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ticulatory oral motor skill for /ta/ and tongue pressure (p < 0.001). No improvements were observed in the control group.

Our results suggest that our oral frailty measures program effectively alleviates oral frailty. Future studies are needed to clarify the impact on preventing physical frailty and improving the nutritional status.

Our results suggest that our oral frailty measures program effectively alleviates oral frailty. Future studies are needed to clarify the impact on preventing physical frailty and improving the nutritional status.Macrophages, the central mediators of innate immune responses, being in the first-line of defense, they have to readily respond to pathogenic or tissue damage signals to initiate the inflammatory cascade. Such rapid responses require energy to support orchestrated production of pro-inflammatory mediators and activation of phagocytosis. Being a cell type that is present in diverse environments and conditions, macrophages have to adapt to different nutritional resources. Thus, macrophages have developed plasticity and are capable of utilizing energy at both normoxic and hypoxic conditions and in the presence of varying concentrations of glucose or other nutrients. Such adaptation is reflected on changes in signaling pathways that modulate responses, accounting for the different activation phenotypes observed. Macrophage metabolism has been tightly associated with distinct activation phenotypes within the range of M1-like and M2-like types. In the context of diseases, systemic changes also affect macrophage metabolism, as in diabetes and insulin resistance, which results in altered metabolism and distinct activation phenotypes in the adipose tissue or in the periphery. In the context of solid tumors, tumor-associated macrophages adapt in the hypoxic environment, which results in metabolic changes that are reflected on an activation phenotype that supports tumor growth. Coordination of environmental and pathogenic signals determines macrophage metabolism, which in turn shapes the type and magnitude of the response. Therefore, modulating macrophage metabolism provides a potential therapeutic approach for inflammatory diseases and cancer.Human and experimental animal data suggest both hyperglycemia and hypoglycemia can lead to altered brain structure and neurocognitive function in type 1 diabetes (T1D). Young children with T1D are prone to extreme fluctuations in glucose levels. The overlap of these potential dysglycemic insults to the brain during the time of most active brain and cognitive development may cause cellular and structural injuries that appear to persist into adult life. Brain structure and cognition in persons with T1D are influenced by age of onset, exposure to glycemic extremes such as severe hypoglycemic episodes, history of diabetic ketoacidosis, persistent hyperglycemia, and glucose variability. Studies using brain imaging techniques have shown brain changes that appear to be influenced by metabolic abnormalities characteristic of diabetes, changes apparent at diagnosis and persistent throughout adulthood. Some evidence suggests that brain injury might also directly contribute to psychological and mental health outcomes. Neurocognitive deficits manifest across multiple cognitive domains. Moreover, impaired executive function and mental health can affect patients' adherence to treatment. This review summarizes the current data on the impact of glycemic extremes on brain structure and cognitive function in youth with T1D and the use of new diabetes technologies that may reduce these complications.

This study investigates the synergistic effects of Gleevec (imatinib) and rapamycin on the proliferative and angiogenic properties of mouse bone marrow-derived endothelial progenitor cells (EPCs).

EPCs were isolated from mouse bone marrow and treated with different concentrations of Gleevec or rapamycin individually or in combination. The cell viability and proliferation were examined using the MTT assay. An analysis of cell cycle and apoptosis was performed using flow cytometry. Formation of capillary-like tubes was examined in vitro, and the protein expression of cell differentiation markers was determined using Western blot analysis.

Gleevec significantly reduced cell viability, cell proliferation, and induced cell apoptosis in EPCs. Rapamycin had similar effects on EPCs, but it did not induce cell apoptosis. The combination of Gleevec and rapamycin reduced the cell proliferation but increased cell apoptosis. Although rapamycin had no demonstratable effect on tube formation, the combined therapy of Gevec and rapamycin therapy may be a promising approach for suppressing cardiovascular disease pathologies associated with angiogenesis.

Gleevec and rapamycin synergistically suppress cell proliferation and tube formation of EPCs by inducing cell apoptosis and endothelial differentiation. Mechanistically, it is likely that rapamycin enhances the proapoptotic and antiangiogenic effects of Gleevec by promoting the endothelial differentiation of EPCs. Given that EPCs are involved in the pathogenesis of some cardiovascular diseases and critical to angiogenesis, pharmacological inhibition of EPC proliferation by combined Gleevec and rapamycin therapy may be a promising approach for suppressing cardiovascular disease pathologies associated with angiogenesis.

The study aimed at investigating the association between the vascular endothelial growth factor A (VEGFA) genetic variants, the VEGFA serum level, and the primary ovarian insufficiency (POI) risk in Chinese Han women.

An age-matched case-control study was implemented in the West China Second Hospital of Sichuan University. Participants/Materials, Setting, Methods Blood samples and clinical information were collected from 240 patients with POI and 261 healthy controls between December 2012 and December 2018 at the West China Second Hospital of Sichuan University. Mutations of VEGFA gene -2578C/A, -1154G/A, 936C/T, and -634C/G were identified by PCR-RFLP. Moreover, VEGFA serum levels in the 2 groups were measured by the enzyme-linked immunosorbent assay (ELISA).

