[Gastric hamartomatous inverted polyps: a clinicopathological analysis of five cases].

Objective: To investigate the endoscopic and histopathological features, diagnosis and differential diagnosis of gastric hamartomatous inverted polyp (GHIP). Methods: Five cases of GHIP were collected at the University Town Hospital of Guangdong Provincial Hospital of Chinese Medicine, Guangzhou, China, from May 2021 to May 2023. The endoscopic, pathological and immunohistochemical features of the 5 GHIP cases were analyzed. The relevant literature was reviewed. Results: There were 3 males and 2 females, aged from 49 to 60 years, with a mean age of 56 years. The lesions were located in the fundus and body of the stomach, and presented as polyps or masses under endoscopy. Microscopically, the lesions were mainly in the submucosa and consisted of lobulated or clustered gastric glandular epithelium surrounded by hyperplastic smooth muscle. In some areas, there were differentiated glandular elements mimicking the normal gastric mucosa. The irregularly dilated glandular elements in the center were lined by hyperplastic foveolar epithelium, while the glands in the periphery were fundic or pyloric glands. In addition, in some areas, the glands showed cystic expansion, disordered arrangement and lack of differentiation. The hyperplastic glandular epithelium included foveolar epithelium, fundic gland and pyloric gland. There were scattered neuroendocrine cells and smooth muscle bundles in the stroma. Immunohistochemically, the tumor cells were positive for MUC5AC, MUC6, Pepsinogen Ⅰ and H+/K+ ATPase ß, but negative for MUC2. The scattered neuroendocrine cells were positive for synaptophysin, and the desmin stain highlighted hyperplastic smooth muscle bundles. One case was classified as type 2 gastric inverted polyp, and 4 cases were classified as type 3. Conclusions: GHIP is a rare gastric polyp with unique histological features. It should be distinguished from inverted hyperplastic polyp, gastritis cystica profunda, adenomyoma, hyperplastic polyps and well-differentiated gastric tubular adenocarcinoma, etc. Improving the understanding of its pathogenesis and diagnostic features can help avoid misdiagnoses.

[Endoplasmic reticulum stress regulates autophagy and tumor necrosis factor-α secretion of RAW264.7 cells induced by silica].

Objective: To investigate the role of endoplasmic reticulum stress (ERS) in the autophagy of RAW264.7 cells induced by SiO(2) and its effect on the secretion of tumor necrosis factor-α. Methods: RAW264.7 cells stimulated by 200 µg/ml SiO(2) were used as an vitro cell model, and different treatment times of SiO(2) were used as variables. They were divided into 0 h treatment group (blank control group) , 6 h, 12 h, 24 h, and 48 h treatment group. The formation of autophagospores was detected by acridine orange and mondane-sulfonate (MDC) staining. Application of real-time quantitative PCR (Real-time PCR) to detect autophagy related molecular Beclin1 mRNA expression and protein immunoblot (Western Blotting) detecting autophagy related proteins LC3Ⅰ, LC3Ⅱ and expression of Beclin1. Real-time PCR and Western blotting were used to detect the expression of ERS specific marker BiP. Secretion of RAW 264.7 cell transforming growth factor-ß1 (TGF-ß1) and tumor necrosis factor-α (TNF-α) was detected by enzyme-linked immunosorbent assay (ELISA) . ERS inhibitors 4-PBA intervention experiment, including blank control group, SiO(2), 1 µmol/L 4-PBA+SiO(2), 10 µmol/L 4-PBA+SiO(2), 20 µmol/L 4-PBA+SiO(2) treatment group, Western blotting testing LC3Ⅰ, LC3Ⅱ and expression of Beclin1 changes. Results: Compared with the control group, SiO(2)-induced fluorescence intensity in RAW264.7 cells was significantly increased, with statistically significant differences (P<0.05) . Compared with control group, with SiO(2) processing time prolonged, LC3Ⅰ, LC3Ⅱ Beclin1 mRNA and protein expression and protein expression increased, 6 h, 24 h, the height of the differences were statistically significant (P<0.05) ; Compared with the control group, the mRNA and protein expression level of BiP reached the peak for 6 h, and the expression level in 6 h, 12 h and 24 h groups increased significantly, and the difference was statistically significant (P<0.05) . Compared with the SiO(2) stimulation group, the LC3Ⅱand Beclin 1 protein levels of RAW264.7 cells were gradually down-regulated by increasing the dose of 4-PBA. With the increase of 4-PBA concentration, the down-regulated levels were more significant, and the difference was statistically significant (P<0.05) . Compared with the SiO(2) stimulation group, the TNF-α secretion level of RAW264.7 cells significantly decreased of 1, 10, 20 µmol/L 4-PBA+SiO(2) treatment group, and the difference was statistically significant (P<0.05) . Conclusion: ERS induced by SiO(2) is involved in the secretion of autophagy and TNF-α in RAW264.7 cells.

