Exploring the effects of acceptable palliative care models on survival time and healthcare expenditure among patients with cancer: a national longitudinal population-based study.

OBJECTIVE: Hospice care ensures better end-of-life quality by relieving terminal symptoms. Prior research has indicated that hospice care could prolong survival and reduce end-of-life medical expenditures among patients with cancer. However, the dearth of studies on the effects of hospice care type and use sequence on survival time and end-of-life medical expenditures substantiates the need for investigation. DATA SOURCES AND STUDY SETTING: Two million random records were obtained from the National Health Insurance Research Database. STUDY DESIGN: We estimated the effects of the type and sequence of hospice care use on survival time and medical expenditures among advanced cancer patients. This was a cross-sectional study. DATA COLLECTION/EXTRACTION METHODS: Patient data were collected from 2 million random records provided by the National Health Insurance Research Database of Taiwan. We included people with cancer and excluded patients under 20 years of age; 2860 patients remained after matching. PRINCIPAL FINDINGS: The results indicated that the average survival time of patients who received inpatient palliative care (1022 days) was significantly shorter than that of patients who did not receive palliative care (P < 0.001), but the health care expenditure during the entire course of cancer therapy was not the lowest. Interestingly, patients who received inpatient palliative care had the lowest health care expenditure at 1 year or month before the end of life (P < 0.001). CONCLUSION: The type and sequence of palliative care affected the survival time and health care expenditures of cancer patients. Receiving palliative care did not prolong survival but rather reduced health care expenditures. The sequence of receiving palliative care significantly affected health care expenditures.

Targeting histone demethylase LSD1 for treatment of deficits in autism mouse models.

Large-scale genetic studies have revealed that the most prominent genes disrupted in autism are chromatin regulators mediating histone methylation/demethylation, suggesting the central role of epigenetic dysfunction in this disorder. Here, we show that histone lysine 4 dimethylation (H3K4me2), a histone mark linked to gene activation, is significantly decreased in the prefrontal cortex (PFC) of autistic human patients and mutant mice with the deficiency of top-ranking autism risk factor Shank3 or Cul3. A brief treatment of the autism models with highly potent and selective inhibitors of the H3K4me2 demethylase LSD1 (KDM1A) leads to the robust rescue of core symptoms of autism, including social deficits and repetitive behaviors. Concomitantly, LSD1 inhibition restores NMDA receptor function in PFC and AMPA receptor-mediated currents in striatum of Shank3-deficient mice. Genome-wide RNAseq and ChIPseq reveal that treatment of Shank3-deficient mice with the LSD1 inhibitor restores the expression and H3K4me2 occupancy of downregulated genes enriched in synaptic signaling and developmental processes. The immediate early gene tightly linked to neuronal plasticity, Egr1, is on the top list of rescued genes. The diminished transcription of Egr1 is recapitulated in PFC of autistic human patients. Overexpression of Egr1 in PFC of Shank3-deficient mice ameliorates social preference deficits. These results have for the first time revealed an important role of H3K4me2 abnormality in ASD pathophysiology, and the therapeutic potential of targeting H3K4me2 demethylase LSD1 or the downstream molecule Egr1 for ASD.

The effects of free Cys residues on the structure, activity, and tetrameric stability of mammalian uricase.

