Effects of Nitrogen Accumulation, Transportation, and Grain Nutritional Quality and Advances in Fungal Endophyte Research in Quinoa (Chenopodium quinoa Willd.) Plants.

This study aims to understand the influence of nitrogen accumulation, fungal endophyte, yield, nitrogen use efficiency, and grain nutritional quality parameters on the yield of quinoa in some areas of China. The endophytic microbial community in plants plays a crucial role in plant growth, development, and health, especially in quinoa plants under different nitrogen fertilizer levels. The results from the present study indicated that appropriate nitrogen application significantly enhanced the nitrogen accumulation and yield of quinoa grains during maturity, increasing by 34.54-42.18% and 14.59-30.71%, respectively. Concurrently, protein content, amylose, total starch, ash, and fat content also increased, with respective growth rates of 1.15-18.18%, 30.74-42.53%, 6.40-12.40%, 1.94-21.94%, and 5.32-22.22%. Our constructed interaction network of bacterial and fungal communities revealed that bacteria outnumbered fungi significantly, and most of them exhibited synergistic interactions. The moderate increase in N150 was beneficial for increasing quinoa yield, achieving nitrogen use efficiency (NUE) of over 20%. The N210 was increased, and both the yield and NUE significantly decreased. This study provides novel insights into the impact of nitrogen fertilizer on quinoa growth and microbial communities, which are crucial for achieving agricultural sustainable development.

Advances in precision therapy of low-grade serous ovarian cancer: A review.

Low-grade serous ovarian carcinoma (LGSOC) is a rare subtype of ovarian cancer that accounts for approximately 6% to 10% of serous ovarian cancers. The clinical treatment of LGSOC is similar to that of high-grade serous ovarian carcinoma, however, its clinical and molecular characteristics are different from those of high-grade serous ovarian carcinoma. This article reviews the research on gene diagnosis, surgical treatment, chemotherapy, and biological therapy of LGSOC, providing reference for clinical diagnosis and treatment of LGSOC. Surgery is the cornerstone of LGSOC treatment and maximum effort must be made to achieve R0 removal. Although LGSOC is not sensitive to chemotherapy, postoperative platinum-based combination chemotherapy remains the first-line treatment option for LGSOC. Additional clinical trials are needed to confirm the clinical benefits of chemotherapy and explore new chemotherapy protocols. Hormone and targeted therapies may also play important roles. Some patients, particularly those with residual lesions after treatment, may benefit from hormone maintenance therapy after chemotherapy. Targeted therapies, such as MEKi, show good application prospects and are expected to change the treatment pattern of LGSOC. Continuing to further study the genomics of LGSOC, identify its specific gene changes, and combine traditional treatment methods with precision targeted therapy based on second-generation sequencing may be the direction for LGSOC to overcome the treatment bottleneck. In future clinical work, comprehensive genetic testing should be carried out for LGSOC patients to accumulate data for future scientific research, in order to find more effective methods and drugs for the treatment of LGSOC.

Testing for quadratic impact of industrial robots on environmental performance and reaction to green technology and environmental cost.

Industrial robots play a crucial role in enhancing productivity but their impact on the environment has produced debates. Some researchers have focused on the relation between industrial robots and energy efficiency (or environmental performance), such as Huang et al. (Energy Econ 107:105837, 2022) and Luan et al. (Sustain Prod Consum 30:870-888, 2022). However, their arguments mainly depend on the assumption of linear relationship between the two. This study infers that there is a nonlinear relationship between them from the theories of energy-saving effect, rebound effect, and scale effect. Our research, using data from 74 countries and regions worldwide between 1997 and 2020, reveals an inverted U-shaped relationship between the use of robots and their environmental impact. This means that the environment benefits from robot use up to a certain point, beyond which it starts to incur damage. Two moderating factors, green technology and environmental cost, are analyzed and tested. Our findings suggest that the high-green-tech left shifts and steepens the inverted U-shaped relationship whereas the high cost right shifts and flattens the relationship. This study explains the influencing mechanism of industrial robots on environmental performance by integrating the energy-saving effect, the rebound effect, and the scale effect. Our findings enrich the understanding of the robot-environment nexus and emphasize the importance of government in balancing robot use and environmental protection.

