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Working at home throughout the COVID-19 pandemic: Impact on writer output and experience.
To examine the effectiveness of biofeedback used in the treatment of adults with Parkinson disease (PD) and dysphagia, define the factors associated with biofeedback treatment outcomes, and inform a theory to guide the implementation of biofeedback in future dysphagia interventions.

A systematic review using a narrative synthesis approach of all published and unpublished studies were sought with no date or language restrictions. Ten electronic databases (EMBASE, PubMed, CINAHL, Web of Science, Scopus, Science Direct, AMED, The Cochrane Database of Systematic Reviews, ProQuest Dissertations and Theses A & I, Google Scholar) were searched from inception to April 2019. This search was updated in January 2020. The methodological quality of included studies was assessed using Downs and Black checklist.

Four studies were included. Acetohydroxamic The methodological quality of the included studies was low with a high risk of bias. Data were analyzed narratively and descriptively. Despite the heterogeneity of the included studies, the findings suggest that interventions incorporating visual biofeedback may have positive effects on swallowing-related quality of life.

Based on these preliminary findings, we provide directions for further research and clinical interventions that incorporate an augmentative biofeedback component of swallowing interventions in people with PD. Future studies should be rigorously designed and set appropriate biofeedback treatment in terms of types, schedules, and timing.
Based on these preliminary findings, we provide directions for further research and clinical interventions that incorporate an augmentative biofeedback component of swallowing interventions in people with PD. Future studies should be rigorously designed and set appropriate biofeedback treatment in terms of types, schedules, and timing.
To explore whether traditional models of cardiovascular disease (CVD) risk prediction correctly predict CVD events across a median 5.7-year follow-up period in individuals with spinal cord injury (SCI) and whether adding SCI-related characteristics (ie, lesion level) to the prediction model can improve the prognostic value.

Retrospective analysis of patient records.

Observation at the start of active rehabilitation of participants in a multicenter cohort study, "Restoration of (Wheelchair) Mobility in SCI Rehabilitation," in the Netherlands.

Patients with SCI (N=200) The patients were 74% men, aged 40±14 years, and with an American Spinal Injury Association (ASIA) impairment score of A through D. Forty percent had tetraplegia, and 69% were motor complete.

Risk profiling/not applicable.

Survival status and cardiovascular morbidity and mortality qwere obtained from medical records. Five-year Framingham Risk Scores (FRS) and the FRS ability to predict events assessed using receiver operating charactein individuals with SCI. Nonetheless, these markers successfully distinguish between SCI individuals at high versus low risk for future CVD events. Our data may have future clinical implications, both related to (cutoff values of) CVD risk factors, but also for (earlier) prescription of (non)pharmacologic strategies against CVD in SCI individuals.
The aim of this study was to evaluate whether computed tomography (CT), magnetic resonance imaging (MRI), and positron emission tomography/computed tomography (PET/CT) can effectively differentiate between malignant and benign palatal lesions.

In total, 59 patients with palatal lesions (32 malignant and 27 benign), who underwent CT, MRI, and/or PET/CT imaging examinations and had histopathological diagnoses, were divided into an analysis group (n=46) and a validation group (n=13). Bone changes adjacent to the lesion, MRI signal intensity, apparent diffusion coefficient (ADC), time to peak enhancement (T
), and maximum standardized uptake values (SUV
) were evaluated in the analysis group. Diagnostic performance was individually assessed for each parameter for differentiating between malignant and benign lesions. A diagnostic decision tree was constructed by using useful parameters and its accuracy tested in the validation group.

The frequency distribution of bone change types and T
differed significantly between malignant and benign lesions. The ADC of malignant lymphoma was significantly lower than that of other lesions. The other parameters did not distinguish between lesion types. The accuracy of the decision tree, constructed by using bone change types, ADC, and T
, was 87.5%.

