bluuebunny/crossref_metadata_2025_split huggingface dataset:
Impact of baseline clinical and radiological features on outcome of chronic rhinosinusitis in granulomatosis with polyangiitis
Authors: Holme Sigrun Skaar , Kilian Karin , Eggesbø Heidi B. , Moen Jon Magnus , Molberg Øyvind 
Published: January 2021

Abstract
Background
Granulomatosis with polyangiitis (GPA) causes a recurring inflammation in nose and paranasal sinuses that clinically resembles chronic rhinosinusitis (CRS) of other aetiologies. While sinonasal inflammation is not among the life-threatening features of GPA, patients report it to have major negative impact on quality of life. A relatively large proportion of GPA patients have severe CRS with extensive damage to nose and sinus structures evident by CT, but risk factors for severe CRS development remain largely unknown. In this study, we aimed to identify clinical and radiological predictors of CRS-related damage in GPA.

Methods
We included GPA patients who had clinical data sets from time of diagnosis, and two or more paranasal sinus CT scans obtained ≥12 months apart available for analysis. We defined time from first to last CT as the study observation period, and evaluated CRS development across this period using CT scores for inflammatory sinus bone thickening (osteitis), bone destructions, and sinus opacifications (here defined as mucosal disease). In logistic regression, we applied osteitis as main outcome measure for CRS-related damage.

Results
We evaluated 697 CT scans obtained over median 5 years observation from 116 GPA patients. We found that 39% (45/116) of the GPA patients remained free from CRS damage across the study observation period, while 33% (38/116) had progressive damage. By end of observation, 32% (37/116) of the GPA patients had developed severe osteitis. We identified mucosal disease at baseline as a predictor for osteitis (odds ratio 1.33), and we found that renal involvement at baseline was less common in patients with severe osteitis at last CT (41%, 15/37) than in patients with no osteitis (60%, 27/45).

Conclusions
In this largely unselected GPA patient cohort, baseline sinus mucosal disease associated with CRS-related damage, as measured by osteitis at the end of follow-up. We found no significant association with clinical factors, but the data set indicated an inverse relationship between renal involvement and severe sinonasal affliction.
Chinese SLE Treatment and Research Group Registry (CSTAR) XIII: prevalence and risk factors for chronic scarring alopecia in patients with systemic lupus erythematosus
Authors: Xiang Yirong , Li Mengtao , Luo Hui , Wang Yanhong , Duan Xinwang , Zhao Cheng , Zhan Feng , Wu Zhenbiao , Li Hongbin , Yang Min , Xu Jian , Wei Wei , Wu Lijun , You Hanxiao , Qian Junyan , Yang Xiaoxi , Huang Can , Zhao Jiuliang , Wang Qian , Leng Xiaomei , Tian Xinping , Zhao Yan , Zeng Xiaofeng 
Published: January 2021

Abstract
Background
Scarring alopecia in systemic lupus erythematosus (SLE) patients caused reduced life quality and prolonged disease course. This case-control study aims to survey the prevalence of scarring alopecia during the disease course of SLE and evaluate the risk factors for scarring alopecia in Chinese SLE patients.

Methods
SLE patients in Chinese SLE treatment and Research group (CSTAR) were recruited. Scarring alopecia was defined according to SLICC/ACR-DI which was collected during follow-up visits or via self-reported questionnaires. We collected demographic characteristics, common comorbidities, autoantibody profiles, disease activity status, major organ involvements, and treatment strategies of these patients at registry. Univariate and multivariate logistic regression analyses were used to investigate the risk factors for scarring alopecia.

Results
We recruited 4792 SLE patients, and 374 (7.80%) patients had scarring alopecia. Mucocutaneous lesions (OR 2.062, p < 0.001), high SLICC/ACR-DI (OR 1.409, p < 0.001), and positive anti-Sm (OR 1.374, p = 0.029) were risk factors for scarring alopecia, while renal (OR 0.714, p = 0.028) and cardio-respiratory involvements (OR 0.347, p = 0.044), and immunosuppressant treatment (OR 0.675, p < 0.001) were significantly negative associated with it.