Forkhead box A2 Promotes Colorectal Cancer Progression and Targets BCL2-Associated X (BAX) Protein.

Background: Colorectal cancer is the third most common malignant tumor in the world and substantial death cases are reported each year. We aimed to explore the molecular mechanism underlying colorectal cancer tumor-igenesis and progression. Methods: The expression levels of Forkhead box A2 (FOXA2) in colorectal cancer tissues were first analyzed using Gene Expression Profiling Interactive Analysis (GEPIA). More multiple in vitro experiments established the role of FOXA2 in colorectal cancer progression. The potential downstream target of FOXA2 was identified by Western blot analysis. Results: FOXA2 expression level was significantly up-modulated in colorectal cancer specimens and cells (P<0.05). Silencing FOXA2 remarkably inhibited colorectal cancer cells growth, invasion and migration. BCL2-associated X (BAX) protein was identified as a potential downstream protein of FOXA2. Conclusion: Our findings demonstrated the essential role of FOXA2 in colorectal cancer progression and identified BAX protein as its potential target.

Novel mRNA Signature for Anti-TNF-α Therapy Primary Response in Patients With Ulcerative Colitis.

BACKGROUND: Ulcerative colitis (UC), an idiopathic, chronic inflammatory disorder of the colonic mucosa, is commonly treated with antitumor necrosis factor α (anti-TNF-α) agents. However, only approximately two-thirds have an initial response to these therapies. METHODS: We integrated gene expression profiling from 3 independent data sets of 79 UC patients before they began anti-TNF-α therapy and calculated the differentially expressed genes between patient response and nonresponse to anti-TNF-α therapy and developed a de novo response-associated transcription signature score (logOR_Score) to demonstrate the predictive capability of anti-TNF-α therapy for therapeutic efficacy. Furthermore, we performed association analysis of the logOR_Score and clinical features, such as disease activity and immune microenvironment. RESULTS: A total of 2522 responsive and 1824 nonresponsive genes were identified from the integrated data set. Responsive genes were significantly enriched in metabolism-related pathways, whereas nonresponsive ones were associated with immune response-related pathways. The logOR_Score enabled the accurate prediction of the therapeutic efficacy of anti-TNF-α in 4 independent patient cohorts and outperformed the predictions made based on 6 transcriptome-based signatures. In terms of clinical features, the logOR_Score correlated highly with the activity of UC. From an immune microenvironment perspective, logOR_Scores of CD8+IL-17+ T cells, follicular B cells, and innate lymphoid cells significantly decreased in inflamed UC tissue. CONCLUSIONS: The de novo response-associated transcription signature may provide novel insights into the personalized treatment of patients with UC. Comprehensive analyses of the response-related subtypes and the association between logOR_Score and clinical features and immune microenvironment may provide insights into the underlying UC pathogenesis.

We developed a de novo response-associated transcription signature score (logOR_Score) to predict the response of patients with UC to anti-TNF-α agents prior to treatment and explored the different response mechanisms of UC.

Short-term and long-term survival outcomes for transrectal specimen extraction after laparoscopic right hemicolectomy: a propensity-score matching study.

Background: Natural orifice specimen extraction surgery (NOSES) has been widely applied to the treatment of colorectal cancer. This study aim to investigate the short-term and survival outcomes of transrectal specimen extraction after laparoscopic right hemicolectomy. Methods: From January 2016 to December 2021, a total of 166 consecutive patients with right colon cancer who underwent laparoscopic right hemicolectomy in Cancer Hospital of Chinese Academy of Medical Sciences and Beijing Hospital were identified. Baseline data, perioperative parameters, anal function, inflammatory indicators and survival outcomes were collected and compared. Results: Totally, 24 patients who underwent transrectal NOSE were matched with 24 patients who received conventional laparoscopic surgery (LAP). Patients in NOSES group had a significantly lower incidence of incision infection (0 vs 20.8%, P=0.048), faster recovery of gastrointestinal function (2.1 vs 3,1 days, P=0.032) compared with those in LAP group. In addition, patients in the NOSE group experienced significantly less postoperative pain on POD1 (2.3 vs 4.4, P<0.001), POD3 (2.1 vs 3.9, P<0.001), and POD5 (1.7 vs 2.8, P=0.011). Regarding to anal function 6 months after surgery, no significant difference was observed in Wexner incontinence scale (9.8 vs 9.5, P=0.559) between the two groups. In terms of indicators of the inflammatory response, there were no significant differences in body temperature, neutrophils, and PCT levels between the two groups. However, CRP levels in the NOSES group on POD 3 (6.9 vs 5.1 mg/L, P=0.016) and POD 5 (3.8 vs 2.6 mg/L, P=0.027) were significantly higher than in the LAP group. With regarded to survival outcomes, patients in the NOSES group were similar to those in the LAP group for 3-year OS (100% vs 91.2%, P=0.949), 3-year DFS (86.2% vs 84.8%, P=0.949), and 3-year LRFS (94.2% vs 88.7%, P=0.549). Conclusion: For total laparoscopic right hemicolectomy, transrectal NOSE is effective and safe, and associated with lower incidence of wound infection, less pain, faster recovery, and similar survival outcomes compared to conventional laparoscopic surgery.

