Cathepsin S (CTSS) in IgA nephropathy: an exploratory study on its role as a potential diagnostic biomarker and therapeutic target.

Introduction: IgA nephropathy (IgAN), a prevalent form of glomerulonephritis globally, exhibits complex pathogenesis. Cathepsins, cysteine proteases within lysosomes, are implicated in various physiological and pathological processes, including renal conditions. Prior observational studies have suggested a potential link between cathepsins and IgAN, yet the precise causal relationship remains unclear. Methods: We conducted a comprehensive bidirectional and multivariable Mendelian randomization (MR) study using publicly available genetic data to explore the causal association between cathepsins and IgAN systematically. Additionally, immunohistochemical (IHC) staining and enzyme-linked immunosorbent assay (ELISA) were employed to evaluate cathepsin expression levels in renal tissues and serum of IgAN patients. We investigated the underlying mechanisms via gene set variation analysis (GSVA), gene set enrichment analysis (GSEA), and immune cell infiltration analysis. Molecular docking and virtual screening were also performed to identify potential drug candidates through drug repositioning. Results: Univariate MR analyses demonstrated a significant link between increased cathepsin S (CTSS) levels and a heightened risk of IgAN. This was evidenced by an odds ratio (OR) of 1.041 (95% CI=1.009-1.073, P=0.012) as estimated using the inverse variance weighting (IVW) method. In multivariable MR analysis, even after adjusting for other cathepsins, elevated CTSS levels continued to show a strong correlation with an increased risk of IgAN (IVW P=0.020, OR=1.037, 95% CI=1.006-1.069). However, reverse MR analyses did not establish a causal relationship between IgAN and various cathepsins. IHC and ELISA findings revealed significant overexpression of CTSS in both renal tissues and serum of IgAN patients compared to controls, and this high expression was unique to IgAN compared with several other primary kidney diseases such as membranous nephropathy, minimal change disease and focal segmental glomerulosclerosis. Investigations into immune cell infiltration, GSEA, and GSVA highlighted the role of CTSS expression in the immune dysregulation observed in IgAN. Molecular docking and virtual screening pinpointed Camostat mesylate, c-Kit-IN-1, and Mocetinostat as the top drug candidates for targeting CTSS. Conclusion: Elevated CTSS levels are associated with an increased risk of IgAN, and this enzyme is notably overexpressed in IgAN patients' serum and renal tissues. CTSS could potentially act as a diagnostic biomarker, providing new avenues for diagnosing and treating IgAN.

Solitary splenic tuberculosis: A case report.

BACKGROUND: Solitary splenic tuberculosis (TB) is unusual and rarely reported. Whether splenic TB is best treated surgically is still controversial. We describe a 73-year-old man with solitary splenic TB and no extrapulmonary TB. CASE SUMMARY: We report the case of a 73-year-old man with solitary splenic TB who complained of emaciation and fatigue. Abdominal computed tomography (CT) images suggested a splenic space-occupying lesion. We then performed a CT-guided splenic biopsy. The postoperative pathological examination revealed splenic TB. The patient took quadruple anti-TB medication. After 1 year, the patient recovered his normal weight and had no feeling of fatigue, and the splenic lesion had shrunk significantly. CONCLUSION: If patients receive combined, appropriate, regular, full-time anti-TB treatment, solitary splenic TB may be cured.

Phase transition and remodeling complex assembly are important for SS18-SSX oncogenic activity in synovial sarcomas.

