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Ultraviolet (UV) radiation is considered to be a potent cell-damaging agent in various cell lineages; however, the effect of UV light-emitting diode (LED) irradiation on human cells remains unclear. The aim of the present study was to examine the effect of UV LED irradiation emitting at 280 nm on cultured HL-60 human leukemia cells, and to explore the underlying mechanisms. HL-60 cells were irradiated with UV LED (8, 15, 30 and 60 J/m2) and incubated for 2 h after irradiation. The rates of cell proliferation and apoptosis, the cell cycle profiles and the mRNA expression of B-cell lymphoma 2 (Bcl-2) were detected using cell counting kit-8, multicaspase assays, propidium iodide staining and reverse transcription-quantitative polymerase chain reaction, respectively. The results showed that UV LED irradiation (8-60 J/m2) inhibited the proliferation of HL-60 cells in a dose-dependent manner. UV LED at 8-30 J/m2 induced dose-dependent apoptosis and G0/G1 cell cycle arrest, and inhibited the expression of Bcl-2 mRNA, while UV LED at 60 J/m2 induced necrosis. In conclusion, 280 nm UV LED irradiation inhibits proliferation and induces apoptosis and necrosis in cultured HL-60 cells. In addition, the cell cycle arrest at the G0/G1 phase and the downregulation of Bcl-2 mRNA expression were shown to be involved in UV LED-induced apoptosis. [ABSTRACT FROM AUTHOR]

Malaria remains as one of the major public health problems worldwide. About 228 million cases occurred in 2018 only, with Africa bearing about 93% of the cases. Asymptomatic population carrying the various forms of the parasite Plasmodium in endemic areas plays an important role in the spread of the disease. To tackle this battle, more sensitive and precise detection kits for malaria are crucial to better control the number of new malaria cases. In this review, we not only discuss some of the available approaches to rapidly detect new malaria cases in endemic areas but also shed light on parallel problems that may affect the detection of individuals infected with the parasite, covering kelch 13 mutation, glucose 6-phosphate dehydrogenase deficiency, and hemoglobin disorders. Available approaches for malaria detection covered in this review are focused on point-of-care tests, including portable polymerase chain reaction and aptamers. [ABSTRACT FROM AUTHOR]

Background: Obesity is a principal risk factor for the development of type 2 diabetes and cardiovascular diseases. Natural plants and/or foods play an important role in the management of obesity. Acalypha australis L. (AAL) is a kind of potherb popular among Asian populations, and it is also consumed as a food ingredient and traditional herbal medicine. Objective: We investigated the effects of water extract from AAL on high-fat-diet (HFD)-induced obese mice and 3T3-L1 adipocytes to develop a new functional food material. Design: Nine-week-old male mice were randomly divided into control (chow diet, n = 6) and HFD (n = 30) group. From 12-weeks onward, mice in the HFD group were further separated into model (saline, 6 mL/kg), simvastatin (0.11 mg/mL, 6 mL/kg), and AAL treatment (low, middle, and high dosage: 300, 600, and 900 mg/kg) group, with 6 animals per group, while mice in the control group were treated with saline (6 mL/ kg). Food intake, body/fat weight, liver/kidney indexes, and lipid profiles were determined. Tissues were fixed with formalin for pathological examination. Western blotting and PCR were performed to evaluate the protein and mRNA expression in 3T3-L1 adipocytes. Oil Red O staining was used to determine lipid accumulation. Results: AAL administration significantly suppressed body weight gain, and reduced fat pad weight and Lee's index in obese mice, but had no effect on liver/kidney index. AAL also reduced serum cholesterol, triglyceride, and LDL-C and increased HDL-C levels. Histological analysis revealed that AAL significantly ameliorated lipid accumulation in the liver and subcutaneous adipose tissue. In vitro, Oil Red O staining showed that AAL inhibited adipose differentiation by down-regulating the gene and protein expression of PPARγ and C/EBPα. AAL also reversed HFD-induced intestinal dysbacteriosis. Conclusion: AAL water-soluble extract has a significant anti-adipogenic effect in the HFD-induced obese mice model. [ABSTRACT FROM AUTHOR]

