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Background The wettability of the target surfaces affects the wetting and deposition of pesticides on them. The properties of leaf surfaces change after infestation by Tetranychus urticae Koch. Studying the surface wettability of T. urticae and the changes in leaf wettability after infestation is important to guide the use of acaricides. Results The body surface of T. urticae is an ellipsoidal crown covered with dense cuticle striations and hairs arranged in different directions, which makes the surface of T. urticae rough and hydrophobic. The abaxial surfaces of the leaves are rougher and more hydrophobic than the adaxial surfaces. After infestation by T. urticae, the faded spots were sunken on the adaxial surface and raised on the abaxial surface, where they had formed new wide peaks and valleys. The adaxial surface became obviously rougher and more hydrophobic, while the roughness of the abaxial surface became slightly larger, and the change in hydrophobicity was not obvious. The contact angles of the studied commercial acaricide on these surfaces were greater than 65° and were affected by the infestation. Reducing the surface tension can allow for better wetting of these surfaces and eliminate changes in leaf wettability. Conclusion The surfaces of kidney bean leaves became more hydrophobic after infestation by T. urticae with hydrophobic surface. The wettability of the acaricide solution should be adjusted according to the changes in leaf wettability. This study has important theoretical guiding significance for improving effective deposition of acaricide.

The present study was undertaken to evaluate the influence of rumen-protected folic acid (RPFA) on slaughter performance, visceral organ and gastrointestinal tract coefficients, and meat quality in lambs. Sixty-six lambs from 120 Hu ewes were selected based on body weight and maternal diets and then assigned to six groups using a randomised block experimental design in a 3 × 2 factorial arrangement. The first factor was folic acid (FA) as RPFA in the maternal diet (0 mg/kg (M0F), 16 mg/kg (M16F) or 32 mg/kg (M32F) on DM basis). The second factor was FA in the lambs’ diet from weaning until slaughter (0 mg/kg (OC) or 4·0 mg/kg (OF)). The results indicated that the addition of 16 mg/kg FA to the maternal diet increased pre-slaughter weight (PSW), dressing and meat percentage, the reticulum and omasum coefficients, length of the jejunum and ileum, tail fat and perirenal fat coefficient and a* value of the meat colour. The addition of RPFA to the lambs’ diet increased PSW, dressing and meat percentage, eye muscle area, abomasum weight, weight and length of the small intestine, but reduced the coefficients of tail fat. An M × O interaction was observed for the weights of heart, lungs, rumen and total stomach, weight and coefficient of omental fat and the girth rib value. Collectively, RPFA in the maternal and lambs’ diet improved slaughter performance and meat quality by stimulating the morphological development of the gastrointestinal tract and the distribution of fat in the body.

The blood pressure (BP) control rate among treated hypertensives in China remains low at 37.5%. The relationship between home blood pressure telemonitoring (HBPT) and BP control is controversial. The authors aimed to investigate the relationship between HBPT and BP control in middle‐aged and elderly hypertensives. In total, 252 hypertension patients aged between 60 and 79 years were enrolled. The patients were given either HBPT through interactive platforms between physicians and patients (telemonitoring group, n = 126) or conventional management (routine management group, n = 126). All patients were followed‐up for 15 months. BP control was defined as home systolic blood pressure

Background The nutrition state plays an important role in the progress of aging. Folate may play a role in protecting mitochondrial (mt) DNA by reducing oxidative stress. Objective The primary aim of this study was to examine the association of mitochondrial oxidative damage with risk of Alzheimer's disease (AD), and to explore the possible role of folate metabolites in this association in a matched case-control study. Methods Serum folate metabolites and mitochondrial function in peripheral blood cells were determined in 82 AD cases and 82 healthy controls, individually matched by age, gender, and education. Results AD patients had lower serum levels of folate and higher homocysteine (Hcy) concentration. AD patients had a reduced mtDNA copy number, higher mtDNA deletions, and increased 8-OHdG content in mtDNA indicative of reduced mitochondrial function. The highest level of mtDNA copy number would decrease the risk of AD (OR = 0.157, 95% CI: 0.058-0.422) compared to the lowest level, independently of serum folate, and Hcy levels. Serum folate levels correlated with low 8-OHdG content in mtDNA both in AD patients and controls, independently of serum Hcy level. Moreover, serum Hcy levels correlated with low copy number in mtDNA both in AD patients and controls, independently of serum folate levels. Conclusion In conclusion, mitochondrial function in peripheral blood cells could be associated with risk of AD independent of multiple covariates. AD patients with a folate deficiency or hyperhomocysteinemia had low mitochondrial function in peripheral blood cells. However, further randomized controlled trials are need to determine a causal effect.

Background Several studies have indicated that inflammatory markers were associated with the risk of mild cognitive impairment (MCI) in type 2 diabetes (T2D). Serum folate was related to MCI as well as inflammation. However, no studies have investigated the association between inflammatory markers and MCI taking account of serum folate level in T2D patients. This study aimed to conduct a case-control study to evaluate the association between inflammatory markers and MCI taking account of serum folate level in Chinese patients with T2D. Methods This study consisted of 126 T2D patients (63 cases with MCI and 63 controls without MCI). Clinical parameters, serum folate, high-sensitivity C-reactive protein (hs-CRP), interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α) were measured. Spearman correlation analysis and logistic regression analysis were used to analyze the association between the inflammatory markers and the risk of MCI in T2D patients. Results There were higher serum hs-CRP, IL-6 and TNF-α in T2D cases with MCI compared with the controls. Serum folate was negatively correlated with hs-CRP, TNF-α, and IL-6 (P

In this research a four-armed amino-tailored tetraphenylethene TPE-NH2 was synthesized, and it could detect heparin (Hep) quantitatively, primarily promoted by the electrostatic interactions between its positively charged amino groups and the sulfates, carboxylates of heparin. On account of the aggregation-induced emission (AIE) nature of tetraphenylethene backbone, the aggregation restricted the rotation of C C single bond through rigidifying the conformation of TPE-NH2, thus making it display intense fluorescence with a broad working range (≤2.0 μg/mL) and a low detection limit (down to 35.89 ng/mL) for heparin. Meanwhile, the TPE-NH2/Hep complex can be further disaggregated by protamine due to the stronger affinity between heparin and protamine, consequently leading to the highly sensitive detection of protamine. What’s more, the low toxicity of TPE-NH2 makes it a potential functional sensor for detecting heparin in the matrix of human serum.

