Changes In Function Research Articles

317 Automated Diffusion Tensor Tractography: Quantitative Tract Counts Predict 90-Day Change in Motor Function by Baseline Deficit in Acute Ischemic Stroke Patients Undergoing Mechanical Thrombectomy

INTRODUCTION: Ischemic stroke causes persistent motor deficits in roughly half of survivors. Although mechanical thrombectomy (MT) optimizes stroke outcomes, not all patients improve. Commercially available diffusion tensor tractography (DTT) software increases access to robust tractometric software. Automation and seamless clinical integration of diffusion tensor imaging (DTI) and tractography protocols standardizes data acquisition in high-throughput and high-resolution manners. METHODS: Between June 2020 and 2021, a total of 28 patients with M1 and M2 ischemic strokes underwent a standardized DTT protocol following MT. Patients were stratified by their baseline deficits, defined as the averaged upper and lower extremity motor testing scores at the time of initial presentation (MTS severe = 0, intermediate = 0.5–3.5, and mild = 4+). Multivariable linear regression analysis included demographics, clinical characteristics, and tractometrics of the lesioned CST with MTS at 90-days as the outcome. RESULTS: There were 12 patients with severe, 12 with intermediate, and 4 with mild baseline deficits. Stratification by baseline deficits revealed no significant difference between mean effected tract counts (5.20, 5.08, and 5.78 in the severe, intermediate, and mild groups, respectively, p = 0.377). When controlling for demographics and clinical characteristics, baseline deficits (β = -0.838, SE = 0.913, p < 0.001) and effected mean tract count (β = 1.755, SE = 0.407, p = 0.001) of the CST significantly predicted the change in MTS at 90-day follow-up (adjusted R2 = 0.727 p = 0.002). CONCLUSIONS: Our study suggests automated tractometrics predict the change in motor function at 90 days when controlling for the patient’s baseline motor deficit. Although larger cohort studies should be conducted, commercially available DTI software could yield novel avenues into rehabilitation optimization for post-stroke patients with persistent motor deficits.

Comprehensive Assessment of Ischemic Stroke in Nonhuman Primates: Neuroimaging, Behavioral, and Serum Proteomic Analysis.

Ischemic strokes, prevalence and impactful, underscore the necessity of advanced research models closely resembling human physiology. Our study utilizes nonhuman primates (NHPs) to provide a detailed exploration of ischemic stroke, integrating neuroimaging data, behavioral outcomes, and serum proteomics to elucidate the complex interplay of factors involved in stroke pathophysiology. We observed a consistent pattern in infarct volume, peaking at 1-month postmiddle cerebral artery occlusion (MCAO) and then stabilized. This pattern was strongly correlated to notable changes in motor function and working memory performance. Using diffusion tensor imaging (DTI), we detected significant alterations in fractional anisotropy (FA) and mean diffusivity (MD) values, signaling microstructural changes in the brain. These alterations closely correlated with the neurological and cognitive deficits that we observed, highlighting the sensitivity of DTI metrics in stroke assessment. Behaviorally, the monkeys exhibited a reliance on their unaffected limb for compensatory movements, a common response to stroke impairment. This adaptation, along with consistent DTI findings, suggests a significant impact of stroke on motor function and spatial perception. Proteomic analysis through MS/MS functional enrichment identified two distinct groups of proteins with significant changes post-MCAO. Notably, MMP9, THBS1, MB, PFN1, and YWHAZ were identified as potential biomarkers and therapeutic targets for ischemic stroke. Our results underscore the complex nature of stroke and advocate for an integrated approach, combining neuroimaging, behavioral studies, and proteomics, for advancing our understanding and treatment of this condition.

Impact of Renal Congestion in Patients With Secondary Mitral Regurgitation After Mitral Transcatheter Edge-to-Edge Repair.

