Effects of losses in the hybrid atom-light interferometer

Enhanced Raman scattering can be obtained by injecting a seeded light field which is correlated with the initially prepared collective atomic excitation. This Raman amplification process can be used to realize atom-light hybrid interferometer. We numerically calculate the phase sensitivities and the signal-to-noise ratios of this interferometer with the method of homodyne detection and intensity detection, and give their differences between this two methods. In the presence of loss of light field and atomic decoherence the measure precision will be reduced which can be explained by the break of the intermode decorrelation conditions of output modesComment: 9 pages, 7 figure

2,2′-[(4,6-Dinitro-1,3-phenyl­ene)dioxy]diacetic acid hemihydrate

The skeletons of both independent mol­ecules of the carboxylic acid hemihydrate, C10H8N2O10·0.5H2O, are approximately planar [maximum deviations 0.642 (3) and 0.468 (1) Å]. The deviations arise from the twisting of the nitro groups with respect to the aromatic rings [dihedral angles = 3.24 (2) and 27.01 (1), and 7.87 (1) and 16.37 (2)° in the two molecules]. The crystal structure features inter­molecular O—H⋯O hydrogen bonds, which the link the dicarboxylic acid and water mol­ecules into a supra­molecular layer network

MiRNA-145 increases therapeutic sensibility to gemcitabine treatment of pancreatic adenocarcinoma cells.

Pancreatic adenocarcinoma is one of the most leading causes of cancer-related deaths worldwide. Although recent advances provide various treatment options, pancreatic adenocarcinoma has poor prognosis due to its late diagnosis and ineffective therapeutic multimodality. Gemcitabine is the effective first-line drug in pancreatic adenocarcinoma treatment. However, gemcitabine chemoresistance of pancreatic adenocarcinoma cells has been a major obstacle for limiting its treatment effect. Our study found that p70S6K1 plays an important role in gemcitabine chemoresistence. MiR-145 is a tumor suppressor which directly targets p70S6K1 for inhibiting its expression in pancreatic adenocarcinoma, providing new therapeutic scheme. Our findings revealed a new mechanism underlying gemcitabine chemoresistance in pancreatic adenocarcinoma cells

Optimization of polysaccharides extracted from Verbena officinalis L and their inhibitory effects on invasion and metastasis of colorectal cancer cells

Purpose: To investigate polysaccharides (PEV) extracted from the aerial part of Verbena officinalis L. and their inhibitory effects on the invasion and metastasis of colorectal cancer (CRC) cells.Methods: PEV was extracted by water and the optimization of extraction conditions was performed using a Box-Benhnken design (BBD). The cell viability was evaluated by 4,5-dimethylthiazol-2-yl)2,5-diphenyltetrazolium bromide (MTT) assay. The effects of PEV on cell adhesion and invasion were evaluated by Transwell invasion, wound healing migration and adhesion assays in vitro. The effects of PEV on the expressions of matrix metalloproteinase-9 (MMP-9), mesenchymal-epithelial transition factor (C-met), E-cadherin (E-CAD), cyclooxygenase-2 (COX-2) and E-prostanoid 2 receptor (EP2) were investigated by western blot.Results: The BBD model was established successfully for the optimization of PEV extraction (p <0.0001). The results indicate that PEV (50, 100 and 200 μg/mL) had significant inhibitory effects on cell invasion and migration of SW480 cells (p < 0.05). PEV also significantly decreased cell adhesion of SW480 cells. By treating with PEV, the expressions of C-met, MMP-9, COX-2 and EP2 were decreased, whereas the expression of E-CAD increased in SW480 cells.Conclusion: RSM is effective for optimizing the extraction conditions of PEV. More importantly, PEV significantly inhibits the invasion and metastasis of SW480 cells by regulating the expression of MMP-9, C-met, E-CAD, COX-2 and EP2. Thus, PEV has the potential to be developed into therapeutic drugs for CRC in the future.Keywords: Polysaccharides, Colorectal cancer, Verbena officinalis, SW480 cell lines, Cell invasion, Metastasi

The effect of vitamin D deficiency during pregnancy on adverse birth outcomes in neonates: a systematic review and meta-analysis

ObjectiveTo systematically evaluate the effect of vitamin D deficiency during pregnancy on neonatal adverse outcomes, such as preterm infants, low birth weight infants (LBWI), and small for gestational age (SGA) infants.MethodsA comprehensive literature search was conducted across multiple databases including PubMed, Embase, Cochrane Library, SinoMed, Wanfang Data Knowledge Service Platform, China National Knowledge Internet (CNKI), and VIP Chinese Science and Technology Journal Database (VIP). Following predefined inclusion and exclusion criteria, two researchers independently screened, extracted data, and assessed the quality of the included studies. Meta-analysis was performed using RevMan 5.4 and Stata 14 software to synthesize the findings.ResultsThis study incorporated 13 cohort studies from 8 different countries and regions, encompassing a total of 55,162 pregnant women, among whom 28,155 were identified as having vitamin D deficiency. The Newcastle-Ottawa Scale (NOS) score ranged from 7–9 points. Meta-analysis results indicated a higher incidence of LBWI (OR = 5.52, 95% CI = 1.31–23.22. P = 0.02) in the group of pregnant women with vitamin D deficiency compared to those with adequate levels. However, there was no statistically significant difference in the likelihood of premature birth (OR = 1.25, 95% CI = 0.78–1.99. P = 0.36) or SGA (OR = 1.47, 95% CI = 0.81–2.68. P = 0.21) among newborns born to mothers with vitamin D deficiency vs. those with sufficient levels of vitamin D. Subgroup analysis based on the timing of maternal blood collection revealed that there was no statistically significant association between vitamin D levels during pregnancy and the incidence of preterm birth across all stages of pregnancy. Furthermore, vitamin D deficiency throughout the entire pregnancy was associated with an increased incidence of neonatal LBWI, whereas vitamin D levels during the first, second, and third trimesters did not demonstrate statistically differences on LBWI. Neonates born to mothers with vitamin D deficiency throughout pregnancy were found to have a higher likelihood of developing SGA. However, there was no statistically significant association between vitamin D levels and the development of SGA during the first and second trimesters.ConclusionsAdequate levels of vitamin D during pregnancy may decrease the incidence of LBWI, although further research is needed to determine its impact on the occurrence of preterm birth and SGA.Systematic Review Registrationhttps://www.crd.york.ac.uk/prospero/display_record.php?ID=CRD42024535950, Identifier: (CRD42024535950)

