Transporters and phytohormones analysis reveals differential regulation of ryegrass (Lolium perenne L.) in response to cadmium and arsenic stresses.

Cadmium (Cd) and arsenic (As) are two highly toxic heavy metals and metalloids that coexist in many situations posing severe threats to plants. Our investigation was conducted to explore the different regulatory mechanisms of ryegrass (Lolium perenne L.) responding to individual and combined Cd and As stresses in hydroponics. Results showed that the ryegrass well-growth phenotype was not affected by Cd stress of 10 mg·L-1. However, As of 10 mg·L-1 caused rapid water loss, proline surge, and chlorosis in shoots, suggesting that ryegrass was highly sensitive to As. Transcriptomic analysis revealed that the transcription factor LpIRO2 mediated the upregulation of ZIP1 and YSL6 that played an important role in Cd tolerance. We found that the presence of As caused the overexpression of LpSWT12, a process potentially regulated by bHLH14, to mitigate hyperosmolarity. Indoleacetic acid (IAA) and abscisic acid (ABA) contents and expression of their signaling-related genes were significantly affected by As stress rather than Cd. We predict a regulatory network to illustrate the interaction between transporters, transcription factors, and signaling transduction, and explain the antagonism of Cd and As toxicity. This present work provides a research basis for plant protection from Cd and As pollution.

Super-enhancer-driven MLX mediates redox balance maintenance via SLC7A11 in osteosarcoma.

Osteosarcoma (OS) is a common type of bone tumor for which there has been limited therapeutic progress over the past three decades. The prevalence of transcriptional addiction in cancer cells emphasizes the biological significance and clinical relevance of super-enhancers. In this study, we found that Max-like protein X (MLX), a member of the Myc-MLX network, is driven by super-enhancers. Upregulation of MLX predicts a poor prognosis in osteosarcoma. Knockdown of MLX impairs growth and metastasis of osteosarcoma in vivo and in vitro. Transcriptomic sequencing has revealed that MLX is involved in various metabolic pathways (e.g., lipid metabolism) and can induce metabolic reprogramming. Furthermore, knockdown of MLX results in disturbed transport and storage of ferrous iron, leading to an increase in the level of cellular ferrous iron and subsequent induction of ferroptosis. Mechanistically, MLX regulates the glutamate/cystine antiporter SLC7A11 to promote extracellular cysteine uptake required for the biosynthesis of the essential antioxidant GSH, thereby detoxifying reactive oxygen species (ROS) and maintaining the redox balance of osteosarcoma cells. Importantly, sulfasalazine, an FDA-approved anti-inflammatory drug, can inhibit SLC7A11, disrupt redox balance, and induce massive ferroptosis, leading to impaired tumor growth in vivo. Taken together, this study reveals a novel mechanism in which super-enhancer-driven MLX positively regulates SLC7A11 to meet the alleviated demand for cystine and maintain the redox balance, highlighting the feasibility and clinical promise of targeting SLC7A11 in osteosarcoma.

Network Pharmacology-Based and Molecular Docking-Based Analysis of Suanzaoren Decoction for the Treatment of Parkinson's Disease with Sleep Disorder.

This study is aimed at exploring the possible mechanism of action of the Suanzaoren decoction (SZRD) in the treatment of Parkinson's disease with sleep disorder (PDSD) based on network pharmacology and molecular docking. Traditional Chinese Medicine Systems Pharmacology (TCMSP) was used to screen the bioactive components and targets of SZRD, and their targets were standardized using the UniProt platform. The disease targets of "Parkinson's disease (PD)" and "Sleep disorder (SD)" were collected by OMIM, GeneCards, and DisGeNET databases. Thereafter, the protein-protein interaction (PPI) network was constructed using the STRING platform and visualized by Cytoscape (3.7.2) software. Then, the DAVID platform was used to analyze the Gene Ontology (GO) enrichment analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway. Cytoscape (3.7.2) software was also used to construct the network of the "herb-component-target-pathway." The core active ingredients and core action targets of the drug were verified by molecular docking using AutoDock software. A total of 135 Chinese herbal components and 41 corresponding targets were predicted for the treatment of PDSD using SZRD. Fifteen important signaling pathways were screened, such as the cancer pathway, TNF signaling pathway, PI3K-AKT signaling pathway, HIF-1 signaling pathway, and Toll-like receptor signaling pathway. The results of molecular docking showed that the main active compounds could bind to the representative targets and exhibit good affinity. This study revealed that SZRD has the characteristics and advantages of "multicomponent, multitarget, and multipathway" in the treatment of PDSD; among these, the combination of the main active components of quercetin and kaempferol with the key targets of AKT1, IL6, MAPK1, TP53, and VEGFA may be one of the important mechanisms. This study provides a theoretical basis for further study of the material basis and molecular mechanism of SZRD in the treatment of PDSD.