The aim of the current study was to investigate the biological effect on T24 cells and human umbilical vein endothelial cells (HUVECs) of transfection with brain-specific angiogenesis inhibitor-1 (BAI-1). The recombinant plasmid pReceiver-M61-BAI-1 was transfected into human superficial bladder tumor cells (T24) and HUVECs, in parallel with the vector control. mRNA and protein expression levels of BAI-1 were then detected by quantitative polymerase chain reaction (qPCR) and western blotting, respectively. Cell apoptosis of T24 cells and HUVECs prior and subsequent to transfection with BAI-1 was analyzed by flow cytometric analysis. Proliferation of T24 cells and HUVECs prior and subsequent to transfection of BAI-1 was assessed by the MTT method. T24 cells and HUVECs transfected with pReceiver-M61-BA1-1 were classed as the experimental group; T24 cells and HUVECs transfected with p-Receiver-M61 were the control group. qPCR and western blotting methods confirmed that there was positive expression of BAI-1 in T24 cells and HUVECs transfected with pReceiver-M61-BAI-1, however BAI-1 was not expressed in T24 cells and HUVECs transfected with pReceiver-M61. The results of the MTT assay demonstrated that absorbance was markedly reduced in HUVECs at 12, 48 and 72 h subsequent to transfection with pReceiver-M61-BAI-1 when compared with that of the control group and in T24 cells transfected with p-Receiver-M61-BAI-1. Furthermore, flow cytometry results also indicated that the apoptotic rate of HUVECs transfected with p-Receiver-M61-BAI-1 was significantly increased compared with that of the control group and T24 cells transfected with p-Receiver-M61-BAI-1. BAI-1 was observed to markedly inhibit the proliferation of vascular endothelial cells in vitro, however, no direct inhibition by BAI-1 was observed in T24 cells. In conclusion, BAI-1 is suggested to be a potential novel therapautic target for the inhibition of tumor neovascularization. [ABSTRACT FROM AUTHOR]

Background: Hepatitis B virus (HBV) infection is a severe health problem in the world; however, there is still no satisfactory therapeutic strategy for the HBV infection. In search for new anti-HBV agents with higher efficiency and less side effects, the anti-HBV activities of traditional Chinese medicine Rheum palmatum L. ethanol extract (RPE) and isolated anthraquinones were evaluated. Methods: The anti-HBV activities of RPE and isolated anthraquinones were demonstrated in a stable HBV-producing cell line HepG2 2.2.15 by using real-time polymerase chain reaction (PCR), enzyme-linked immunosorbent assay (ELISA) and Southern blot analysis. Results: RPE could inhibit HBV-DNA production and HBsAg expression in a dose-dependent manner. The concentration of 50% HBV-DNA inhibition (IC50) of RPE was calculated at 212.36 ± 11 μg/ml. Six anthraquinones were isolated from RPE by using RP-HPLC. Five free anthraquinones showed weakly or slightly inhibitory activities against HBV. The only combined anthraquinone chrysophanol 8-O-β-D-glucoside exhibited significant activity against HBV DNA production and antigens expression with an IC50 value of 36.98 ± 2.28 μg/ml on HBV DNA inhibition. Endogenous HBV DNA polymerase activity assay indicated that chrysophanol 8-O-β-D-glucoside might be a potential inhibitor of the HBV DNA polymerase. Conclusions: The results suggested that RPE could effectively inhibit HBV. The combined anthraquinone chrysophanol 8-O-β-D-glucoside is the major active compound in RPE and could be a promising candidate for the development of new anti-HBV drugs in the treatment of HBV infection. Copyright © 2007 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Alzheimer's disease (AD) is a chronic progressive neurodegenerative disorder. However, its pathogenetic mechanism is still poorly understood. An increasing number of studies have evidenced the important role of long noncoding RNAs (lncRNAs) in AD. The aim of the current study was to investigate the effect and molecular mechanism of the lncRNA X‐inactive specific transcript (XIST) in AD. Bilateral common carotid artery occlusion (2VO) was used to induce an AD model in mice. Hydrogen peroxide (H2O2) was used to induce an AD model in N2a cells. The lncRNA XIST, miR‐124, and BACE1 messenger RNA expression levels were detected by a real‐time polymerase chain reaction. The BACE1 protein expression level was detected by western blot and immunofluorescence assay. The Aβ1–42 expression level was detected using an enzyme‐linked immunosorbent assay kit. The expression level of lncRNA XIST was significantly upregulated in AD models, both in vivo and in vitro. Silencing of lncRNA XIST negatively regulated miR‐124 and positively regulated BACE1 expression in N2a cells, which is attenuated by cotransfection of anti‐miR‐124 oligodeoxyribonucleotide (AMO‐124). Silencing of lncRNA XIST reversed the effect of H2O2 on miR‐124, BACE1, and Aβ1–42 expression in N2a cells, which was reversed by cotransfection of AMO‐124. Silencing of lncRNA XIST attenuated AD‐related BACE1 alteration through miR‐124. LncRNA XIST may be a new potential target for the treatment of AD. [ABSTRACT FROM AUTHOR]