Expression and Prognostic Value of RAD51 in Adenocarcinoma at the Gastroesophageal Junction.

Background: The RAD51 recombinase is involved in homologous recombination and DNA repair. However, the association of RAD51 with the prognosis of adenocarcinoma at the gastroesophageal junction (ACGEJ) is not clear. We aimed to investigate the association of RAD51 with ACGEJ prognosis. Methods: The difference in the expression level of RAD51 between ACGEJ tumors and control tissues in the microarray datasets (GSE159721, GSE74553, and GSE96669) were compared. The online Kaplan-Meier plotter survival analysis and meta-analysis were used to analyze the association of RAD51 with overall survival in pan-cancers. MiRNAs targeting RAD51 were identified and their expression profiles in ACGEJ tumors were analyzed. Functional enrichment analysis was performed for miRNAs of RAD51. Results: RAD51 was upregulated in ACGEJ tumors compared with control tissues (P < 0.05). High RAD51 level was correlated with a poor prognosis in stomach adenocarcinoma and esophageal cancer. The meta-analysis showed that high RAD51 level was correlated with a poor prognosis in TCGA pan-cancers (P = 0.03). Six regulatory miRNAs of RAD51, including hsa-miR-182, hsa-miR-221, and hsa-miR-34a, were downregulated in ACGEJ tumor tissues and were associated with pathways including "fatty acid biosynthesis" and "viral carcinogenesis". Conclusion: RAD51 is a potent prognostic biomarker in ACGEJ. MiRNAs including hsa-miR-182, hsa-miR-221, and hsa-miR-34a might play crucial roles in ACGEJ by regulating the RAD51 gene.

Retraction Notice to: lncRNA GAS5 Inhibits Cell Migration and Invasion and Promotes Autophagy by Targeting miR-222-3p via the GAS5/PTEN-Signaling Pathway in CRC.

[This retracts the article DOI: 10.1016/j.omtn.2019.06.009.].

Oral zero-valent-molybdenum nanodots for inflammatory bowel disease therapy.

Inflammatory bowel disease (IBD) affects millions of people each year. The overproduction of reactive oxygen species (ROS) plays a critical role in the progress of IBD and will be a potential therapeutic target. Here, we synthesize a kind of oral zero-valent-molybdenum nanodots (ZVMNs) for the treatment of IBD by scavenging ROS. These ultrasmall ZVMNs can successfully pass through the gastric acid and then be absorbed by the intestine. It has been verified that ZVMNs can down-regulate the quantity of ROS and reduce colitis in a mouse IBD model without distinct side effects. In addition, RNA sequencing reveals a further mechanism that the ZVMNs can protect colon tissues from oxidative stress by inhibiting the nuclear factor κB signaling pathway and reducing the production of excessive pro-inflammatory factors. Together, the ZVMNs will offer a promising alternative treatment option for patients suffering from IBD.

Bcl-xL DNAzymes promote radiosensitivity and chemosensitivity in colorectal cancer cells via enhancing apoptosis.