FBXW7 inhibited cell proliferation and invasion regulated by miR-27a through PI3K/AKT signaling pathway and epithelial-to-mesenchymal transition in oral squamous cell carcinoma.

OBJECTIVE: Our purpose was to detect the molecular mechanism of F-box and WD repeat domain containing 7 (FBXW7) in regulating cell growth and metastasis of oral squamous cell carcinoma (OSCC). PATIENTS AND METHODS: Real Time-quantitative Polymerase Chain Reaction (RT-qPCR) and Western blot were applied to calculate the messenger ribonucleic acid (mRNA) and protein levels of genes and miR-27a. The proliferation and invasive abilities were measured by methyl thiazolyl tetrazolium (MTT) and transwell assays. The. Kaplan-Meier method was conducted to evaluate the 5-year overall survival of oral squamous cell carcinoma patients. RESULTS: FBXW7 was downregulated while miR-27a was upregulated in OSCC tissues and cells compared with the corresponding adjacent tissues. Downregulation of FBXW7 or upregulation of miR-27a in OSCC tissues predicted poor outcome of OSCC patients. FBXW7 suppressed the growth through the phosphatidylinositol 3-hydroxy kinase/protein kinase B (PI3K/AKT) signaling pathway in OSCC cell line HSC3. FBXW7 inhibited the invasion-mediated epithelial-mesenchymal transition (EMT) in HSC3 cells. The expression of FBXW7 was mediated by miR-27a by directly binding to the 3'-untranslated region (3'-UTR) of FBXW7 in HSC3 cells. MiR-27a reversed partial roles of FBXW7 on the proliferation and invasion in OSCC cells. CONCLUSIONS: FBXW7 was mediated by miR-27a and could inhibit the proliferation through the PI3K/AKT pathway and invasion-mediated EMT in OSCC cell line. The newly identified miR-27a/FBXW7/PI3K/AKT axis provides novel insights into the pathogenesis of osCC.

MiR-421 expression independently predicts unfavorable overall survival in patients with esophageal adenocarcinoma.

OBJECTIVE: This study aimed to examine the prognostic value of miR-421 in terms of overall survival (OS) and recurrence free survival (RFS) in ESAD and its potential regulatory network. PATIENTS AND METHODS: An in-silico analysis was conducted using data from large databases, including The Cancer Genome Atlas-Esophageal Carcinoma (TCGA-ESCA), Starbase 3.0 and GeneMANIA. RESULTS: Both esophageal adenocarcinoma (ESAD) and esophageal squamous cell carcinoma (ESCC) tissues had significantly upregulate miR-421 expression, compared with adjacent normal tissues. Upregulated miR-421 expression was associated with shorter OS, but not RFS in ESAD. In patients with ESCC, no difference in miR-421 expression was observed regards to OS or RFS status. Univariate and multivariate analysis showed that high miR-421 expression was independently associated with shorter OS (HR: 2.77, 95%CI: 1.41-5.46, p<0.01), after adjustment of histological grade and pathological stages. The predicted regulatory network of miR-421 in ESAD includes both tumor suppressors and oncogenes, which makes the role of miR-421 quite mysterious in this cancer. CONCLUSIONS: MiR-421 expression might serve as a valuable prognostic biomarker in patients with ESAD. But future molecular studies are required to explore the exact regulatory effect of it.