Oncoprotein SS18-SSX is a hallmark of synovial sarcomas. However, as a part of the SS18-SSX fusion protein, SS18's function remains unclear. Here, we depict the structures of both human SS18/BRG1 and yeast SNF11/SNF2 subcomplexes. Both subcomplexes assemble into heterodimers that share a similar conformation, suggesting that SNF11 might be a homologue of SS18 in chromatin remodeling complexes. Importantly, our study shows that the self-association of the intrinsically disordered region, QPGY domain, leads to liquid-liquid phase separation (LLPS) of SS18 or SS18-SSX and the subsequent recruitment of BRG1 into phase-separated condensates. Moreover, our results show that the tyrosine residues in the QPGY domain play a decisive role in the LLPS of SS18 or SS18-SSX. Perturbations of either SS18-SSX LLPS or SS18-SSX's binding to BRG1 impair NIH3T3 cell transformation by SS18-SSX. Our data demonstrate that both LLPS and assembling into chromatin remodelers contribute to the oncogenic activity of SS18-SSX in synovial sarcomas.

Overexpression of FOXD2-AS1 enhances proliferation and impairs differentiation of glioma stem cells by activating the NOTCH pathway via TAF-1.

Emerging data have highlighted the importance of long noncoding RNAs (lncRNAs) in exerting critical biological functions and roles in different forms of brain cancer, including gliomas. In this study, we sought to investigate the role of lncRNA FOXD2 adjacent opposite strand RNA 1 (FOXD2-AS1) in glioma cells. First, we used sphere formation assay and flow cytometry to select U251 glioma stem cells (GSCs). Then, we quantified the expression of lncRNA FOXD2-AS1, TATA-box binding protein associated factor 1 (TAF-1) and NOTCH1 in glioma tissues and GSCs, as well as the expression of GSC stem markers, OCT4, SOX2, Nanog, Nestin and CD133 in GSCs. Colony formation assay, sphere formation assay, and flow cytometry were used to evaluate GSC stemness. Next, the correlations among lncRNA FOXD2-AS1, TAF-1 and NOTCH1 were investigated. LncRNA FOXD2-AS1, TAF-1 and NOTCH1 were found to be elevated in glioma tissues and GSCs, and silencing lncRNA FOXD2-AS1 inhibited stemness and proliferation, while promoting apoptosis and differentiation of GSCs. LncRNA FOXD2-AS1 overexpression also led to increased NOTCH1 by recruiting TAF-1 to the NOTCH1 promoter region, thereby promoting stemness and proliferation, while impairing cell apoptosis and differentiation. Mechanistically, lncRNA FOXD2-AS1 elevation promoted glioma in vivo by activating the NOTCH signalling pathway via TAF-1 upregulation. Taken together, the key findings of our investigation support the proposition that downregulation of lncRNA FOXD2-AS1 presents a viable and novel molecular candidate for improving glioma treatment.

Role and Mechanism of lncRNA-pvt1 in the Pathogenesis of Acute Lymphoblastic Leukemia in Children.

Objective: To investigate the role and mechanism of lncRNA-pvt1 in the pathogenesis of childhood acute lymphoblastic leukemia (ALL). Methods: The expression of lncRNA-pvt1 in bone marrow tissues of ALL patients after initial diagnosis and complete remission was detected by RT-PCR to explore its possible involvement in the pathogenesis of ALL. The proliferation and apoptosis of Jurkat cells transfected with lncRNA-pvt1 were observed by MTT and flow cytometry. Results: lncRNA-pvt1 expression was upregulated in bone marrow of ALL patients. Knockdown of lncRNA-pvt1 inhibited Jurkat cell proliferation and increased its apoptosis rate. Conclusion: Silencing lncRNA-pvt1 expression can inhibit the development of ALL.

Palmitate induces fat accumulation via repressing FoxO1-mediated ATGL-dependent lipolysis in HepG2 hepatocytes.