MiR-143 acts as a tumor suppressor by targeting N-RAS and enhances temozolomide-induced apoptosis in glioma.

Therapeutic applications of microRNAs (miRNAs) in RAS-driven glioma were valuable, but their specific roles and functions have yet to be fully elucidated. Here, we firstly report that miR-143 directly targets the neuroblastoma RAS viral oncogene homolog (N-RAS) and functions as a tumor-suppressor in glioma. Overexpression of miR-143 decreased the expression of N-RAS, inhibited PI3K/AKT, MAPK/ERK signaling, and attenuated the accumulation of p65 in nucleus of glioma cells. In human clinical specimens, miR-143 was downregulated where an adverse with N-RAS expression was observed. Furthermore, overexpression of miR-143 decreased glioma cell migration, invasion, tube formation and slowed tumor growth and angiogenesis in a manner associated with N-RAS downregulation in vitro and in vivo. Finally, miR-143 also sensitizes glioma cells to temozolomide (TMZ),the first-line drug for glioma treatment. Taken together, for the first time, our results demonstrate that miR-143 plays a significant role in inactivating the RAS signaling pathway through the inhibition of N-RAS, which may provide a novel therapeutic strategy for treatment of glioma and other RAS-driven cancers

Essential oil from Chenopodium ambrosioides L. induces mitochondrial-mediated pathway and endoplasmic reticulum stress-related apoptosis in human liver cancer SMMC-7721 cells

Purpose: To evaluate the cytotoxic effect of essential oil derived from Chenopodium ambrosioides L. in Sichuan Province on human liver cancer SMMC-7721 cells, as well as its possible molecular mechanisms.Methods: Cytotoxicity was characterized by MTT assay and transmission electron microscopy (TEM) of SMMC-7721 cells ultrastructure. The apoptotic effect of the essential oil was evaluated by changes in mitochondrial membrane potential and Western blot assay.Results: MTT assay data indicate that the essential oil was cytotoxic to SMMC-7721 cells, while TEN revealed that there were vacuoles and nucleus fragmentation in the SMMC-7721 cell cytosol, cell swelling, and a large amount of leakage. Mitochondrial membrane potential assay and Western Blot data indicate that the essential oil induced cell apoptosis.Conclusion: The essential oil of Chenopodium ambrosioides L. in Sichuan Province seems to induce apoptosis of human liver cancer SMMC-7721 cells via the mitochondrial-mediated pathway and endoplasmic reticulum stress. Thus, this plant requires further investigation as a potential source of ananti-liver cancer drug. Keywords: Chenopodium ambrosioides Essential oil; Anti-tumor activity, Liver cancer Apoptosis, SMMC-7721 cell

In vitro Studies and Clinical Observations Imply a Synergistic Effect Between Epstein-Barr Virus and Dengue Virus Infection

Dengue virus (DENV) infection can lead to a complex spectrum of clinical outcomes, ranging from asymptomatic infection to life-threatening severe dengue. The reasons for thus drastically varying manifestations of the disease remain an enigma. Herein, we reported an original discovery of the synergistic effect between preexisting Epstein–Barr virus (EBV) infection and DENV superinfection in vitro and of a strong correlation of these two viruses in the clinical samples from dengue patients. We showed that (I) DENV-2 infection of an EBV-positive cell line (EBV + Akata cell) reactivated EBV, and it could be blocked by wortmannin treatment. (II) Examination of human peripheral blood mononuclear cell (PBMC) samples from dengue patients revealed significantly elevated cell-associated EBV DNA copy number at the time of hospitalization vs. at the time of disease recovery in most individuals. (III) EBV infection promoted DENV propagation in both EBV-hosting B cells and indirectly in THP-1 cells, supported by the following evidence: (A) EBV + Akata cells were more permissive to DENV-2 infection compared with Akata cells harboring no EBV virus (EBV- Akata cells). (B) Low-molecular weight fraction secreted from EBV + Akata cells could enhance DENV-2 propagation in monocytic THP-1 cells. (C) While reactivation of EBV in EBV + Akata cells further increased DENV-2 yield from this cell line, pharmacological inhibition of EBV replication by acyclovir had the opposite effect. To our knowledge, this is the first investigation demonstrating a positive correlation between EBV and DENV in vitro and in human biospecimens