Background In recent years, long noncoding RNAs (lncRNAs) have been reported frequently to play important roles in specific cancers, including high-grade serous ovarian cancer (HGSOC). PVT1 is an important oncogenic lncRNA highly expressed in various cancers. However, little is known about the role of PVT1 in HGSOC and underlying mechanisms. Methods The expression levels of PVT1 and HER2/3 in HGSOC tissue and adjacent normal tissue were determined by qRT-PCR. MTT and transwell assays were used to identify the effects of PVT1 cell proliferation and migration respectively. Dual-luciferase reporter assay and RIP experiment were carried out to verify target genes of PVT1. ChIP experiment was used to identify that HER2 was transcription factor of PVT1. Results Our results showed that PVT1 expression was up-regulation in human HGSOC specimens and promoted ovarian cancer cell proliferation and migration. We further validated that HER2 was a direct transcription factor for facilitating PVT1 expression. In return, PVT1 enhanced HER2 transcript stability. Moreover, bioinformatics analysis and dual luciferase reporter assay results uncovered that PVT1 functioned as a competing endogenous RNA (ceRNA) for miR-1301-3p to promote cell proliferation and migration by increasing HER3 expression. Conclusions Taken together, our results showed that PVT1, controlled by HER2, elevated HER2 and HER3 expression to promote HGSOC progression. Thus, PVT1 can be regarded as a vital diagnostic biomarker for HGSOC and a potential novel therapeutic target.

Endothelial cell injury and apoptosis play a primary role in the pathogenesis of atherosclerosis. Moreover, accumulating evidence indicates that oxidative injury is an important risk factor for endothelial cell damage. In addition, low folate levels are considered a contributing factor to promotion of vascular disease because of the deregulation of DNA methylation. We aimed to investigate the effects of folic acid on injuries induced by oxidative stress that occur via an epigenetic gene silencing mechanism in ApoE knockout mice fed a high-fat diet and in human umbilical vein endothelial cells treated with oxidized low-density lipoprotein (ox-LDL). We assessed how folic acid influenced the levels of 8-hydroxy-2′-deoxyguanosine (8-OHdG, an oxidative DNA damage marker) and cellular apoptosis in in vivo and in vitro models. Furthermore, we analyzed DNA methyltransferase (DNMT) activity, vascular peroxidase 1 (VPO1) expression, and promoter methylation in human umbilical vein endothelial cells. Our data showed that folic acid reduced 8-OHdG levels and decreased apoptosis in the aortic tissue of ApoE−/− mice. Likewise, our in vitro experiments showed that folic acid protects against endothelial dysfunction induced by ox-LDL by reducing reactive oxygen species (ROS)-derived oxidative injuries, 8-OHdG content, and the apoptosis ratio. Importantly, this effect was indirectly caused by increased DNMT activity and altered DNA methylation at VPO1 promoters, as well as changes in the abundance of VPO1 expression. Collectively, we conclude that folic acid supplementation may prevent oxidative stress-induced apoptosis and suppresses ROS levels through downregulating VPO1 as a consequence of changes in DNA methylation, which may contribute to beneficial effects on endothelial function., Graphical abstract fx1, Highlights • Folic acid reduces oxidative stress-induced injuries in atherosclerosis. • Folic acid decreases 8-OHdG levels and apoptosis in vivo and in vitro. • Folic acid supplementation increases DNMT levels and regulates VPO1 expression. • VPO1 expression is modulated by epigenetic silencing via promoter methylation.

AIM Microalbuminuria (MA) has been demonstrated as a biomarker for microvascular dysfunction. This study is aimed to evaluate the association of glycaemic status with MA in prehypertensive and ideal BP subjects and to evaluate the interaction between glycaemic and blood pressure status as risk factors for MA prevalence. METHODS 1059 subjects aged 40-70 with non-hypertension who were recruited from six districts of Tianjin were divided into a prehypertensive group (622 cases) and an ideal blood BP group (437 cases). Subjects of the prehypertensive group and the ideal BP group were divided respectively into three subgroups: normoglycaemia subgroup, prediabetes subgroup and diabetes subgroup. The prevalence of MA in the above three subgroups of subjects with prehypertension and ideal BP were assessed. We performed a statistical analysis for interaction test between glycaemia and BP status on microalbuminuria in the overall study sample by a multivariate logistic regression model. The association of glycaemic status (defined as normoglycaemia, prediabetes, and diabetes) with MA was evaluated separately in prehypertensive and ideal BP subjects. RESULTS Results showed that the prevalence of MA in both prehypertensive and ideal BP groups rose with the increasing of classification of glycaemic level of subgroups (32.6%, 18.3%, 14.8% vs. 23.1%, 16.2%, 13.4%), the differences in prehypertensive group were statistically significant (Pearson χ2 = 15.24, P < 0.001). The ORs (95% CI) of MA were 1.25 (0.86-1.83) for prediabetes and 2.56 (1.62-4.03) for diabetes in the fully adjusted model. There was no interaction between prediabetes and BP status regarding MA (P = 0.237) but we found a significant interaction between diabetes and BP status (P < 0.001). In the prehypertensive group, multivariate logistic regression models showed that the diabetes subgroup had a significant association with MA, and the adjusted odds ratio of the diabetes subgroup to the normoglycaemia subgroup was 2.68 (95%CI 1.54-4.67) (P < 0.001). However, there was no significant association of glycaemic status with MA in the ideal BP group. Stratified analysis by a multivariate logistic regression model in the whole study population showed that people with both prehypertension and diabetes had the highest risk of MA (adjusted OR = 2.50, 95%CI 1.16-5.36; P = 0.019), compared with those with ideal BP and normoglycaemia (reference group). CONCLUSIONS Our findings suggest that there was a statistically significant association between diabetes and microalbuminuria only in prehypertensive subjects. In addition, our study highlights the interaction between prehypertension and diabetes as a risk factor for MA.

Homocysteine may be responsible for vascular endothelial cell injury, which occurs early in the pathology of cardiovascular disease. Homocysteine metabolism requires enzymatic interaction with vitamins such as folic acid, vitamin B12, and vitamin B6. We hypothesized that folic acid alleviated homocysteine-induced vascular injury by regulating the metabolic pathway of apoptosis. Human umbilical vein endothelial cells were incubated for 48 h with folic acid at the concentrations of 0-1000 nmol/L, in combination with either 1000 μmol/L homocysteine or vehicle for the first 24 h. We then assessed cell viability and apoptosis by methyl thiazolyl tetrazolium assay and flow cytometry, respectively. To further investigate how folic acid influenced cell apoptosis, we also analyzed the activities of caspase-3/7 and the mRNA and protein expressions of BCL2, BAX, TP53, CASP3, and CASP8 in human umbilical vein endothelial cells. We showed that folic acid increased cell viability and decreased apoptosis in a dose-dependent manner, and that this effect was mediated by decreased caspase-3/7 activity, upregulated BCL2/BAX ratio, and downregulated TP53, CASP3, and CASP8 expressions. Thus, we conclude that folic acid inhibits cell apoptosis and ameliorates homocysteine toxicity by regulating the expression of apoptosis-related genes in human umbilical vein endothelial cells.

