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Anthelmintics are drugs used for controlling pathogenic helminths in animals and plants. The natural compound betaine and the recently developed synthetic compound monepantel are both anthelmintics that target the acetylcholine receptor ACR-23 and its homologs in nematodes. Here, we present cryo-electron microscopy structures of ACR-23 in apo, betaine-bound, and betaine- and monepantel-bound states. We show that ACR-23 forms a homo-pentameric channel, similar to some other pentameric ligand-gated ion channels (pLGICs). While betaine molecules are bound to the classical neurotransmitter sites in the inter-subunit interfaces in the extracellular domain, monepantel molecules are bound to allosteric sites formed in the inter-subunit interfaces in the transmembrane domain of the receptor. Although the pore remains closed in betaine-bound state, monepantel binding results in an open channel by wedging into the cleft between the transmembrane domains of two neighboring subunits, which causes dilation of the ion conduction pore. By combining structural analyses with site-directed mutagenesis, electrophysiology and in vivo locomotion assays, we provide insights into the mechanism of action of the anthelmintics monepantel and betaine.
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The relationship between prevalence of infection and severe outcomes such as hospitalisation and death changed over the course of the COVID-19 pandemic. Reliable estimates of the infection fatality ratio (IFR) and infection hospitalisation ratio (IHR) along with the time-delay between infection and hospitalisation/death can inform forecasts of the numbers/timing of severe outcomes and allow healthcare services to better prepare for periods of increased demand. The REal-time Assessment of Community Transmission-1 (REACT-1) study estimated swab positivity for Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) infection in England approximately monthly from May 2020 to March 2022. Here, we analyse the changing relationship between prevalence of swab positivity and the IFR and IHR over this period in England, using publicly available data for the daily number of deaths and hospitalisations, REACT-1 swab positivity data, time-delay models, and Bayesian P-spline models. We analyse data for all age groups together, as well as in 2 subgroups: those aged 65 and over and those aged 64 and under. Additionally, we analysed the relationship between swab positivity and daily case numbers to estimate the case ascertainment rate of England's mass testing programme. During 2020, we estimated the IFR to be 0.67% and the IHR to be 2.6%. By late 2021/early 2022, the IFR and IHR had both decreased to 0.097% and 0.76%, respectively. The average case ascertainment rate over the entire duration of the study was estimated to be 36.1%, but there was some significant variation in continuous estimates of the case ascertainment rate. Continuous estimates of the IFR and IHR of the virus were observed to increase during the periods of Alpha and Delta's emergence. During periods of vaccination rollout, and the emergence of the Omicron variant, the IFR and IHR decreased. During 2020, we estimated a time-lag of 19 days between hospitalisation and swab positivity, and 26 days between deaths and swab positivity. By late 2021/early 2022, these time-lags had decreased to 7 days for hospitalisations and 18 days for deaths. Even though many populations have high levels of immunity to SARS-CoV-2 from vaccination and natural infection, waning of immunity and variant emergence will continue to be an upwards pressure on the IHR and IFR. As investments in community surveillance of SARS-CoV-2 infection are scaled back, alternative methods are required to accurately track the ever-changing relationship between infection, hospitalisation, and death and hence provide vital information for healthcare provision and utilisation.
Subject(s)
COVID-19 , Humans , COVID-19/epidemiology , SARS-CoV-2 , Bayes Theorem , Pandemics , England/epidemiology , HospitalizationABSTRACT
Recent studies have provided insights into the pathogenesis of coronavirus disease 2019 (COVID-19)1-4. However, the longitudinal immunological correlates of disease outcome remain unclear. Here we serially analysed immune responses in 113 patients with moderate or severe COVID-19. Immune profiling revealed an overall increase in innate cell lineages, with a concomitant reduction in T cell number. An early elevation in cytokine levels was associated with worse disease outcomes. Following an early increase in cytokines, patients with moderate COVID-19 displayed a progressive reduction in type 1 (antiviral) and type 3 (antifungal) responses. By contrast, patients with severe COVID-19 maintained these elevated responses throughout the course of the disease. Moreover, severe COVID-19 was accompanied by an increase in multiple type 2 (anti-helminths) effectors, including interleukin-5 (IL-5), IL-13, immunoglobulin E and eosinophils. Unsupervised clustering analysis identified four immune signatures, representing growth factors (A), type-2/3 cytokines (B), mixed type-1/2/3 cytokines (C), and chemokines (D) that correlated with three distinct disease trajectories. The immune profiles of patients who recovered from moderate COVID-19 were enriched in tissue reparative growth factor signature A, whereas the profiles of those with who developed severe disease had elevated levels of all four signatures. Thus, we have identified a maladapted immune response profile associated with severe COVID-19 and poor clinical outcome, as well as early immune signatures that correlate with divergent disease trajectories.