Conclusions
The prevalence of scarring alopecia in SLE patients is 7.80%. Active treatment strategies should be adopted to prevent scarring alopecia occurring.
Evaluation of microRNA-223 and microRNA-125a expression association with STAT3 and Bcl2 genes in blood leukocytes of CLL patients: a case–control study
Authors: Davari Nader , Ahmadpour Fatemeh , Kiani Ali Asghar , Azadpour Mozhgan , Asadi Zari Tahannejad 
Published: January 2021

Abstract
Objective
In chronic lymphocytic leukemia (CLL), lack of expression or dysregulation of some special miRs disrupts apoptosis of malignant cells; thereby miR expression can enhance cell proliferation, disease progression and decrease patient survival.

Results
30 CLL patients and 20 healthy individuals participated in the study. RNA was extracted to evaluate the expression of miR-125, miR-223, BCL-2 and signal transducer and transcription 3 activator (STAT3) genes; quantitative Real Time- PCR (Q-RT-PCR) was performed. MiR-125a and miR-223 expression decreased in the patients compared to the control group (P-Value:0.001). BCL-2 and STAT3 which are the target genes of these two miRs, showed increased expression, in the patients compared to the control subjects (P-Value: 0.001 and P-Value: 0.64 respectively). A significant reverse relationship was found between miR-125a and BCl-2 expression and WBC count. Significantly, miR-223 expression was associated with smoking in patients (P-Value: 0.007). Also, these miRs may have regulatory effects by controlling white blood cell (WBC) production based on the inverse correlation with WBC count and hemoglobin (Hb) concentration. Finally, miR-223 can be used as a prognostic factor in CLL patients; miR-125a may be useful for evaluating the therapeutic approaches based on the inverse link with BCl-2.
Proteomic characterization of hydatid cyst fluid: two-dimensional electrophoresis (2-DE) setup through optimizing protein extraction
Authors: Sedaghat Bahareh , Hajjaran Homa , Sadjjadi Fatemeh Sadat , Heidari Soudabeh , Sadjjadi Seyed Mahmoud 
Published: January 2021

Abstract
Objective
Proper characterization of hydatid cyst fluid (HCF) is useful for diagnostic and follow up purposes of cystic echinococcosis/hydatidosis, which is an important zoonotic disease. In this regard, proteomics methods are very helpful. The present study was conducted to compare three protein extraction methods for HCF collected from sheep liver hydatid cysts including, trichloracetic acid (TCA)/Acetone precipitation, TCA/Acetone along with dialysis, and combination of 2-D Clean-up Kit and dialysis followed by two-dimensional electrophoresis (2-DE), to achieve better resolution in the proteomic characterization of HCF proteins.

Results
The 2-DE of TCA/Acetone products showed a lot of smears in the background of gels; TCA/Acetone with dialysis showed greatly reduced smears while the 2-D Clean-up Kit together with dialysis showed sharp spots and least smears. Three-dimensional images of separated spots created by Progenesis SameSpots software showed the best result was achieved by 2-D Clean-up Kit and dialysis.
Kidney function and dementia risk in community-dwelling older adults: the Shanghai Aging Study
Authors: Wang Mengjing , Ding Ding , Zhao Qianhua , Wu Wanqing , Xiao Zhenxu , Liang Xiaoniu , Luo Jianfeng , Chen Jing 
Published: January 2021

Abstract
Background
Association between kidney dysfunction and dementia has been studied in western cohorts, but with inconsistent conclusions which may be due to the different measurements of kidney function. We aim to verify the hypothesis that lower levels of kidney function would be associated with increased risk of incident dementia in Chinese elderly.

Methods
One thousand four hundred twelve dementia-free participants aged 60 years or older from the Shanghai Aging Study were enrolled and followed up for 5.3 years on average. Glomerular filtration rate (GFR) was calculated by using combined creatinine–cystatin C CKD-EPI (Chronic Kidney Disease Epidemiology Collaboration) equation. Diagnoses of incident dementia and Alzheimer’s disease (AD) were established using DSM-IV and NINCDS-ADRDA criteria based on medical, neurological, and neuropsychological examinations to each participant. Cox proportional regression was used to analyze the association of baseline GFRcrcys levels with incident dementia/AD, adjusting age, gender, education years, APOE-ε4, diabetes, hypertension, baseline Mini-Mental State Examination score, and proteinuria.