[The clinical characteristics, diagnosis and treatment of patients with gout in China].

Objective: To investigate the demographic characteristics, clinical features, diagnosis and treatment of patients with gout in China. Methods: Clinical data of 6 814 patients with gout from 100 hospitals in 27 provinces, municipalities or autonomous regions in China were collected and analyzed. Results: (1) The ratio of male to female in patients with gout was 14.7∶1. The mean age of onset was (48.8±15.1) years old. Mean serum urate level was (526.7±132.3) µmol/L. Patients' education background was of U-shaped distribution; (2) Hypertension was the most common comorbidity [15.8%(1 079/6 814)], then overweight or obesity [51.9%(3 536/6 814)]; (3) Alcohol and high-purine food intake were dominant triggering factors in men. The diagnosis of gout was made after onset in majority of patients with cardinal symptom arthralgia. Most patients had the disease less than 5 years, and the longer the course, the more flares in the previous year of entry; (4) Febuxostat was the mostly used urate-lowering medication. 20.7%(1 412/6 814), 10.8%(739/6 814) and 3.9%(265/6 814) of patients were followed up in 4 weeks, 12 weeks and 24 weeks after registration, and 18.9%(267/1 412), 29.1%(215/739) and 38.1%(101/265) of them reached the control target of serum urate levels, respectively. After treatment, patients' liver function was not affected, but serum creatinine levels decreased significantly. Conclusions: The proportion of gout patients who reach target serum urate level is very low. Further steps including education and survey need to be carried on.

Inhibition of JMJD6 expression reduces the proliferation, migration and invasion of neuroglioma stem cells.

Neuroglioma is the most common form of human primary malignant brain tumor, more and more studies recently showed only a small subpopulation of glioma cells which called glioma stem cells have true tumorigenic potential. Meanwhile, it was reported the overexpression of JMJD6 protein is closely involvement with the occurrence and development of multiple tumors, and JMJD6 is required for the differentiation of multiple organ, tissues and cells during embryogenesis. However, the influence of JMJD6 overexpression on neuroglioma development is unclear now. Hence, to explore the effects of JMJD6 expression on neuroglioma, we firstly isolated glioma stem cells by using CD133 MicroBead Kit, and identified via neurosphere-forming assay and Immunofluorescence staining. At the same time, we investigated the effects and mechanism of JMJD6 on the proliferation, migration and invasion of glioma stem cells through MTT, transwell assays and the Cignal finder cancer 10-pathway reporter array. The results demonstrated that the glioma neurosphere cells positively expressed stem cell marker SOX2, neuroectodermal stem cell marker Nestin, and also expressed astrocytes marker GFAP and neurons marker ß-tubulin III fter FBS-induced differentiation for a week, which proved the glioma neurosphere cells have the self-renewal and multipotential differentiation capacity. Moreover, shRNA lentiviral vector mediated knockdown of JMJD6 in glioma stem cells led to decreased proliferation, migration and invasion, the underlying molecular mechanism is related to the weaken of Wnt signaling pathway and strengthen of p53 signaling pathway.

Effect of GJB2 235delC and 30-35delG genetic polymorphisms on risk of congenital deafness in a Chinese population.