Renal congestion is a potential prognostic factor in patients with heart failure and recently, assessment has become possible with intrarenal Doppler ultrasonography (IRD). The association between renal congestion assessed by IRD and outcomes after mitral transcatheter edge-to-edge repair (TEER) is unknown, so we aimed to clarify renal congestion and its prognostic implications in patients with mitral regurgitation (MR) who underwent TEER using MitraClip system.Methods and Results: Patients with secondary MR who underwent TEER and were assessed for intrarenal venous flow (IRVF) by IRD were classified according to their IRVF pattern as continuous or discontinuous. Of the 105 patients included, 78 patients (74%) formed the continuous group and 27 (26%) were the discontinuous group. Kaplan-Meier analysis revealed significant prognostic power of the IRVF pattern for predicting the composite outcome of all-cause death and heart failure rehospitalization (log-rank P=0.0257). On multivariate Cox regression analysis, the composite endpoint was independently associated with the discontinuous IRVF pattern (hazard ratio, 3.240; 95% confidence interval, 1.300-8.076; P=0.012) adjusted using inverse probability of treatment weighting. IRVF patterns strongly correlated with clinical outcomes without changes in renal function. Thus, they may be useful for risk stratification after mitral TEER for patients with secondary MR.

Increased connections among soil microbes and microfauna enhances soil multifunctionality along a long‐term restoration chronosequence

Abstract The functional role of soil microbes in the restoration of degraded lands is greatly influenced by interactions within and between microbial communities, as well as by soil organisms at higher trophic levels (microfauna). However, little is known about how changes in connection patterns among soil microbes and their co‐existing microfauna contribute to associated changes in soil function over the ecosystem restoration process. In this study, the effects of afforestation and natural regeneration approaches on connection patterns among soil microbes and their co‐existing microfauna were assessed in ex‐arable lands on the Loess Plateau in China along a 50‐year restoration chronosequence. The relationships between soil network connections, microbial functional associations, and multiple soil functions (e.g. multifunctionality) were assessed quantitatively. Although both afforestation and natural regeneration approaches enhance connections among soil microbes and their co‐existing microfauna compared to recently abandoned sites, connection trends were opposed between these two approaches across the restoration chronosequence. Afforestation resulted in a higher number of soil microbial and microfauna species with a unimodal connection pattern, while natural regeneration resulted in a continuous increase in soil network connections over the progress of succession. These increases in soil network connections, particularly those of soil microfauna‐microbe and microbial inter‐kingdom connections, corresponded to enhanced microbial functional associations. This result is corroborated by significant correlations between microbial functional genes encoding different central functional pathways, which, in turn, were positively correlated with soil multifunctionality. Synthesis and applications. Changes in the connections among soil microbes and their co‐existing microfauna were positively associated with changes in soil multifunctionality, mediated by microbial functional associations. While in the early restoration stages, soil networks following afforestation contained more connections than those following natural regeneration, in later restoration stages, the number of connections of the afforestation network declined and was eventually surpassed by those following natural regeneration. These findings raise concerns about the ecological sustainability of afforestation measures in historic grasslands on the Loess Plateau, suggesting that natural regeneration is the preferred approach to achieve long‐term ecological restoration success.

Food additives and brain complications: A risk to public health

Food additives comprise the amounts of xenobiotics that are known to affect the physiological metabolic pathways of living tissues. Although organic and inorganic chemicals are considered xenobiotics, organic compounds, the basic chemical entity for most constituents, are reported to be responsible for 80-90% xenobiotics-induced toxicity. Food additives have been the major source of generating these harmful toxins in the human population. Exposure to xenobiotics via dietary habits, environment or medication is inexorable in living creatures. Reports have shown the bidirectional interaction between xenobiotics and biological systems. When ingested, xenobiotics induce physiological, biochemical or pathological changes in the biological system. One study reported that exposure to titanium dioxide nanoparticles can cause cytotoxicity of glial cells and hippocampal neurons, leading to brain damage and changes in hippocampal function, which plays a vital role in the process of memory and learning. Therefore, the complexity and limited plasticity of the brain has always challenged researchers to seek solutions to neuronal and cognitive problems. Including new compounds in the food in the form of pesticides, preservatives, additives, and coloring agents in daily meals is the latest aspect of gene-environment interaction. The sporadic cause of neurodegenerative diseases and its epidemiological distribution can be better understood and countermeasures can be applied only if this relationship is represented quantitatively. Hence, this review focuses on the effect of food additives as xenobiotics, which leads to the potential for a compromised nervous system.