BACKGROUND: RNA-cleaving deoxyribozymes (DNAzymes) are catalytic deoxyribonucleic acid molecules that have become a promising new class of gene suppressors by binding and cleaving target mRNA. This study investigated whether DNAzymes targeting Bcl-xL enhanced the effectiveness of radiotherapy and chemotherapy in colorectal cancer (CRC) cells. METHODS: Two types of CRC cells, SW480 and SW837, were transfected with five DNAzymes. Cell viability, Bcl-xL expression and apoptosis were examined. SW480 xenograft model was used to examine the combined effects of Bcl-xL DNAzymes and 5-FU (or X-rays) on tumor growth. RESULTS: Three Bcl-xL DNAzymes, DT882, DT883, and DT884 were identified to be effective in suppressing Bcl-xL expression and causing cell apoptosis. Furthermore, DT882 combined with 5-FU or radiotherapy addictively promoted cell apoptosis and significantly inhibited the growth of SW480 xenografts in vivo. CONCLUSIONS: These results suggest that Bcl-xL DNAzymes can enhance the radiosensitivity and chemosensitivity in CRC cells via inducing apoptosis.

Erratum: Isoliquiritigenin induces apoptosis of human bladder cancer T24 cells via a cyclin-dependent kinase-independent mechanism.

[This corrects the article DOI: 10.3892/ol.2017.6159.].

The impact of novel coronavirus SARS-CoV-2 among healthcare workers in hospitals: An aerial overview.

The ongoing outbreak of COVID-19, caused by the novel coronavirus SARS-CoV-2, places healthcare workers at an increased risk of infection as they are in close contact with patients. In this article, we report an overview of cases of infected healthcare workers in China and Italy during the early periods of the COVID-19 epidemic. China's coronavirus response highlights the importance of implementing effective public health strategies. The authorities worldwide therefore, need to be extremely cautious when they implement stringent protective measures that safeguard healthcare workers in hospitals and counteract the threats created by the pandemic.

lncRNA GAS5 Inhibits Cell Migration and Invasion and Promotes Autophagy by Targeting miR-222-3p via the GAS5/PTEN-Signaling Pathway in CRC.

Colorectal cancer (CRC) is a frequently occurring lethal disorder with heterogeneous outcomes and drug responses. Recent studies have demonstrated that long non-coding RNAs (lncRNAs) play a critical role in carcinogenesis. Hence, the aim of this study was to investigate the role of lncRNA growth arrest-specific 5 (GAS5) in CRC cells via mediation of the microRNA-222-3p (miR-222-3p)/GAS5/phosphatase and tensin homolog (PTEN)-signaling pathway. HCT116 and SW480 cells were collected and treated with small interfering (si)-lncRNA GAS5, overexpressing (oe)-lncRNA GAS5, miR-222-3p mimic, miR-222-3p inhibitor, or si-lncRNA GAS5 + miR-222-3p mimic. The miR-222-3p level and mRNA and protein levels of GAS5, Beclin1, light-chain 3B (LC3B), PTEN, and Akt were detected. Besides, cell migration, invasion, and apoptosis as well as acidic vesicular organelles (AVOs) were examined respectively. Xenografts in nude mice were also performed to detect tumorigenesis in vivo. Results suggested that the downregulation of lncRNA GAS5 decreased the expressions of Beclin1, LC3B, and PTEN. When treated with oe-lncRNA GAS5 or miR-222-3p inhibitor, HCT116 and SW480 cells exhibited suppressed invasion and migration abilities and increased apoptotic cells and autophagosome and AVO activities. Moreover, overexpression of GAS5 inhibited the tumorigenesis of CRC cells in vivo. Taken together, lncRNA GAS5 upregulated the expression of PTEN by functioning as a competing endogenous RNA (ceRNA) of miR-222-3p, thus inhibiting CRC cell migration and invasion and promoting cell autophagy.

Capecitabine versus 5-fluorouracil in neoadjuvant chemoradiotherapy of locally advanced rectal cancer: A meta-analysis.