Background The association of vitamin D status and inflammation prediabetes mellitus (PreDM) individuals has not been investigated. We investigated the association of serum 25-hydroxyvitamin D 3 (25(OH) D 3 ) with adipokines and inflammatory markers in persons with PreDM. Methods In this cross-sectional study, we stratified 418 nondiabetic subjects as having PreDM or normal fasting glucose (NFG), and divided PreDM or NFG subjects into vitamin D sufficient, vitamin D insufficient and vitamin D deficient subgroups. 25(OH) D 3 concentrations were determined by HPLC. Serum tumor necrosis factor-α (TNF-α), interleiukin-6 (IL-6) and high-sensitivity C-reactive protein (hs-CRP), adiponectin, leptin and resistin were measured by ELISA. Results In the PreDM group, compared with those in the vitamin D sufficient subgroup, vitamin D insufficient subgroup and vitamin D deficient subgroup had higher concentrations of hs-CRP and leptin ( P P 3 concentrations were inversely associated with hs-CRP and leptin concentrations after adjusted the BMI only in the PreDM group ( P 3 concentration (β = − 0.174 and β = − 0.171, respectively). Conclusions 25(OH) D 3 status in PreDM individuals was inversely correlated with concentrations of hs-CRP and leptin, suggesting their involvement in the inflammation response between vitamin D status and PreDM.

Increasing evidence shows that cancer stem cells are responsible for drug resistance and relapse of tumors. In breast cancer, human epidermal growth factor receptor 2 (HER2) induces Herceptin resistance by inducing cancer stem cells. In the present study, we explored the effect of HER2 on cancer stem cells induction and drug sensitivity of ovarian cancer cell lines. First, we found that HER2 overexpression (HER2 OE) induced, while HER2 knockdown (HER2 KD) decreased CD44+/CD24− population. Consistently, HER2 expression was closely correlated with the sphere formation efficiency (SFE) of ovarian cancer cells. Second, we found that NFκB inhibition by specific inhibitor JSH23 or siRNA targetting subunit p65 dramatically impaired the induction of ovarian cancer stem cells by HER2, indicating that NFκB mediated HER2-induced ovarian cancer stem cells. Third, we found that HER2 KD significantly attenuated the tumorigenicity of ovarian cancer cells. Further, we found that HER2 inhibition increased drastically the sensitivity of ovarian cancer cells to doxorubicin (DOX) or paclitaxel (PTX). Finally, we examined the correlation between HER2 status and stem cell-related genes expression in human ovarian tumor tissues, and found that expressions of OCT4, COX2, and Nanog were higher in HER2 positive tumors than in HER2 negative tumors. Consistently, the 5-year tumor-free survival rate of HER2 positive patients was dramatically lower than HER2 negative patients. Taken together, our data indicate that HER2 decreases drug sensitivity of ovarian cancer cells via inducing stem cell-like property.

Objective. Both hypertension and subclinical thyroid dysfunction (STD) have high prevalence and clinical importance, but their relationship is still a matter of debate. We aimed to explore gender-specific difference on the association between hypertension and STD in Chinese. Methods. We recruited 13,380 ostensible healthy participants (8,237 men and 5,143 women). The associations between hypertension and STD were analyzed on a gender-based setting after dividing STD into subclinical hypothyroidism, subclinical hyperthyroidism and further subgrouped euthyroidism. Crude and adjusted odds ratios of STD for hypertension were analyzed by binary logistic regression. Results. An increasing trend of hypertension prevalence was found along with aging in both genders. Yet, higher male hypertension prevalence was found until 65 years, and then it intersected with female hypertension prevalence. Women had significantly higher propensity for STD than men. Yet, in elderly participants, this gender-specific difference became less obvious. We displayed detrimental effects for subclinical hypothyroidism in both genders after multiple-covariate adjustments, yet no such effects were shown for subclinical hyperthyroidism. Moreover, females with subclinical hypothyroidism were more likely to be associated with hypertension than males, and the corresponding odds ratios were 1.619 (P<0.01) and 1.557 (P<0.05), respectively. For systolic blood pressure, the adjusted odds ratios were 1.371 (P<0.05) and 1.154 (P>0.05), and for diastolic blood pressure, 1.604 (P<0.01) and 1.564 (P<0.01), respectively. Conclusion. We demonstrate that hypertension is associated with subclinical hypothyroidism, but not with subclinical hyperthyroidism. Moreover, females with subclinical hypothyroidism are more likely to be associated with hypertension than males.

Introduction Myasthenia gravis (MG) is an autoimmune disease in which antibodies directly target components of the neuromuscular junction, causing neuromuscular conduction damage that leads to muscle weakness. The current pharmaceutical treatment for MG is still not ideal to address the problems of disease progression, high recurrence rate, and drug side effects. Clinical observations suggest that traditional Chinese medicine (TCM) can strengthen immunity and improve symptoms of MG patients, delay the progression of the disease, reduce or even prevent the need for immunosuppressive therapy when used in combination with acetylcholinesterase inhibitors or low-dose prednisone, as well as improve the quality of life of patients. The Qiangji Jianli Capsule (QJC) is a combination of medicinal herbs which is used in traditional Chinese medicine. Since MG is a rare disorder, randomized controlled trials comparing large cohorts are difficult to conduct. Therefore, we proposed to aggregate data from a small series of N-of-1 trials to assess the effect of the Chinese medical prescription QJC, which strengthens the spleen and nourishes Qi, as an add-on treatment for MG with spleen and stomach Qi deficiency syndrome. Methods and analysis Single-center, randomized, double-blind, multiple crossover N-of-1 studies will compare QJC versus placebo in 5 adult MG patients with spleen and stomach Qi deficiency syndrome. Patients will undergo 3 cycles of two 4-week intervention periods. According to the treatment schedule, patients will continue to be treated with pyridine bromide tablets, prednisone acetate, tablets and/or tacrolimus capsules throughout the entire trial. Each period consisting of 4-week oral add-on treatment with QJC will be compared with 4-week add-on treatment with a placebo. The primary endpoints are quantitative myasthenia gravis (QMG) test; measurement of the amount of Treg cells and cytokines such as interferon-γ (IFN-γ), interleukin-4 (IL-4), interleukin-17A (IL-17A), and transforming growth factor-β (TGF-β); and corticosteroid or immunosuppressive agent dosage. Secondary outcome measures: Clinical: Evaluation of the effect of TCM syndromes; MG-activities of daily living (MG-ADL) scales; adverse events. Ethics and dissemination This study was approved by The First Affiliated Hospital of Guangzhou University of Chinese Medicine (GZUCM), No. ZYYECK[2019]038. The results will be published in a peer-reviewed publication. Regulatory stakeholders will comment on the suitability of the trial for market authorization and reimbursement purposes. Trial registration: Chinese Clinical Trial Register, ID: ChiCTR2000033516. Registered on 3 June 2020, http://www.chictr.org.cn/showprojen.aspx?proj=54618.