Effect of outpatient cardiac rehabilitation on motor function and health-related quality of life in stroke survivors

BackgroundOutpatient cardiac rehabilitation (CR) is a promising tool for improving functional outcome in stroke survivors, however, evidence for improving emotional health is limited. We aimed to clarify the effects of outpatient CR following in-hospital stroke rehabilitation on health-related quality of life (HRQOL) and motor function. MethodsPatients with acute ischemic stroke or transient ischemic attack discharged directly home were recruited, and 128 patients who fulfilled criteria for insurance coverage of CR were divided into the CR (+) group (n = 46) and CR (-) group (n = 82). All patients underwent in-hospital stroke rehabilitation, and within 2 months after stroke onset, patients in the CR (+) group started a 3-month outpatient CR program of supervised sessions. Changes of motor function and HRQOL assessed by the short form-36 version 2 (SF-36) from discharge to 3 months post-discharge were compared between the two groups. ResultsTwenty-six patients in the CR (+) group completed the program and 66 patients in the CR (-) group were followed up at a 3-month examination. Least-square mean changes in 6-minute walk distance and isometric knee extension muscle strength were significantly higher in the CR (+) group than the CR (-) group (52.6 vs. 16.3 m; 10.1 vs. 3.50 kgf/kg). Improvement of HRQOL at 3 months was not observed in the CR (+) group. ConclusionsOutpatient CR following in-hospital stroke rehabilitation within 2 months after stroke onset improved exercise tolerance and functional strength but not HRQOL assessed by the SF-36 after completion of CR in the present cohort.

Effects of Intranasal Dantrolene Nanoparticles on Brain Concentration and Behavior in PS19 Tau Transgenic Mice.

Repurposing dantrolene to treat Alzheimer's disease has been shown to be effective in amyloid transgenic mouse models but has not been examined in a model of tauopathy. The effects of a nanoparticle intranasal formulation, the Eagle Research Formulation of Ryanodex (ERFR), in young adult and aged wild type and PS19 tau transgenic mice was investigated. The bioavailability of intranasal ERFR was measured in 2 and 9-11-month-old C57BL/6J mice. Blood and brain samples were collected 20 minutes after a single ERFR dose, and the plasma and brain concentrations were analyzed. Baseline behavior was assessed in untreated PS19 tau transgenic mice at 6 and 9 months of age. PS19 mice were treated with intranasal ERFR, with or without acrolein (to potentiate cognitive dysfunction), for 3 months, beginning at 2 months of age. Animal behavior was examined, including cognition (cued and contextual fear conditioning, y-maze), motor function (rotarod), and olfaction (buried food test). The dantrolene concentration in the blood and brain decreased with age, with the decrease greater in the blood resulting in a higher brain to blood concentration ratio. The behavioral assays showed no significant changes in cognition, olfaction, or motor function in the PS19 mice compared to controls after chronic treatment with intranasal ERFR, even with acrolein. Our studies suggest the intranasal administration of ERFR has higher concentrations in the brain than the blood in aged mice and has no serious systemic side effects with chronic use in PS19 mice.

Impact of Insulin-Induced Relative Hypoglycemia on Vascular Insulin Sensitivity and Central Hemodynamics in Prediabetes.

Relative hypoglycemia (RH) is linked to sympathetic responses that can alter vascular function in individuals with type 2 diabetes. However, less is known about the role of RH on hemodynamics or metabolic insulin sensitivity in prediabetes. Determine if RH alters peripheral endothelial function or central hemodynamics to a greater extent in those with prediabetes (PD) versus normoglycemia (NG). Seventy adults with obesity were classified using ADA criteria as PD (n=34 (28F); HbA1c=6.02±0.1%) or NG (n=36 (30F); HbA1c=5.4±0.0%). Brachial artery endothelial function, skeletal muscle capillary perfusion, and aortic waveforms were assessed at 0 and 120min of a euglycemic clamp (40 mU/m2/min, 90 mg/dl). Plasma nitrate/nitrite and endothelin-1 (ET-1) were measured as surrogates of nitric oxide-mediated vasodilation and vasoconstriction, respectively. RH was defined as the drop in glucose (%) from fasting to clamp steady state. There were no differences in age, weight, or VO2max between groups. PD had higher HbA1c (P<0.01) and a greater drop in glucose in response to insulin (14 vs. 8%; P=0.03). Further, heart rate (HR) increased in NG compared to PD (P<0.01), while forward wave (Pf) decreased in PD (P=0.04). Insulin also tended to reduce arterial stiffness (cfPWV) in NG versus PD (P=0.07), despite similar increases in pre-occlusion diameter (P=0.02), blood flow (P=0.02), and lower augmentation index (AIx75) (P≤0.05). Compared with NG, insulin-induced RH corresponded with a blunted rise in HR and drop in Pf during insulin infusion in adults with PD, independent of changes in peripheral endothelial function.