Congenital deafness is a serious and irreversible condition in humans. The GJB2 gene is implicated in the pathogenesis of autosomal recessive nonsyndromic hearing loss. Its 235delC and 30-35delG polymorphisms are reported to be associated with risk of hereditary deafness. However, the effect of the interaction between GJB2 235delC and 30-35delG and environmental factors on congenital deafness has not been described. Therefore, we performed a case-control study to investigate the influence of these polymorphisms on congenital deafness risk, and their interaction with maternal and other environmental factors in the development of this disease. Between March 2014 and May 2015, 118 patients with congenital deafness and 242 healthy controls were enrolled into our study. Compared with the GG genotype, the adjusted odds ratios (ORs) [and 95% confidence intervals (CIs)] for the 235delC GC and CC genotypes were 4.66 (1.77-13.07) and 8.28 (2.06-47.52), respectively. Individuals harboring the GC+CC genotypes were at a greatly increased risk of congenital deafness compared to those with the GG genotype (OR = 5.65, 95%CI = 2.54-13.18). However, no significant relationship was established between the 30-35delG variant and this disease. The 235delC polymorphism exhibited an interaction with use of aminoglycoside antibiotics during pregnancy in conferring susceptibility to congenital deafness (chi-square = 8.76, P = 0.003). In conclusion, our study suggests that the GJB2 235delC polymorphism, but not the 30-35delG variant, contributes to congenital deafness susceptibility in the Chinese population examined, and demonstrates an interaction with consumption of aminoglycoside antibiotics during pregnancy in exerting this effect.

The correlation of leptin/leptin receptor gene polymorphism and insulin-like growth factor-1 and their impact on childhood growth hormone deficiency.

OBJECTIVE: Growth hormone deficiency (GHD) is the most common cause for childhood dwarfism. Currently, the significance of insulin-like growth factor-1 (IGF-1) in diagnosis of GHD is still debatable. Due to the possible correlation between leptin (LEP) and GHD pathogenesis, this study investigated the gene polymorphism of LEP and its receptor (LEPR) genes, along with serum IGF-1 and LEP levels in GHD patients. This study attempted to illustrate the correlation between gene polymorphism and GHD pathogenesis. PATIENTS AND METHODS: A case-control study was performed using 180 GHD children in addition to 160 healthy controls. PCR-DNA sequencing method was employed for genotyping various polymorphism loci of LEP and LEPR genes in both GHD and healthy individuals. Serum IGF-1 and LEP levels were also determined. RESULTS: Results revealed a statistically significant difference between the levels of IGF-1 and LEP in the serum samples collected from patients in the GHD and the control groups. Both IGF-1 and LEP levels were found to be correlated with polymorphism at rs7799039 loci of LEP gene, in which GG and GA genotypes carriers had higher serum IGF-1 levels when compared to AA genotype carriers. CONCLUSIONS: GHD pathogenesis is well correlated with the LEP and IGF-1 levels in the both of which were mediated by the gene polymorphism at rs7799039 loci of LEP gene.

Serum soluble CD40 ligand levels after acute intracerebral hemorrhage.

BACKGROUND: Soluble CD40 ligand (sCD40L) is associated with inflammation. This study aimed to assess the prognostic value of sCD40L for clinical outcomes of acute intracerebral hemorrhage (ICH) patients. MATERIALS AND METHODS: The serum sCD40L levels of 110 patients and 110 age- and gender-matched healthy controls were measured using sandwich immunoassays. The relationships between serum sCD40L levels and 1-week mortality, 6-month mortality, 6-month overall survival, 6-month unfavorable outcome (modified Rankin Scale score >2), and ICH severity including hematoma volume and National Institutes of Health Stroke Scale (NIHSS) score were assessed using multivariate analysis. RESULTS: Compared with healthy controls, ICH patients had higher serum sCD40L levels. Serum sCD40L levels were correlated positively with hematoma volumes and NIHSS scores using a multivariate linear regression. Multivariate analysis results indicated that sCD40L was identified an independent predictor of 1-week mortality, 6-month mortality, 6-month unfavorable outcome and 6-month overall survival. sCD40L also showed high predictive performances for 1-week mortality, 6-month mortality and 6-month unfavorable outcome based on receiver operating characteristic curve. CONCLUSIONS: Elevated serum sCD40L levels are independently associated with ICH severity and clinical outcomes. And sCD40L has potential to be a good prognostic biomarker of ICH.

Exploring the significance of sex hormone-binding globulin examination in the treament of women with polycystic ovarian syndrome (PCOS).