Mammalian uricases contain four conserved cysteine (Cys) residues, but little is known about their structures and functions. In this study, we first confirmed that all four Cys residues are free and not involved in disulfide bond formation, using canine uricase as a model protein. Cys residues had a greater effect on stability than on activity based on single Cys-to-Ser (serine) substitutions. Circular dichroism (CD) and homology modeling indicated that C188S reduces ß-sheet contents and inter- and intra-subunit hydrophobic interaction, potentially impairing the core tetrameric ß-barrel structure of the tunneling-fold protein, and ultimately decreased the tetrameric stability. Additionally, the inactivation of C188S during the stability tests may be a complex process involving depolymerization followed by irregular aggregation. Double mutations or thiol blockage of Cys188 and Cys195 significantly disrupted the formation and stability of tetrameric uricase, which may be mediated by the free thiols in Cys residues. The present results demonstrated that the free Cys residues are essential for tetrameric formation and stability in mammalian uricase. This implies that free cysteine residues, although not involved in disulfide bonding, may play important structural roles in certain proteins, underscoring the significance of the hydrophobic characteristics of the free thiols in Cys residues. KEY POINTS: • Four Cys residues are not involved in disulfide bonding in mammalian uricase. • The hydrophobicity of free thiols is critical for tetrameric stability in uricase. • Free Cys residues can serve structural roles without involving in disulfide bonds.

Association between 14 candidate genes, PM2.5, and affective disorders: a study of the Taiwan Biobank.

BACKGROUND: Most studies have focused on the risk factors, treatment, and care of affective psychosis, and several have reported a relationship between ambient air quality and this psychosis. Although an association has been reported between psychosis and genes, studies mainly explored the associations between one type of psychosis and one gene; few have identified genes related to affective psychosis. This study investigates the genetic and environmental factors of affective psychosis. METHODS: In this retrospective longitudinal study, 27 604 participants aged 30-70 were selected from Taiwan Biobank. The participants' propensity scores were calculated based on their demographic information, and propensity score matching was performed to divide the participants into an experimental (i.e., affective psychosis) and control group at a 1:5 ratio. Plink was used to analyze the major and minor types of gene expression related to affective psychosis, and PM2.5 exposure was incorporated into the analyses. RESULTS: According to the generalized estimating equation analysis results, 8 single nucleotide polymorphisms (SNPs) belonging to the ANK3, BDNF, CACNA1C, and GRID1 genotypes were significantly correlated with depressive disorder (P < .001), with the majority belonging to the ANK3 and CACNA1C. A total of 5 SNPs belonging to the CACNA1C, GRID1, and SIRT1 genotypes were significantly correlated with bipolar disorder (P < .001), with the majority belonging to the CACNA1C. No significant correlation was identified between ambient air pollution and affective psychosis. CONCLUSIONS: CACNA1C and GRID1 are common SNP genotypes for depressive disorder and bipolar disorder and should be considered associated with affective psychosis.

Disparities in the medical expenditures of patients with cancer and concomitant mental disorder: analyzing the effects of diagnosis sequence order.

BACKGROUND: Cancer is the leading cause of death in Taiwan. Medical expenditures related to cancer accounted for 44.8% of all major illness insurance claims in Taiwan. Prior research has indicated that the dual presence of cancer and mental disorder in patients led to increased medical burden. Furthermore, patients with cancer and concomitant mental disorder could incur as much as 50% more annual costs than those without. Although previous studies have investigated the utilization of patients with both diseases, the effects of morbidity sequence order on patient costs are, however, uncertain. This study explored medical expenditures linked with the comorbidity of cancer and mental disorder, with a focus on the impact of diagnosis sequence order. METHODS: This population-based retrospective matched cohort study retrieved patients with cancer and mental disorder (aged ≥ 20 years) from the Ministry of Health and Welfare Data Science Center 2005-2015 database. 321,045 patients were divided based on having one or both diseases, as well as on the sequence of mental disorder and cancer diagnosis. Study subjects were paired with comparison counterparts free of both diseases using Propensity Score Matching at a 1:1 ratio. Annual Cost per Patient Linear Model (with a log-link function and gamma distribution) was used to assess the average annual cost, covarying for socio-demographic and clinical factors. Binomial Logistic Regression was used to evaluate factors associated with the risk of high-utilization. RESULTS: The "Cancer only" group had higher adjusted mean annual costs (NT$126,198), more than 5-times that of the reference group (e^ß: 5.45, p < 0.001). However, after exclusion of patients with non-cancer and inclusion of diagnosis sequence order for patients with cancer and concomitant mental disorder, the post-cancer mental disorder group had the highest expenditures at over 13% higher than those diagnosed with only cancer on per capita basis (e^ß: 1.13, p < 0.001), whereas patients with cancer and any pre-existing mental disorder incurred lower expenditures than those with only cancer. The diagnosis of post-cancer mental disorder was significantly associated with high-utilization (OR = 1.24; 95% CI: 1.047-1.469). Other covariates associated with high-utilizer status included female sex, middle to old age, and late stage cancer. CONCLUSION: Presence of mental disorder prior to cancer had a diminishing effect on medical utilization in patients, possibly indicating low medical compliance or adherence in patients with mental disorder on initial treatments after cancer diagnosis. Patients with post-cancer mental disorder had the highest average annual cost. Similar results were found in the odds of reaching high-utilizer status. The follow-up of cancer treatment for patients with pre-existing mental disorders warrants more emphasis in an attempt to effectively allocate medical resources.