Isorhamnetin ameliorates cisplatin-induced acute kidney injury in mice by activating SLPI-mediated anti-inflammatory effect in macrophage

Objective Isorhamnetin (IH) has been reported to have significant anti-inflammatory effects in various diseases, but its role and mechanism in AKI remain unclear. This study aimed to explore the potential role and mechanism of isorhamnetin in inhibiting macrophage related inflammation and improving AKI injury. Methods We established an AKI mouse model by intraperitoneal injection of cisplatin in vivo, and constructed an inflammatory cell model by stimulating RAW264.7 cells with LPS. Creatinine and urea nitrogen were measured to evaluate the changes of renal function in AKI mice. The changes of renal pathological structure were observed by H&E staining. The inflammatory factor-related proteins and RNA expression levels were detected by Western blot and real time PCR. Results Isorhamnetin protected the kidney from cisplatin induced AKI and significantly inhibited the mRNA and protein levels of inflammatory cytokines (IL-1β, IL-6, and TNF-α) both in AKI kidney and LPS-stimulated RAW264.7 cells. Interestingly, the data also demonstrated that isorhamnetin significantly upregulated the expression of secretory leukocyte peptidase inhibitor (SLPI), an anti-inflammatory factor, in AKI kidney and LPS-stimulated macrophages, as well as inhibited the M1 macrophage and activated M2 macrophage in vitro. Blocking of SLPI by siRNA activated Mincle-associated inflammatory signaling in macrophages, and the inhibitory effect of isorhamnetin on inflammation was significantly attenuated. Conclusion Isorhamnetin inhibits macrophage inflammation and protects kidney in AKI may be related to downregulating Mincle/Syk/NF-κB-maintained macrophage phenotype by activating SLPI.

Modulation of the expression of connexins 37, 40, and 43 in endothelial cells in a culture.

Connexin (Cx) 37, 40, and 43 are implicated in vascular function, specifically in the electrical coupling of endothelial cells and vascular smooth-muscle cells. In the present study, we investigated whether factors implicated in vascular dysfunction can modulate the gene expression of Cx37, Cx40, and Cx43 and whether this is associated with changes in endothelial layer barrier function in human microvascular endothelial cells (HMEC-1). First, HMEC-1 were subjected to stimuli for 4 and 8h. We tested their responses to DETA-NONOate, H2O2, high glucose, and angiotensin II, none of which relevantly affected the transcription of the connexin genes. Next, we tested inflammatory factors IL-6, interferon gamma (IFNγ), and TNFα. IFNγ (10ng/mL) consistently induced Cx40 expression at 4 and 8 h to 10-20-fold when corrected for the control. TNFα and IL-6 resulted in small but significant depressions of Cx37 expression at 4h. Two JAK inhibitors, epigallocatechin-3-gallate (EGCG) (100-250μM) and AG490 (100-250μM), dose-dependently inhibited the induction of Cx40 expression by IFNγ. Subsequently, HMEC-1 were subjected to 10ng/mL IFNγ for 60h, and intercellular and transcellular impedance was monitored by electric cell-substrate impedance sensing (ECIS). In response to IFNγ, junctional-barrier impedance increased more than cellular-barrier impedance; this was prevented by AG490 (5μM). In conclusion, IFNγ can strongly induce Cx40 expression and modify the barrier properties of the endothelial cell membrane through the JAK/STAT pathway. Moreover, the Cx37, Cx40, and Cx43 expression in endothelial cells is stable and, apart from IFNγ, not affected by a number of factors implicated in endothelial dysfunction and vascular diseases.

Visual outcome of 25 Gauge vitrectomy for acute post operative infectious endophthalmitis.