Bone change types, ADC values, and T
are useful for differentiating between malignant and benign palatal lesions.
Bone change types, ADC values, and Tpeak are useful for differentiating between malignant and benign palatal lesions.As a critical regulator of the cell cycle, cyclin-dependent kinase (CDK) inhibitor p21 or p21 is involved in the development of cardiac hypertrophy and heart failure. Calcitriol, or 1,25(OH)2D3, the bioactive form of vitamin D (VD), can activate p21 expression and attenuate cardiac hypertrophy. To simulate cardiac hypertrophy in vitro and ex vivo, respectively, mice and cardiomyocytes were treated with isoproterenol (ISO). Moreover, the p21 signaling pathway was examined in ISO + VD and ISO + VD p21 inhibitor-treated cardiomyocytes. We found that calcitriol treatment led to a significant decrease in cardiac size and the mRNA levels of atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) in ISO-treated mice. Furthermore, the surface area of cardiomyocytes and the expression of ANP and BNP were decreased, and the expression of p21 was increased in the ISO + VD group compared with those in the ISO group. Furthermore, the surface area of cardiomyocytes and the expression of ANP and BNP were markedly upregulated in the ISO + VD p21 inhibitor group relative to the ISO + VD group, whereas the difference was not statistically significant compared with those of the ISO p21 inhibitor group. Therefore, our findings indicate that 1,25(OH)2D3 protects against cardiac hypertrophy in mice through upregulating p21 expression.Colon cancer is still a major disease plaguing humans. In this study, we evaluated the synergistic antitumor effects of the combination of BRD4 inhibitor JQ1 and docosahexaenoic acid (DHA) in colon cancer. We demonstrated that simultaneous exposure to JQ1 and DHA resulted in strong synergistic antiproliferative and proapoptotic effects related to inhibition of expression of c-Myc and activation of NF-κB in colon cancer cell lines. At the same time, the synergetic anticancer effect had been confirmed in vivo. For in vivo experiments, JQ1 and DHA resulted in more significant tumor growth inhibition (53.7%) in a human colon cancer HCT116 xenograft model, comparing with the moderate inhibition in JQ1-treated (31.9%) or DHA-treated groups (20.3%). Because DHA is the predominant component of fish oil, our data suggest that this nontoxic dietary supplement could be administered with BRD4 inhibitor during therapy for CRC, which lay an important foundation for the development of therapeutic regimens for CRC.Pharmacological modulation of the Janus kinase (JAK) family has achieved clinically meaningful therapeutic outcomes for the treatment of inflammatory and hematopoietic diseases. Several JAK1 selective compounds are being investigated clinically to determine their anti-inflammatory potential. We used recombinant enzymes and primary human lymphocytes to assess the JAK1 specificity of itacitinib (INCB039110) and study inhibition of signal transducers and activators of transcription (STAT) signaling. Rodent models of arthritis and inflammatory bowel disease were subsequently explored to elucidate the efficacy of orally administered itacitinib on inflammatory pathogenesis. Itacitinib is a potent and selective JAK1 inhibitor when profiled against the other JAK family members. Upon oral administration in rodents, itacitinib achieved dose-dependent pharmacokinetic exposures that highly correlated with STAT3 pharmacodynamic pathway inhibition. Itacitinib ameliorated symptoms and pathology of established experimentally-induced arthritis in a dose-dependent manner. Furthermore, itacitinib effectively delayed disease onset, reduced symptom severity, and accelerated recovery in three distinct mouse models of inflammatory bowel disease. Low dose itacitinib administered via cannula directly into the colon was highly efficacious in TNBS-induced colitis but with minimal systemic drug exposure, suggesting localized JAK1 inhibition is sufficient for disease amelioration. Itacitinib treatment in an acute graft-versus-host disease (GvHD) model rapidly reduced inflammatory markers within lymphocytes and target tissue, resulting in a marked improvement in disease symptoms. This is the first manuscript describing itacitinib as a potent and selective JAK1 inhibitor with anti-inflammatory activity across multiple preclinical disease models. These data support the scientific rationale for ongoing clinical trials studying itacitinib in select GvHD patient populations.GDF11 has been reported to play a critical role in rejuvenating hypertrophy heart, skeletal muscle, and blood vessel regeneration in aged mice. Whether GDF11 can regulate autophagy in cardiomyocytes remains largely unknown. Thus, the purpose of the present study was to investigate the effects of GDF11 on cardiomyocyte autophagy induced by hypoxia, in addition to the underlying mechanisms. By using the MTT assay, Flow cytometry assay, LIVE/DEAD® Viability/Cytotoxicity Kit Stains and TUNEL assay, we found that exogenous GDF11 decreased apoptosis caused by prolonged hypoxia in cardiomyocytes. The expression of GDF11 was decreased obviously both in the cardiac tissue of myocardial infarction mice and the hypoxia treated cardiomyocytes. Protein levels of cleaved caspase-3, p-AMPK, SQSTM1, LC3B-I/II and GDF11 were detected by western blot. Autophagosomes and autolysosomes were identified by confocal laser microscopy after transfecting with the mRFP-eGFP-LC3 plasmids. Antibody against GDF11 (anti-GDF11) was used to inhibit the function of GDF11. At the molecular level, exogenous GDF11 increased AMPK function and enhanced autophagy activity. Anti-GDF11 inhibited autophagy and aggravated hypoxia-induced apoptosis in cardiomyocytes. Thus, GDF11 might be a potential target for myocardial infarction therapy.
This study sought to assess the relationship between E/e' and exercise capacity in patients with chronic kidney disease (CKD) and evaluate its prognostic role.

Patients with CKD have diastolic dysfunction, reduced physical fitness, and elevated risk of cardiovascular disease.

Patients with stage 3 and 4 CKD without previous cardiac disease underwent resting and exercise stress echocardiograms with assessment of exercise E/e'. Patients were compared to age-, sex-, and risk factor-matched control individuals and were followed annually for 5 years for cardiovascular death and major adverse cardiovascular event(s) (MACE). Exercise capacity was assessed as metabolic equivalents (METs), with reduced exercise capacity defined as METs of≤7. Raised exercise E/e' was defined as >13.

A total of 156 patients with CKD (age 62.8 ± 10.6 years; male 62%) were compared to 156 matched control individuals. Patients with CKD were more likely to be anemic (p<0.01) and had increased left ventricular mass (p<0.01), larger left atrial volumes (p<0.
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