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This study investigated the impact of stroke on the control of upper limb endpoint force during isokinetic exercise, a dynamic force-generating task, and its association with stroke-affected muscle synergies. Three-dimensional upper limb endpoint force and electromyography of shoulder and elbow muscles were collected from sixteen chronic stroke survivors and eight neurologically intact adults. Participants were instructed to control the endpoint force direction during three-dimensional isokinetic upper limb movements. The endpoint force control performance was quantitatively evaluated in terms of the coupling between forces in orthogonal directions and the complexity of the endpoint force. Upper limb muscle synergies were compared between participants with varying levels of endpoint force coupling. The stroke survivors generating greater force abnormality than the others exhibited interdependent activation profiles of shoulder- and elbow-related muscle synergies to a greater extent. Based on the relevance of synergy activation to endpoint force control, this study proposes isokinetic training to correct the abnormal synergy activation patterns post-stroke. Several ideas for implementing effective training for stroke-affected synergy activation are discussed.

Cardiovascular disease (CVD) is the leading cause of death around the world, warranting an increasing number of studies for its treatment. Among all of its therapeutical strategies, engineered exosomes are attracting growing attention due to their excellent biocompatibility, non-immunogenicity, and favorable plasticity. Despite its increasing popularity, there is yet to be a bibliometric analysis regarding the application of exosomes in CVD treatment. Therefore, the present study assessed the current trends in engineered exosomes in treating CVD by conducting a bibliometric analysis. All associated literatures published between years 2002–2022 were collected, through the Web of Science Core Collection. Our results showed that related studies robustly increased in 2020, followed by a gradual increase from 2020 to 2022, indicating that this field attracted growing attention. Additionally, we described critical network of countries, institutions, authors, top-cited references, and keywords. The present bibliometric study provides systematic observations on engineering exosomes in treating CVD, reveals potential challenges and future direction for additional studies, and may inspire more researchers to commit to investigating treatments for CVD.

Abstract Base treatment and metal doping were evaluated as means of enhancing the photocatalytic activity of ZrO2 nanoparticles (NPs) via the generation of oxygen vacancies (OvS), and the sites responsible for this enhancement were identified and characterized by spectroscopic and microscopic techniques. We confirmed that OvS produced by base treatment engaged in photocatalytic activity for organic pollutant degradation, whereas surface defects introduced by Cr-ion doping engaged in oxidative catalysis of molecules. Moreover, we verified that base-treated ZrO2 NPs outperformed their Cr-ion doped counterparts as photocatalysts using in situ X-ray photoelectron spectroscopy and scanning transmission electron microscopy coupled with electron energy loss spectroscopy (STEM-EELS). Thus, our study provides valuable information on the origin of the enhanced photocatalytic activity of modified ZrO2 NPs and demonstrates the practicality of in situ spectroscopy and STEM-EELS for the evaluation of highly efficient metal oxide photocatalysts.

Platelets and their subcellular components (e.g., dense granules) are essential components in hemostasis. Understanding their chemical heterogeneities at the sub-micrometer scale, particularly their activation during hemostasis and production of platelet-derived extracellular vesicles, may provide important insights into their mechanisms; however, this has rarely been investigated, mainly owing to the lack of appropriate chemical characterization tools at nanometer scale. Here, the use of scanning transmission X-ray microscopy (STXM) combined with X-ray absorption near edge structure (XANES) to characterize human platelets and their subcellular components at the carbon K-edge and calcium L2,3-edge, is reported. STXM images can identify not only the spatial distribution of subcellular components in human platelets, such as dense granules (DGs) with sizes of ~200 nm, but also their granule-to-granule chemical heterogeneities on the sub-micrometer scale, based on their XANES spectra. The calcium distribution map as well as the principal component analysis of the STXM image stacks clearly identified the numbers and locations of the calcium-rich DGs within human platelets. Deconvolution of the carbon K-edge XANES spectra, extracted from various locations in the platelets, showed that amide carbonyl and carboxylic acid functional groups were mainly found in the cytoplasm, while ketone-phenol-nitrile-imine, aliphatic, and carbonate functional groups were dominant in the platelet DGs. These observations suggest that platelet DGs are most likely composed of calcium polyphosphate associated with adenosine triphosphate (ATP) and adenosine diphosphate (ADP), with significant granule-to-granule variations in their compositions, while the cytoplasm regions of platelets contain significant amounts of proteins.