The correlation between the change in foveal thickness measured using optical coherence tomography (OCT) following surgery for infectious endophthalmitis and preoperative and postoperative visual acuity is uncertain, and there are few pertinent studies on this topic. We explored the variations in macular thickness using OCT after emergency vitrectomy for post-cataract infectious endophthalmitis and the relationship between macular thickness with changes in visual function. We included 10 cases of post-cataract infectious endophthalmitis. Each patient underwent 25-G vitrectomy. The infection in all 10 patients was under control and visual function improved. Postoperative vitreous humor culture was positive in 8 patients, including 7 cases of coagulase-negative Staphylococcus epidermidis and 1 case of Lactobacillus acidophilus. The average age of these 10 patients was 71.60 ± 8.71 years (P< 0.05, two-tailed). There was no significant correlation between time 2 (the time of onset after cataract surgery) and visual prognosis. The average time 1 (the time of the vitrification surgery caused by the onset of the disease) was 1.45 ± 0.76 days (P< 0.05, two-tailed). The postoperative 3dVA ranged from 0.20 to 3.00, with an average visual acuity of 1.87 ± 1.12, which was superior to the preoperative value (P< 0.01, two-tailed). The correlation between the post3dVA and post 1mVA was significant. The post 1mVA ranged from 0.05 to 2.20, with an average visual acuity of 0.94 ± 0.74 (P< 0.05, two-tailed). The correlation between post 1mVA and post3mVA was significant. Also, paired t-tests comparing preoperative and postoperative visual acuity revealed a significant correlation (P< 0.05, two-tailed). The post3mVA was 0-1.00 with an average visual acuity of 0.44 ± 0.41. The postoperative foveal thickness ranged from 176.00 to 514.00 μm, with an average thickness of 281.10 ± 113.12 μm. Emergency 25-G minimally invasive vitrectomy can improve visual acuity and decrease the reoperation rate for patients who have acquired post-cataract infectious endophthalmitis. There were significant correlations between age, disease onset to operation time, preoperative and postoperative visual acuity, and postoperative macular thickness.

Cldn4 overexpression promotes penile cavernous smooth muscle cell fibrotic response via the JNK signaling pathway.

Erectile dysfunction (ED), defined as the inability to achieve or maintain a penile erection sufficient to satisfy sexual behavior, is prevalent worldwide. Using previous research, bioinformatics, and experimental confirmation, we aimed to discover genes that contribute to ED through regulating hypoxia in corpus cavernosum smooth muscle cells (CCSMCs). We used the Gene Expression Omnibus to acquire the sequencing data of the corpus cavernosum transcriptome for diabetic ED and nerve injury type ED rats. We intersected the common differentially expressed genes. Further verification was performed using single cell sequencing. Real-time quantitative polymerase chain reaction and immunofluorescence were used to investigate whether the differentially expressed genes are found in the corpus cavernosum. We used induced hypoxia to assess cell viability changes, and we developed a lentivirus overexpressing Cldn4 for in vitro and in vivo experiments to measure changes in JNK signaling, fibrosis, hypoxia, and erectile function. Our results indicate that targeting the JNK pathway and decreasing local hypoxia may be better options for therapeutic intervention to improve erectile function. We identified Cldn4 and found its expression increased in the corpora cavernosa of the 2 datasets. In addition, we found that hypoxia can increase the expression of Cldn4, activate the JNK signaling pathway, and exacerbate fibrosis in CCSMCs. Cldn4 overexpression in CCSMCs activated the JNK signaling pathway and increased fibrotic protein expression. Last, rat corpus cavernosum overexpressing Cldn4 activated the JNK signaling pathway, increased local fibrosis, and impaired erectile function. Through bioinformatics and in vitro and in vivo experiments, we found that Cldn4 has a negative effect on ED, and targeting Cldn4 may provide new ideas for ED treatment. Although we have identified Cldn4 as a potential target for ED treatment, we have only conducted preliminary validation on CCMSCs, and we still need to further validate in other cell lines. CCSMC hypoxia leads to increased Cldn4, in both nerve injury and diabetic ED rat models, and promotes fibrosis by activating the JNK signaling pathway.

Microglial Activation and Progression of Nigrostriatal Dysfunction in Isolated REM Sleep Behavior Disorder.