Subject(s)
Coronavirus Infections/immunology , Coronavirus Infections/physiopathology , Cytokines/analysis , Pneumonia, Viral/immunology , Pneumonia, Viral/physiopathology , Adult , Aged , Aged, 80 and over , COVID-19 , Cluster Analysis , Cytokines/immunology , Eosinophils/immunology , Female , Humans , Immunoglobulin E/analysis , Immunoglobulin E/immunology , Interleukin-13/analysis , Interleukin-13/immunology , Interleukin-5/analysis , Interleukin-5/immunology , Male , Middle Aged , Pandemics , T-Lymphocytes/cytology , T-Lymphocytes/immunology , Viral Load , Young AdultABSTRACT
SUMMARYWithin weeks of the first report of acquired immunodeficiency syndrome (AIDS) in 1981, it was observed that these patients often had Kaposi sarcoma (KS), a hitherto rarely seen skin tumor in the USA. It soon became apparent that AIDS was also associated with an increased incidence of high-grade lymphomas caused by Epstein-Barr virus (EBV). The association of AIDS with KS remained a mystery for more than a decade until Kaposi sarcoma-associated herpesvirus (KSHV) was discovered and found to be the cause of KS. KSHV was subsequently found to cause several other diseases associated with AIDS and human immunodeficiency virus (HIV) infection. People living with HIV/AIDS continue to have an increased incidence of certain cancers, and many of these cancers are caused by EBV and/or KSHV. In this review, we discuss the epidemiology, virology, pathogenesis, clinical manifestations, and treatment of cancers caused by EBV and KSHV in persons living with HIV.
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Phe-Met-Arg-Phe-amide (FMRFamide)-activated sodium channels (FaNaCs) are a family of channels activated by the neuropeptide FMRFamide, and, to date, the underlying ligand gating mechanism remains unknown. Here we present the high-resolution cryo-electron microscopy structures of Aplysia californica FaNaC in both apo and FMRFamide-bound states. AcFaNaC forms a chalice-shaped trimer and possesses several notable features, including two FaNaC-specific insertion regions, a distinct finger domain and non-domain-swapped transmembrane helix 2 in the transmembrane domain (TMD). One FMRFamide binds to each subunit in a cleft located in the top-most region of the extracellular domain, with participation of residues from the neighboring subunit. Bound FMRFamide adopts an extended conformation. FMRFamide binds tightly to A. californica FaNaC in an N terminus-in manner, which causes collapse of the binding cleft and induces large local conformational rearrangements. Such conformational changes are propagated downward toward the TMD via the palm domain, possibly resulting in outward movement of the TMD and dilation of the ion conduction pore.