Results
A total of 113 (8%) and 84 (7%) participants developed dementia and AD. Comparing to participants with high GFRcrcys (≥ 80 ml/min/1.73 m2), participants with low (< 67 ml/min/1.73 m2) and moderate GFRcrcys (67 ≤ GFR < 80 ml/min/1.73 m2) had increased risk of incident dementia with hazard ratios (HRs) of 1.87 (95% CI 1.02–3.44) and 2.19 (95% CI 1.21–3.95) after adjustment for confounders, respectively. Low (HR = 2.27 [95%CI 1.10–4.68]) and moderate (HR = 2.14 [95% CI 1.04–4.40]) GFRcrcys at baseline was also independently associated with incident AD after adjustments when comparing to high GFRcrcys. The significant association between GFRcrcys and dementia risk was observed in female but not in male participants.

Conclusions
GFRcrcys may be considered as a marker of an individual’s vulnerability to the increased risk of cognitive decline.
Important differences between hypertensive middle-aged women and men in cardiovascular autonomic control—a critical appraisal
Authors: Philbois Stella V. , Facioli Tábata P. , Gastaldi Ada C. , Rodrigues Jhennyfer A. L. , Tank Jens , Fares Thauane H. , Rodrigues Karine P. , Souza Hugo C. D. 
Published: January 2021

Abstract
Background
Normotensive premenopausal women show a vagal predominance of cardiac autonomic modulation, whereas age-matched men show a predominance of sympathetic modulation. However, some women develop systemic arterial hypertension (SAH) even with preserved ovarian function. Our hypothesis is that these women may have cardiovascular autonomic parameters similar to those of hypertensive men, even when subjected to pharmacological treatment. We aimed to investigate cardiovascular autonomic control and baroreflex sensitivity (BRS) in hypertensive premenopausal women and age-matched men.

Methods
One hundred volunteers between 18 and 45 years of age were assigned to two groups (50 participants each): a hypertensive group including patients with a history of SAH for at least 6 months (25 men and 25 women), who were under treatment with monotherapy (losartan, 25–50 mg/kg); and a normotensive group (25 men and 25 women). Anthropometric, hemodynamic, metabolic, and autonomic cardiovascular assessments were performed focusing on BRS, autonomic modulation of heart rate variability (HRV), and blood pressure variability (BPV).

Results
On HRV analysis, women showed higher values of high-frequency (HF) oscillations in absolute and normalized units, lower values ​of low-frequency (LF) in normalized units, and lower LF/HF ratio, as compared with men. When the normotensive and hypertensive groups were compared, hypertensive groups showed lower values ​of total variance and of LF and HF bands in absolute units. On BRS, hypertensive groups showed lower values than the normotensive group.

Conclusion
Regardless of blood pressure control through pharmacological treatment, hypertensive patients continued to have reduced HRV compared to normotensive, and hypertensive men had more autonomic impairment than hypertensive premenopausal women.
Epigenetic regulation of satellite cell fate during skeletal muscle regeneration
Authors: Massenet Jimmy , Gardner Edward , Chazaud Bénédicte , Dilworth F. Jeffrey 
Published: January 2021

AbstractIn response to muscle injury, muscle stem cells integrate environmental cues in the damaged tissue to mediate regeneration. These environmental cues are tightly regulated to ensure expansion of muscle stem cell population to repair the damaged myofibers while allowing repopulation of the stem cell niche. These changes in muscle stem cell fate result from changes in gene expression that occur in response to cell signaling from the muscle environment.Integration of signals from the muscle environment leads to changes in gene expression through epigenetic mechanisms. Such mechanisms, including post-translational modification of chromatin and nucleosome repositioning, act to make specific gene loci more, or less, accessible to the transcriptional machinery. In youth, the muscle environment is ideally structured to allow for coordinated signaling that mediates efficient regeneration. Both age and disease alter the muscle environment such that the signaling pathways that shape the healthy muscle stem cell epigenome are altered. Altered epigenome reduces the efficiency of cell fate transitions required for muscle repair and contributes to muscle pathology. However, the reversible nature of epigenetic changes holds out potential for restoring cell fate potential to improve muscle repair in myopathies.In this review, we will describe the current knowledge of the mechanisms allowing muscle stem cell fate transitions during regeneration and how it is altered in muscle disease. In addition, we provide some examples of how epigenetics could be harnessed therapeutically to improve regeneration in various muscle pathologies.
Upregulation of DUSP6 impairs infectious bronchitis virus replication by negatively regulating ERK pathway and promoting apoptosis
Authors: Wang Huan , Liu Dingxiang , Sun Yingjie , Meng Chunchun , Tan Lei , Song Cuiping , Qiu Xusheng , Liu Weiwei , Ding Chan , Ying Liao 
Published: January 2021