OBJECTIVES: To explore whether sex hormone-binding globulin (SHBG) and free androgen index (FAI) can be seen as therapeutic effect indexes of women with polycystic ovarian syndrome (PCOS). MATERIALS AND METHODS: The body mass index (BMI), basal sexual hormones, SHBG, fasting blood glucose (FBG), and fasting insulin (FINS) were collected from 579 women with PCOS, were divided into two groups according to BMI: obese group (n = 145) and non-obese group (n = 434), according to homeostasis model assessment of insulin status (HOMA-IR). Patients were then divided into four groups: A: non-obese without insulin resistance (n = 174), B: non-obese with insulin resistance (n = 260), C: obese without insulin resistance (n = 34), D: obese with insulin resistance (n = 111). A and B groups received Diane-35 alone, C and D groups received Diane-35 plus metformin for three months. Then clomiphene citrate and HMAG were used to induce ovulation then compared ovulation rate and pregnancy outcome. RESULTS: FAI decreased significantly and SHBG increased significantly in all groups. In A group FINS and HOMA-IR increased significantly (p < 0.05), but in B and D groups FINS and HOMA-IR decreased significantly (p < 0.05). After treatment the ovulation rate in non-obese group was higher than obese group (p < 0.01). Compared with non-ovulation patients, SHBG increased significantly and FAI decreased significantly in the patient with ovulation. Regarding the pregnancy outcome, FAI decreased significantly in delivery patients than spontaneous abortion patients. Furthermore, SHBG increased significantly. CONCLUSION: It was important to check SHBG and FAI during the treatment of PCOS patient. They could be used to assess whether the treatment was effective and as a guidance of clinical medication.

SAHA attenuates sevoflurane-induced learning and memory impairments in fetal mice.

Previous studies have found that children with multiple exposures to anesthesia at an early age are at increased risk of learning and memory impairment. Sevoflurane is the most commonly used inhalational anesthetic for general anesthesia in children. Multiple exposures to sevoflurane have been shown to induce neuroinflammation, inhibit neurogenesis, and cause subsequent learning and memory impairments in fetal mice. Histone-tail acetylation has been implicated in memory formation. In this study, we employed suberanilohydroxamic acid (SAHA), an inhibitor of histone deacetylases, to treat sevoflurane-induced learning and memory impairments. Six-day-old C57BL/6 mice were exposed to sevoflurane for 2 h daily for 3 days. Morris water maze test performed to evaluate learning and memory impairments and the expression of genes related in to synaptic remodeling/plasticity, or regulated by neuronal activity or the cell cycle were detected by real-time PCR. We found that SAHA attenuated sevoflurane-induced learning and memory impairments in fetal mice. Our findings suggest that SAHA may have potential as a therapeutic agent for preventing or treating the neurotoxicity associated with anesthesia.

A model to predict 3-month mortality risk of acute-on-chronic hepatitis B liver failure using artificial neural network.

Model for end-stage liver disease (MELD) scoring was initiated using traditional statistical technique by assuming a linear relationship between clinical features, but most phenomena in a clinical situation are not linearly related. The aim of this study was to predict 3-month mortality risk of acute-on-chronic hepatitis B liver failure (ACHBLF) on an individual patient level using an artificial neural network (ANN) system. The ANN model was built using data from 402 consecutive patients with ACHBLF. It was trained to predict 3-month mortality by the data of 280 patients and validated by the remaining 122 patients. The area under the curve of receiver operating characteristic (AUROC) was calculated for ANN and MELD-based scoring systems. The following variables age (P < 0.001), prothrombin activity (P < 0.001), serum sodium (P < 0.001), total bilirubin (P = 0.015), hepatitis B e antigen positivity rate (P < 0.001) and haemoglobin (P < 0.001) were significantly related to the prognosis of ACHBLF and were selected to build the ANN. The ANN performed significantly better than MELD-based scoring systems both in the training cohort (AUROC = 0.869 vs 0.667, 0.591, 0.643, 0.571 and 0.577; P < 0.001, respectively) and in the validation cohort (AUROC = 0.765 vs 0.599, 0.563, 0.601, 0.521 and 0.540; P ≤ 0.006, respectively). Thus, the ANN model was shown to be more accurate in predicting 3-month mortality of ACHBLF than MELD-based scoring systems.