Interplay of m6 A and histone modifications contributes to temozolomide resistance in glioblastoma.

BACKGROUND: Despite the development of new treatment protocols for glioblastoma (GBM), temozolomide (TMZ) resistance remains a primary hindrance. Previous studies, including our study, have shown that aberrant N6-methyladenosine (m6 A) modification is implicated in GBM pathobiology. However, the roles and precise mechanisms of m6 A modification in the regulation of TMZ resistance in GBM remain unclear. METHODS: m6 A individual-nucleotide-resolution cross-linking and immunoprecipitation sequencing (miCLIP-seq) was performed to identify m6 A modification of transcripts in TMZ-resistant and -sensitive tumors. To explore the role of METTL3 in TMZ resistance, TMZ-resistant GBM cells were transfected with METTL3 shRNA or overexpression lentivirus and then assessed by cell viability, tumor sphere formation, and apoptosis assays. An intracranial GBM xenograft model was developed to verify the effect of METTL3 depletion during TMZ treatment in vivo. ATAC-seq, ChIP-qPCR, and dual-luciferase reporter assays were carried out to verify the role of SOX4/EZH2 in the modulation of METTL3 expression upon TMZ treatment. RESULTS: We demonstrated that TMZ treatment upregulated the expression of the m6 A methyltransferase METTL3, thereby increasing m6 A modification of histone modification-related gene transcripts. METTL3 is required to maintain the features of GBM stem cells. When combined with TMZ, METTL3 silencing suppressed orthotopic TMZ-resistant xenograft growth in a cooperative manner. Mechanistically, TMZ induced a SOX4-mediated increase in chromatin accessibility at the METTL3 locus by promoting H3K27ac levels and recruiting RNA polymerase II. Moreover, METTL3 depletion affected the deposition of m6 A on histone modification-related gene transcripts, such as EZH2, leading to nonsense-mediated mRNA decay. We revealed an important role of EZH2 in the regulation of METTL3 expression, which was via an H3K27me3 modification-independent manner. CONCLUSIONS: Our findings uncover the fundamental mechanisms underlying the interplay of m6 A RNA modification and histone modification in TMZ resistance and emphasize the therapeutic potential of targeting the SOX4/EZH2/METTL3 axis in the treatment of TMZ-resistant GBM.

Pharmacological Inhibition of Core Regulatory Circuitry Liquid-liquid Phase Separation Suppresses Metastasis and Chemoresistance in Osteosarcoma.

Liquid-liquid phase-separated (LLPS) transcriptional factor assemblies at super-enhancers (SEs) provide a conceptual framework for underlying transcriptional control in mammal cells. However, the mechanistic understanding of LLPS in aberrant transcription driven by dysregulation of SEs in human malignancies is still elusive. By integrating SE profiling and core regulatory circuitry (CRC) calling algorithm, the CRC of metastatic and chemo-resistant osteosarcoma is delineated. CRC components, HOXB8 and FOSL1, produce dense and dynamic phase-separated droplets in vitro and liquid-like puncta in cell nuclei. Disruption of CRC phase separation decreases the chromatin accessibility in SE regions and inhibits the release of RNA polymerase II from the promoter of SE-driven genes. Importantly, absence of CRC key component causes a reduction in osteosarcoma tumor growth and metastasis. Moreover, it is shown that CRC condensates can be specifically attenuated by the H3K27 demethylase inhibitor, GSK-J4. Pharmacological inhibition of the CRC phase separation results in metastasis suppression and re-sensitivity to chemotherapy drugs in patient-derived xenograft model. Taken together, this study reveals a previously unknown mechanism that CRC factors formed LLPS condensates, and provides a phase separation-based pharmacological strategy to target undruggable CRC components for the treatment of metastatic and chemo-resistant osteosarcoma.