A Chinese telemedicine-dialogue dataset annotated for named entities.

BACKGROUND: A large collection of dialogues between patients and doctors must be annotated for medical named entities to build intelligence for telemedicine. However, since most patients involved in telemedicine deliver related named entities in informal and long multiword expressions, it is challenging to tag their telemedicine dialogue data. This study aims to address this issue. METHODS: With the telemedicine dialogue dataset for obstetrics and gynecology taken from haodf.com, we developed guidelines and followed a two-round procedure to tag six types of named entities, including disease, symptom, time, pharmaceutical, operation, and examination. Additionally, we developed four deep-learning models based on this dataset to establish a benchmark for named-entity recognition (NER). RESULTS: The distilled obstetrics and gynecology dataset contains 2,383 consultations between doctors and patients, of which 13,411 sentences were from doctors, and 17,929 were from patients. With 63,560 named entities in total, the average number of characters per named entity is 4.33. The experimental results suggest that LatticeLSTM performs best on our dataset in terms of accuracy, precision, recall, and F score. CONCLUSION: Compared with other datasets, this dataset offers three novel facets. This study offers intricately tagged long multiword expressions for medical named entities. Second, this study is one of the first attempts to mark temporal entities in a medical dataset. Third, this annotated dataset is balanced across the six types of labels, which we believe will play a considerable role in expanding telemedicine artificial intelligence.

Behavioral, circuitry, and molecular aberrations by region-specific deficiency of the high-risk autism gene Cul3.

Cullin 3 (Cul3) gene, which encodes a core component of the E3 ubiquitin ligase complex that mediates proteasomal degradation, has been identified as a true high-risk factor for autism. Here, by combining behavioral, electrophysiological, and proteomic approaches, we have examined how Cul3 deficiency contributes to the etiology of different aspects of autism. Heterozygous mice with forebrain Cul3 deletion displayed autism-like social interaction impairment and sensory-gating deficiency. Region-specific deletion of Cul3 leads to distinct phenotypes, with social deficits linked to the loss of Cul3 in prefrontal cortex (PFC), and stereotypic behaviors linked to the loss of Cul3 in striatum. Correlated with these behavioral alterations, Cul3 deficiency in forebrain or PFC induces NMDA receptor hypofunction, while Cul3 loss in striatum causes a cell type-specific alteration of neuronal excitability in striatal circuits. Large-scale profiling has identified sets of misregulated proteins resulting from Cul3 deficiency in different regions, including Smyd3, a histone methyltransferase involved in gene transcription. Inhibition or knockdown of Smyd3 in forebrain Cul3-deficient mice ameliorates social deficits and restores NMDAR function in PFC. These results have revealed for the first time a potential molecular mechanism underlying the manifestation of different autism-like behavioral deficits by Cul3 deletion in cortico-striatal circuits.

Characterizing the Onset Potential Distribution of Pt/C Catalyst Deposition by a Total Internal Reflection Imaging Method.