The tumour necrosis factor-α-238A allele increases the risk of chronic HBV infection in European populations.

Tumour necrosis factor-α (TNF-α) plays a pivotal role in viral clearance and host immune response to hepatitis B virus (HBV) infection, of which the production capacity in individuals is demonstrated to be influenced by a single nucleotide polymorphism within the promoter region of TNF-α genes. However, there have been conflicting results reported in previous studies on TNF-α-238 and TNF-α-863 gene promoter polymorphisms in chronic HBV infection. To derive a more precise estimation of their relationship, we searched Pubmed (January, 1966-August, 2010) and China Biological Medicine Database (January, 1978-August, 2010) and carried out a meta-analysis involving nineteen studies that included 5245 chronic HBV infection cases and 3181 controls describing G238A genotypes, and eleven studies totalling 3576 cases and 2044 controls describing C863A genotypes. The overall meta-analysis did not suggest significant associations of TNF-α-238 and TNF-α-863 gene promoter polymorphisms with chronic HBV infection. However, in subgroup analysis by ethnicity, it indicated that TNF-α-238A allele carriers (GA + AA) in European populations had an increased risk of developing chronic HBV infection (OR = 2.22, 95% CI: 1.07-4.58, P = 0.032; OR = 4.46, 95% CI: 1.75-11.38, P = 0.002, respectively), when compared with spontaneous recovered and healthy populations, respectively. However, no significant associations were found in Asian populations in all genetic models. So, we draw the conclusion that the TNF-α-238A allele may increase the risk of chronic HBV infection in European populations.

Tumour necrosis factor-α-857T allele reduces the risk of hepatitis B virus infection in an Asian population.

Tumour necrosis factor-α (TNF-α) plays a pivotal role in hepatitis B virus (HBV) clearance and host immune response determining the chronicity of HBV infection. However, studies of the association between TNF-α-857 polymorphism and chronic HBV infection have reported conflicting results. So a meta-analysis was carried out to draw a more precise conclusion. Pubmed (January, 1966-March, 2011) and the China Biological Medicine Database (January, 1978-March, 2011) were searched using the keywords TNF-α gene polymorphism in combination with HBV infection without language restriction. Fourteen studies including 4929 chronic HBV infection cases and 2702 controls describing the C857T genotype were included in the meta-analysis. All fourteen studies focussed on an Asian population. The overall meta-analysis suggested that TNF-α-857T allele reduced the risk of chronic HBV infection in the Asian population (OR = 0.82, 95% CI: 0.71-0.95, P = 0.008) when compared with a spontaneously recovered population. In the sensitivity analyses of the groups obeying Hardy-Weinberg equilibrium (HWE), without the largest study population and without the smallest study population, a similar association was revealed (OR = 0.81, 95% CI: 0.68-0.98, P = 0.043; OR = 0.77, 95% CI: 0.68-0.87, P = 0.0001; OR = 0.81, 95% CI: 0.70-0.95, P = 0.009, respectively). However, when compared with a healthy population, no significant association was found in the Asian population in all groups. So, we draw the conclusion that the TNF-α-857T allele reduces the risk of chronic HBV infection in this Asian population.

Construction of the HBV S-ecdCD40L fusion gene and effects of HBV S-ecdCD40L modification on function of dendritic cells.