The Early Diagnostic Value of Serum Interleukin-8 in Esophagogastric Junction Adenocarcinoma.

BACKGROUND: Esophagogastric junction adenocarcinoma (EJA) is one of the most common malignant tumors of digestive tract with high mortality worldwide. Given a lack of early diagnosis biomarkers, the prognosis of EJA is poor. Non-invasive biomarkers for early-stage EJA are urgently required. OBJECTIVE: We aimed at evaluating the early diagnostic value of serum interleukin-8 (IL-8) level in EJA patients. METHODS: The IL-8 mRNA expression data were analyzed based on the stomach cardia adenocarcinoma samples of The Cancer Genome Atlas (TCGA) database. Enzyme-linked immunosorbent assay (ELISA) was used to measure the concentration of serum IL-8 in 95 EJA patients and 95 normal controls enrolled from 2 different cancer hospitals. The diagnostic accuracy of serum IL-8 was evaluated by applying Mann-Whitney U test and receiver operating characteristic (ROC) curve. RESULTS: The mRNA expression levels and serum levels of IL-8 in EJA group were significantly higher than those in the normal group (all P < 0.001). The areas under the ROC curve (AUC) were 0.661 (95% CI, 0.583-0.740) and 0.745 (95% CI, 0.606-0.885), with the sensitivities of 43.2% (95% CI, 33.2%-53.7%) and 66.7% (95% CI, 46.0%-82.8%) and the specificities of 87.4% (95% CI, 78.6%-93.1%) in EJA group and early-EJA group, respectively, when the optimal cutoff value was 109.086 pg/mL. The clinical data analysis showed there were significant correlations between patient genders, depth of invasion, lymph node metastasis, TNM stage and the serum level of IL-8 (all P < 0.05). CONCLUSIONS: Serum IL-8 represents a potential diagnostic biomarker to identify early-stage EJA.

Identifying SLC27A5 as a potential prognostic marker of hepatocellular carcinoma by weighted gene co-expression network analysis and in vitro assays.

BACKGROUND: The incidence and mortality rates of hepatocellular carcinoma are among the highest of all cancers all over the world. However the survival rates are relatively low due to lack of effective treatments. Efforts to elucidate the mechanisms of HCC and to find novel prognostic markers and therapeutic targets are ongoing. Here we tried to identify prognostic genes of HCC through co-expression network analysis. METHODS: We conducted weighted gene co-expression network analysis with a microarray dataset GSE14520 of HCC from Gene Expression Omnibus database and identified a hub module associated with HCC prognosis. Function enrichment analysis of the hub module was performed. Clinical information was analyzed to select candidate hub genes. The expression profiles and survival analysis of the selected genes were performed using additional datasets (GSE45267 and TCGA-LIHC) and the hub gene was identified. GSEA and in vitro experiments were conducted to further verify the function of the hub gene. RESULTS: Genes in the hub module were mostly involved in the metabolism pathway. Four genes (SLC27A5, SLC10A1, PCK2 and FMO4) from the module were identified as candidate hub genes according to correlation analysis with prognostic indicators. All these genes were significantly down-regulated in tumor tissues compared with non-tumor tissues in additional datasets. After survival analysis and network construction, SLC27A5 was selected as a prognostic marker. GSEA analysis and in vitro assays suggested that SLC27A5 downregulation promoted tumor cell migration via enhancing epithelial-mesenchymal transition. CONCLUSION: SLC27A5 is a potential biomarker of HCC and SLC27A5 downregulation promoted HCC progression by enhancing EMT.

Oleate Ameliorates Palmitate-Induced Impairment of Differentiative Capacity in C2C12 Myoblast Cells.