Using 11 C-(R)-PK11195-PET, we found increased microglia activation in isolated REM sleep behavior disorder (iRBD) patients. Their role remains to be clarified. The objective is to assess relationships between activated microglia and progression of nigrostriatal dysfunction in iRBD. Fifteen iRBD patients previously scanned with 11 C-(R)-PK11195 and 18 F-DOPA-PET underwent repeat 18 F-DOPA-PET after 3 years. 18 F-DOPA Ki changes from baseline were evaluated with volumes-of-interest and voxel-based analyses. Significant 18 F-DOPA Ki reductions were found in putamen and caudate. Reductions were larger and more widespread in patients with increased nigral microglia activation at baseline. Left nigral 11 C-(R)-PK11195 binding at baseline was a predictor of 18 F-DOPA Ki reduction in left caudate (coef = -0.0426, P = 0.016). Subjects with increased baseline 11 C-(R)-PK11195 binding have greater changes in nigrostriatal function, suggesting a detrimental rather than protective effect of microglial activation. Alternatively, both phenomena occur in patients with prominent nigrostriatal dysfunction without a causative link. The clinical and therapeutic implications of these findings need further elucidation. © 2024 The Authors. Movement Disorders published by Wiley Periodicals LLC on behalf of International Parkinson and Movement Disorder Society.

Chronic Pain-Related Cognitive Deficits: Preclinical Insights into Molecular, Cellular, and Circuit Mechanisms.

Cognitive impairment is a common comorbidity of chronic pain, significantly disrupting patients' quality of life. Despite this comorbidity being clinically recognized, the underlying neuropathological mechanisms remain unclear. Recent preclinical studies have focused on the fundamental mechanisms underlying the coexistence of chronic pain and cognitive decline. Pain chronification is accompanied by structural and functional changes in the neural substrate of cognition. Based on the developments in electrophysiology and optogenetics/chemogenetics, we summarized the relevant neural circuits involved in pain-induced cognitive impairment, as well as changes in connectivity and function in brain regions. We then present the cellular and molecular alternations related to pain-induced cognitive impairment in preclinical studies, mainly including modifications in neuronal excitability and structure, synaptic plasticity, glial cells and cytokines, neurotransmitters and other neurochemicals, and the gut-brain axis. Finally, we also discussed the potential treatment strategies and future research directions.

Effects of age and diet consistency on the expression of myosin heavy-chain isoforms on jaw-closing and jaw-opening muscles in a rat model.

Skeletal craniofacial morphology can be influenced by changes in masticatory muscle function, which may also change the functional profile of the muscles. To investigate the effects of age and functional demands on the expression of Myosin Heavy-Chain (MyHC) isoforms in representative jaw-closing and jaw-opening muscles, namely the masseter and digastric muscles respectively. Eighty-four male Wistar rats were divided into four age groups, namely an immature (n = 12; 4-week-old), early adult (n = 24; 16-week-old), adult (n = 24; 26-week-old) and mature adult (n = 24; 38-week-old) group. The three adult groups were divided into two subgroups each based on diet consistency; a control group fed a standard (hard) diet, and an experimental group fed a soft diet. Rats were sacrificed, and masseter and digastric muscles dissected. Real-time quantitative polymerase chain reaction was used to compare the mRNA transcripts of the MyHC isoforms-Myh7 (MyHC-I), Myh2 (MyHC-IIa), Myh4 (MyHC-IIb) and Myh1 (MyHC-IIx)-of deep masseter and digastric muscles. In the masseter muscle, hypofunction increases Myh1 (26, 38 weeks; p < .0001) but decreases Myh4 (26 weeks; p = .046) and Myh2 (26 weeks; p < .0001) expression in adult rats. In the digastric muscle, hypofunction increases Myh1 expression in the mature adult rats (38 weeks; p < .0001), while Myh2 expression decreases in adult rats (26 weeks; p = .021) as does Myh4 (26 weeks; p = .001). Myh7 expression is increased in the digastric muscle of mature adult rats subjected to hypofunction (38 weeks; p = <.0001), while it is very weakly expressed in the masseter. In jaw-opening and jaw-closing muscles, differences in myosin expression between hard- and soft-diet-fed rats become evident in adulthood, suggesting that long-term alteration of jaw function is associated with changes in the expression of MyHC isoforms and potential fibre remodelling. This may give insight into the role of function on masticatory muscles and the resultant craniofacial morphology.