Little is known of the relationships between dietary patterns and cardiovascular risk factors in China. We therefore designed a 3-year longitudinal study to evaluate the impacts of dietary patterns on changes in these factors among Chinese women. A total of 1,028 subjects who received health examination in 2011 and 2014 were recruited. Three major dietary patterns ("vegetable pattern", "meat pattern", and "animal offal-dessert-and-alcohol pattern") were derived by principal component analysis based on validated food frequency questionnaires. Cardiovascular risk factors were standardized to create within-cohort z-scores and the changes in them were calculated as the differences between 2011 and 2014. Relationships between dietary patterns and changes in cardiovascular risk factors were assessed using general linear model. After adjustment for potential confounders, changes in total cholesterol and fasting blood glucose decreased across the tertiles of vegetable pattern (p for trend = 0.01 and 0.04, respectively). While, changes in diastolic blood pressure, total cholesterol and low density lipoprotein cholesterol increased across the tertiles of animal offal-dessert-and-alcohol pattern (p for trend = 0.02, 0.01, and 0.02, respectively). The findings suggest that vegetable pattern was beneficially related to cardiovascular risk factors, whereas animal offal-dessert-and-alcohol pattern was detrimental related to these factors among apparently healthy Chinese women.

Background In absence of curative treatments for dementia with type 2 diabetes mellitus (T2DM), mild cognitive impairment (MCI) in T2DM, the preclinical transitional states of dementia with T2DM has attracted dramatic attention. Our study was to estimate the prevalence and distribution of MCI in T2DM subjects from China, and identify influencing factors of subjects in MCI with T2DM. Methods In the present study, we performed cluster random sampling of 8213 people aged 65 years and older in Tianjin, a metropolitan city, located in northern China. All participants were interviewed and screened for T2DM. 1109 subjects with T2DM were initially screened with American Diabetes Association criteria for diagnosis of diabetes mellitus and were diagnosed with MCI and dementia according to the criteria of DSM-IIIR. The prevalence of MCI and dementia in subjects with T2DM were compared with that in ordinary subjects. Logistic regression analyses were performed to evaluate risk of MCI with T2DM. Results Among all 8213 subjects, overall MCI and dementia with T2DM prevalence were 13.5% and 2.34%, respectively. Compared with ordinary subjects, the prevalence of MCI in the present study was more frequent than the prevalence of MCI for the general population in almost each age group. In the univariate analyses, among all diabetic subjects, compared with cognitive intactly subjects, MCI subjects had significantly higher levels of age, current smoking, mean waist circumference, duration from onset of diabetes, insulin intake, systolic BP, fasting plasma glucose (FPG), glycosylated hemoglobin (HbA1c) and immunoreactive insulin (IRI). In multivariate logistic regression analyses, variables including current smoking, duration from onset of diabetes, FPG, HbA1c and IRI were significantly associated with increased risk for MCI with T2DM, the ORs were 1.36,1.33,1.17,1.25 and 1.33, respectively (all P Conclusions The present study confirms the high prevalence of MCI with T2DM among the elderly population of China. T2DM is related to a higher risk of MCI in a population with a high prevalence of this disorder and may aggravate the clinical picture as a concomitant factor.

A novel Zn 2+ ion chemosensor 1 has been developed based on deoxycholic acid and salen motifs, and this chemosensor can be used in test-strips and living cells imaging for Zn 2+ ion through a turn-on effect. Moreover, the resulting [ 1 ·Zn 2+ ] complex exhibits turn-off response toward H 2 PO 4 − ion, thus leading to the fabrication of an INHIBIT (INH) logic gate using Zn 2+ ion and H 2 PO 4 − ion as inputs and the emission of 1 as outputs, respectively. This line of research not only enriches the library of Zn 2+ ion sensors, but also expands the applications of natural products-based chemosensors.

Objective. Both hyperuricemia and hypertension have important clinical implications, but their relationship in terms of gender and age is still a matter of debate. In this study, we aimed to explore gender- and age-specific differences in this association between hyperuricemia and hypertension in a Chinese population. Methods. A total of 78596 ostensibly healthy subjects (47781 men and 30815 women) were recruited. The association between hyperuricemia and hypertension was analyzed by multivariate logistic regression, and the analyses were stratified by gender and age. Results. Overall prevalence of hypertension and hyperuricemia was significantly higher in males than in females. Increasing trends of hypertension prevalence in both genders as well as hyperuricemia prevalence in females were found along with aging. However, males showed a reduced trend in hyperuricemia prevalence with aging. Higher hypertension and hyperuricemia prevalence was found in young and middle-aged men than in women, but not in elderly people older than 70 years. Significantly increased risk of hypertension from hyperuricemia was found only in men with an adjusted odds ratio of 1.131 (P<0.01), especially in the middle-aged male participants. However, such significant results were not found in women. Similarly, hyperuricemia was also an independent risk factor of increased systolic blood pressure and diastolic blood pressure in males, but not in females. Conclusion. We observed significantly higher overall prevalence of hyperuricemia and hypertension in men than in women. Men with hyperuricemia (particularly in middle age) had a significantly increased susceptibility of hypertension, while this significant association was not observed in women.

To identify characteristics of neuropsychological function among elderly individuals with Type 2 diabetes mellitus with mild cognitive impairment (T2DM-MCI) and evaluate domain-specific effects of T2DM on cognition.This was a cross-sectional study conducted in Tianjin, China. MCI subjects (n=246) and controls were identified in elderly individuals with diabetes, and groups were matched in a 1:1 ratio for sex, age and educational level. Cognitive function was assessed using WAIS-III (block design, digit span), Trail Making Test A, Trail Making Test B, WMS-III (word list learning, logical memory), verbal fluency and MMSE. We used multivariable logistic regression to find diabetic factors associated with MCI.The mean MMSE score was 22.73 ± 2.32 in subjects with T2DM-MCI, versus 26.71 ± 2.43 in subjects cognitive normal (P0.001). Executive and visuospatial functions were more impaired in individuals with T2DM-MCI than in those without, as assessed using block design (P0.001), digit span test (P0.001), and Trails B (P0.001). For memory, subjects with T2DM-MCI did worse than those cognitive normal on the word learning list delayed recall (P=0.015). Diabetic-related factors such as longer duration of T2DM, higher HbA1c, insulin treatment was associated with a lower level of cognitive functioning using MMSE, block design, delayed recall and Trails B test.T2DM should be considered a risk factor for MCI. This risk may be associated with duration of diabetes, use of glucose-lowering medications, degree of glucose control. To decrease risk of MCI, it is important to monitor glucose control and adjust medications appropriately in elderly patients.