A common observation in metabolic disorders and aging is the elevation of free fatty acids (FFAs), which can form ectopic fat deposition and result in lipotoxicity. Ectopic fat deposition of skeletal muscle has been recognized as an important component of aging, frailty, and sarcopenia. Previous studies have suggested that lipotoxicity caused by FFAs mainly stemmed from saturated fatty acids and decreased unsaturated/saturated fatty acid ratio in serum are also observed among metabolic disorder patients. However, the different effects of saturated fatty acids and unsaturated fatty acids on skeletal muscle are not fully elucidated. In this study, we verified that palmitate (PA), a saturated fatty acid, could lead to impaired differentiative capacity of C2C12 myoblasts by affecting Pax7, MyoD, and myogenin (MyoG), which are master regulators of lineage specification and the myogenic program. Then, oleate (OA), a monounsaturated fatty acid, were added to culture medium together with PA. Results showed that OA could ameliorate the impairment of differentiative capacity in C2C12 myoblast cells. In addition, we found PI3K/Akt signaling pathway played an important role during the process by RNA sequencing and bioinformatics analysis. The positive effect of OA on myoblast differentiative capacity disappeared if PI3K inhibitor LY294002 was added. In conclusion, our study showed that PA could destroy differentiative capacity of C2C12 myoblasts by affecting the expression of Pax7, MyoD, and MyoG, and OA could improve this impairment through PI3K/Akt signaling pathway.

Overcoming therapeutic failure in osteosarcoma via Apatinib-encapsulated hydrophobic poly(ester amide) nanoparticles.

Anti-angiogenic tyrosine kinase inhibitors (TKIs) have been proved to be effective in prolonging progression-free survival in advanced osteosarcoma. However, osteosarcoma stem-like cells persist for a long time and ultimately cause disease recurrence and therapy resistance. Here, we reveal that inefficient accumulation of Apatinib, an anti-angiogenic TKI, induces the expression of ribosome-associated genes in osteosarcoma, and confers apoptosis resistance. An engineered nanoscale delivery system based on hydrophobic poly(ester amide) has been established to effectively deliver Apatinib to improve the treatment. Notably, the considerable uptake by osteosarcoma cells enables this nanodrug to distribute increasingly inside the tumor. Furthermore, the delivered nano-Apatinib can suppress osteosarcoma stemness and enhance osteosarcoma stem-like cell apoptosis, and overcomes the crucial bottleneck of the unfavorable stem-like cell residue for TKI therapy. Importantly, nano-Apatinib significantly inhibits the osteosarcoma stem-like cell-derived tumor growth in contrast with free Apatinib, with minimal side effects. These results suggest that this Apatinib-loaded nano delivery system may serve as a promising strategy to solve the issue of TKI therapeutic resistance existing in advanced osteosarcoma.

JMJD3 regulates CD4 T cell trafficking by targeting actin cytoskeleton regulatory gene Pdlim4.

Histone H3K27 demethylase, JMJD3 plays a critical role in gene expression and T-cell differentiation. However, the role and mechanisms of JMJD3 in T cell trafficking remain poorly understood. Here we show that JMJD3 deficiency in CD4+ T cells resulted in an accumulation of T cells in the thymus, and reduction of T cell number in the secondary lymphoid organs. We identified PDLIM4 as a significantly down-regulated target gene in JMJD3-deficient CD4+ T cells by gene profiling and ChIP-seq analyses. We further showed that PDLIM4 functioned as an adaptor protein to interact with S1P1 and filamentous actin (F-actin), thus serving as a key regulator of T cell trafficking. Mechanistically, JMJD3 bound to the promoter and gene body regions of Pdlim4 gene and regulated its expression by interacting with zinc finger transcription factor KLF2. Our findings have identified Pdlim4 as a JMJD3 target gene that affects T-cell trafficking by cooperating with S1P1, and provided insights into the molecular mechanisms by which JMJD3 regulates genes involved in T cell trafficking.

Clinical Application of 25-MHz Ultrasound Biomicroscopy for Lens Opacity Degree Measurements in Phacoemulsification.