A catalytic electrode with extraordinary performances for hydrogen evolution reaction (HER) should achieve a low onset potential of the bulk electrode, as well as its uniform distribution. Herein, a total internal reflection imaging (TIRi) method to characterize the onset potential distribution of the catalytic electrode surface is presented. When the potential scans toward negative in a linear sweep voltammetry, the equivalent refractive index of the electrolyte on the electrode surface will decrease due to H2 microbubbles generation, leading to the increase in optical intensity. Analysis of the relationship between the optical intensity and potential in each region results in the onset potential distribution. The TIRi method reveals poor uniformity and repeatability in the catalytic electrodes which are fabricated by depositing Pt/C catalysts on a porous carbon support with polymer binders (e.g., Nafion). Further electrochemical stability test also shows poor durability, whose HER onset potential deteriorates from the edge to the middle of these catalytic electrodes. The present TIRi method realizes direct visualization of the activity distribution on the bulk electrode surface, which provides a powerful tool for better fabrication and evaluation of large-area HER electrodes in industrial energy devices.

In situ detection of electrochemical reaction by weak measurement.

In the field of electrochemical energy storage systems, the use of in situ detection technology helps to study the mechanism of electrochemical reaction. Our group has previously in situ detected the electrochemical reaction in vanadium flow batteries by total internal reflection (TIR) imaging. In order to further improve the detection resolution, in this study, the weak measurement (WM) method was introduced to in situ detect the electrochemical reaction during the linear sweep voltammetry or the cyclic voltammetry tests with quantitative measurement of the absolute current density, which lays a foundation for replacing the TIR for two-dimensional imaging of electrochemical reactions in vanadium flow batteries, oxygen/hydrogen evolution reaction, surface treatments, electrochemical corrosion and so on.

Correction: Amelioration of autism-like social deficits by targeting histone methyltransferases EHMT1/2 in Shank3-deficient mice.

A correction to this paper has been published and can be accessed via a link at the top of the paper.

Amelioration of autism-like social deficits by targeting histone methyltransferases EHMT1/2 in Shank3-deficient mice.

Many of the genes disrupted in autism are identified as histone-modifying enzymes and chromatin remodelers, most prominently those that mediate histone methylation/demethylation. However, the role of histone methylation enzymes in the pathophysiology and treatment of autism remains unknown. To address this, we used mouse models of haploinsufficiency of the Shank3 gene (a highly penetrant monogenic autism risk factor), which exhibits prominent autism-like social deficits. We found that histone methyltransferases EHMT1 and EHMT2, as well as histone lysine 9 dimethylation (specifically catalyzed by EHMT1/2), were selectively increased in the prefrontal cortex (PFC) of Shank3-deficient mice and autistic human postmortem brains. Treatment with the EHMT1/2 inhibitor UNC0642 or knockdown of EHMT1/2 in PFC induced a robust rescue of autism-like social deficits in Shank3-deficient mice, and restored NMDAR-mediated synaptic function. Activity-regulated cytoskeleton-associated protein (Arc) was identified as one of the causal factors underlying the rescuing effects of UNC0642 on NMDAR function and social behaviors in Shank3-deficient mice. UNC0642 treatment also restored a large set of genes involved in neural signaling in PFC of Shank3-deficient mice. These results suggest that targeting histone methylation enzymes to adjust gene expression and ameliorate synaptic defects could be a potential therapeutic strategy for autism.

Inhibition of EHMT1/2 rescues synaptic and cognitive functions for Alzheimer's disease.