The role of homocysteine (Hcy) in the pathogenesis of coronary artery disease (CAD) is controversial, as decreased Hcy levels have not demonstrated consistent clinical benefits. Recent studies propose that S-adenosylhomocysteine (SAH), and not Hcy, plays a role in cardiovascular disease (CVD). We aimed to assess the relationship between plasma SAH and coronary artery lesions. Participants (n=160; aged 40-80years) with chest pain and suspected CAD underwent coronary angiography (CAG) for assessment of coronary artery stenosis, and were assigned to either the atherosclerosis (AS) or CAD group. Plasma SAH and S-adenosylmethionine (SAM) concentrations were measured and the association between coronary artery lesions and SAH was assessed. SAH levels were significantly higher in the CAD group (23.09±2.4nmol/L) than in the AS group (19.2±1.5nmol/L). While the AS group had higher values for SAM/SAH (5.1±0.7 vs. 4.1±1.1), levels of SAM, Hcy, folate, and vitamin B12 were similar in the two groups. Coronary artery lesions were associated with SAH (β=11.8 [95% CI: 5.88, 17.7, P

Atherosclerosis is a chronic disease that can seriously endanger human life. Folic acid supplementation modulates several disorders, including atherosclerosis, via its antiapoptotic and antioxidative properties. This study investigated whether folic acid alleviates atherogenesis by restoring homocysteine levels and antioxidative capacity in atherosclerosis Wistar rats. To this end, 28 Wistar rats were randomly divided into 4 groups (7 rats/group) as follows: (i) wild-type group, fed only the AIN-93 semi-purified rodent diet (folic acid: 2.1 mg/kg); (ii) high-fat + folic acid-deficient group (HF+DEF) (folic acid: 0.2 mg/kg); (iii) high-fat + normal folic acid group (folic acid: 2.1 mg/kg); and (iv) high-fat + folic acid-supplemented group (folic acid: 4.2 mg/kg). After 12 weeks, histopathological changes in the atherosclerotic lesions of the aortic arch were determined. In addition, serum folate levels, plasma homocysteine levels, plasma S-adenosyl-homocysteine levels, antioxidant status, oxidant status, and lipid profiles were evaluated. The results show aggravated atherosclerotic lesions in the HF+DEF group. Folic acid supplementation increased concentrations of serum folate. Further, folic acid supplementation increased high-density lipoprotein-cholesterol, decreased plasma homocysteine levels, and improved antioxidant capacity in atherogenic rats. These findings are consistent with the hypothesis that folic acid alleviates atherogenesis by reducing plasma homocysteine levels and improving antioxidant capacity in rats fed a high-fat diet.

Type 2 diabetes is a risk factor for Alzheimer’s disease and mild cognitive impairment. Folate insufficiency fosters a decline in the sole methyl donor, S-adenosylmethionine, and decreases methylation potential, which is associated with Alzheimer’s disease in non-diabetic patients. However, little is known in diabetic patients. We analyzed plasma levels of S-adenosylmethionine, S-adenosylhomocysteine and serum level of folate in 100 elderly type 2 diabetic patients with and without mild cognitive impairment. S-adenosylmethionine/S-adenosylhomocysteine ratio was used to reflect the methylation potential. Patients with mild cognitive impairment had significantly lower levels of S-adenosylmethionine, folate and S-adenosylmethionine/S-adenosylhomocysteineratios. Furthermore, logistic regression analysis indicated the plasma S-adenosylmethionine, S-adenosylmethionine/S-adenosylhomocysteine ratio and serum folate (OR, 0.96, 0.698, 0.72, respectively; p

The proliferative response of neural stem cells (NSCs) to folate may play a critical role in the development, function and repair of the central nervous system. It is important to determine the dose-dependent effects of folate in NSC cultures that are potential sources of transplantable cells for therapies for neurodegenerative diseases. To determine the optimal concentration and mechanism of action of folate for stimulation of NSC proliferation in vitro , NSCs were exposed to folic acid or 5-methyltetrahydrofolate (5-MTHF) (0–200 μmol/L) for 24, 48 or 72 h. Immunocytochemistry and methyl thiazolyl tetrazolium assay showed that the optimal concentration of folic acid for NSC proliferation was 20–40 μmol/L. Stimulation of NSC proliferation by folic acid was associated with DNA methyltransferase (DNMT) activation and was attenuated by the DNMT inhibitor zebularine, which implies that folate dose-dependently stimulates NSC proliferation through a DNMT-dependent mechanism. Based on these new findings and previously published evidence, we have identified a mechanism by which folate stimulates NSC growth.

Periodontal diseases comprise mixed bacterial infections mainly caused by Gram‑negative anaerobic bacteria. Lipopolysaccharides (LPS) are important virulence factors and periodontal pathogens, which change local cytokine levels and promote osteoblast apoptosis, thereby leading to an imbalance in bone remodeling mechanisms and accelerating bone loss. Calcitonin gene‑related peptide (CGRP) is a vasoactive neuropeptide that is released from sensory nerves and has a positive effect on osteoblast proliferation and differentiation. In addition, this small molecule peptide is an important immune regulator in the inflammatory response. The aim of the present study was to assess the in vitro effects of CGRP on Porphyromonas gingivalis (Pg)LPS‑induced osteoblast apoptosis. Osteoblast cultures were stimulated either with various concentrations of PgLPS (0, 25, 50, 100, 500 and 1,000 ng/ml) for 48 h or with 500 ng/ml PgLPS for various lengths of time (0, 6, 12, 24, 48 and 72 h). The PgLPS‑stimulated cells were pretreated with different concentrations of CGRP (0, 1, 10, 100 and 1,000 nM) and cell viability and apoptotic rates were measured by Cell Counting kit‑8 assays and flow cytometry, respectively. CGRP, cleaved (c)‑Caspase‑8 and c‑Caspase‑3 protein expression levels were analyzed by western blotting. Changes in cytokine expression levels, which included tumor necrosis factor (TNF)‑α, interleukin (IL)‑1β, IL‑6, monocyte chemotactic protein (MCP)‑1 and MCP‑2, were measured by ELISA. PgLPS was demonstrated to inhibit osteoblast viability and promote apoptosis in a time‑ and concentration‑dependent manner. CGRP expression was revealed to reduce PgLPS‑induced cytostatic activity and apoptosis in osteoblasts. CGRP also suppressed the PgLPS‑induced release of TNF‑α and inhibited the activation of c‑Caspase‑3 and c‑Caspase‑8, thus preventing apoptosis in osteoblasts. CGRP may be an important neuropeptide in bone remodeling and may reduce osteoblast apoptosis in inflammatory conditions. These results may provide a solid foundation for CGRP to serve as a new target for the treatment of periodontitis.

Zika virus (ZIKV) infection has become an emerging concern of global public health. Several recent studies provide new insights into the evolution and diversity of ZIKV, with important implications for ongoing surveillance and control measures.

The aim of this study was to compare the effect of high fruit and soybean products diet and standard diet interventions on serum uric acid (SUA) in asymptomatic hyperuricemia adults. A total of 187 Chinese adults (20-59 years old) with asymptomatic hyperuricemia participated in this randomized trial and were assigned to receive the standard diet recommended by guideline (group 1) and high fruit and soybean products diet (group 2) for 3 months. The outcome of SUA was assessed before and at the end of the intervention period. After 3 months, the SUA in group 1 and group 2 was significant reduced, whereas the SUA was not significantly changed in-between groups. These data suggest that over a 3-month period, although the high fruit and soybean products diet and standard diet interventions yield no different effects on SUA, the high fruit and soybean products dietary intervention could be an effective alternative to a standard diet for achieving clinically important reductions in SUA for asymptomatic hyperuricemia patients.