Subject(s)
Ion Channel Gating , Neuropeptides , FMRFamide/metabolism , FMRFamide/pharmacology , Cryoelectron Microscopy , Neuropeptides/metabolism , Sodium Channels/chemistry , Sodium Channels/metabolismABSTRACT
Chronic varicella zoster virus (VZV) infection induced neuroinflammatory condition is the critical pathology of post-herpetic neuralgia (PHN). The immune escape mechanism of VZV remains elusive. As to mice have no VZV infection receptor, herpes simplex virus type 1 (HSV-1) infection is a well established PHN mice model. Transcriptional expression analysis identified that the protein arginine methyltransferases 6 (Prmt6) was upregulated upon HSV-1 infection, which was further confirmed by immunofluorescence staining in spinal dorsal horn. Prmt6 deficiency decreased HSV-1-induced neuroinflammation and PHN by enhancing antiviral innate immunity and decreasing HSV-1 load in vivo and in vitro. Overexpression of Prmt6 in microglia dampened antiviral innate immunity and increased HSV-1 load. Mechanistically, Prmt6 methylated and inactivated STING, resulting in reduced phosphorylation of TANK binding kinase-1 (TBK1) and interferon regulatory factor 3 (IRF3), diminished production of type I interferon (IFN-I) and antiviral innate immunity. Furthermore, intrathecal or intraperitoneal administration of the Prmt6 inhibitor EPZ020411 decreased HSV-1-induced neuroinflammation and PHN by enhancing antiviral innate immunity and decreasing HSV-1 load. Our findings revealed that HSV-1 escapes antiviral innate immunity and results in PHN by upregulating Prmt6 expression and inhibiting the cGAS-STING pathway, providing novel insights and a potential therapeutic target for PHN.
Subject(s)
Herpesvirus 1, Human , Membrane Proteins , Neuralgia, Postherpetic , Nucleotidyltransferases , Protein-Arginine N-Methyltransferases , Up-Regulation , Animals , Protein-Arginine N-Methyltransferases/metabolism , Protein-Arginine N-Methyltransferases/genetics , Protein-Arginine N-Methyltransferases/antagonists & inhibitors , Mice , Membrane Proteins/metabolism , Membrane Proteins/genetics , Nucleotidyltransferases/metabolism , Nucleotidyltransferases/genetics , Neuralgia, Postherpetic/metabolism , Neuralgia, Postherpetic/immunology , Mice, Inbred C57BL , Immunity, Innate , Humans , Mice, Knockout , Male , Interferon Regulatory Factor-3/metabolism , Interferon Regulatory Factor-3/genetics , Herpes Simplex/immunology , Microglia/metabolism , Microglia/immunology , Protein Serine-Threonine KinasesABSTRACT
Multiple myeloma (MM) is a rarely curable malignancy of plasma cells. MM expresses B cell maturation antigen (BCMA). We developed a fully human anti-BCMA chimeric antigen receptor (CAR) with a heavy-chain-only antigen-recognition domain, a 4-1BB domain, and a CD3ζ domain. The CAR was designated FHVH33-CD8BBZ. We conducted the first-in-humans clinical trial of T cells expressing FHVH33-CD8BBZ (FHVH-T). Twenty-five patients with relapsed MM were treated. The stringent complete response rate (sCR) was 52%. Median progression-free survival (PFS) was 78 weeks. Of 24 evaluable patients, 6 (25%) had a maximum cytokine-release syndrome (CRS) grade of 3; no patients had CRS of greater than grade 3. Most anti-MM activity occurred within 2-4 weeks of FHVH-T infusion as shown by decreases in the rapidly changing MM markers serum free light chains, urine light chains, and bone marrow plasma cells. Blood CAR+ cell levels peaked during the time that MM elimination was occurring, between 7 and 15 days after FHVH-T infusion. C-C chemokine receptor type 7 (CCR7) expression on infusion CD4+ FHVH-T correlated with peak blood FHVH-T levels. Single-cell RNA sequencing revealed a shift toward more differentiated FHVH-T after infusion. Anti-CAR antibody responses were detected in 4 of 12 patients assessed. FHVH-T has powerful, rapid, and durable anti-MM activity.