Muscle atrophy is a common complication of many chronic diseases including heart failure, cancer cachexia, aging, etc. Unhealthy habits and usage of hormones such as dexamethasone can also lead to muscle atrophy. However, the underlying mechanisms of muscle atrophy are not completely understood. Non-coding RNAs (ncRNAs), such as microRNAs (miRNAs), long ncRNAs (lncRNAs), and circular RNAs (circRNAs), play vital roles in muscle atrophy. This review mainly discusses the regulation of ncRNAs in muscle atrophy induced by various factors such as heart failure, cancer cachexia, aging, chronic obstructive pulmonary disease (COPD), peripheral nerve injury (PNI), chronic kidney disease (CKD), unhealthy habits, and usage of hormones; highlights the findings of ncRNAs as common regulators in multiple types of muscle atrophy; and summarizes current therapies and underlying mechanisms for muscle atrophy. This review will deepen the understanding of skeletal muscle biology and provide new strategies and insights into gene therapy for muscle atrophy.

ObjectiveRehabilitation is essential in reducing stroke disability and should be performed as early as possible. Exercise is an established and effective rehabilitation method; however, its implementation has been limited as its very early use exacerbates cerebral injury and is restricted by patients' unstable conditions and disabilities. Remote ischemic conditioning (RIC) is a passive and accessible therapy in acute phases of stroke and appears to have similar neuroprotective effects as exercise. This study assessed the safety and feasibility of the novel rehabilitation strategy—early RIC followed by exercise (RICE) in acute ischemic stroke (AIS).MethodsWe conducted a single-center, double-blinded, randomized controlled trial with AIS patients within 24 h of stroke onset or symptom exacerbation. All enrolled patients were randomly assigned, at a ratio of 1:1, to either the RICE group or the sham-RICE group (sham RIC with exercise). Each group received either RIC or sham RIC within 24 h after stroke onset or symptom exacerbation, once a day, for 14 days. Both groups started the exercise routine on day 4, twice daily, for 11 total days. The safety endpoints included clinical deterioration, recurrence of stroke, hemorrhagic transformation, complications, and adverse events resulting from RICE during hospitalization. The efficacy endpoints [Modified Rankin Scale (mRS) score, National Institutes of Health Stroke Scale (NIHSS) score, Barthel Index, and walking ability] were evaluated at admission and 90 days after stroke onset.ResultsForty AIS patients were recruited and completed the study. No significant differences in baseline characteristics were found between the two groups, which included risk factors, stroke severity at admission, pre-morbid disability, and other special treatments. No significant differences were found in the safety endpoints between two groups. Excellent recovery (mRS 0–2) at 3 months was obtained in 55% of the patients with RICE as compared 40% in sham group, but it did not reach a significant level.ConclusionsRICE was safe and feasible for AIS patients, and seems to be a promising early stroke rehabilitation. The results of this study suggest a need for a future randomized and controlled multicenter trial with a larger sample size to determine the efficacy of RICE.

Abstract Background Abnormal intermuscular coordination limits the motor capability of stroke-affected upper limbs. By evaluating the intermuscular coordination in the affected limb under various biomechanical task constraints, the impact of a stroke on motor control can be analyzed and intermuscular coordination-based rehabilitation strategies can be developed. In this study, we investigated upper limb intermuscular coordination after a stroke during isokinetic movements. Methods Sixteen chronic stroke survivors and eight neurologically intact individuals were recruited. End-point forces and electromyographic activities of the shoulder and elbow muscles were measured while the participants performed isokinetic upper limb movements in a three-dimensional space. Intermuscular coordination of the stroke survivors and the control participants was quantified in the form of muscle synergies. Then, we compared the number, composition, and activation coefficients of muscle synergies and the end-point force between the groups. The correlation between the alteration of muscle synergies and the level of motor impairment was investigated. Results Four and five muscle synergies in the stroke and control groups were observed, respectively. The composition of muscle synergies was comparable between the groups, except that the three heads of the deltoid muscle were co-activated and formed one synergy in the stroke group, whereas those muscles formed two synergies in the control group. When the number of muscle synergies between the groups matched, the comparable composition of muscle synergies was observed in both groups. Alternatively, the modulation of synergy activation coefficients was altered after a stroke. The severity of motor impairments was negatively correlated with the similarity of the post-stroke synergies with respect to the mean control synergies. Conclusions Stroke-affected upper limbs seemed to modularize the activation of the shoulder and elbow muscles in a fairly similar way to that of neurologically intact individuals during isokinetic movements. Compared with free (i.e., unconstrained) movement, exercise under biomechanical constraints including the isokinetic constraint might promote the activation of muscle synergies independently in stroke survivors. We postulated the effect of biomechanical constraints on the intermuscular coordination and suggested a possible intermuscular coordination-based rehabilitation protocol that provides the biomechanical constraint appropriate to a trainee throughout the progress of rehabilitation.