The aim of the present study was to determine if the excitatory amino acid homocysteine (Hcy) alters ERK signaling and cell proliferation in fetal neural stem cells (NSCs) in vitro. NSCs were isolated from fetal rats and grown in serum-free suspension medium. The cells were identified as NSCs by their expression of immunoreactive Sox2. NSCs were assigned to one of four treatment groups: vehicle control, low-dose Hcy group (Hcy-L, medium contained 30 μmol/L Hcy), middle-dose Hcy group (Hcy-M, 100 μmol/L Hcy) and high-dose Hcy group (Hcy-H, 300 μmol/L Hcy). Cell proliferation was evaluated by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. Protein expression levels of ERK1/2 and phosphorylated ERK1/2 were detected by Western blot. The effects of Hcy on NSC death, including apoptosis, were assessed by using flow cytometry and trypan blue exclusion. The results showed that NSCs grew as neurospheres in the serum-free medium. Hcy decreased ERK1/2 protein phosphorylation and NSC proliferation, but it did not induce cell death or apoptosis within the concentration from 30 to 300 μmol/L. The above results are consistent with the hypothesis that Hcy decreases fetal NSC proliferation by inhibiting ERK signaling.

OBJECTIVE To evaluate core needle biopsy (CNB) as a mini-mally invasive method to examine breast lesions and discuss the clinical significance of subsequent immunohistochemistry (IHC) analysis. METHODS The clinical data and pathological results of 235pa-tients with breast lesions, who received CNB before surgery, were analyzed and compared. Based on the results of CNB done before surgery, 87 out of 204 patients diagnosed as invasive carcinoma were subjected to immunodetection for p53, c-erbB-2, ER and PR. The morphological change of cancer tissues in response to chemo-therapy was also evaluated. RESULTS In total of 235 cases receiving CNB examination,204 were diagnosed as invasive carcinoma, reaching a 100% consistent rate with the surgical diagnosis. Sixty percent of the cases diag-nosed as non-invasive carcinoma by CNB was identified to have the presence of invading elements in surgical specimens, and simi-larly, 50% of the cases diagnosed as atypical ductal hyperplasia by CNB was confirmed to be carcinoma by the subsequent result of excision biopsy. There was no significant difference between the CNB biopsy and regular surgical samples in positive rate of im-munohistochemistry analysis (p53, c-erbB-2, ER and PR; P > 0.05). However, there was signifi cant difference in the expression rate of p53 and c-erbB-2 between the cases with and without morphologi-cal change in response to chemotherapy ( P < 0.05). In most cases with p53 and c-erbB-2 positive, there was no obvious morphologi-cal change after chemotherapy. CONCLUSION CNB is a cost-eff ective diagnostic method with minimal invasion for breast lesions, although it still has some limi-tations. Immunodetection on CNB tissue is expected to have great significance in clinical applications.

Although a simple linear progression model for breast cancer has already been proposed, its validity still remains controversial. Especially, the genetic and molecular features of breast cancer at different stages during the development and progression, as well as their relationship, have rarely been studied under the same experimental conditions simultaneously. According to these limitations in this research area, the current study applied comparative genomic hybridization technique to investigate genomic changes in 15 cases of breast atypical ductal hyperplasia (ADH), 15 cases of ductal carcinomas in situ (DCIS), and 15 cases of invasive ductal carcinomas (IDC) and the relationship among the genetic changes. Thirty commonly altered regions that were identified included known (gains of 1q,8q, 17q,20q,Xq and losses of 8p,13q,16q,17p,22q) and several uncharacterized (gains of 2q,5p, 10p,12q,16p,18q, etc. and losses of 11p13-pter,11q,14q,Xp, etc). The overall frequency of copy number losses was higher in IDC than that in DCIS (P = 0.013). ADH showed more frequent gain of 17q than that in IDC (P = 0.007), and IDC exhibited a higher frequency for the loss of 22q than that in ADH (P = 0.018). On one hand, several common genomic changes shared by ADH, DCIS, and IDC make a linear relationship for these three lesions possible. On the other hand, the heterogeneity has also showed clonal diversification and different pathways of breast cancer progression. The regions of chromosomal copy number alterations may bring new insights into the strategy for tumor progression blocking and the discovery of new potential targets for breast cancer treatment.

Objective To explore the expression of β-tubulin in premalignant lesions and carcinomas of the breast, and to observe the relationship of its expression with breast cancer pathological features.

Objective To investigate the correlation of E2F-1, Rb and ER expression with peripheral papilloma (Peri-PM) and ductal carcinoma in situ of the breast (DCIS), and further explore some molecular mechanisms of the canceration of Peri-PM.

Hyperuricemia is an independent risk factor for hypertension. This study aims to investigate whether SUA predicts 2-year incidence of hypertension in population with pre-hypertension and ideal blood pressure in Tianjin, China.In this population-based prospective study, we analyzed 608 subjects (455 women) aged 40-70 with non-hypertension (SBP140 mmHg and DBP90 mmHg) who were recruited with stratified cluster sampling method across six districts of Tianjin in 2011-2012. Participants were divided into pre-hypertensive group (group P) and ideal blood pressure group (group I) according to their first physical examination. After 2 years follow-up, the second physical examination was taken on the same crowd. The 2-year hypertension incidence rate in group P (35.6%) was higher than that of group I (8.3%) (p0.05). In group P, the hypertension incidence rate increased with the increase of SUA quartiles. Multivariate logistic regression analysis showed that the odd ratio (OR) between the highest SUA quartile group and the lowest SUA quartile group in group P were 2.02 (1.04-3.92), 3.34 (1.10-10.04) in men and 2.43 (1.08-5.45) in women (p0.05). However, there is no significant correlation between SUA and the risk for hypertension incidence in group I. Multiple linear regression showed that the SBP increased 0.017 mmHg with the increasing of 1 μmol/L deviation of SUA in group P.SUA levels predict SBP elevation and hypertension incidence in population with pre-hypertension, however, do not predict the DBP elevation in pre-hypertensive population as well as change of BP in ideal blood pressure population.