Subject(s)
Multiple Myeloma , Receptors, Chimeric Antigen , Humans , Multiple Myeloma/genetics , Receptors, Chimeric Antigen/metabolism , T-Lymphocytes , Immunotherapy, Adoptive , Bone Marrow/metabolismABSTRACT
Electrocatalysis is considered promising in renewable energy conversion and storage, yet numerous efforts rely on catalyst design to advance catalytic activity. Herein, a hydrodynamic single-particle electrocatalysis methodology is developed by integrating collision electrochemistry and microfluidics to improve the activity of an electrocatalysis system. As a proof-of-concept, hydrogen evolution reaction (HER) is electrocatalyzed by individual palladium nanoparticles (Pd NPs), with the development of microchannel-based ultramicroelectrodes. The controlled laminar flow enables the precise delivery of Pd NPs to the electrode-electrolyte interface one by one. Compared to the diffusion condition, hydrodynamic collision improves the number of active sites on a given electrode by 2 orders of magnitude. Furthermore, forced convection enables the enhancement of proton mass transport, thereby increasing the electrocatalytic activity of each single Pd NP. It turns out that the improvement in mass transport increases the reaction rate of HER at individual Pd NPs, thus a phase transition without requiring a high overpotential. This study provides new avenues for enhancing electrocatalytic activity by altering operating conditions, beyond material design limitations.
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BACKGROUND: This study aimed to investigate the relationship between signal regulatory protein gamma (SIRPG) and tumor immune microenvironment phenotypes or T cell mediated-adaptive antitumor immunity, and its predictive value for response to PD-1 blockade in cancers. METHODS: Pan-cancer analysis of SIRPG expression and immune deconvolution was performed using transcriptomic data across 33 tumor types. Transcriptomic and clinical data from 157 patients with non-small-cell lung cancer (NSCLC) and melanoma received PD-1 blockade were analyzed. Expression characteristics of SIRPG were investigated using single-cell RNA sequencing (scRNA-seq) data of 103,599 cells. The effect of SIRPG expression was evaluated via SIRPG knockdown or overexpression in Jurkat T cells. RESULTS: The results showed that most cancers with high SIRPG expression had significantly higher abundance of T cells, B cells, NK cells, M1 macrophages and cytotoxic lymphocytes and increased expression level of immunomodulatory factors regulating immune cell recruitment, antigen presentation, T cell activation and cytotoxicity, but markedly lower abundance of neutrophils, M2 macrophages, and myeloid-derived suppressor cells. High SIRPG expression was associated with favorable response to PD-1 blockade in both NSCLC and melanoma. scRNA-seq data suggested SIRPG was mainly expressed in CD8+ exhausted T and CD4+ regulatory T cells, and positively associated with immune checkpoint expression including PDCD1 and CTLA4. In vitro test showed SIRPG expression in T cells could facilitate expression of PDCD1 and CTLA4. CONCLUSION: High SIRPG expression is associated with an inflamed immune phenotype in cancers and favorable response to PD-1 blockade, suggesting it would be a promising predictive biomarker for PD-1 blockade and novel immunotherapeutic target.
Subject(s)
Immune Checkpoint Inhibitors , Programmed Cell Death 1 Receptor , Tumor Microenvironment , Humans , Tumor Microenvironment/immunology , Immune Checkpoint Inhibitors/therapeutic use , Immune Checkpoint Inhibitors/pharmacology , Programmed Cell Death 1 Receptor/antagonists & inhibitors , Programmed Cell Death 1 Receptor/metabolism , Carcinoma, Non-Small-Cell Lung/immunology , Carcinoma, Non-Small-Cell Lung/metabolism , Carcinoma, Non-Small-Cell Lung/pathology , Carcinoma, Non-Small-Cell Lung/drug therapy , Lung Neoplasms/immunology , Lung Neoplasms/metabolism , Lung Neoplasms/pathology , Lung Neoplasms/genetics , Biomarkers, Tumor/metabolism , Melanoma/immunology , Melanoma/metabolism , Melanoma/geneticsABSTRACT
Since the first discovery of the fatigue phenomenon in the late 1830s, efforts to fight against fatigue failure have continued. Here we report a fatigue resistance phenomenon in nano-TiB2-decorated AlSi10Mg enabled by additive manufacturing. This fatigue resistance mechanism benefits from the three-dimensional dual-phase cellular nanostructure, which acts as a strong volumetric nanocage to prevent localized damage accumulation, thus inhibiting fatigue crack initiation. The intrinsic fatigue strength limit of nano-TiB2-decorated AlSi10Mg was proven to be close to its tensile strength through the in situ fatigue tests of a defect-free microsample. To demonstrate the practical applicability of this mechanism, printed bulk nano-TiB2-decorated AlSi10Mg achieved fatigue resistance more than double those of other additive manufacturing Al alloys and surpassed those of high-strength wrought Al alloys. This strategy of additive-manufacturing-assisted nanostructure engineering can be extended to the development of other dual-phase fatigue-resistant metals.