Cerebral venous thrombosis (CVT) is a rare type of venous thromboembolism (VTE). It is an important cause of stroke in young adults and children. Severe CVT, which is characterized by cerebral venous infarction or hemorrhage, seizures, or disturbance of consciousness, has more severe clinical manifestations and a worse prognosis. It is commonly believed that the onset of severe CVT gave credit to venous return disorder, with the underlying pathogenesis remaining unclear. There is increasing evidence suggesting that an inflammatory response is closely associated with the pathophysiology of severe CVT. Preclinical studies have identified the components of neuroinflammation, including microglia, astrocytes, and neutrophils. After CVT occurrence, microglia are activated and secrete cytokines (e.g., interleukin-1β and tumor necrosis factor-α), which result in a series of brain injuries, including blood-brain barrier disruption, brain edema, and cerebral venous infarction. Additionally, astrocytes are activated at the initial CVT stage and may interact with microglia to exacerbate the inflammatory response. The extent of cerebral edema and neutrophil recruitment increases temporally in the acute phase. Further, there are also changes in the morphology of inflammatory cells, expression of inflammatory mediators, and inflammatory pathway molecules with CVT progression. Lately, some clinical research suggested that some inflammation-related biomarkers are of great value in assessing the course, severity, and prognosis of severe CVT. Moreover, basic and clinical research suggested that anti-inflammatory therapy might hold promise in severe CVT. This study reviews the current literature regarding the involvement of inflammation in the pathophysiology and anti-inflammatory interventions of severe CVT, which would contribute to informing the pathophysiology mechanism and laying a foundation for exploring novel severe CVT therapeutic strategies.

ObjectiveThe present study sought to differentiate multiple sclerosis and neuromyelitis optica spectrum disorder patients at their first attack by describing and distinguishing their clinical features, radiographic characteristics, and immunologic characteristics of serum and cerebrospinal fluid.MethodsWe retrospectively studied 58 patients with multiple sclerosis (MS) and 52 patients with neuromyelitis optica spectrum disorder (NMOSD) by referencing brainstem lesions as the prodromal events. Their demographics and presentation at the time of the first attack was evaluated including their gender, age, clinical features of the first attack, the expanded disability status scale (EDSS), brainstem lesion(s) by head MRI, and immunological indices of serum and cerebrospinal fluid.ResultsThe NMOSD group had more female patients (4.8 vs. 1.9, p < 0.05), and was older than the MS group (37.81 ± 16.60 vs. 27.57 ± 11.17, p

ObjectivesTo explore the alterations in immune cell composition in peripheral blood in patients with acute ischemic stroke (AIS) based on their age group.MethodsPatients with imaging confirmed AIS were enrolled from April 2019 to January 2020 and were divided into three groups according to their ages: 65 years (group-C). Blood samples were collected immediately when the patients were admitted to our ward prior to any intervention. Flow cytometry was used to analyze immune cell composition in peripheral blood.ResultsA total of 41 eligible patients were included for final analysis. Among the three groups, the proportions of CD56+ CD16dim NK cells were least to greatest in group-B, group-A, then group-C, respectively. With increasing age, there was a decrease in the proportion of CD3+ T-cells (group-A vs. group-C, P = 0.016) and CD3+CD4+ T-cells (group-C vs. group-A, P = 0.008; group-C vs. group-B P = 0.026). Meanwhile, no significant differences in proportions of monocytes and B cells were observed.ConclusionsThe compositions of immune cells in peripheral blood of AIS patients were distinct when divided by age groups. Differences in immune cell ratios may affect clinical outcomes and foreshadows possible need for customized treatment of AIS in different age groups.