PURPOSE: To evaluate the correlation between lens opacity degrees and phacoemulsification cumulated dissipated energy (CDE) values in patients with age-related cataract by applying 25-MHz panoramic ultrasound biomicroscopy (UBM). METHODS: This observational study was conducted in 227 patients (294 eyes) with age-related cataract. Patient ages ranged from 45 to 91 years. According to the lens images acquired by 25-MHz UBM, the objective indexes of lens opacity degrees were determined by using the ImageJ software. The correlation between lens opacity degrees (pixel units) and CDE values of phacoemulsification were mainly analyzed. RESULTS: The means of measurements were as follows: preoperative LogMAR corrected distance visual acuity, anterior chamber depth, and central lens thickness was 1.10 ± 0.61, 2.52 ± 0.51, and 4.34 ± 0.60 mm, respectively. The mean 25-MHz UBM-measured lens opacity degree was 101.30 ± 19.70 pixel units, and the mean CDE value was 9.74 ± 9.10. There was a linear correlation between pixel units and the CDE value, as well as LogMAR corrected distance visual acuity (r = 0.38 and 0.50, respectively; both P < 0.05). Age correlated with anterior chamber depth and lens thickness (r = -0.18 and 0.16, respectively; both P < 0.05) but not with pixel units (r = -0.08, P > 0.05). CONCLUSION: The 25-MHz UBM has significant advantages in displaying the opacity feature of age-related cataract. The 25-MHz UBM combined with ImageJ software can be used to evaluate the opacity degree of age-related cataract quantitatively and may help predict the phacoemulsification parameters in cataract surgery. TRANSLATIONAL RELEVANCE: Combination of the lens ultrasonic image and image analysis software enables researchers to evaluate lens opacity degree quantitatively and predict the parameters of phacoemulsification surgery.

Expression of New York esophageal squamous cell carcinoma 1 and its association with Foxp3 and indoleamine-2,3-dioxygenase in microenvironment of nonsmall cell lung cancer.

Lung cancer is one of the most prevalent and fatal cancer worldwide. The traditional treatments including surgery, radiotherapy, chemotherapy and targeted therapy are not satisfactory because of severe side effects and/or relapse. Genetically engineered T-cell-based immunotherapy for malignant cancer shows promise in recent clinical trials. T-cell receptor (TCR)-engineered T cells targeting New York esophageal squamous cell carcinoma 1 (NY-ESO-1) have been employed in a number of clinical trials for late stage melanoma, synovial sarcoma, multiple myeloma and other malignancies. Owing to the significant efficacy and controllable side effect, NY-ESO-1 has been considered as one of the most ideal TCR-engineered T cell therapy (TCR-T) cell target for solid tumors, including nonsmall cell lung cancer (NSCLC). However, the incidence of NY-ESO-1 expression and its relationship with immunosuppressive microenvironment of NSCLC are largely unclear. In this study, we analyzed the expression of NY-ESO-1 and two key immune regulators, Forkhead box P3 (Foxp3) and indoleamine-2,3-dioxygenase (IDO), in 156 NSCLC specimens by immunohistochemistry. Our results showed that NY-ESO-1 positive rate is 28.1% (44/156) and significantly higher in distal metastasis (P = 0.012) and late stage (P = 0.019) NSCLC patients. In addition, we found that NY-ESO-1 expression was positively associated with Foxp3 level but not IDO. These findings implied the potential role of NY-ESO-1 in tumor immune escape of NSCLC and indicated the requirement to remove Treg cells in TCR-T cell therapy for NSCLC patients.

Treatment of metastatic non-small cell lung cancer with NY-ESO-1 specific TCR engineered-T cells in a phase I clinical trial: A case report.

This article presented a case of a human leukocyte antigen (HLA)-A2-positive patient with advanced cancer/testis antigen New York esophageal squamous cell carcinoma-1 (NY-ESO-1) expressing lung adenocarcinoma (LADC) who received adoptive cell therapy of T cell receptor engineered-T cells (TCR-T cells) targeting the cancer-testis antigen NY-ESO-1. The appropriate clinical and laboratory assessments were conducted to investigate the safety and efficacy of this therapy for this lung cancer patient. The patient had a clinical response to and was well-tolerated with this therapy in the clinical trial. In addition, a preliminary evaluation of the safety of NY-ESO-1 TCR-T cell therapy was performed in four patients with non-small cell lung cancer (NSCLC) enrolled in a clinical trial. It was well-tolerated and did not observe any serious adverse events post-infusion. Fever, anemia, and a decrease in white blood cell count were common adverse events, which were likely due to the TCR-T cell therapy. Two patients had clinical responses to NY-ESO-1 TCR-T cell therapy, including the 44-year-old female patient with LADC, who achieved a short-term partial response for 4 months, improved in Karnofsky performance status, and had a recovery of drug sensitivity. This suggests that TCR-T cell therapy targeting NY-ESO-1 antigen may be beneficial for HLA-A2-positive late-stage patients with NY-ESO-1-expressing NSCLC.

Optimal incision sites to reduce corneal aberration variations after small incision phacoemulsification cataract surgery.