In this study, we evaluated the prognostic value of plasma galectin-3 levels in patients with coronary heart disease (CHD) and chronic heart failure (HF) and selected 261 CHD patients who were consecutively admitted to our hospital. The enrolled chronic HF patients included HF patients with preserved ejection fraction (HFpEF) and reduced ejection fraction (HFrEF). Patients without HF served as the control group. Galectin-3 and B-type natriuretic peptide (BNP) levels were determined and the primary endpoint was the composite of all-cause mortality and rehospitalization with 12-month follow-up. Plasma galectin-3 levels were higher in HF patients compared with non-HF patients (P < 0.001). Receiver operating characteristic (ROC) analyses for diagnosis of HF showed that galectin-3 had the greatest area under the curve (AUC) of 0.756 (P < 0.001), with an optimal cutoff of 10.8 ng/mL, yielding a sensitivity of 81.7% and a specificity of 61.7%. Follow-up ROC analyses of galectin-3 for outcome prediction showed an optimal cutoff of 17.8 ng/ mL, yielding a sensitivity of 97.3% and a specificity of 77.6%. Galectin-3 yielded an AUC of 0.899 (P < 0.001), whereas the AUC of BNP was 0.633 (P = 0.022). Galectin-3 led to an AUC of 0.931 (P < 0.001) for HFpEF and an AUC of 0.882 (P < 0.001) for HFrEF. Cox proportional hazards regression analysis revealed that galectin-3 was an independent prognostic predictor for chronic HF, especially for HFpEF patients (RR: 1.231, 95% CI: 1.066-1.442). In summary, plasma galectin-3 levels were increased in CHD HF patients and were an independent predictor of all-cause mortality and rehospitalization. In HFpEF patients galectin-3 levels correlated stronger with outcomes than in HFrEF patients.

Recent efforts have revealed the microRNA (miRNA) pathways in the pathogenesis of Alzheimer's disease (AD). Epidemiological studies have revealed an association between folic acid deficiency and AD risk. However, the effects of folic acid deficiency on miRNA expression in AD animals have not been observed. We aimed to find if folic acid deficiency may enhance amyloid-β (Aβ) peptide deposition and regulate amyloid-associated miRNAs and their target genes expression in APP/PS1 mice. APP/PS1 mice and N2a cells were treated with folic acid-deficient diet or medium. Cognitive function of mice was assessed using the Morris water maze. miRNA profile was tested by polymerase chain reaction (PCR) array. Different expressional miRNAs were validated by real-time PCR. The deposition of Aβ plaques was evaluated by immunohistochemistry and enzyme-linked immunosorbent assay. APP and BACE1 proteins in mice brain and N2a cells were determined by Western blot. Folic acid deficiency aggravated amyloid pathology in AD mice. The AD+FD group showed shorter time spent in the target zone during the probe test. Analysis of miRNAs predicted to target these genes revealed several miRNA candidates that were differentially modulated by folic acid deficiency. In APP/PS1 mice brains and N2a cells with folic acid-deficient treatment, miR-106a-5p, miR-200b-3p and miR-339-5p were down-regulated, and their target genes APP and BACE1 were up-regulated. In conclusion, folic acid deficiency can enhance Aβ accumulation in APP/PS1 mice brain and decrease amyloid-associated miRNAs expression.

High incidence rate of Alzheimer's disease (AD) is observed in patients with type 2 diabetes. Aggregated β-amyloid (Aβ) and hyperphosphorylated tau are the hallmarks of AD. Hyperphosphorylated tau has been detected in diabetic animals as well as in diabetic patients. Folates mediate the transfer of one carbon unit, required in various biochemical reactions. The effect of folate on tau phosphorylation in diabetic models still remains unknown. In this study, we investigated the effect and mechanism of folic acid on hyperphosphorylation of tau in streptozotocin (STZ)-induced diabetic mice. Diabetic mice induced by STZ, at the age of 10 weeks, were administered with three levels of folic acid: folic acid-deficient diet, diet with normal folic acid content, and 120 μg/kg folic acid diet for 8 weeks. Levels of serum folate and blood glucose were monitored. Tau phosphorylation, protein phosphatase 2A (PP2A) methylation, and Glycogen synthase kinase 3β (GSK-3β) phosphorylation were detected using Western blot. The S-adenosyl methionine:S-adenosyl homocysteine ratio (SAM:SAH) in brain tissues was also determined. DNA methyltransferase (DNMT) mRNA expression levels were detected using real-time PCR. Folic acid reduced tau hyperphosphorylation at Ser396 in the brain of diabetes mellitus (DM) mice. In addition, PP2A methylation and DNMT1 mRNA expression were significantly increased in DM mice post folic acid treatment. GSK-3β phosphorylation was not regulated by folic acid administration. Folic acid can reduce tau phosphorylation by regulating PP2A methylation in diabetic mice. These results support that folic acid can serve as a multitarget neuronal therapeutic agent for treating diabetes-associated cognitive dysfunction.

Background Because human diets are composed of a wide variety of nutrients that may work synergistically to prevent or promote disease, assessing dietary nutrient intake status may be informative. The purpose of this study was to assess the dietary nutrient intake status of Chinese adults with metabolic syndrome (MetS) and to evaluate its possible role in MetS. Methods This case–control study was conducted from March 2010 to January 2011. A total of 123 patients with MetS and 135 controls participated in this study at the Health Examination Center of Heping District in Tianjin, China. Dietary intake was estimated by 24-h dietary recalls. We used principal component factor analysis to derive nutrient groups from 17 major nutrients. We examined the odds ratios and 95% confidence intervals using logistic regression models to test the relationship between tertiles of dietary nutrient pattern and MetS. Results There were 4 major dietary nutrient patterns in this study: “vitamin B group”, “protein and lipids”, “vitamin E and minerals”, and “antioxidant vitamins”. After adjustment for potential confounders, the highest tertile of the nutrient pattern factor score for the “vitamin B group” (odds ratio: 0.16; 95% confidence interval: 0.05–0.47) was negatively associated with MetS compared with the lowest tertiles. No relationships were found between other dietary nutrient patterns and MetS. Conclusions The “vitamin B group” pattern was inversely associated with MetS in Chinese adults. This finding supports the hypothesis that the “vitamin B group” pattern may have a potentially beneficial effect on the prevention of MetS.

In this study, we conducted a case-control study to evaluate the association of major dietary patterns and asymptomatic hyperuricemia taking account of blood lipids in Chinese adults. 187 cases with confirmed asymptomatic hyperuricemia and 187 controls were frequency matched on age, gender and area of residence. We conducted factor analysis using dietary information from a validated food frequency questionnaire to derive dietary patterns. The association between major dietary patterns and asymptomatic hyperuricemia was assessed by logistic regression analysis. Three major dietary patterns were found: 1) "animal products and fried food," 2) "western," 3) "soybean products and fruit." In multivariate analyses the "animal products and fried food" pattern score was associated with an odds ratio (OR) of 2.15 (95% CI, 1.22-3.76) compared with the lowest tertile. The OR for the top tertile of score for "soybean products and fruit" pattern was 0.32 (95% CI, 0.19-0.57) compared with the lowest tertile of "soybean products and fruit" pattern score. The significant association of these two patterns and asymptomatic hyperuricemia persisted after further adjusting for blood lipids. On the other hand, the "western" pattern was not associated with asymptomatic hyperuricemia. We observed a positive relationship between the "animal products and fried food" pattern and asymptomatic hyperuricemia, and a negative relationship between the "soybean products and fruit" pattern and asymptomatic hyperuricemia, independent of blood lipids.