Obesity is closely associated with non-alcoholic fatty liver disease (NAFLD), and elevated serum palmitate is the link between obesity and excessive hepatic lipid accumulation. Forkhead box O-1 (FoxO1) is one of the FoxO family members of transcription factors and can stimulate adipose triglyceride lipase (ATGL) and suppress its inhibitor G0/G1 switch gene 2 (G0S2) expression in the liver. However, previous researches have also shown conflicting results regarding the role of FoxO1 in hepatic lipid accumulation. We therefore examined the role of FoxO1 as a downstream suppressor to palmitate-stimulated hepatic steatosis. Palmitate significantly promoted lipid accumulation but inhibited lipid decomposition in human HepG2 hepatoma cells. Palmitate also significantly reduced FoxO1, ATGL and its activator comparative gene identification-58 (CGI-58) expression but increased peroxisome proliferator-activated receptorγ (PPARγ) and its target gene G0S2 expression. FoxO1 overexpression significantly increased palmitate-inhibited ATGL and CGI-58 expression but reduced palmitate-stimulated PPARγ and its target gene G0S2 expression. FoxO1 overexpression also inhibited lipid accumulation and promoted lipolysis in palmitate-treated hepatocytes. Overall, these results indicate that FoxO1-mediated ATGL-dependent lipolysis may be an effective molecular mechanism in protecting hepatocytes from palmitate-induced fat accumulation.

Swimming exercise activates aortic autophagy and limits atherosclerosis in ApoE-/- mice.

BACKGROUND: The aim of this study was to investigate the beneficial effect of swimming exercise on autophagy and atherosclerosis in mice aorta, so as to clarify the possible causal relationship between autophagy activation and atherosclerosis. METHODS: The body weight was monitored regularly. Hematoxylin-eosin staining and Oil Red O staining was conducted to observe vascular morphology and plaque burden respectively. The levels of serum total cholesterol (TC), triglyceride (TG), soluble intercellular adhesion molecule-1 (sICAM-1), matrix metalloproteinase-9 (MMP-9) and interleukin-6 (IL-6) was examined via Enzyme-linked immu-nosorbent assays (ELISA). The mRNA expression level of autophagy markers, including LC3 and Beclin-1, was examined by real-time quantitative polymerase chain reaction (RT-PCR). The expressions of LC3-II/LC3-I and Beclin-1 are detected by Western blotting and immunohistochemistry. RESULTS: Compared with the model group, long-term swimming exercise decreased the weight gain of ApoE-/- mice, improved the structural disorder of artery, reduced the load of atherosclerotic lesion, and attenuated the concentrations of serum TC, TG, sICAM-1, MMP-9, and IL-6. In addition, the expression of autophagy markers LC3 and Beclin-1 increased significantly at the mRNA and protein levels. CONCLUSION: Long-term swimming exercise could activate the autophagy and reduce atherosclerotic lesion in the aorta of ApoE-/- mice. Autophagy activation may be one of the mechanisms by which atherosclerosis is improved through exercise.

The Role of Akt2 in the Protective Effect of Fenofibrate against Diabetic Nephropathy.

Fenofibrate (FF) protects against diabetic nephropathy (DN) in type 1 diabetic (T1D) mice by upregulating the expression of fibroblast growth factor 21 (FGF21), leading to the activation of the Akt-mediated Nrf2 antioxidant pathways. Here, we examined which isoforms of Akt contribute to FF activation of FGF21-mediated renal protection by examining the phosphorylation and expression of three isoforms, Akt1, Akt2, and Akt3. T1D induced by a single intraperitoneal dose of streptozotocin (STZ) resulted in reduced phosphorylation of one isoform, Akt2, but FF treatment increased renal Akt2 phosphorylation in these and normal mice, suggesting a potential and specific role for renal Akt2 in FF protection against T1D. This was further confirmed using in vitro cultured HK-2 human kidney tubule cells exposed to high glucose (HG) with siRNA silencing of the Akt2 gene and STZ-induced diabetic Akt2-knockout mice with and without 3-month FF treatment. In normal HK-2 cells exposed to HG for 24 hours, FF completely prevented cell death, reduced total Akt expression and glycogen synthase kinase (GSK)-3ß phosphorylation, increased nuclear accumulation of Fyn, and reduced nuclear Nrf2 levels. These positive effects of FF were partially abolished by silencing Akt2 expression. Similarly, FF abolished T1D-induced renal oxidative stress, inflammation, and renal dysfunction in wild-type mice, but was only partially effective in Akt2-KO mice. Furthermore, FF treatment stimulated phosphorylation of AMPKα, an important lipid metabolism mediator, which in parallel with Akt2 plays an important role in FF protection against HG-induced HK-2 cells oxidative stress and damage. These results suggest that FF protects against DN through FGF21 to activate both Akt2/GSK-3ß/Fyn/Nrf2 antioxidants and the AMPK pathway. Therefore, FF could be repurposed for the prevention of DN in T1D patients.