Relationship between thyroid function changes with work-/night-shifts and history of thyroid pathology among health personnel

The study aim was to analyze the relationship between functional thyroid pathology and the exposure to work shifts / night shifts, and describe the most prevalent thyroid disorders based on the type of shift. Cross-sectional study performed in the emergency department of a hospital in Almeria (Spain). Relationships between thyroxine and thyrotropin levels (TSH) and work shifts, professional category and history of thyroid pathology were analyzed. The study included 133 workers; 80.5% female, average age was 46.11 years (38 - 65), and 52% were part of the nursing staff; thyroid disorders were more frequent in female participants. Most participants (81.2%) had rotating shifts schedules and 11.3% night shifts (12.1% female and 7.7% male). Thyroid alterations were found in 27% of the participants (usually elevated TSH levels and normal thyroxine levels), particularly in those doing night shifts (61.1%). TSH alterations were more frequent in individuals doing night shifts than in rotating shifts (53.3 vs 13.0%; p<0.001). Individuals working night shifts had mean TSH values in the normal range, although significantly higher than the individuals in the rest of the shifts; thyroxine levels were found to be similar. No thyroid disorders were found in day shift participants. Night shift and a history of thyroid pathology were independent predictors of thyroid disorders. Night shift schedules and history of thyroid disorders are more frequent in female, both related to the presence of thyroid disorders, indicating the need to include the evaluation of these disorders in health surveillance programs and analyze gender differences.

Suppressing Trap‐Assisted Nonradiative Recombination via Interface Modification for Achieving Efficient Organic Solar Cells

AbstractTrap states in organic solar cells (OSCs) can capture free charges, leading to a reduction in current density and significant energy loss. Since charge collection is primarily dependent on the interface layer, minimizing trap states at interfaces can effectively suppress energy losses, a topic that has been rarely explored. Herein, an interface strategy is proposed by combining Me‐4PACz and PEDOT:PSS to mitigate the trap‐assisted nonradiative recombination at the hole transport layer (HTL). OSCs based on the Me‐4PACz/PEDOT:PSS exhibit reduced trap densities and low energy losses compared to devices fabricated with a single‐layer HTL. This reduction can be attributed to a lower nonradiative recombination rate during hole transport at the interface. Changes in the work function of the two interlayers due to contact result in the existence of a built‐in potential inside the composite interlayer, promoting charge collection and reducing energy loss from charge recombination. Furthermore, the composite HTL interface induces vertical phase separation of active layer, leading to significant improvements of the fill factor for OSCs. As a result, high power conversion efficiencies (PCEs) of 18.70% and 19.02% are achieved for binary all‐polymer solar cells and polymer donor/small molecule acceptor solar cells, respectively.

Validation of the Japanese version of the Social Functioning in Dementia scale and COVID-19 pandemic's impact on social function in mild cognitive impairment and mild dementia.

We aimed to psychometrically evaluate and validate a Japanese version of the Social Functioning in Dementia scale (SF-DEM-J) and investigate changes in social function in people with dementia during the coronavirus disease-19 (COVID-19) pandemic. We interviewed people with mild cognitive impairment (MCI) and mild dementia and their caregivers during June 2020-March 2021 to validate patient- and caregiver-rated SF-DEM-J and compared their scores at baseline (April 2020 to May 2020) and at 6-8 months (January 2021 to March 2021) during a time of tighter COVID-19 restrictions. The neuropsychology clinic in the Department of Psychiatry at Osaka University Hospital and outpatient clinic in the Department of Psychiatry and Neurology at Daini Osaka Police Hospital, Japan. 103 dyads of patients and caregivers. SF-DEM-J, Mini-Mental State Examination, Neuropsychiatric Inventory, UCLA Loneliness Scale, and Apathy Evaluation Scale. The scale's interrater reliability was excellent and test-retest reliability was substantial. Content validity was confirmed for the caregiver-rated SF-DEM-J, and convergent validity was moderate. Caregiver-rated SF-DEM-J was associated with apathy, irritability, loneliness, and cognitive impairment. The total score of caregiver-rated SF-DEM-J and the score of Section 2, "communication with others," significantly improved at 6-8 months of follow-up. The SF-DEM-J is acceptable as a measure of social function in MCI and mild dementia. Our results show that the social functioning of people with dementia, especially communicating with others, improved during the COVID-19 pandemic, probably as a result of adaptation to the restrictive life.