Epigenetic dysregulation, which leads to the alteration of gene expression in the brain, is suggested as one of the key pathophysiological bases of ageing and neurodegeneration. Here we found that, in the late-stage familial Alzheimer's disease (FAD) mouse model, repressive histone H3 dimethylation at lysine 9 (H3K9me2) and euchromatic histone methyltransferases EHMT1 and EHMT2 were significantly elevated in the prefrontal cortex, a key cognitive region affected in Alzheimer's disease. Elevated levels of H3K9me2 were also detected in the prefrontal cortex region of post-mortem tissues from human patients with Alzheimer's disease. Concomitantly, H3K9me2 at glutamate receptors was increased in prefrontal cortex of aged FAD mice, which was linked to the diminished transcription, expression and function of AMPA and NMDA receptors. Treatment of FAD mice with specific EHMT1/2 inhibitors reversed histone hyper-methylation and led to the recovery of glutamate receptor expression and excitatory synaptic function in prefrontal cortex and hippocampus. Chromatin immunoprecipitation-sequencing (ChIP-seq) data indicated that FAD mice exhibited genome-wide increase of H3K9me2 enrichment at genes involved in neuronal signalling (including glutamate receptors), which was reversed by EHMT1/2 inhibition. Moreover, the impaired recognition memory, working memory, and spatial memory in aged FAD mice were rescued by the treatment with EHMT1/2 inhibitors. These results suggest that disrupted epigenetic regulation of glutamate receptor transcription underlies the synaptic and cognitive deficits in Alzheimer's disease, and targeting histone methylation enzymes may represent a novel therapeutic strategy for this prevalent neurodegenerative disorder.

The ADHD-linked human dopamine D4 receptor variant D4.7 induces over-suppression of NMDA receptor function in prefrontal cortex.

The human dopamine D4 receptor (hD4R) variants with long tandem repeats in the third intracellular loop have been strongly associated with attention deficit hyperactivity disorder (ADHD) and risk taking behaviors. To understand the potential molecular mechanism underlying the connection, we have investigated the synaptic function of human D4R polymorphism by virally expressing the ADHD-linked 7-repeat allele, hD4.7, or its normal counterpart, hD4.4, in the prefrontal cortex (PFC) of D4R knockout mice. We found that hD4R bound to the SH3 domain of PSD-95 in a state-dependent manner. Activation of hD4.7 caused more reduction of NR1/PSD-95 binding and NR1 surface expression than hD4.4 in PFC slices. Moreover, the NMDAR-mediated excitatory postsynaptic currents (NMDAR-EPSC) in PFC pyramidal neurons were suppressed to a larger extent by hD4.7 than hD4.4 activation. Direct stimulation of NMDARs with the partial agonist d-cycloserine prevented the NMDAR hypofunction induced by hD4.7 activation. Moreover, hD4.7-expressing mice exhibited the increased exploratory and novelty seeking behaviors, mimicking the phenotypic hallmark of human ADHD. d-cycloserine administration ameliorated the ADHD-like behaviors in hD4.7-expressing mice. Our results suggest that over-suppression of NMDAR function may underlie the role of hD4.7 in ADHD, and enhancing NMDAR signaling may be a viable therapeutic strategy to ADHD humans carrying the D4.7 allele.

In Situ Mapping of Activity Distribution of V(II)/V(III) and Onset Potential Distribution of Hydrogen Evolution Side Reaction in Vanadium Flow Batteries.

Vanadium flow batteries (VFBs) face a challenge with the low reaction rates of the V(II)/V(III) redox couple, which limits the performance of VFBs. Additionally, the negative electrode in VFBs is often accompanied by the persistent hydrogen evolution reaction (HER), which is difficult to eliminate. Therefore, understanding the spatial distribution of activity on the negative electrode and the HER side reaction on the electrode surface is of critical importance. This study proposes a weak measurement imaging method to characterize the spatial distribution of surface activity and HER onset potential on the negative electrode in VFBs). This method enables the visualization and in situ detection of key parameters such as the absolute values of |ipa |, |ipc |, |∆E|, |ipc /ipa |, and the HER onset potential. By comparing three different types of graphite felts with varying activity levels, it validates the feasibility of this method. Furthermore, electrochemical stability tests are conducted to study the electrodes repeatability, uniformity, and durability. This method holds promise in guiding the design of electrodes with enhanced activity, good reversibility, minimized HER side reactions, and uniform distribution.