AbstractElucidating virus-cell interactions is fundamental to understanding viral replication and identifying targets for therapeutic control of viral infection. The extracellular signal-regulated kinase (ERK) pathway has been shown to regulate pathogenesis during many viral infections, but its role during coronavirus infection is undetermined. Infectious bronchitis virus is the representative strain of Gammacoronavirus, which causes acute and highly contagious diseases in the poultry farm. In this study, we investigated the role of ERK1/2 signaling pathway in IBV infection. We found that IBV infection activated ERK1/2 signaling and the up-regulation of phosphatase DUSP6 formed a negative regulation loop. Pharmacological inhibition of MEK1/2-ERK1/2 signaling suppressed the expression of DUSP6, promoted cell death, and restricted virus replication. In contrast, suppression of DUSP6 by chemical inhibitor or siRNA increased the phosphorylation of ERK1/2, protected cells from apoptosis, and facilitated IBV replication. Overexpression of DUSP6 decreased the level of phospho-ERK1/2, promoted apoptosis, while dominant negative mutant DUSP6-DN lost the regulation function on ERK1/2 signaling and apoptosis. In conclusion, these data suggest that MEK-ERK1/2 signaling pathway facilitates IBV infection, probably by promoting cell survival; meanwhile, induction of DUSP6 forms a negative regulation loop to restrict ERK1/2 signaling, correlated with increased apoptosis and reduced viral load. Consequently, components of the ERK pathway, such as MEK1/2 and DUSP6, represent excellent targets for the development of antiviral drugs.
CNS glucose metabolism in Amyotrophic Lateral Sclerosis: a therapeutic target?
Authors: Tefera Tesfaye Wolde , Steyn Frederik J. , Ngo Shyuan T. , Borges Karin 
Published: January 2021

AbstractAmyotrophic lateral sclerosis (ALS) is a fatal progressive neurodegenerative disorder primarily characterized by selective degeneration of both the upper motor neurons in the brain and lower motor neurons in the brain stem and the spinal cord. The exact mechanism for the selective death of neurons is unknown. A growing body of evidence demonstrates abnormalities in energy metabolism at the cellular and whole-body level in animal models and in people living with ALS. Many patients with ALS exhibit metabolic changes such as hypermetabolism and body weight loss. Despite these whole-body metabolic changes being observed in patients with ALS, the origin of metabolic dysregulation remains to be fully elucidated. A number of pre-clinical studies indicate that underlying bioenergetic impairments at the cellular level may contribute to metabolic dysfunctions in ALS. In particular, defects in CNS glucose transport and metabolism appear to lead to reduced mitochondrial energy generation and increased oxidative stress, which seem to contribute to disease progression in ALS. Here, we review the current knowledge and understanding regarding dysfunctions in CNS glucose metabolism in ALS focusing on metabolic impairments in glucose transport, glycolysis, pentose phosphate pathway, TCA cycle and oxidative phosphorylation. We also summarize disturbances found in glycogen metabolism and neuroglial metabolic interactions. Finally, we discuss options for future investigations into how metabolic impairments can be modified to slow disease progression in ALS. These investigations are imperative for understanding the underlying causes of metabolic dysfunction and subsequent neurodegeneration, and to also reveal new therapeutic strategies in ALS.
Biological functions of m6A methyltransferases
Authors: Gu Jianzhong , Zhan Yu , Zhuo Lvjia , Zhang Qin , Li Guohua , Li Qiujie , Qi Shasha , Zhu Jinyu , Lv Qun , Shen Yingying , Guo Yong , Liu Shuiping , Xie Tian , Sui Xinbing 
Published: January 2021

AbstractM6A methyltransferases, acting as a writer in N6-methyladenosine, have attracted wide attention due to their dynamic regulation of life processes. In this review, we first briefly introduce the individual components of m6A methyltransferases and explain their close connections to each other. Then, we concentrate on the extensive biological functions of m6A methyltransferases, which include cell growth, nerve development, osteogenic differentiation, metabolism, cardiovascular system homeostasis, infection and immunity, and tumour progression. We summarize the currently unresolved problems in this research field and propose expectations for m6A methyltransferases as novel targets for preventive and curative strategies for disease treatment in the future.
Is COPD associated with increased risk for microaspiration in intubated critically ill patients?
Authors:   for the MicroCOPD study group, Degroote Thècle , Jaillette Emmanuelle , Reignier Jean , Zerimech Farid , Girault Christophe , Brunin Guillaume , Chiche Arnaud , Lacherade Jean-Claude , MIRA Jean-Paul , Maboudou Patrice , Balduyck Malika , Nseir Saad 
Published: January 2021