Background: Mycoplasma-related vaginitis gradually has been growing as a threat in adults--genitourinary infection contributes to funisitis, spontaneous abortion, and low birth weight. Until now, use of loop-mediated isothermal amplification (LAMP) to detect Ureaplasma urealyticum (UU), Mycoplasma hominis (MH), or Mycoplasma genitalium (MG) has been reported by some researchers. However, previous studies focused on purified DNA as the template for LAMP assay, which is usually extracted via commercial kit. Methods: We developed a LAMP assay for rapid detection of UU, MH, and MG genital mycoplasmas using a simple boiling method for DNA extraction, in a cohort of pregnant women with mycoplasma-related vaginitis. We monitored amplicons with the naked eye using SYBR Green I. Results: The cohort in our study showed a prevalence of 22.6% in pregnant women, as detected by UU-LAMP assay. Compared to the polymerase chain reaction (PCR) test with purified DNA, the sensitivity of the UU-LAMP in clinical specimens with crude DNA was 87.5% (95% confidence interval [CI], 64.6%->99.9). For crude DNA specimens, UU-LAMP was more sensitive and reliable than PCR, with a higher agreement rate (96.8%) and Youden index value (0.88). Conclusions: As a point-of-care test, LAMP is a useful, specific, and efficient way to detect genital mycoplasmas in resource-limited settings, especially for crude DNA. [ABSTRACT FROM AUTHOR]

Background: Cholesterol accumulation causes pancreatic beta cell lipotoxicity and dysfunction. Cholesteryl ester transfer protein (CETP) plays an important role in blood lipid homeostasis. However, its role in tissue lipid metabolism remains unclear. We hypothesized that plasma CETP impact cholesterol homeostasis in the beta cells, thus damaging their functions. Methods: The adipose tissue-specific CETP expression transgenic (aP2-CETPTg) mice, characterized by high CETP levels in the circulation, were used in this study. Pancreatic islet cholesterol and beta cell function were assessed in mice. We further measured mRNA levels of the genes involved in beta cell proliferation and differentiation, inflammation and cholesterol metabolism. TUNEL assay was applied to investigate beta cell apoptosis in islets. Results: The aP2-CETPTg mice exhibited glucose intolerance, lower plasma insulin concentrations but increased insulin sensitivity compared with wild type mice. In addition, glucose-stimulated insulin secretion from isolated pancreatic islets significantly decreased, and free cholesterol significantly increased. Moreover, the number and size of islets from aP2-CETPTg mice were significantly decreased. Genes involved in beta cell proliferation, such as Pdx1 and BETA2, were down-regulated; genes involved in inflammation and ER stress, such as IL-1β, CHOP, and Xbp1 were up-regulated, in line with an increase of beta cell apoptosis. Conclusions: Plasma CETP causes free cholesterol accumulation in islets which could contribute to beta cell dysfunction. Thus, CETP inhibition could be a novel protective strategy for dyslipidemia related to diabetes and obese. [ABSTRACT FROM AUTHOR]