Physical exercise is a promising rehabilitative strategy for acute ischemic stroke. Preclinical trials suggest that exercise restores cerebral blood circulation and re-establishes the blood–brain barrier's integrity with neurological function and motor skill improvement. Clinical trials demonstrated that exercise improves prognosis and decreases complications after ischemic events. Due to these encouraging findings, early exercise rehabilitation has been quickly adopted into stroke rehabilitation guidelines. Unfortunately, preclinical trials have failed to warn us of an adverse effect. Trials with very early exercise rehabilitation (within 24 h of ischemic attack) found an inferior prognosis at 3 months. It was not immediately clear as to why exercise was detrimental when performed very early while it was ameliorative just a few short days later. This review aimed to explore the potential mechanisms of harm seen in very early exercise administered to acute ischemic stroke patients. To begin, the mechanisms of exercise's benefit were transposed onto the current understanding of acute ischemic stroke's pathogenesis, specifically during the acute and subacute phases. Then, exercise rehabilitation's mechanisms were compared to that of remote ischemic conditioning (RIC). This comparison may reveal how RIC may be providing clinical benefit during the acute phase of ischemic stroke when exercise proved to be harmful.

Background: Air pollution is one of the greatest public health concerns worldwide. In order to understand its mechanism of harm, we investigated the effects of diesel exhaust particles (DEPs), one of the major constituents of ambient air pollutants, on reactive cell viability, oxygen stress, autophagy, and apoptosis. Materials and Methods: In in vitro human umbilical vein endothelial cell (HUVEC) model, cells were exposed to freshly dispersed DEP preparations at 0, 12.5, 25, 50, 100, or 200 µg/mL for 24 h or at 50 µg/mL DEP for 1, 3, 6, 12, or 24 h. Cell survival and oxidative stress were determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, activity of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (NOX), and generation of reactive oxygen species (ROS). Protein expressions of autophagy (Beclin-1, p62, and light chain 3 [LC3]-II) and apoptosis (Bcl2 and Bax) were assayed by Western blotting. Results: DEP induced a significant dose-dependent and temporal decrease in cell viability and increase in ROS generation and NOX activity, in association with decreased or increased protein levels of p62 or Beclin-1, as well as conversion of the LC3 in a dose-dependent manner. DEP increased pro-apoptotic protein Bax and decreased anti-apoptotic protein Bcl2. Conclusions: These results demonstrated that DEP exposure induced cytotoxicity, oxidative stress, autophagy, and apoptosis in HUVECs. Novel insight into the mechanisms of cardiovascular diseases caused by air pollution may be provided through these findings.

Stroke is one of the leading causes of mortality and morbidity worldwide, and yet, current treatment is limited to thrombolysis through either t-PA or mechanical thrombectomy. While therapeutic hypothermia has been adopted in clinical contexts such as neuroprotection after cardiac resuscitation and neonatal hypoxic-ischemic encephalitis, it is yet to be used in the context of ischemic stroke. The lack of ameliorative effect in ischemic stroke patients may be tied to the delayed cooling induction onset. In the trials where the cooling was initiated with significant delay (mostly systemic cooling methods), minimal benefit was observed; on the other hand, when cooling was initiated very early (mostly selective cooling methods), there was significant efficacy. Another timing factor that may play a role in amelioration may be the onset of cooling relative to thrombolysis therapy. Current understanding of the pathophysiology of acute ischemic injury and ischemia-reperfusion injury suggests that hypothermia before thrombolysis may be the most beneficial compared to cooling initiation during or after reperfusion. As many of the systemic cooling methods tend to require longer induction periods and extensive, separate procedures from thrombolysis therapy, they are generally delayed to hours after recanalization. On the other hand, selective cooling was generally performed simultaneously to thrombolysis therapy. As we conduct and design therapeutic hypothermia trials for stroke patients, the key to their efficacy may lie in quick and early cooling induction, both respective to the symptom onset and thrombolysis therapy.

Oxygen vacancies (Vo) present in CeO2 nanoparticles (NPs) can effectively boost their photocatalytic activity under ultraviolet (UV) light. To improve photocatalytic performance, Cr- and Fe-doped CeO2 NPs with increased Vo were prepared using a simple method of doping Cr and Fe ions into CeO2 NPs, which was confirmed by an in-depth analysis of the structural and electronic changes. Through photocatalytic degradation (PCD) experiments with 5-hydroxymethylfurfural (HMF), we found that the PCD rates of the two doped CeO2 NPs were faster than that of the CeO2 NPs. In addition, the conversion of HMF to 2,5-furandicarboxylic acid (FDCA) using the doped CeO2 NPs occurred only through the mechanism of the selective oxidation to 5-hydroxymethyl-2-furancarboxylic acid (HMFCA), exhibiting better efficiency than using CeO2 NPs.