AIM: To analyze the effect of steep meridian small incision phacoemulsification cataract surgery on anterior, posterior and total corneal wavefront aberration. METHODS: Steep meridian small incision phacoemulsification cataract surgery was performed in age-related cataract patients which were divided into three groups according to the incision site: 12 o'clock, 9 o'clock and between 9 and 12 o'clock (BENT) incision groups. The preoperative and 3-month postoperative root mean square (RMS) values of anterior, posterior and total corneal wavefront aberration including coma, spherical aberration, and total higher-order aberrations (HOAs), were measured by Pentacam scheimpflug imaging. The mean preoperative and postoperative corneal wavefront aberrations were documented. RESULTS: Total corneal aberration and total lower-order aberrations decreased significantly in three groups after operation. RMS value of total HOAs decreased significantly postoperatively in the 12 o'clock incision group (P<0.001). Corneal spherical aberration was statistically significantly lower after steep meridian small incision phacoemulsification cataract surgery in BENT incision group (P<0.05) and Pearson correlation analysis indicated that spherical aberration changes had no significant relationship with total astigmatism changes in all three corneal incision location. CONCLUSION: Corneal incision of phacoemulsification cataract surgery can affect corneal wavefront aberration. The 12 o'clock corneal incision eliminated more HOAs and the spherical aberrations decreased in BENT incision group obviously when we selected steep meridian small incision. Cataract lens replacement using wavefront-corrected intraocular lens combined with optimized corneal incision site would improve ocular aberration results.

The relationship between disability-adjusted life years of cataracts and ambient erythemal ultraviolet radiation in China.

BACKGROUND: Cataracts are one of the major public health problems worldwide. Ultraviolet radiation (UVR) is one of the risk factors for cataract development. We analyzed the relationship between disability-adjusted life year (DALY) rates of cataracts and UVR exposure in China. METHODS: DALY rates of cataracts and UVR exposure in 31 regions of China were calculated based on data from the Second China National Sample Survey on Disability and the United States' National Aeronautics and Space Administration database. The relationship between the DALY rates of cataracts and UVR was estimated by Spearman rank correlation analysis and linear regression analysis. RESULTS: The elderly (≥ 65 years) had higher DALY rates of cataracts than the whole population. The DALY rate of cataracts in the agricultural population was higher than that observed in the non-agricultural population. The DALY rates of cataracts were positively associated with UVR The DALY rates of cataracts in regions with higher UVR were higher than those in regions with lower UVR. An increase in the daily ambient erythemal UVR of 1000 J/m(2) was associated with an increase in the DALY rates of cataracts by 92 DALYs/100 000 (R(2) = 0.676) among the whole population, 34 DALYs/100 000 among the population < 65 years old (R(2) = 0.423), 607 DALYs/100 000 among the population aged 65-74 years (R(2) = 0.617), and by 1342 DALYs/100 000 among the population ≥ 75 years old (R(2) = 0.758). CONCLUSIONS: DALY rates of cataracts increased with increases in UVR exposure in 31 regions of China. Greater exposure to UVR increases the disease burden of cataracts in the whole population, especially in the elderly and among the agricultural population.

The distribution of biologically effective UV spectral irradiances received on a manikin face that cause erythema and skin cancer.

Solar ultraviolet (UV) radiation is a major cause of erythema and skin cancer in humans and the face is one of the highest risk sites. Biologically effective UV irradiation (UVBE) is wavelength-dependent, and risk assessment has been demonstrated based on the value of the received UV radiation. Therefore, this study measured the face skin exposure to UV spectral irradiance using a spectroradiometer and a head manikin, which were weighted by action spectra to calculate the UVBE that causes erythema (UVBEery), non-melanoma (UVBEnon-mel), human squamous cell cancer (UVBEh-SCC), and DNA damage (UVBEDNA-d). We determined that the biologically effective UVB and UVA irradiances on clear sky days had peak values at 65-73° SEA (8-9 UVI) and 55-68° SEA (6-7 UVI), respectively. In the 10-30° SEA range, the highly skin-damaging wavelengths were all observed at 300 nm. However, in the 30-60°, 60-81°, and 10-81° SEA ranges, the highly skin damaging wavelengths were 300 nm, 304 nm and 300 nm for UVBEery, respectively; 304 nm, 306 nm and 304 nm for UVBEnon-mel, respectively; all 305 nm for UVBEh-SCC, and two small peaks at 302 nm and 312 nm for UVBEDNA-d.