Background Because of the shared transmission routes, co-infection with human immunodeficiency virus (HIV) and hepatitis C virus (HIV) is very common. Accumulated clinical evidence showed that one could alter the infectious course of the other virus in HIV and HCV co-infected individuals. However, little is known on the molecular basis of HIV/HCV interactions and their modulations on hosts. Methods In this study, treatment-naive HIV, HCV mono-/co-infected individuals with CD4+ T cell counts >300/μl were recruited and their gene expression profiles were investigated by microarray assays. The differentially expressed genes were identified and validated by quantitative real-time PCR (qRT-PCR). To further understand the biological meanings of the gene expression profiles in these three groups, GSEA analysis (version 2.0, Broad Institute http://www.broad.mit.edu/gsea) was performed. Results By gene set enrichment analysis, we revealed that gene sets of cell cycle progression, innate immune response and some transcription factors in CD4+ T cells were mainly affected by HIV; while genes associated with GPCR signaling were the major targets of HCV. Metabolic pathways were modulated by both HCV and HIV viruses. Conclusions This study for the first time offers gene profiling basis for HCV/HIV mono-/co- infections in human beings. HIV infection displayed the great impact on transcription profile of CD4+ T cells in HIV/HCV co-infected individuals. Genes related to cell cycle arrest were significantly mediated by HIV which may lead to dysfunction of CD4+ T cells and acceleration of HCV-related disease progression in the co-infections. [ABSTRACT FROM AUTHOR]

The widely used pseudorabies virus (PRV) Bartha-K61 vaccine has played a key role in the eradication of PRV. Since late 2011, however, a disease characterized by neurologic symptoms and a high number of deaths among newborn piglets has occurred among Bartha-K61-vaccinated pigs on many farms in China. Clinical samples from pigs on 15 farms in 6 provinces were examined. The PRV gE gene was detectable by PCR in all samples, and sequence analysis of the gE gene showed that all isolates belonged to a relatively independent cluster and contained 2 amino acid insertions. A PRV (named HeN1) was isolated and caused transitional fever in pigs. In protection assays, Bartha-K61 vaccine provided 100% protection against lethal challenge with SC (a classical PRV) but only 50% protection against 4 challenges with strain HeN1. The findings suggest that Bartha-K61 vaccine does not provide effective protection against PRV HeN1 infection. [ABSTRACT FROM AUTHOR]

The prag01 gene (GenBank accession no. EU073017) was cloned from Culex pipiens pallens. An open reading frame of 270 bp was found to encode a putative 89-amino-acid protein which has the highest homology with Culex quinquefasciatus and Anopheles funestus. Real-time quantitative PCR analysis demonstrated that the transcription level of prag01 gene in deltamethrin-resistant strain was 1.65-fold higher than in deltamethrin-susceptible strain of C. pipiens pallens. Overexpression of prag01 gene in the mosquito C6/36 cells showed better prolification than the cells with empty vector when treated by deltamethrin. Our data for the first time approved that prag01 gene might play some role in the development of deltamethrin resistance in C. pipiens pallens. [ABSTRACT FROM AUTHOR]

Pyrethroid insecticides have been extensively used in China and worldwide for public health pest control. Accurate resistance monitoring is essential to guide the rational use of insecticides and resistance management. Here we examined the nucleotide diversity of the para-sodium channel gene, which confers knockdown resistance (kdr) in Culex pipiens pallens mosquitoes in China. The sequence analysis of the para-sodium channel gene identified L1014F and L1014S mutations. We developed and validated allele-specific PCR and the real-time TaqMan methods for resistance diagnosis. The real-time TaqMan method is more superior to the allele-specific PCR method as evidenced by higher amplification rate and better sensitivity and specificity. Significant positive correlation between kdr allele frequency and bioassay-based resistance phenotype demonstrates that the frequency of L1014F and L1014S mutations in the kdr gene can be used as a molecular marker for deltamethrin resistance monitoring in natural Cx. pipiens pallens populations in the East China region. The laboratory selection experiment found that L1014F mutation frequency, but not L1014S mutation, responded to deltamethrin selection, suggesting that the L1014F mutation is the key mutation conferring resistance to deltamethrin. High L1014F mutation frequency detected in six populations of Cx. pipens pallens suggests high prevalence of pyrethroid resistance in Eastern China, calling for further surveys to map the resistance in China and for investigating alternative mosquito control strategies. [ABSTRACT FROM AUTHOR]