The -1154G>A and 936C>T variants of the VEGFA gene were significantly associated with POI (the adjusted odds ratio [OR] = 2.17 and 95% confidence interval [CI] = 1.07-4.43 for the former; the adjusted OR = 2.74 and 95% CI = 1.18-6.34 for theshould be cautiously considered.

Our study indicates an association between the VEGFA -1154G/A, 936C/T variants, and susceptibility to POI in Chinese Han women. Reduced levels of VEGFA may be a potential mechanism for the de-velopment of POI.

Our study indicates an association between the VEGFA -1154G/A, 936C/T variants, and susceptibility to POI in Chinese Han women. Reduced levels of VEGFA may be a potential mechanism for the de-velopment of POI.Both absolute and relative brain sizes vary greatly among and within the major vertebrate lineages. Scientists have long debated how larger brains in primates and hominins translate into greater cognitive performance, and in particular how to control for the relationship between the noncognitive functions of the brain and body size. One solution to this problem is to establish the slope of cognitive equivalence, i.e., the line connecting organisms with an identical bauplan but different body sizes. The original approach to estimate this slope through intraspecific regressions was abandoned after it became clear that it generated slopes that were too low by an unknown margin due to estimation error. Here, we revisit this method. We control for the error problem by focusing on highly dimorphic primate species with large sample sizes and fitting a line through the mean values for adult females and males. We obtain the best estimate for the slope of circa 0.27, a value much lower than those constructed using all mammal species and close to the value expected based on the genetic correlation between brain size and body size. FDI-6 cell line We also find that the estimate of cognitive brain size based on cognitive equivalence fits empirical cognitive studies better than the encephalization quotient, which should therefore be avoided in future studies on primates and presumably mammals and birds in general. The use of residuals from the line of cognitive equivalence may change conclusions concerning the cognitive abilities of extant and extinct primate species, including hominins.

Social distance, quarantine, pathogen testing, and other preventive strategies implemented during CO-VID-19 pandemic may negatively influence the management of acute ischemic stroke (AIS).

The current study aimed to evaluate the impacts of COVID-19 pandemic on treatment delay of AIS in China.

This study included patients with AIS admitted in 2 hospitals in Jiangsu, China. Patients admitted before and after the COVID-19 pandemic outbreak (January 31, 2020, as officially announced by the Chinese government) were screened to collect sociodemographic data, medical history information, and symptom onset status from clinical medical records and compared for pre- (measured as onset-to-door time [ODT]) and posthospital delay (measured as door-to-needle time [DNT]). The influencing factors for delayed treatment (indicated as onset-to-needle time >4.5 h) were analyzed with multivariate logistic regression analysis.

A total of 252 patients were included, of which 153 (60.7%) were enrolled before and 99 (39.3%shorten the delay so that the outcomes of stroke could be improved.

COVID-19 pandemic has remarkable impacts on the management of AIS. Both pre- and posthospital delays were prolonged significantly, and proportion of patients arrived within the 4.5-h time window for intravenous thrombolysis treatment was decreased. Given that anti-COVID-19 measures are becoming medical routines, efforts are warranted to shorten the delay so that the outcomes of stroke could be improved.

Critical aspects of time of feed initiation, advancement, and volume of feed increment in preterm neonates remain largely unanswered.

Medline , Embase, CENTRAL and CINAHL were searched from inception until 25th September 2020. Network meta-analysis with the Bayesian approach was used. Randomized controlled trials (RCTs) evaluating preterm neonates ≤32 weeks were included. Feeding regimens were divided based on the following categories initiation day early (<72 h), moderately early (72 h-7 days), and late (>7 days); advancement day early (<72 h), moderately early (72 h-7 days), and late (>7 days); increment volume small volume (SV) (<20 mL/kg/day), moderate volume (MoV) (20-< 30 mL/kg/day), and large volume (≥30 mL/kg/day); and full enteral feeding from the first day. Sixteen regimens were evaluated. Combined outcome of necrotizing enterocolitis (NEC) stage ≥ II or mortality before discharge was the primary outcome.

A total of 39 studies enrolled around 6,982 neonates. Early initiation (EI) with moderately early or late advancement using MoV increment enteral feeding regimens appeared to be most efficacious in decreasing the risk of NEC or mortality when compared to EI and early advancement with SV increment (risk ratio [95% credible interval] 0.39 [0.12, 0.95]; 0.34 [0.10, 0.86]) (GRADE-very low).

Early initiated, moderately early, or late advanced with MoV increment feeding regimens might be most appropriate in decreasing the risk of NEC stage ≥II or mortality. In view of the certainty of evidence being very low, adequately powered RCTs evaluating these 2 strategies are warranted.

Early initiated, moderately early, or late advanced with MoV increment feeding regimens might be most appropriate in decreasing the risk of NEC stage ≥II or mortality. In view of the certainty of evidence being very low, adequately powered RCTs evaluating these 2 strategies are warranted.