Sex differences in progression of diabetic nephropathy in OVE26 type 1 diabetic mice.

AIMS: OVE26 mice (FVB background), genetically overexpressing calmodulin in pancreatic beta cells, develop early onset type 1 diabetes, leading to progressive diabetic nephropathy (DN), with features of established human DN. The role of gender in characteristics of renal lesions has remained unexplored. METHODS: Male and female OVE26 mice were compared to age and sex matched wild-type, nondiabetic FVB mice at ages of 4, 12, 24 and 36 weeks. Nephropathy was examined by measuring urine albumin-to-creatinine ratio, histopathology, expression of pathological markers and immunochemistry in the same cohort of mice. RESULTS: Progression of diabetic kidney disease was evident first in the OVE26 glomerulus, initially as mesangial matrix expansion at 4 weeks followed by loss of podocytes, glomerular volume expansion and severe albuminuria at 12 weeks. Tubule dilation and initiation of interstitial fibrosis did not become significant until 24 weeks. T-lymphocyte infiltration into the renal parenchyma appeared at 36 weeks. OVE26 female mice developed more advanced DN than male OVE26 mice, such as more severe albuminuria, greater podocyte loss, additional fibrosis and significantly more inflammatory cell infiltration. The female OVE26 mice had lowest level of plasma estradiol in all 36 weeks old mice, as well as renal estrogen receptors. CONCLUSIONS: This demonstration of the role of gender, combined with the detailed characterization of DN progression illustrates the value of OVE26 mice for understanding gender effects on DN and provides the basis for researchers to better select the age and sex of OVE26 mice in future studies of type 1 DN. RESEARCH IN CONTEXT: What is already known about this subject? What is the key question? What are the new findings? How might this impact on clinical practice in the foreseeable future?

Clopidogrel Reduces Fibronectin Accumulation and Improves Diabetes-Induced Renal Fibrosis.

Hyperglycemia-induced renal fibrosis causes end-stage renal disease. Clopidogrel, a platelet inhibitor, is often administered to decrease cardiovascular events in diabetic patients. We investigated whether clopidogrel can reduce diabetes-induced renal fibrosis in a streptozotocin-induced type 1 diabetes murine model and fibronectin involvement in this protective response. Diabetic and age-matched controls were sacrificed three months after the onset of diabetes, and additional controls and diabetic animals were further treated with clopidogrel or vehicle for three months. Diabetes induced renal morphological changes and fibrosis after three months. Clopidogrel, administered during the last three months, significantly decreased blood glucose, collagen and fibronectin expression compared to vehicle-treated diabetic mice. Diabetes increased TGF-ß expression, inducing fibrosis via Smad-independent pathways, MAP kinases, and Akt activation at three months but returned to baseline at six months, whereas the expression of fibronectin and collagen remained elevated. Our results suggest that activation of TGF-ß, CTGF, and MAP kinases are early profibrotic signaling events, resulting in significant fibronectin accumulation at the early time point and returning to baseline at a later time point. Akt activation at the three-month time point may serve as an adaptive response in T1D. Mechanisms of clopidogrel therapeutic effect on the diabetic kidney remain to be investigated as this clinically approved compound could provide novel approaches to prevent diabetes-induced renal disease, therefore improving patients' survival.

Myosin Heavy Chain 10 (MYH10) Gene Silencing Reduces Cell Migration and Invasion in the Glioma Cell Lines U251, T98G, and SHG44 by Inhibiting the Wnt/ß-Catenin Pathway.

