentin, a type III intermediate filament, is highly expressed in aggressive epithelial cancers and is associated with increased rates of metastasis. We show that vimentin is causally required for lung cancer metastasis using a genetic mouse model of lung adenocarcinoma (LSL-KrasG12D;Tp53fl/fl, termedKPV+/+) crossed with vimentin-null mice (thereby creatingKPV−/−mice). BothKPV+/+andKPV−/−mice developed lung tumors, yetKPV−/−mice had delayed tumorigenesis and prolonged survival.KPV+/+cells implanted in the flank metastasized to the lung whileKPV−/−cells did not, providing additional evidence that vimentin is required for metastasis. Differential expression analysis of RNA-seq data demonstrated thatKPV−/−cells had suppressed expression of genes that drive epithelial-to-mesenchymal transition, migration, and invasion, processes that are critical to the metastatic cascade. Integrative metabolomic and transcriptomic analysis revealed altered glutaminolysis, withKPV−/−cells accumulating glutathione, leading to impaired cell motility in response to oxidative stress. Together, these results show that loss of vimentin impairs epithelial-to-mesenchymal transition and regulation of the oxidative stress response, resulting in decreased metastasis in murine lung adenocarcinoma.