Objective: Exercise rehabilitation is an effective therapy in reducing the disability rate after stroke and should be carried out as early as possible. However, very early rehabilitation exercise exacerbates brain injury and is difficult to conduct in stroke patients due to their weakened and potentially disabled state. It is valuable to explore additional early rehabilitation strategies. Remote Ischemic Conditioning (RIC) is a novel therapy designed to protect vital organs from severe lethal ischemic injury by transient sublethal blood flow to non-vital organs, including the distal limbs, in order to induce endogenous protection. RIC has previously been conducted post-stroke for neuroprotection. However, whether combined early RIC and exercise (RICE) therapy enhances stroke rehabilitation remains to be determined.Methods: This is a single-center, double-blinded, randomized controlled trial that will enroll acute ischemic stroke patients within 24 h of symptom onset or symptom exacerbation. All enrolled patients will be randomly assigned to either the RICE group (exercise with RIC) or the control group (exercise with sham RIC) at a ratio of 1:1, with 20 patients in each group. Both groups will receive RIC or sham RIC within 24 h after stroke onset or symptom exacerbation, once a day, for 14 days. All patients will begin exercise training on the fourth day, twice a day, for 11 days. Their neurological function [Modified Rankin Scale (mRS) score, National Institutes of Health Stroke Scale (NIHSS) score, Barthel Index, and walking ability], infarct volume (nuclear magnetic resonance, MRI), and adverse events will be evaluated at different time points in their post-stroke care.Results: The primary outcome is safety, measured by the incidence of any serious RICE-related adverse events and decreased adverse events during hospitalization. The secondary outcome is a favorable prognosis within 90 days (mRS score < 2), determined by improvements in the mRS score, NIHSS score, Barthel Index, walking ability after 90 days, and infarct volume after 12 ± 2 days.Conclusion: This study is a prospective randomized controlled trial to determine the rehabilitative effect of early RIC followed by exercise on patients with acute ischemic stroke.Trial Registration:www.chictr.org.cn, identifier: ChiCTR2000041042

Stroke is a leading threat to human life. Metabolic dysfunction of glucose may play a key role in stroke pathophysiology. Pharmacological hypothermia (PH) is a potential neuroprotective strategy for stroke, in which the temperature is decreased safely. The present study determined whether neuroprotective PH with chlorpromazine and promethazine (C + P), plus dihydrocapsaicin (DHC) improved glucose metabolism in acute ischemic stroke. A total of 208 adult male Sprague Dawley rats were randomly divided into the following groups: sham, stroke, and stroke with various treatments including C + P, DHC, C + P + DHC, phloretin (glucose transporter (GLUT)-1 inhibitor), cytochalasin B (GLUT-3 inhibitor), TZD (thiazolidinedione, phosphoenolpyruvate carboxykinase (PCK) inhibitor), and apocynin (nicotinamide adenine dinucleotide phosphate oxidase (NOX) inhibitor). Stroke was induced by middle cerebral artery occlusion (MCAO) for 2 h followed by 6 or 24 h of reperfusion. Rectal temperature was monitored before, during, and after PH. Infarct volume and neurological deficits were measured to assess the neuroprotective effects. Reactive oxygen species (ROS), NOX activity, lactate, apoptotic cell death, glucose, and ATP levels were measured. Protein expression of GLUT-1, GLUT-3, phosphofructokinase (PFK), lactate dehydrogenase (LDH), PCK1, PCK2, and NOX subunit gp91 was measured with Western blotting. PH with a combination of C + P and DHC induced faster, longer, and deeper hypothermia, as compared to each alone. PH significantly improved every measured outcome as compared to stroke and monotherapy. PH reduced brain infarction, neurological deficits, protein levels of glycolytic enzymes (GLUT-1, GLUT-3, PFK and LDH), gluconeogenic enzymes (PCK1 and PCK2), NOX activity and its subunit gp91, ROS, apoptotic cell death, glucose, and lactate, while raising ATP levels. In conclusion, stroke impaired glucose metabolism by enhancing hyperglycolysis and gluconeogenesis, which led to ischemic injury, all of which were reversed by PH induced by a combination of C + P and DHC.