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Remission durability following single-antigen targeted chimeric antigen receptor (CAR) T-cells is limited by antigen modulation, which may be overcome with combinatorial targeting. Building upon our experiences targeting CD19 and CD22 in B-cell acute lymphoblastic leukemia (B-ALL), we report on our phase 1 dose-escalation study of a novel murine stem cell virus (MSCV)-CD19/CD22-4-1BB bivalent CAR T-cell (CD19.22.BBζ) for children and young adults (CAYA) with B-cell malignancies. Primary objectives included toxicity and dose finding. Secondary objectives included response rates and relapse-free survival (RFS). Biologic correlatives included laboratory investigations, CAR T-cell expansion and cytokine profiling. Twenty patients, ages 5.4 to 34.6 years, with B-ALL received CD19.22.BBζ. The complete response (CR) rate was 60% (12 of 20) in the full cohort and 71.4% (10 of 14) in CAR-naïve patients. Ten (50%) developed cytokine release syndrome (CRS), with 3 (15%) having ≥ grade 3 CRS and only 1 experiencing neurotoxicity (grade 3). The 6- and 12-month RFS in those achieving CR was 80.8% (95% confidence interval [CI]: 42.4%-94.9%) and 57.7% (95% CI: 22.1%-81.9%), respectively. Limited CAR T-cell expansion and persistence of MSCV-CD19.22.BBζ compared with EF1α-CD22.BBζ prompted laboratory investigations comparing EF1α vs MSCV promoters, which did not reveal major differences. Limited CD22 targeting with CD19.22.BBζ, as evaluated by ex vivo cytokine secretion and leukemia eradication in humanized mice, led to development of a novel bicistronic CD19.28ζ/CD22.BBζ construct with enhanced cytokine production against CD22. With demonstrated safety and efficacy of CD19.22.BBζ in a heavily pretreated CAYA B-ALL cohort, further optimization of combinatorial antigen targeting serves to overcome identified limitations (www.clinicaltrials.gov #NCT03448393).
Subject(s)
Burkitt Lymphoma , Lymphoma, B-Cell , Precursor Cell Lymphoblastic Leukemia-Lymphoma , Receptors, Chimeric Antigen , Animals , Antigens, CD19 , Cytokine Release Syndrome , Cytokines , Humans , Immunotherapy, Adoptive/adverse effects , Immunotherapy, Adoptive/methods , Mice , Receptors, Antigen, T-Cell/genetics , Receptors, Chimeric Antigen/genetics , Recurrence , T-LymphocytesABSTRACT
Not available.
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Not available.
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BACKGROUND: Cognitive impairment and dementia are severe public health issues in aging populations, which can be exacerbated by insufficient or unhealthy dietary intake. Food (in)security status is linked to cognitive function among older adults, but the relationship is complex and can vary by sociodemographic characteristics. OBJECTIVE: This article aimed to investigate the association between food insecurity and cognitive function among United States older adults and explore potential variations by race and ethnicity groups. METHODS: We prospectively examined changes in cognitive function and incidence of cognitive impairment alongside the presence of self-reported food insecurity among older adults of different racial and ethnic groups. Data were from the 2012-2018 Health and Retirement Study (HRS) and the 2013 Health Care and Nutrition Study (HCNS), including N = 6,638 United States adults aged 50 years and older. Food insecurity was measured by a self-reported United States Household Food Security Survey Module, and cognitive function was assessed by the modified version of the Telephone Interview for Cognitive Status. RESULTS: Results showed that 17% of United States older adults reported food insecurity in the 2013 HCNS. Compared with food secure older adults, those reporting food insecurity experienced worsened cognitive functioning over time (B = -0.63, p < .001), and they were more likely to have onset of cognitive impairment (OR= 1.46, p < .001) in the 6-y observation. Compared with non-Hispanic White older adults, being non-Hispanic Black, non-Hispanic Other, or Hispanic was associated with 2.96, 2.09, or 1.26 odds (p < .001) of cognitive impairment (2012-2018), respectively. Older adults of racial and ethnic minority groups also had higher risks of experiencing the double burden of cognitive impairment alongside food insecurity compared with non-Hispanic White older adults. CONCLUSION: Findings underscore racial and ethnic structural disparities in food security and cognitive health in the United States aging population.