BACKGROUND The myosin heavy chain 10 or MYH10 gene encodes non-muscle myosin II B (NM IIB), and is involved in tumor cell migration, invasion, extracellular matrix (ECM) production, and epithelial-mesenchymal transition (EMT). This study aimed to investigate the effects of the MYH10 gene on normal human glial cells and glioma cell lines in vitro, by gene silencing, and to determine the signaling pathways involved. MATERIAL AND METHODS The normal human glial cell line HEB, and the glioma cell lines, U251, T98G, and SHG44 were studied. Plasmid transfection silenced the MYH10 gene. The cell counting kit-8 (CCK-8) assay evaluated cell viability. Cell migration and invasion were evaluated using scratch and transwell assays. Western blot measured the protein expression levels, and quantitative real-time polymerase chain reaction (qRT-PCR) was used to detect the mRNA expression levels, for MYH10, metastasis-associated protein 1 (MTA-1), matrix metalloproteinase (MMP)-1, MMP-9, tissue inhibitor of metalloproteinases 2 (TIMP2), collagen 1, E-cadherin, vimentin, Wnt3a, ß-catenin, and cyclin D1. RESULTS The MYH10 gene was overexpressed in U251, T98G, and SHG44 cells. MYH10 expression was down-regulated following siMYH10 plasmid interference, which also inhibited glioma cell migration and invasion. MYH10 gene silencing resulted in reduced expression of MTA-1, MPP-2, MMP-9 and vimentin, and increased expression of TIMP-2, E-cadherin and collagen 1 at the protein and mRNA level, and inhibited the Wnt/ß-catenin pathway. CONCLUSIONS In human glioma cell lines, silencing the MYH10 gene reduced cell migration and invasion, by inhibiting the Wnt/ß-catenin pathway, which may regulate the ECM and inhibit EMT in human glioma.

The beneficial effects of Zn on Akt-mediated insulin and cell survival signaling pathways in diabetes.

Zinc is one of the essential trace elements and participates in numerous physiological processes. Abnormalities in zinc homeostasis often result in the pathogenesis of various chronic metabolic disorders, such as diabetes and its complications. Zinc has insulin-mimetic and anti-diabetic effects and deficiency has been shown to aggravate diabetes-induced oxidative stress and tissue injury in diabetic rodent models and human subjects with diabetes. Akt signaling pathway plays a central role in insulin-stimulated glucose metabolism and cell survival. Anti-diabetic effects of zinc are largely dependent on the activation of Akt signaling. Zn is also an inducer of metallothionein that plays important role in anti-oxidative stress and damage. However, the exact molecular mechanisms underlying zinc-induced activation of Akt signaling pathway remains to be elucidated. This review summarizes the recent advances in deciphering the possible mechanisms of zinc on Akt-mediated insulin and cell survival signaling pathways in diabetes conditions. Insights into the effects of zinc on epigenetic regulation and autophagy in diabetic nephropathy are also discussed in the latter part of this review.

Metallothionein Is Downstream of Nrf2 and Partially Mediates Sulforaphane Prevention of Diabetic Cardiomyopathy.

We have reported that sulforaphane (SFN) prevented diabetic cardiomyopathy in both type 1 and type 2 diabetes (T2DM) animal models via the upregulation of nuclear transcription factor erythroid 2-related factor 2 (Nrf2) and metallothionein (MT). In this study, we tested whether SFN protects the heart from T2DM directly through Nrf2, MT, or both. Using Nrf2-knockout (KO), MT-KO, and wild-type (WT) mice, T2DM was induced by feeding a high-fat diet for 3 months followed by a small dose of streptozotocin. Age-matched controls were given a normal diet. Both T2DM and control mice were then treated with or without SFN for 4 months by continually feeding a high-fat or normal diet. SFN prevented diabetes-induced cardiac dysfunction as well as diabetes-associated cardiac oxidative damage, inflammation, fibrosis, and hypertrophy, with increases in Nrf2 and MT expressions in the WT mice. Both Nrf2-KO and MT-KO diabetic mice exhibited greater cardiac damage than WT diabetic mice. SFN did not provide cardiac protection in Nrf2-KO mice, but partially or completely protected the heart from diabetes in MT-KO mice. SFN did not induce MT expression in Nrf2-KO mice, but stimulated Nrf2 function in MT-KO mice. These results suggest that Nrf2 plays the indispensable role for SFN cardiac protection from T2DM with significant induction of MT and other antioxidants. MT expression induced by SFN is Nrf2 dependent, but is not indispensable for SFN-induced cardiac protection from T2DM.