While it is well-known that pre-stroke exercise conditioning reduces the incidence of stroke and the development of comorbidities, it is unclear whether post-stroke exercise conditioning is also neuroprotective. The present study investigated whether exercise postconditioning (PostE) induced neuroprotection and elucidated the involvement of SIRT1 regulation on the ROS/ER stress pathway. Adult rats were subjected to middle cerebral artery occlusion (MCAO) followed by either: (1) resting; (2) mild exercise postconditioning (MPostE); or (3) intense exercise postconditioning (IPostE). PostE was initiated 24 h after reperfusion and performed on a treadmill. At 1 and 3 days thereafter, we determined infarct volumes, neurological defects, brain edema, apoptotic cell death through measuring pro- (BAX and Caspase-3) and anti-apoptotic (Bcl-2) proteins, and ER stress through the measurement of glucose-regulated protein 78 (GRP78), inositol-requiring 1α (IRE1α), protein kinase RNA-like endoplasmic reticulum kinase (PERK), activating transcription factor 6 (ATF6), C/EBP homologous protein (CHOP), Caspase-12, and SIRT1. Proteins were measured by Western blot. ROS production was detected by flow cytometry.Compared to resting rats, both MPostE and IPostE significantly decreased brain infarct volumes and edema, neurological deficits, ROS production, and apoptotic cell death. MPostE further increased Bcl-2 expression and Bcl-2/BAX ratio as well as BAX and Caspase-3 expressions and ROS production (*p < 0.05). Both PostE groups saw decreases in ER stress proteins, while MPostE demonstrated a further reduction in GRP78 (***p < 0.001) and Caspase-12 (*p < 0.05) expressions at 1 day and IRE1α (**p < 0.01) and CHOP (*p < 0.05) expressions at 3 days. Additionally, both PostE groups saw significant increases in SIRT1 expression.In this study, both mild and intense PostE levels induced neuroprotection after stroke through SIRT1 and ROS/ER stress pathway. Additionally, the results may provide a base for our future study regarding the regulation of SIRT1 on the ROS/ER stress pathway in the biochemical processes underlying post-stroke neuroprotection. The results suggest that mild exercise postconditioning might play a similar neuroprotective role as intensive exercise and could be an effective exercise strategy as well.

Various assistive devices like exoskeletons have been developed to aid the growing number of disabled people. Recent studies have started to explore using soft rather than rigid components to create lightweight and unobtrusive systems that can be more easily adopted by the general population. However, there is a tradeoff between compliance and power in these systems. We investigated the physiological benefits of using an inconspicuous, soft and passive assistive device which would avoid bulkiness, heaviness and user discomfort. We chose to assist the sit-to-stand (STS) maneuver because it is a common activity of daily living (ADL). STS is also recognized as one of the most challenging ADLs due to the high knee torque required, and the primary limiting factor is known to be knee extensor strength. Thus, the objective of this research was to develop and evaluate an unobtrusive knee assist wear called X-tights that could aid knee extension during STS using only soft and passive components. This was accomplished by routing elastic bands across the lower extremity. Thirty-one healthy participants performed STS tests with and without the X-tights, while metabolic cost and muscle activity were recorded. Metabolic power significantly decreased, by 3.2 ± 1.5% (P = 0.04), when utilizing the X-tights during the STS, while there was no statistically significant differences in muscle activity. The present work introduces a new soft and passive assist wear that can be worn inconspicuously under normal clothing, and we demonstrate promising results for the future development and integration of soft assistive technology for daily life.

Obesity is a highly prevalent public health concern, attributed to multifactorial causes and limited in treatment options. Several comorbidities are closely associated with obesity such as the development of type 2 diabetes mellitus (T2DM), cardiovascular and cerebrovascular diseases, and nonalcoholic fatty liver disease (NAFLD). Bariatric surgery, which can be delivered in multiple forms, has been remarked as an effective treatment to decrease the prevalence of obesity and its associated comorbidities. The different types of bariatric surgery create a variety of new pathways for food to metabolize in the body and truncate the stomach’s caliber. As a result, only a small quantity of food is tolerated, and the body mass index noticeably decreases. This review describes the improvements of obesity and its comorbidities following bariatric surgery and their mechanism of improvement. Additionally, endocrine function improvements after bariatric surgery, which contributes to the patients’ health improvement, are described, including the role of glucagon-like peptide-1 (GLP-1), fibroblast growth factors 19 and 21 (FGF-19, FGF-21), and pancreatic peptide YY (PYY). Lastly, some of the complications of bariatric surgery, including osteoporosis, iron deficiency/anemia, and diarrhea, as well as their potential mechanisms, are described.