Relationship of Perivascular Space Markers With Incident Dementia in Cerebral Small Vessel Disease.

Recent studies, using diffusion tensor image analysis along the perivascular space (DTI-ALPS), suggest impaired perivascular space (PVS) function in cerebral small vessel disease, but they were cross-sectional, making inferences on causality difficult. We determined associations between impaired PVS, measured using DTI-ALPS and PVS volume, and cognition and incident dementia. In patients with lacunar stroke and confluent white matter hyperintensities, without dementia at baseline, recruited prospectively in a single center, magnetic resonance imaging was performed annually for 3 years, and cognitive assessments, including global, memory, executive function, and processing speed, were performed annually for 5 years. We determined associations between DTI-ALPS and PVS volume with cerebral small vessel disease imaging markers (white matter hyperintensity volume, lacunes, and microbleeds) at baseline and with changes in imaging markers. We determined whether DTI-ALPS and PVS volume at baseline and change over 3 years predicted incident dementia. Analyses were controlled for conventional diffusion tensor image metrics using 2 markers (median mean diffusivity [MD] and peak width of skeletonized MD) and adjusted for age, sex, and vascular risk factors. A total of 120 patients, mean age 70.0 years and 65.0% male, were included. DTI-ALPS declined over 3 years, while no change in PVS volume was found. Neither DTI-ALPS nor PVS volume was associated with cerebral small vessel disease imaging marker progression. Baseline DTI-ALPS was associated with changes in global cognition (β=0.142, P=0.032), executive function (β=0.287, P=0.027), and long-term memory (β=0.228, P=0.027). Higher DTI-ALPS at baseline predicted a lower risk of dementia (hazard ratio, 0.328 [0.183-0.588]; P<0.001), and this remained significant after including median MD as a covariate (hazard ratio, 0.290 [0.139-0.602]; P<0.001). Change in DTI-ALPS predicted dementia conversion (hazard ratio, 0.630 [0.428-0.964]; P=0.048), but when peak width of skeletonized MD and median MD were entered as covariates, the association was not significant. There was no association between baseline PVS volume, or PVS change over 3 years, and conversion to dementia. DTI-ALPS predicts future dementia risk in patients with lacunar strokes and confluent white matter hyperintensities. However, the weakening of the association between change in DTI-ALPS and incident dementia after controlling for peak width of skeletonized MD and median MD suggests part of the signal may represent conventional diffusion tensor image metrics. PVS volume is not a predictor of future dementia risk.

Hemodialysis Patients with High-Flow Arteriovenous Fistulas: An Evaluation of the Impact on Cardiac Function.

: Patients undergoing hemodialysis often experience changes in cardiac function when they have a high-flow arteriovenous fistula (AVF). This study aimed to assess the effect of high-flow AVFs on cardiac function in patients undergoing hemodialysis. : A longitudinal study was conducted on hemodialysis patients with high-flow AVFs. Echocardiographic parameters, such as left ventricular ejection fraction (LVEF), left atrial diameter (LAD), left ventricular end-diastolic dimension (LVEDD), right ventricular end-diastolic dimension (RVEDD), inferior vena cava diameter (IVCD), systolic blood pressure, and diastolic blood pressure, were measured and compared before and after AVF creation. : One hundred hemodialysis patients with high-flow AVFs (mean age: 55.95±13.39 years, mean body mass index: 24.71±3.43 kg/m²) were studied. LVEF significantly decreased (51.10%±5.39% to 47.50%±5.79%), while LAD, LVEDD, and IVCD significantly increased after AVF creation (P<0.05). Systolic (132.49±16.42 mmHg to 146.60±17.43 mmHg) and diastolic (79.98±8.40 mmHg to 83.33±9.68 mmHg) blood pressure substantially rose post-fistularization (P<0.001). Notably, LVEF reduction was more significant in brachio-cephalic AVFs (46.29%±4.24%) compared to distal radio-cephalic or snuffbox AVFs (49.17%±7.15%) (P=0.014). : High-flow AVFs can significantly affect echocardiographic parameters in hemodialysis patients, thereby increasing the risk of cardiac failure. Close cardiac monitoring may be necessary for early intervention. Distal AVFs may be preferable in patients with decreased cardiac function.