BACKGROUND: The differences in efficacy between capecitabine and 5-fuorouracil (5-FU) in neoadjuvant chemoradiotherapy (CRT) of locally advanced rectal cancer (LARC) are not well recognized. We performed this meta-analysis to analyze the effect of capecitabine and 5-FU on neoadjuvant CRT to more accurately understand the differences between the 2 drugs. METHODS: MEDLINE, EMBASE, Cochrane Library, China National Knowledge Infrastructure, and Wanfang Database were performed to identify all published studies investigating the efficacy of capecitabine in neoadjuvant CRT of LARC versus 5-FU before August, 2017. Primary endpoint was the odds ratio (OR) for improving pathological complete response (pCR) rate of patients with LARC. Secondary endpoints were the ORs of efficiency for downstaging tumor and increasing R0 resection in patients with LARC. Safety analyses were also performed. The OR was the principal measurement of effect, which was calculated as capecitabine group versus 5-FU group, and was presented as a point estimate with 95% confidence intervals (CIs). All calculations and statistical tests were performed using RevMan 5.3 software. RESULTS: In all, 2916 patients with LARC enrolled in the 10 studies were divided into capecitabine group (n = 1451) and 5-FU group (n = 1465). The meta-analysis showed that capecitabine improved pCR (OR 1.34, 95% CI 1.10-1.63), and R0 resection rate (OR 1.92, 95% CI 1.10-3.36). There were no statistically significant differences either in overall downstaging rate (OR 1.31, 95% CI 0.79-2.16) or in the tumor downstaging rate (OR 1.24, 95% CI 0.79-1.92), but there was a significant difference of the nodal downstaging rate between the 2 groups (OR 1.68, 95% CI 1.11-2.54). There was no statistically significant difference in sphincter preservation rate between the 2 groups (OR 1.36, 95% CI 0.96-1.92). No obvious safety concerns about mortality and complications were raised in these studies. There were no statistically significant differences in 3-year disease-free-survival (OR 1.29, 95% CI 0.75-2.20), and in grade 3 to 4 acute toxicity during CRT (OR 0.63, 95% CI 0.31-1.30). CONCLUSIONS: Compared with 5-FU-based neoadjuvant CRT, capecitabine-based neoadjuvant CRT can safely improve pCR, nodal down-staging, ad R0 resection of patients with LARC.

Prognostic and predictive value of long non-coding RNA GAS5 and mircoRNA-221 in colorectal cancer and their effects on colorectal cancer cell proliferation, migration and invasion.

BACKGROUND: LncRNA and microRNA play an important role in the development of human cancers; they can act as a tumor suppressor gene or an oncogene. LncRNA GAS5, originating from the separation from tumor suppressor gene cDNA subtractive library, is considered as an oncogene in several kinds of cancers. The expression of miR-221 affects tumorigenesis, invasion and metastasis in multiple types of human cancers. However, there's very little information on the role LncRNA GAS5 and miR-221 play in CRC. Therefore, we conducted this study in order to analyze the association of GAS5 and miR-221 with the prognosis of CRC and preliminary study was done on proliferation, metastasis and invasion of CRC cells. In the present study, we demonstrate the predictive value of long non-coding RNA GAS5 (lncRNA GAS5) and mircoRNA-221 (miR-221) in the prognosis of colorectal cancer (CRC) and their effects on CRC cell proliferation, migration and invasion. METHODS: One hundred and fifty-eight cases with CRC patients and 173 cases of healthy subjects that with no abnormalities, who've been diagnosed through colonoscopy between January 2012 and January 2014 were selected for the study. After the clinicopathological data of the subjects, tissue, plasma and exosomes were collected, lncRNA GAS5 and miR-221 expressions in tissues, plasma and exosomes were measured by reverse transcription quantitative polymerase chain reaction (RT-qPCR). The diagnostic values of lncRNA GAS5 and miR-221 expression in tissues, plasma and exosomes in patients with CRC were analyzed using receiver operating characteristic curve (ROC). Lentiviral vector was constructed for the overexpression of lncRNA GAS5, and SW480 cell line was used for the transfection of the experiment and assigned into an empty vector and GAS5 groups. The cell proliferation, migration and invasion were tested using a cell counting kit-8 assay and Transwell assay respectively. RESULTS: The results revealed that LncRNA GAS5 was upregulated while the miR-221 was downregulated in the tissues, plasma and exosomes of patients with CRC. The results of ROC showed that the expressions of both lncRNA GAS5 and miR-221 in the tissues, plasma and exosomes had diagnostic value in CRC. While the LncRNA GAS5 expression in tissues, plasma and exosomes were associated with the tumor node metastasis (TNM) stage, Dukes stage, lymph node metastasis (LNM), local recurrence rate and distant metastasis rate, the MiR-221 expression in tissues, plasma and exosomes were associated with tumor size, TNM stage, Dukes stage, LNM, local recurrence rate and distant metastasis rate. LncRNA GAS5 and miR-221 expression in tissues, plasma and exosomes were found to be independent prognostic factors for CRC. Following the overexpression of GAS5, the GAS5 expressions was up-regulated and miR-221 expression was down-regulated; the rate of cell proliferation, migration and invasion were decreased.