Abstract The modified TiO2 nanoparticles (NPs) to enhance their catalytic activities by doping them with the five transition metals (Cr, Mn, Fe, Co, and Ni) have been investigated using various surface analysis techniques such as scanning electron microscopy (SEM), Raman spectroscopy, scanning transmission X-ray microscopy (STXM), and high-resolution photoemission spectroscopy (HRPES). To compare catalytic activities of these transition metal-doped TiO2 nanoparticles (TM-TiO2) with those of TiO2 NPs, we monitored their performances in the catalytic oxidation of 2-aminothiophenol (2-ATP) by using HRPES and on the oxidation of 2-ATP in aqueous solution by taking electrochemistry (EC) measurements. As a result, we clearly investigate that the increased defect structures induced by the doped transition metal are closely correlated with the enhancement of catalytic activities of TiO2 NPs and confirm that Fe- and Co-doped TiO2 NPs can act as efficient catalysts.

While reduced graphene oxide (rGO) is used widely as a catalyst, its catalytic activity can be improved significantly by modifying it with a metal. In this study, we compared the photocatalytic and catalytic properties of base-treated rGO particles and transition-metal-ion-doped rGO based on the oxidation reaction of thiophenol and the photocatalytic degradation of 4-chlorophenol. Since the two catalytic activities are related to the changes in the electronic structure of rGO, X-ray photoemission spectroscopy, X-ray absorption spectroscopy, and Raman spectroscopy were performed. When rGO was doped with Mn2+ ions, its catalytic properties improved with respect to both reactions. The changes in the electronic structure of rGO are attributed to the formation of defect structures on the rGO surface via a reaction between the doped Mn2+ ions and oxygen of the rGO surface. Thus, the results show that the doping of rGO with Mn ions in the +2-charge state (stable oxide form: MnO) enhances its catalytic and photocatalytic activities. Hence, this study provides new insights into the use of defect-controlled rGO as a novel catalyst.

Abstract To compare the catalytic oxidation activities of reduced graphene oxide (rGO) and rGO samples doped with five different transition metals (TM-rGO), we determine their effects on the oxidation of L-cysteine (Cys) in aqueous solution by performing electrochemistry (EC) measurements and on the photocatalytic oxidation of Cys by using high-resolution photoemission spectroscopy (HRPES) under UV illumination. Our results show that Cr-, Fe-, and Co-doped rGO with 3+ charge states (stable oxide forms: Cr3+, Fe3+, and Co3+) exhibit enhanced catalytic activities that are due to the charge states of the doped metal ions as we compare them with Cr-, Fe-, and Co-doped rGO with 2+ charge states. Graphical Abstract The SEM images and the corresponding EC measurements for (a) Cr3+, (b) Fe3+, and (c) Co3+ doped rGO

Motor disabilities limiting the mobility of limbs affect the quality of lives of people with neural injuries. Among various types of motor disabilities, abnormal intermuscular coordination is commonly observed from people with severe impairment. The concept of muscle synergy, defined as characteristic muscle co-activation patterns activated to produce complex motor behavior, has been applied to assess the alteration in intermuscular coordination in pathological populations. This study presents the development of a robotic system named KAIST upper limb synergy investigation system (KULSIS), for accurate measurement of intermuscular synergies while providing the convenient experimental setup. It provides full force/moment measurements for isometric force generation tasks at various upper limb postures and reaching tasks in a three-dimensional workspace. It is composed of: a three-degree-of-freedom gimbaled handle to adjust the orientation of the handle to accommodate potential hand-wrist deformity, a linear actuator that moves the handle for reaching tasks; a five-degree-of-freedom mechanism for positioning and adjusting the orientation of the linear actuator. The design was evaluated in terms of the workspace of the handle, mechanical stiffness and force/moment measurement accuracy. The position/force measurement is synchronized with electromyographic measurements. Muscle synergy patterns, activated during four isokinetic reaching motions, were also assessed as preliminary data using KULSIS from ten healthy subjects.