Folic acid (FA) stimulates neural stem cell (NSC) proliferation in vitro and enhances hippocampal neurogenesis in rats after middle cerebral artery occlusion (MCAO). The effect of FA supplementation on exogenous NSCs transplanted in MCAO rats was observed to determine if FA can stimulate NSC replacement after focal cerebral ischemia. Rats were randomly assigned to 3 groups: MCAO; MCAO and exogenous NSC transplantation (MCAO+NSCs); and MCAO, NSC transplantation and FA (MCAO+NSCs+FA). FA (0.8 mg/kg) or vehicle was administered by gavage daily for 28 days before MCAO and 23 days afterward. NSCs were labeled with superparamagnetic iron oxide (SPIO) and bromodeoxyuridine (BrdU) prior to transplantation into the striatum, contralateral to the ischemic zone, at 2 days post-MCAO. Magnetic resonance imaging tracking and fluorescent immunohistochemistry, as well as measurement of serum folate concentration, were performed at intervals up to 21 days after transplantation. FA supplementation caused sustained increases of 400–600% in serum folate concentration. Magnetic resonance images indicated that SPIO-labeled NSCs were more abundant at the transplantation and ischemic brain sites in MCAO+NSCs+FA rats than in MCAO+NSCs rats. Similarly, immunohistochemistry showed that the numbers of Sox-2/BrdU double positive cells at the transplantation and ischemic sites were higher in the rats that received FA. In conclusion, after focal cerebral ischemia, FA supplementation stimulates transplanted NSCs to proliferate and migrate to ischemic sites.

The relation between serum uric acid and metabolic syndrome is observed not only with frank hyperuricemia but also with serum uric acid levels within the normal range. The current “normal” range set for hyperuricemia often fails to identify patients with potential metabolic disorders. We investigate the association between serum uric acid within the normal range and incident metabolic syndrome risk, and further to determine the optimal cut-off value of serum uric acid for the diagnosis or prediction of metabolic syndrome. A total of 7399 Chinese adults (2957 men and 4442 women; ≥20 years) free of metabolic syndrome were followed for 3 years. During the 3-year follow-up, 1190 normouricemic individuals developed metabolic syndrome (16.1%). After adjusting the associated variables, the top quartile of serum uric acid levels was associated with higher metabolic syndrome development compared with the bottom quartile in men (hazard ratio (HR), 1.29; p

Centrosome abnormalities occur frequently in various tumors and can cause chromosomal instability and eventually promote cancer development. We investigated the chromosome aberrations associated with centrosome abnormalities in 30 cases of breast cancer, combining immunohistochemical staining and comparative genomic hybridization. Except for some common chromosome alterations (including gains of 1q, 8q, 17q, 20q, and Xq and losses of 8p, 11q, 13q, 14q, 16q, 17p, 22q, and Xp) that have also been seen more frequently in other studies, we discovered some new changes that have rarely been reported, including gains at 2p, 5p, 10p, 15q, 16p, 18q, 21q, and 22q and losses at 6p, 8p23, 11p13-pter, 13q34, and 14q32-qter. We also identified some changes (such as gains of 17q, 20q, and Xq and losses of 17p, 13q, and 14q) harboring candidate genes. We also explored the expression of centrosome protein in different molecular subtypes of breast cancer. Our findings provide a new way to explore the molecular mechanisms of breast tumorigenesis and accordingly potential new targets for therapy for this disease.

Minichromosome maintenance proteins are novel proliferative markers that have been proposed as diagnostic markers in many cancers. We evaluated the potential role of minichromosome maintenance protein 2 as a screening biomarker and compared it with proliferating cell nuclear antigen and Ki67 in a population survey of esophageal squamous cell carcinoma. A total of 299 esophageal samples from a high-risk region in China, including 171 from an endoscopy population survey, 30 from brushing cytology, and 98 from surgery and autopsy, underwent immunostaining with minichromosome maintenance protein 2, proliferating cell nuclear antigen, and Ki67 antibodies. Minichromosome maintenance protein 2 expression was confined to the proliferative compartment of normal and abnormal esophageal epithelium and particularly manifested in the surface layer of dysplasia and carcinoma in situ. The expression of proliferating cell nuclear antigen and Ki67 was positively correlated with that of minichromosome maintenance protein 2 (r(s)0.39, P.01); but their positive nuclei seldom reached the surface layer, and the labeling indices were significantly lower than those for minichromosome maintenance protein 2 in dysplasia (P.05) and carcinoma in situ (P.001). The sensitivity and specificity of minichromosome maintenance protein 2 in diagnosing dysplasia were 91.3% and 61.8%, respectively, higher than those for proliferating cell nuclear antigen (88.4% and 47.1%) and Ki67 (78.3% and 57.8%). Nine of 10 cancer and paracancerous surface-brushing samples expressed minichromosome maintenance protein 2, and the detection was higher than that for proliferating cell nuclear antigen (8/10 and 7/10) and Ki67 (7/10 and 7/10). However, none of 10 normal surface-brushing samples expressed the 3 markers. Minichromosome maintenance protein 2 is more sensitive and specific than proliferating cell nuclear antigen and Ki67 in indicating esophageal dysplasia. Minichromosome maintenance protein 2 immunostaining combined with surface brushing could be valuable in screening patients at high risk of cancer in mass surveys.

The purpose of our study was to investigate the temporal malignant tumor incidence rates among the 70,000 residents at the relatively isolated Nanao Island in South China Sea. The data on all malignant tumor cases from Nanao Cancer Registry during 1995-2004 were coded, computerized, and analyzed using the software SPSS10.0. The tumor incident cases, crude incident rate, age-standardized incidence rate, their sex distribution and temporal trend were assessed. A total of 1450 new cancer cases (990 males and 460 females) were identified. The annual average age-standardized incidence rate (ASR) of malignant tumors was 208.18/100,000. The age-standardized incidence rate of the ten leading cancers in both sexes combined per 100,000 population were 74.47 for esophageal cancer (EC), 34.81 for cardiac cancer (CC), 25.66 for liver cancer, 26.01 for lung cancer, 18.52 for stomach cancer, 4.45 for nasopharyngeal cancer, 3.91 for breast cancer, 2.53 for colon/rectum cancer, 2.45 for bladder cancer and 1.92 for pancreatic cancer. These ten types of cancers make up to 93% of all cancer cases, with EC and CC being the most prevalent and making up 52% of the total cases. The incidence rates of esophagus, liver, lung, breast, nasopharyngeal, and colon/rectum cancers showed increasing trends during the period from 1995 to 2004 in Nanao Island. Astounding the EC ASR were 72-150/100,000 among male and 26-64/100,000 among female in Nanao Island during 1995-2004. The EC incidence rate in Nanao population is among the highest across the world, which suggests that there are potential genetic and/or environmental factors affecting this particular population.