Short-term memory capacity analysis of Lu3Fe4Co0.5Si0.5O12-based spin cluster glass towards reservoir computing.

Reservoir computing is a brain heuristic computing paradigm that can complete training at a high speed. The learning performance of a reservoir computing system relies on its nonlinearity and short-term memory ability. As physical implementation, spintronic reservoir computing has attracted considerable attention because of its low power consumption and small size. However, few studies have focused on developing the short-term memory ability of the material itself in spintronics reservoir computing. Among various magnetic materials, spin glass is known to exhibit slow magnetic relaxation that has the potential to offer the short-term memory capability. In this research, we have quantitatively investigated the short-term memory capability of spin cluster glass based on the prevalent benchmark. The results reveal that the magnetization relaxation of Co, Si-substituted Lu3Fe5O12 with spin glass behavior can provide higher short-term memory capacity than ferrimagnetic material without substitution. Therefore, materials with spin glass behavior can be considered as potential candidates for constructing next-generation spintronic reservoir computing with better performance.

Diminished activity-dependent BDNF signaling differentially causes autism-like behavioral deficits in male and female mice.

Autism spectrum disorder (ASD) is a group of neurodevelopmental disorders with strong genetic heterogeneity and more prevalent in males than females. Recent human genetic studies have identified multiple high-risk genes for ASD, which produce similar phenotypes, indicating that diverse genetic factors converge to common molecular pathways. We and others have hypothesized that activity-dependent neural signaling is a convergent molecular pathway dysregulated in ASD. However, the causal link between diminished activity-dependent neural signaling and ASD remains unclear. Brain-derived neurotrophic factor (BDNF) is a key molecule mediating activity-dependent neural signaling. We therefore hypothesize that diminished activity-dependent BDNF signaling could confer autism-like behavioral deficits. Here, we investigated the effect of diminished activity-dependent BDNF signaling on autism-like behavioral deficits by using mice with genetic knock-in of a human BDNF methionine (Met) allele, which has decreased activity-dependent BDNF release without altering basal BDNF level. Compared with wild-type (WT) controls, diminished activity-dependent BDNF signaling similarly induced anxiety-like behaviors in male and female mice. Notably, diminished activity-dependent BDNF signaling differentially resulted in autism-like social deficits and increased self-grooming in male and female mice, and male mice were more severe than female mice. Again, sexually dimorphic spatial memory deficits were observed in female BDNF+/Met mice, but not in male BDNF+/Met mice. Our study not only reveals a causal link between diminished activity-dependent BDNF signaling and ASD-like behavioral deficits, but also identifies previously underappreciated sex-specific effect of diminished activity-dependent BDNF signaling in ASD. These mice with genetic knock-in of the human BDNF Met variant provide a distinct mouse model for studying the cellular and molecular mechanisms underlying diminished activity-dependent neural signaling, the common molecular pathway dysregulated in ASD.

Inhibition of histone methyltransferase Smyd3 rescues NMDAR and cognitive deficits in a tauopathy mouse model.

Pleiotropic mechanisms have been implicated in Alzheimer's disease (AD), including transcriptional dysregulation, protein misprocessing and synaptic dysfunction, but how they are mechanistically linked to induce cognitive deficits in AD is unclear. Here we find that the histone methyltransferase Smyd3, which catalyzes histone H3 lysine 4 trimethylation (H3K4me3) to activate gene transcription, is significantly elevated in prefrontal cortex (PFC) of AD patients and P301S Tau mice, a model of tauopathies. A short treatment with the Smyd3 inhibitor, BCI-121, rescues cognitive behavioral deficits, and restores synaptic NMDAR function and expression in PFC pyramidal neurons of P301S Tau mice. Fbxo2, which encodes an E3 ubiquitin ligase controlling the degradation of NMDAR subunits, is identified as a downstream target of Smyd3. Smyd3-induced upregulation of Fbxo2 in P301S Tau mice is linked to the increased NR1 ubiquitination. Fbxo2 knockdown in PFC leads to the recovery of NMDAR function and cognitive behaviors in P301S Tau mice. These data suggest an integrated mechanism and potential therapeutic strategy for AD.