Potential health benefits of controlling dust emissions in Beijing.

Although the adverse impact of fine particulate matter (i.e., PM2.5) on human health has been well acknowledged, little is known of the health effects of its specific constituents. Over the past decade, the annual average dust concentrations in Beijing were approximately ∼14 µg m(-3), a value that poses a great threat to the city's 20 million residents. In this study, we quantify the potential long-term health damages in Beijing resulting from the dust exposure that occurred from 2000 to 2011. Each year in Beijing, nearly 4000 (95% CI: 1000-7000) premature deaths may be associated with long-term dust exposure, and ∼20% of these deaths are attributed to lung cancer. A decomposition analysis of the inter-annual variability of premature deaths in Beijing indicates that dust concentrations determine the year-to-year tendency, whereas population growth and lung cancer mortality rates drive the increasing tendency of premature death. We suggest that if Beijing takes effective measures towards reducing dust concentrations (e.g., controlling the resuspension of road dust and the fugitive dust from construction sites) to a level comparable to that of New York City's, the associated premature deaths will be significantly reduced. This recommendation offers "low-hanging fruit" suggestions for pollution control that would greatly benefit the public health in Beijing.

Metallothionein plays a prominent role in the prevention of diabetic nephropathy by sulforaphane via up-regulation of Nrf2.

Sulforaphane (SFN) prevents diabetic nephropathy (DN) in type 1 diabetes via up-regulation of nuclear factor (erythroid-derived 2)-like 2 (Nrf2). However, it has not been addressed whether SFN also prevents DN from type 2 diabetes or which Nrf2 downstream gene(s) play(s) the key role in SFN renal protection. Here we investigated whether Nrf2 is required for SFN protection against type 2 diabetes-induced DN and whether metallothionein (MT) is an Nrf2 downstream antioxidant using Nrf2 knockout (Nrf2-null) mice. In addition, MT knockout mice were used to further verify if MT is indispensable for SFN protection against DN. Diabetes-increased albuminuria, renal fibrosis, and inflammation were significantly prevented by SFN, and Nrf2 and MT expression was increased. However, SFN renal protection was completely lost in Nrf2-null diabetic mice, confirming the pivotal role of Nrf2 in SFN protection from type 2 diabetes-induced DN. Moreover, SFN failed to up-regulate MT in the absence of Nrf2, suggesting that MT is an Nrf2 downstream antioxidant. MT deletion resulted in a partial, but significant attenuation of SFN renal protection from type 2 diabetes, demonstrating a partial requirement for MT for SFN renal protection. Therefore, the present study demonstrates for the first time that as an Nrf2 downstream antioxidant, MT plays an important, though partial, role in mediating SFN renal protection from type 2 diabetes.

Decreased vascular endothelial growth factor expression is associated with cell apoptosis in low-dose aspirin-induced gastric mucosal injury.