Effect of inhibiting Beclin-1 expression on autophagy, proliferation and apoptosis in colorectal cancer.

The present study aimed to investigate the molecular mechanisms and effect of Beclin-1 on autophagy, proliferation and apoptosis in the colorectal cancer (CRC) HCT116 and SW620 cells. Beclin-1 was silenced by RNA interference (RNAi) in HTC116 and SW620 cells. Reverse transcription-polymerase chain reaction and western blot were used to measure the expression of Beclin-1. The percentage of apoptotic cells was analyzed by cell counting kit-8 (CCK-8) and flow cytometry (FCM). Cell cycle and cell proliferation were analyzed by FCM and the MTT assay. The present study created 3 groups in the two cell lines, consisting of the targeting siRNA (TS) group, in which Beclin-1 was partially silenced, non-specific siRNA (NS) group and control group (CG; without transfection). By siRNA transfection, the mRNA and protein level of Beclin-1 in the TS group were significantly inhibited compared with the NS group and CG (P<0.05). After 0, 24, 48 and 72 h, the survival rate of the cells in the TS group was significantly decreased compared with the survival rate of the cells in the NS group and CG, as detected by CCK-8 methods (P<0.05). FCM and MTT results showed the apoptotic rate of the cells in the TS group was significantly decreased compared with the rate in the NS group and CG (P<0.05), and the proliferation of the cells in the NS group was evidently increased compared with the CG. In conclusion, Beclin-1 played an important role in regulating autophagy, proliferation and apoptosis in HCT116 and SW620 cells. The inhibition of Beclin-1 by RNAi suppressed the autophagic activity and proliferation, but promoted apoptosis in CRC cells. Beclin-1 was the new target of gene therapy for CRC.

Isoliquiritigenin induces apoptosis of human bladder cancer T24 cells via a cyclin-dependent kinase-independent mechanism.

The aim of the present study was to investigate whether an increase in cyclin-dependent kinase 2 (CDK2) activity is involved in apoptosis of human bladder cancer T24 cells induced by isoliquiritigenin (ISL). The viability of T24 cells was estimated using a sulforhodamine B assay. Cell morphological changes were examined using Hoechst 33258 staining. The apoptotic rate was determined by staining cells with Annexin V-fluorescein isothiocyanate and propidium iodide labeling. The mitochondrial membrane potential (ΔΨm) was measured using 5,5,6,6-tetrachloro-1,1, 3,3-tetraethyl benzimidazole carbocyanine iodide. Alterations in the apoptosis-related regulators B-cell lymphoma-2 (Bcl-2), Bcl-2-associated X protein (Bax), Bcl-2-interacting mediator of cell death (Bim), apoptotic protease-activating facter-1 (Apaf-1), caspase-9 and caspase-3 were determined using reverse transcription-polymerase chain reaction (PCR) and quantitative PCR methods. Western blot analysis was used to detect the expression of Bcl-2, Bax and caspase-3. CDK2 activity was measured using a spectrometric assay. Following treatment with ISL (between 30 and 70 µg/ml) for 24 h, typical apoptotic morphological changes were observed in T24 cells, exhibiting an edge set of chromosomes, nuclear condensation, nuclear fragmentation and other morphological features. Treatment with ISL increased the apoptotic ratio of T24 cells in a concentration-dependent manner and induced a decrease in the ΔΨm in a time-dependent manner. Treatment with ISL upregulated the expression of Bax, Bim, Apaf-1, caspase-9 and caspase-3, downregulated the expression of Bcl-2, and increased CDK2 activity. MK-8776 (an inhibitor of CDK2) antagonized the apoptosis induced by ISL, and, compared with treatment with ISL alone, pretreatment with MK-8776 inhibited the decrease in ΔΨm, downregulated the mRNA expression of Bax, Bim, Apaf-1, caspase-9 and caspase-3, and upregulated Bcl-2 mRNA expression. Western blot analysis demonstrated that, with increasing ISL concentration, the Bcl-2 expression level was significantly decreased (P<0.05), whereas caspase-3 and Bax expression levels were significantly increased (P<0.01). These results indicated that ISL treatment caused a significant decrease in the proliferation rate and increase in apoptosis of T24 cells. The mechanism by which ISL induces T24 cell apoptosis in vitro may be associated with an increase in CDK2 activity, downregulation of the ΔΨm and activation of caspase-3/caspase-9-mediated mitochondrial apoptotic signaling pathways.