Despite advances in the preparation of metal oxide (MO) nanoparticles (NPs) as catalysts for various applications, concerns about the biosafety of these particles remain. In this study, we prepared transition metal-doped cerium oxide (TM@CeO2; TM = Cr, Mn, Fe, Co, or Ni) nanoparticles and investigated the mechanism underlying dopant-dependent toxicity in HaCaT human keratinocytes. We show that doping with Cr or Co but not Fe, Mn, or Ni increased the toxicity of CeO2 NPs in dose- and time-dependent manners and led to apoptotic cell death. Interestingly, while both undoped and transition metal-doped NPs increased intracellular reactive oxygen species (ROS), toxic Cr@CeO2 and Co@CeO2 NPs failed to induce the expression of NRF2 (nuclear factor erythroid 2-related factor 2) as well as its downstream target genes involved in the antioxidant defense system. Moreover, activation of NRF2 transcription was correlated with dynamic changes in H3K4me3 and H3K27me3 at the promoter of NRF2, which was not observed in cells exposed to Cr@CeO2 NPs. Furthermore, exposure to relatively non-toxic Fe@CeO2 NPs, but not the toxic Cr@CeO2 NPs, resulted in increased binding of MLL1 complex, a major histone lysine methylase mediating trimethylation of histone H3 lysine 4, at the NRF2 promoter. Taken together, our findings strongly suggest that failure of cells to respond to oxidative stress is critical for dopant-dependent toxicity of CeO2 NPs and emphasize that careful evaluation of newly developed NPs should be preceded before industrial or biomedical applications.

We demonstrated that Fe/Cr doped and pH-modified CeO2 nanoparticles (NPs) exhibit enhanced photocatalytic performance as compared to bare CeO2 NPs, using photocatalytic degradation. To assess the toxicity level of these double-modified CeO2 NPs on the human skin, they were introduced into HaCaT cells. The results of our conventional cellular toxicity assays (neutral red uptake and 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide for assays) indicated that Cr@CeOx NPs prompt severe negative effects on the viability of human cells. Moreover, the results obtained by scanning transmission X-ray microscopy and bio-transmission electron microscope analysis showed that most of the NPs were localized outside the nucleus of the cells. Thus, serious genetic toxicity was unlikely. Overall, this study highlights the need to prevent the development of Cr@CeOx NP toxicity. Moreover, further research should aim to improve the photocatalytic properties and activity of these NPs while accounting for their stability issues.

The structures and stability levels of leucine (Leu) and tyrosine (Tyr) adsorbed on a Cu(110) surface, at initial levels of coverage (less than 0.25 monolayer), were investigated using reflection−absorption infrared spectroscopy and high-resolution photoemission spectroscopy (HRPES), as well as by performing density functional theory calculations. At an initial coverage, the O−H dissociation bonded structure was indicated from the spectral results to be the most favorable structure for Leu adsorbed on the Cu(110) surface, whereas the O−H dissociated-N dative bonded structure was most favorable for adsorbed Tyr. These models were further supported by the results of experiments, in which the systems were exposed to other molecules and HRPES was used to monitor whether the amine or carboxylic groups of the adsorbed amino acids became reactive.

High-resolution photoemission spectroscopy (HRPES) measurements were collected and density functional theory (DFT) calculations were performed to track the exposure-dependent variation of the adsorption structure of 2-thiophenecarboxaldehyde (C4H3SCHO: TPCA) on the Ge(100) 2 × 1 reconstructed surface at room temperature. In an effort to identify the most probable adsorption structures on the Ge(100)-2 × 1 reconstructed surface, we deposited TPCA molecules at low exposure and at high exposure and compared the differences between the electronic features measured using HRPES. The HRPES data suggested three possible adsorption structures of TPCA on the Ge(100)-2 × 1 reconstructed surface, and DFT calculations were used to determine the plausibility of these structures. HRPES analysis corroborated by DFT calculations, indicated that an S-dative bonded structure is the most probable adsorption structure at relatively low exposure levels, the [4 + 2] cycloadduct structure is the second most probable structure, and the [2 + 2]-C=O cycloadduct structure is the least probable structure on the Ge(100)-2 × 1 reconstructed surface at relatively high exposure levels.