Reconfigurable magnon interference by on-chip dynamic wavelength conversion.

Spin waves (SWs), an ultra-low power magnetic excitation in ferro or antiferromagnetic media, have tremendous potential as transport less data carriers for post-CMOS technology using their wave interference properties. The concept of magnon interference originates from optical interference, resulting in a historical taboo of maintaining an identical wavevector for magnon interference-based devices. This makes the attainment of on-chip design reconfigurability challenging owing to the difficulty in phase tuning via external fields. Breaking the taboo, this study explores a novel technique to systematically control magnon interference using asymmetric wavevectors from two different SW modes (magnetostatic surface SWs and backward volume magnetostatic SWs) in a microstructured yttrium iron garnet crossbar. Using this system, we demonstrate phase reconfigurability in the interference pattern by modulating the thermal landscape, modifying the dispersion of the interfering SW modes. Thus, we manifest that such a tunable interference can be used to implement reconfigurable logic gates operating between the XNOR and XOR modes by using symmetric and asymmetric interference, respectively.

Association between use of different long-term care services and risks of mental disorder and mortality as well as medical utilization.

Objective: This study sought to investigate mental disorder and mortality risks and medical utilization among various long-term care (LTC) services and examine the associated factors. Methods: This retrospective cohort study used data from the National Health Insurance Research Database of the entire population of Taiwan recorded between 2006 and 2017. A total of 41,407 patients using LTC (study group) were identified and propensity score-matched with 41,407 LTC nonusers (control group) at a ratio of 1:1 according to sex, age, salary-based premium, comorbidity index score, and urbanization level. Patients were divided into four groups according to LTC service type. The age distribution was as follows: 50-60 years (10.47%), 61-70 years (14.48%), 71-80 years (35.59%), and 81 years and older (39.45%). The mean age was 70.18 years and 53.57% of female participants were included. The major statistical methods were the Cox proportional hazards model and the general linear model (GLM). Results: Users of both institutional and inhome LTC services had the highest risk of mental disorder [adjusted hazard ratio (aHR) = 3.2]. The mean mortality rate in LTC nonusers was 46.2%, whereas that in LTC users was 90.4%, with the highest found among the users of both institutional and inhome LTC (90.6%). The institutional LTC users had the shortest survival time (4.1 years). According to the adjusted Cox model analysis, the odds of mortality was significantly higher among institutional LTC users than among inhome LTC users (aHR = 1.02). After the adjustment of covariates, adjusted GLM model results revealed that the annual medical expenditure per capita of LTC nonusers was NT$46,551, which was 1.6 times higher that of LTC users. Conclusion: Users of both institutional and inhome LTC services have higher risk of mental disorder, shorter survival time, and lower medical utilization.

Real-time detection of acetone gas molecules at ppt levels in an air atmosphere using a partially suspended graphene surface acoustic wave skin gas sensor.

To improve the quality of modern life in the current society, low-power, highly sensitive, and reliable healthcare technology is necessary to monitor human health in real-time. In this study, we fabricated partially suspended monolayer graphene surface acoustic wave gas sensors (G-SAWs) with a love-mode wave to effectively detect ppt-level acetone gas molecules at room temperature. The sputtered SiO2 thin film on the surface of a black 36°YX-LiTaO3 (B-LT) substrate acted as a guiding layer, effectively reducing the noise and insertion loss. The G-SAWs exhibited enhanced gas response towards acetone gas molecules (800 ppt) in a real-time atmosphere. The high sensitivity of the G-SAW sensor can be attributed to the elasticity and surface roughness of the SiO2 film. In addition, the G-SAW sensor exhibited rapid response and recovery at room temperature. This study provides a potential strategy for diagnosing different stages of diabetes in the human body.