Selection and antitumor activity of anti-Bcl-2 DNAzymes.

Apoptosis pathway has become one of the important targets for therapeutic exploration for cancer therapy. The increased Bcl-2 protein level and phosphorylation is implicated in a decreased chemotherapeutic response in many cancers. BCL-2 inhibitors have been developed as direct inducers of apoptosis. However, resistance to BCL2 inhibitors has been emerging and thus considerable effort has been made to seek novel approaches to BCL2 suppression. In this report we describe an in vitro DNAzyme selection strategy resulting in molecules that are effective in suppressing expression of the target gene BCL-2 in vitro. A 3'-inverted modification was shown to significantly increase the DNAzyme stability in serum and the modified DNAzyme delivered by an osmotic pump chemosensitized human prostate cancer to Taxol in vivo. Thus this study provides an alternative strategy for potential BCL-2-targetd therapy.

Durable Antibacterial and Nonfouling Cotton Textiles with Enhanced Comfort via Zwitterionic Sulfopropylbetaine Coating.

A rapid, environment-friendly, and cost-effective finishing method has been developed for cotton textiles by using zwitterionic NCO-sulfopropylbetaine as the antibacterial finishing agent through covalent bond. The sulfopropylbetaine-finished cotton textile exhibits durable broad-spectrum antibacterial and nonfouling activity, improved mechanical properties, and enhanced comfort.

Licochalcone A induces T24 bladder cancer cell apoptosis by increasing intracellular calcium levels.

Licochalcone A (LCA) has been reported to significantly inhibit cell proliferation, increase reactive oxygen species (ROS) levels, and induce apoptosis of T24 human bladder cancer cells via mitochondria and endoplasmic reticulum (ER) stress-triggered signaling pathways. Based on these findings, the present study aimed to investigate the mechanisms by which LCA induces apoptosis of T24 cells. Cultured T24 cells were treated with LCA, and cell viability was measured using the sulforhodamine B assay. Apoptosis was detected by flow cytometry with Annexin V/propidium iodide staining, and by fluorescent microscopy with Hoechst 33258 staining. The levels of intracellular free calcium ions were determined using Fluo-3 AM dye marker. Intracellular ROS levels were assessed using the 2',7'-dichlorodihydrofluorescein diacetate probe assay. The mitochondrial membrane potential was measured using 5,5',6,6'-tetrachloro-1,1',3,3'-tetraethyl benzimidazole carbocyanine iodide. Furthermore, the mRNA expression levels of B­cell lymphoma (Bcl)­extra large, Bcl­2­associated X protein, Bcl­2­interacting mediator of cell death, apoptotic protease activating factor­1 (Apaf­1), calpain 2, cysteinyl aspartate specific proteinase (caspase)­3, caspase­4 and caspase­9 were determined using reverse transcription semiquantitative and quantitative polymerase chain reaction analyses. Treatment with LCA inhibited proliferation and induced apoptosis of T24 cells, and increased intracellular Ca2+ levels and ROS production. Furthermore, LCA induced mitochondrial dysfunction, decreased mitochondrial membrane potential, and increased the mRNA expression levels of Apaf­1, caspase­9 and caspase­3. Exposure of T24 cells to LCA also triggered calpain 2 and caspase­4 activation, resulting in apoptosis. These findings indicated that LCA increased intracellular Ca2+ levels, which may be associated with mitochondrial dysfunction. In addition, the ER stress pathway may be considered an important mechanism by which LCA induces apoptosis of T24 bladder cancer cells.