The relationship between the disability prevalence of cataracts and ambient erythemal ultraviolet radiation in China.

In Western countries, ultraviolet (UV)-induced skin cancer has been studied extensively regarding the high incidence of skin cancers in the white population; however, for people of color, cataracts are the main public health issue in relation to increased ambient ultraviolet radiation (UVR). To our knowledge, few studies have been conducted examining the relationship between cataracts and ambient UVR in China. In this study, we aimed to explore the relationship between and the factors influencing the disability prevalence of cataracts and annual ambient erythemal UVR exposure in 31 regions of China. The data used to determine the disability prevalence of cataracts was obtained from the Second China National Sample Survey on Disability. The regional annual erythemal UVR was calculated using Geographic Information System (GIS) methods based on data from the National Aeronautics and Space Administration (NASA) database. The relationship between the disability prevalence of cataracts and the annual ambient erythemal UVR was examined by using logistic regression. Both the age-standardized disability prevalence of cataracts (OR = 3.97, 95%CI 1.30-12.13, per 100KJ/m(2) increase in annual ambient erythemal UVR) and the disability prevalence of cataracts among a population ≥65 years old (OR = 3.97, 95%CI 1.30-12.13, per 100KJ/m(2) increase in annual ambient erythemal UVR) were higher in association with higher ambient erythemal UVR. Regions with higher urbanization and educational levels had lower disability prevalence of cataracts. We found positive associations of the age-standardized disability prevalence of cataracts and the disability prevalence of cataracts among a population ≥65 years old with ambient erythemal UVR in 31 regions of China.

Ground-based observations of ultraviolet and total solar radiation in Shenyang, northeast China.

OBJECTIVE: This work explores the diurnal variation of Solar ultraviolet radiation (UVR) and total solar radiation (TSR) in northeast China, using daily observations of UVR and TSR in Shenyang. METHODS: UVR and TSR measurements were carried out from March 1st, 2006 to December 31st, 2009 in Shenyang, Liaoning province, China (41°51' N, 123°27' E). RESULTS: Both TSR and UVR showed seasonal variation, reaching the highest levels in summer and the lowest in winter. They showed the greatest fluctuation in summer and autumn. The irradiance of TSR and UVR on clear days around the equinoxes and solstices increased substantially compared with the mean seasonal irradiance, especially in autumn. The whole day accumulated dose of UVR in winter was far less than that during the middle part of a summer day (i.e. between 10:00 and 14:00). It was also less than the accumulated summer dose of morning and afternoon (i.e. between 8:00 and 10:00 and 14:00 and 16:00). CONCLUSION: The instant irradiance and daily accumulated amount of UVR are low in Shenyang, especially in autumn and winter. Thus concern about the health effects arising because shortage of UVR in northeast China is warranted.

Diurnal variations in solar ultraviolet radiation on horizontal and vertical plane.

BACKGROUND: In general, measurements of solar ultraviolet (UV) radiation are related to horizontal surfaces. While the humans walking and standing outdoors expose to the natural solar UV radiation, their eyes, cheeks, extremities, trunks, or many other anatomical sites are close to vertical plane and random orient to different directions. In this study, we characterized the diurnal variations in solar UV on horizontal and vertical plane which may be helpful to obtain more relevant information on UV exposure of humans. METHODS: The UV exposure on vertical and horizontal plane were measured using Solar-UV Sensors in Shenyang (41°51″N, 123°27″E) and Sanya (18°19'N, 109°42'E), PR China. RESULTS: As the well known, the diurnal variations in solar UV on horizontal plane in a sunny day exhibited unimodal distributions, reached a single UV peak exposure at around solar noon. However, the diurnal variations on vertical plane presented bimodal distributions, with two peaks in summer in Shenyang and Sanya, and a unimodal distribution in winter in Shenyang. In spring and autumn in Shenyang, the UV exposure around noon were slightly flat with no significant peaks but relative high. When the Solar Elevation Angle (SEA) is about 40°, the vertical plane may potentially receiving maximal unweighted total solar UV radiation exposures. CONCLUSION: The results potentially showed that the protection of some vertical and near-vertical anatomical sites of human body from high UV exposure should not only focused on the periods of before and after noon especially in high SEA places.