Abstract
Background
Although COPD patients are at higher risk for aspiration when breathing spontaneously, no information is available on the risk for microaspiration in invasively ventilated COPD patients. The aim of our study was to determine the relationship between COPD and abundant microaspiration in intubated critically ill patients.

Methods
This was a retrospective analysis of prospectively collected data, provided by 3 randomized controlled trials on microaspiration in critically ill patients receiving invasive mechanical ventilation for more than 48 h. Abundant microaspiration was defined as the presence of pepsin and or alpha-amylase at significant levels in tracheal aspirates. In all study patients, pepsin and alpha-amylase were quantitatively measured in all tracheal aspirates collected during a 48-h period. COPD was defined using spirometry criteria.

Results
Among the 515 included patients, 70 (14%) had proven COPD. Pepsin and alpha-amylase were quantitatively measured in 3873 and 3764 tracheal aspirates, respectively. No significant difference was found in abundant microaspiration rate between COPD and non-COPD patients (62 of 70 patients (89%) vs 366 of 445 (82%) patients, p = 0.25). Similarly, no significant difference was found in abundant microaspiration of gastric contents (53% vs 45%, p = 0.28), oropharyngeal secretions (71% vs 71%, p = 0.99), or VAP (19% vs 22%, p = 0.65) rates between the two groups. No significant difference was found between COPD and non-COPD patients in duration of mechanical ventilation, ICU length of stay, or ICU mortality.

Conclusions
Our results suggest that COPD is not associated with increased risk for abundant microaspiration in intubated critically ill patients.
Lung ultrasound score predicts outcomes in COVID-19 patients admitted to the emergency department
Authors:   the COVID U. S. P. Registry Team, de Alencar Julio Cesar Garcia , Marchini Julio Flavio Meirelles , Marino Lucas Oliveira , da Costa Ribeiro Sabrina Correa , Bueno Cauê Gasparotto , da Cunha Victor Paro , Lazar Neto Felippe , Brandão Neto Rodrigo Antonio , Souza Heraldo Possolo 
Published: January 2021

Abstract
Background
During the COVID-19 pandemic, creating tools to assess disease severity is one of the most important aspects of reducing the burden on emergency departments. Lung ultrasound has a high accuracy for the diagnosis of pulmonary diseases; however, there are few prospective studies demonstrating that lung ultrasound can predict outcomes in COVID-19 patients. We hypothesized that lung ultrasound score (LUS) at hospital admission could predict outcomes of COVID-19 patients. This is a prospective cohort study conducted from 14 March through 6 May 2020 in the emergency department (ED) of an urban, academic, level I trauma center. Patients aged 18 years and older and admitted to the ED with confirmed COVID-19 were considered eligible. Emergency physicians performed lung ultrasounds and calculated LUS, which was tested for correlation with outcomes. This protocol was approved by the local Ethics Committee number 3.990.817 (CAAE: 30417520.0.0000.0068).

Results
The primary endpoint was death from any cause. The secondary endpoints were ICU admission and endotracheal intubation for respiratory failure. Among 180 patients with confirmed COVID-19 who were enrolled (mean age, 60 years; 105 male), the average LUS was 18.7 ± 6.8. LUS correlated with findings from chest CT and could predict the estimated extent of parenchymal involvement (mean LUS with < 50% involvement on chest CT, 15 ± 6.7 vs. 21 ± 6.0 with > 50% involvement, p < 0.001), death (AUC 0.72, OR 1.13, 95% CI 1.07 to 1.21; p < 0.001), endotracheal intubation (AUC 0.76, OR 1.17, 95% CI 1.09 to 1.26; p < 0.001), and ICU admission (AUC: 0.71, OR 1.14, 95% CI 1.07 to 1.21; p < 0.001).

Conclusions
In COVID-19 patients admitted in ED, LUS was a good predictor of death, ICU admission, and endotracheal intubation.