Aims: To clarify the incidence of multicentric occurrence (MO) and intrahepatic metastasis (IM) for hepatocellular carcinoma (HCC) related to hepatitis B virus in China and to identify the differences between them.Methods: Histopathologic and genetic features of primary and recurrent tumors in 160 cases with HCC were analyzed. The two groups, the origin of which was definitely determinable as of multicentric occurrence or as of intrahepatic metastasis, were analyzed for their disease-free survival and clinicopathological differences.Results: According to histopathological findings, 27.5% and 59.4% patients were considered to be MO and IM, respectively. By comparing the genetic information of loss of heterozygosity and microsatellite instability for 10 different markers between primary and recurrent tumor, 30.0% and 63.8% patients with recurrent HCC were considered to be MO and IM, respectively. In total, 126 cases with unanimous conclusions from the histopathological and genetic method were selected and divided into the MO group (37 cases) and the IM group (89 cases). Analysis of stepwise regression identified that recurrence time, grading, portal vein invasion, tumor number, and Child's stage were the most important discriminating factors between MO and IM (p < 0.05). As for their prognosis, Kaplan-Meier and log rank test showed that the disease-free survival in the MO group was significantly better than in the IM group (p = 0.002).Conclusions: Combined analysis of histopathological and genetic analysis may reflect more exactly the nature of recurrent HCC. The incidence of MO in China is lower than in other countries--30% compared to up to 50% in Japan [Morimoto et al., Journal of Hepatology 39:215-221, 2003; Yamamoto et al., Hepatology 29;1446-1452, 1999]. Recurrence time, tumor grading, portal vein invasion, tumor number, and Child's stage are the most important discriminating factors between MO and IM. The prognosis (disease-free survival) of patients with MO compared to IM is significantly better. [ABSTRACT FROM AUTHOR]

Repetitive mild traumatic brain injury (rmTBI; eg, sports concussions) is a common injury that has been shown to result in significant cognitive impairment and yet, current targeted therapies for rmTBI are lacking. There is a paucity of preclinical and clinical data regarding NMDAR antagonist efficacy in the rmTBI setting. Evidence from other injury models indicates that strategies mitigating N-methyl-daspartate (NMDA) receptor (NMDAR)-mediated excitotoxicity might mitigate rmTBI-induced neurologic deficits. This is particularly attractive as NMDAR antagonists are widely-available and already in clinical use. Thus, we investigated whether a posttraumatic NMDAR blockade protects against adverse functional and histopathological sequelae in an established mouse rmTBI model. Immediately after the last rmTBI injury (5 injuries in 5 days), mice were randomized to receive memantine treatment or vehicle. Functional outcomes were assessed by motor, anxiety/impulsivity and mnemonic behavioral tests. At the synaptic level, NMDAR-dependent long-term potentiation (LTP) was assessed in isolated neocortical slices. At the molecular level, the magnitude of microgliosis and tau hyper-phosphorylation was tested by immunostaining, while NMDAR subunit expression was evaluated by western blot and polymerase chain reaction (PCR). Compared to injured vehicle treated mice, injured memantine treated mice had partially mitigated APP upregulation and reductions in tau phosphorylation. Memantine also ameliorated deficits in LTP and a decline in NMDARs. Furthermore, treatment with memantine in injured mice reduced moicrogliosis after rmTBI. Finally, Open Field testing showed that injured, memantine-treated mice spent less time in the wall zone compared to injured vehicle treated mice. Elevated Plus Maze also revealed that injured, memantine-treated mice performed more like sham mice compared to injured, vehicle-treated mice. No improvement in learning and memory was observed in the injured, memantine-treated group. Our results indicate that early treatment of memantine ameliorates TBI-mediated histopathological changes at the molecular and electrophysiological levels. Furthermore, memantine improves certain behavioral outcomes after rmTBI. This data raises the prospects for therapeutic, post-concussive NMDAR antagonism. Further evaluation of the therapeutic window and dosing for treatment is warranted. [ABSTRACT FROM AUTHOR]