BACKGROUND: The use of low-dose aspirin (LDA) has emerged as an important cause of gastrointestinal ulcers. The aim of this study was to investigate the association between LDA-induced gastric mucosal injury and the expression of vascular endothelial growth factor (VEGF) and cell apoptosis in elderly Chinese patients. METHODS: A total of 136 patients aged 60 to 80 years with LDA-induced (100 mg/d for at least 1 month) gastric mucosal injury and 48 age-matched healthy subjects were enrolled in this study. The patients were divided into a low-severity group and a high-severity group based on their modified Lanza scale scores. Biopsy specimens of gastric mucosa from all participants were subjected to immunohistochemical staining for VEGF expression and terminal deoxynucleotidyl transferase dUTP nick end labeling staining for cell apoptosis. Staining indices and apoptotic indices were applied to assess VEGF expression level and the extent of cell apoptosis. RESULTS: VEGF expression decreased significantly in the 2 patient groups, whereas the extent of cell apoptosis significantly increased compared with the control group. Furthermore, Spearman's correlation coefficients suggest that VEGF expression levels and the extent of cell apoptosis in gastric mucosae shared a significant correlation with the severity of LDA-induced gastric mucosal injury. Receiver operating characteristics analysis further confirmed these results. CONCLUSIONS: Our findings provide important clues as to the underlying molecular mechanism behind gastric mucosal injury resulting from exposure to LDA in elderly adults, and also suggest that interventions specifically targeting the pathways associated with angiogenesis and apoptosis may help facilitate the healing process.

Screening for novel protein targets of indomethacin in HCT116 human colon cancer cells using proteomics.

Non-steroidal anti-inflammatory drugs, such as indomethacin (IN), inhibit colorectal cancer (CRC) growth through cyclooxygenase (COX)-independent mechanisms, however, the precise biological mechanisms are not completely understood. The aim of the present study was to investigate new molecular factors potentially associated with IN in HCT116 human CRC cells, which do not express COX, using a proteomic approach. The total proteins from the IN-treated and untreated groups were separated by immobilized pH gradient-based two-dimensional gel electrophoresis. The differentially-expressed proteins were identified by peptide mass fingerprint (PMF) based on matrix-assisted laser desorption/ionization time of flight mass spectrometry. The PMF maps were searched in the SWISS-PROT/TrEMBL database using the PeptIdent software. Between the IN-treated and untreated groups, a total of 45 differential protein spots were detected and 15 differentially-expressed proteins were identified by PMF. IN downregulated Wnt1-inducible signaling pathway protein 1, Bcl-2-related protein A1 and mitogen-activated protein kinase, inhibited HCT116 cell growth and induced apoptosis. In conclusion, IN may exert its effects on CRC to induce HCT116 cell apoptosis and suppress growth through COX-independent pathways.

[Investigation on occupational hazards of ultraviolet light, sunscreen awareness and behaviors in Wuhan city traffic police].

OBJECTIVE: To understand the awareness of occupational hazards to ultraviolet (UV) and sunscreen awareness, protective measures in Wuhan City traffic police on duty outside. METHODS: The investigation included questionnaire survey in Wuhan City 367 traffic police on duty outside, talk with them face to face, fill in the questionnaires, and medical examine skin of exposed parts of body of them and 134 Wuhan City administration staffs. RESULTS: They understand UV harm to the human body and skin well (94.8% of them know that UV harm to skin), did not understand sun skin care and protective measures enough, and did not adopt enough sun skin care and protective measures (only 3.8% of them use sun skin care more than twice); but contrast to older persons, younger traffic police had better understanding of UV radiation damage on the human body and the skin, and sunscreen products and protective measures, paid more attention to sunscreen, and had less chance of sunburn (in the past 5 years, 18.3% of younger traffic police had sunburnt more than 3 times, but for older traffic police, the number is 30.3%). Traffic police had more skin problems than administration staffs in exposed parts of body (Traffic police face appears oily and large pores, facial pigmentation spots, face telangiectasia, deep wrinkles crude rates respectively were 73.7%, 40.4%, 36.5%, 10.4%, but for administration staffs, the numbers respectively were 26.1%, 15.7%, 15.7%, 1.5%). CONCLUSION: UV can induce skin problems in exposed parts of body. The traffic police should be enhanced the publicity and education on UV-related knowledge and occupational hazards, especially for older traffic police.