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Cognitive Dysfunction , Ethnicity , Food Insecurity , Minority Groups , Racial Groups , Aged , Humans , Middle Aged , Cognition , Food Supply , United States/epidemiology , Cognitive Dysfunction/epidemiologyABSTRACT
Microglia induced chronic inflammation is the critical pathology of Neuropathic pain (NP). Metabolic reprogramming of macrophage has been intensively reported in various chronic inflammation diseases. However, the metabolic reprogramming of microglia in chronic pain remains to be elusive. Here, we reported that immuno-metabolic markers (HIF-1α, PKM2, GLUT1 and lactate) were related with increased expression of PRMT6 in the ipsilateral spinal cord dorsal horn of the chronic construction injury (CCI) mice. PRMT6 deficiency or prophylactic and therapeutic intrathecal administration of PRMT6 inhibitor (EPZ020411) ameliorated CCI-induced NP, inflammation and glycolysis in the ipsilateral spinal cord dorsal horn. PRMT6 knockout or knockdown inhibited LPS-induced inflammation, proliferation and glycolysis in microglia cells. While PRMT6 overexpression exacerbated LPS-induced inflammation, proliferation and glycolysis in BV2 cells. Recent research revealed that PRMT6 could interact with and methylate HIF-1α, which increased HIF-1α protein stability. In sum, increased expression of PRMT6 exacerbates NP progress by increasing glycolysis and neuroinflammation through interacting with and stabilizing HIF-1α in a methyltransferase manner, which outlines novel pathological mechanism and drug target for NP.
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Microglia , Neuralgia , Mice , Animals , Microglia/metabolism , Lipopolysaccharides/pharmacology , Lipopolysaccharides/metabolism , Inflammation/metabolism , Neuralgia/metabolism , GlycolysisABSTRACT
This image article presents a single patient receiving a reconstructed fibular bony peak (BP) for guided bone regeneration (GBR) with a customized titanium mesh. The patient was informed and understood the objectives and signed a written informed consent document before surgery.
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Rational design of γ-alumina-based catalysts relies on an extensive understanding of the distribution of hydroxyl groups on the surface of γ-alumina and their physicochemical properties, which remain unclear and challenging to determine experimentally due to the structural complexity. In this work, by means of DFT and thermodynamic calculations, various hydroxylation modes of γ-alumina (110) and (100) surfaces at different OH coverages were evaluated, based on which a thermodynamic model to reflect the relationship between temperature and the surface structure was established and the stable hydroxylation modes under experimental conditions were predicted. This enables us to identify the experimentally measured IR spectra. The effect of hydroxyl coverages on the surface Lewis acidity was then analyzed, showing that the presence of hydroxyl groups could promote the Lewis acidity of neighboring Al sites. This work provides fundamental insights into the molecular level understanding of the surface properties of γ-alumina and benefits the rational design of alumina-based catalysts.