We examined the effect of dendritic cells engineered to express an HBV S antigen CD40L fusion gene (HBV S-ecdCD40L). The DNA of HBV S gene and the cDNA of the extracellular domain of human CD40 ligand were linked by cloning. Peripheral blood mononuclear cells (PBMC) from healthy adults were incubated and induced into dendritic cells (DC) in presence of granulocyte/macrophage colony-stimulating factor (GM-CSF) and interleukin-4(IL-4). The DCs were transfected the novel construct, and the impact of the expressed clone assessed. We find that, compared with control groups, modification of DCs with HBV S-ecdCD40L fusion gene resulted in the activation of DCs with upregulated expression of immunologically important cell surface molecules (CD80, CD86 and HLA-DR) and proinflammatory cytokines (IL-12). The DCs modified with HBV S-ecdCD40L are able to stimulate enhanced allogeneic T-cell proliferation in vitro. Thus, the fusion gene HBV S-ecdCD40L can promote DC's activation and enhance its function and may prove to be the foundation for a new type of hepatitis B vaccine.

Photoprotection by tocopherol submicron emulsion against UV-mediated damage in HaCaT cells.

alpha-Tocopherol is a lipophilic vitamin E that shows antioxidative, antiaging and antiphotodamage activity. Nanometer biotechnology is more widely used in the entrainment system of drug carriers and the development for new pharmaceutical preparations. Ultraviolet irradiation to human skin in the long term can result in photoaging and photocarcinogenesis. The purpose of this study was to observe the biological features of tocopherol submicron emulsion (vitE SME) and to clarify the roles of vitE SME on UVB-induced photodamage in HaCaT keratinocytes (KC). VitE SME was prepared by high-pressure homogenization and microemulsion technique. HaCaT KC was incubated in the culture medium supplied with 1/200 and 1/400 of VitE SME prior to different dosages of UVB irradiation. The vitamin E amount in the culture medium was measured by high-performance liquid chromatography (HPLC). Cell growth and cellular viability was detected by MTT assay. The amount of vitamin E remaining in the culture medium significantly decreased during the first 8 h, and less than 10% can be detected by the terminal experiment (24 h). No cytotoxicity effect of tocopherol NM on HaCat KC was observed. In contrast to the control group, the cellular viability of VitE SME-treated group increased 44.22% by 24 h. Compared with irradiated groups without VitE SME, cell proliferation decreased by 17.77% and 40.42% when the HaCaT KC was irradiated with 30 mJ/cm(2) and 90 mJ/cm(2) UVB irradiation, respectively. VitE SME has no toxicity to cell culture system and is characterized by stable release and penetration. Pre-incubation with VitE SME can partly reduce UV-induced cell damage, and the photoprotective efficiency to UVB irradiation also shows time dependence.

Indirect validation of benzene exposure assessment by association with benzene poisoning.

We present a validation study of a quantitative retrospective exposure assessment method used in a follow-up study of workers exposed to benzene. Assessment of exposure to benzene was carried out in 672 factories in 12 cities in China. Historical exposure data were collected for 3179 unique job titles. The basic unit for exposure assessment was a factory/work unit/job title combination over seven periods between 1949 and 1987. A total of 18,435 exposure estimates was developed, using all available historical information, including 8477 monitoring data. Overall, 38% of the estimates were based on benzene monitoring data. The highest time-weighted average exposures were observed for the rubber industry (30.7 ppm) and for rubber glue applicators (52.6 ppm). Because of its recognized link with benzene exposure, the association between a clinical diagnosis of benzene poisoning and benzene exposure was evaluated to validate the assessment method that we used in the cohort study. Our confidence in the assessment method is supported by the observation of a strong positive trend between benzene poisoning and various measures, especially recent intensity of exposure to benzene.

Mortality among benzene-exposed workers in China.

A large cohort of 74,828 benzene-exposed and 35,805 nonexposed workers employed between 1972 and 1987 in 12 cities in China was followed to determine mortality from all causes. Benzene-exposed study subjects were employed in a variety of occupations including coating applications, and rubber, chemical, and shoe production. Mortality was slightly increased among workers with greater cumulative exposure to benzene (ptrend < 0.05), but this excess was largely due to cancer deaths (ptrend < 0.01). Deaths due to lymphatic and hematopoietic malignancies (ptrend = 0.01) and lung cancer (ptrend = 0.01) increased with increasing cumulative exposure to benzene. Investigations continue to relate benzene exposure to specific lymphatic and hematopoietic malignancies and other causes of death.