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BACKGROUND: Multifaceted SARS-CoV-2 interventions have modified exposure to air pollution and dynamics of respiratory diseases. Identifying the most vulnerable individuals requires effort to build a complete picture of the dynamic health effects of air pollution exposure, accounting for disparities across population subgroups. METHODS: We use generalized additive model to assess the likely changes in the hospitalisation and mortality rate as a result of exposure to PM2.5 and O3 over the course of COVID-19 pandemic. We further disaggregate the population into detailed age categories and illustrate a shifting age profile of high-risk population groups. Additionally, we apply multivariable logistic regression to integrate demographic, socioeconomic and climatic characteristics with the pollution-related excess risk. RESULTS: Overall, a total of 1,051,893 hospital admissions and 34,954 mortality for respiratory disease are recorded. The findings demonstrate a transition in the association between air pollutants and hospitalisation rates over time. For every 10 µg/m3 increase of PM2.5, the rate of hospital admission increased by 0.2% (95% CI: 0.1-0.7%) and 1.4% (1.0-1.7%) in the pre-pandemic and dynamic zero-COVID stage, respectively. Conversely, O3-related hospitalization rate would be increased by 0.7% (0.5-0.9%) in the pre-pandemic stage but lowered to 1.7% (1.5-1.9%) in the dynamic zero-COVID stage. Further assessment indicates a shift of high-risk people from children and young adolescents to the old, primarily the elevated hospitalization rates among the old people in Lianyungang (RR: 1.53, 95%CI: 1.46, 1.60) and Nantong (RR: 1.65, 95%CI: 1.57, 1.72) relative to those for children and young adolescents. Over the course of our study period, people with underlying diseases would have 26.5% (22.8-30.3%) and 12.7% (10.8-14.6%) higher odds of having longer hospitalisation and over 6 times higher odds of deaths after hospitalisation. CONCLUSIONS: Our estimates provide the first comprehensive evidence on the dynamic pollution-health associations throughout the pandemic. The results suggest that age and underlying diseases collectively determines the disparities of pollution-related health effect across population subgroups, underscoring the urgency to identifying the most vulnerable individuals to air pollution.
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Air Pollution , Respiration Disorders , Respiratory Tract Diseases , Adolescent , Child , Humans , Pandemics , Respiratory Tract Diseases/epidemiology , Air Pollution/adverse effects , Particulate Matter/adverse effectsABSTRACT
Despite rising numbers of only children in China, little is known about their family dynamics and well-being in adulthood-for example, how often they marry other only children and whether those in siblingless families have worse or better health than others. Theoretical expectations produce opposing predictions: siblings might provide social and emotional support and reduce parental caregiving pressures, but only children might receive more support from parents and grandparents. Using the 2010 China Family Panel Study, we examine marital sorting on Chinese adults' number of siblings and test whether sibling availability and sibling sorting are associated with subjective physical and mental health. Despite general perceptions that China has an exceedingly high prevalence of adults with no siblings that might produce very small families, results demonstrate a low prevalence of siblingless couples (i.e., both spouses are only children). Married adults with no siblings or siblings-in-law have better subjective physical health but similar levels of subjective mental health relative to their counterparts with siblings. The health advantages of siblingless marital unions are greater for rural and female adults. Declining sibling prevalence in China will shape future family demographic dynamics but appears less detrimental to population health than sometimes assumed.
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Health Status , Mental Health , Siblings , Humans , Female , Male , China , Adult , Middle Aged , Family Characteristics , Socioeconomic Factors , Marriage/statistics & numerical data , Sex Factors , Young Adult , Sociodemographic Factors , East Asian PeopleABSTRACT
OBJECTIVES: This study examined the associations between sensory impairment (SI), lack of social contact during the COVID-19 pandemic, and depressive symptoms among Americans aged 50 and above. METHODS: We employed data from the 2018 and 2020 Health and Retirement Study (N = 13,460) to examine four SI groups: no SI, visual impairment (VI) only, hearing impairment (HI) only, and dual sensory impairment (DSI). First, multilevel models were employed to estimate the associations between SI and depressive symptoms before and during the pandemic using the full dataset (N = 13,460). Second, linear regression models were employed to estimate the moderation effect of lack of social contact during the pandemic using the 2020 wave data only (N = 4,133). RESULTS: Among older adults, 15.60% had VI only, 10.16% had HI only, and 9.66% had DSI. All SI groups reported significantly more depressive symptoms than the no SI group. The differences between older adults with VI and DSI and those without SI regarding depressive symptoms narrowed during the pandemic. There was no statistically significant moderation effect of lack of social contact for SI and depressive symptoms. CONCLUSION: Older adults with SI faced mental health challenges and demonstrated psychological resilience during the pandemic. Future research should examine other risk factors that may modify the relationship between SI and mental health during public health crises.