Solution-Induced Degradation of the Silicon Nanobelt Field-Effect Transistor Biosensors.

Field-effect transistor (FET)-based biosensors are powerful analytical tools for detecting trace-specific biomolecules in diverse sample matrices, especially in the realms of pandemics and infectious diseases. The primary concern in applying these biosensors is their stability, a factor directly impacting the accuracy and reliability of sensing over extended durations. The risk of biosensor degradation is substantial, potentially jeopardizing the sensitivity and selectivity and leading to inaccurate readings, including the possibility of false positives or negatives. This paper delves into the documented degradation of silicon nanobelt FET (NBFET) biosensors induced by buffer solutions. The results highlight a positive correlation between immersion time and the threshold voltage of NBFET devices. Secondary ion mass spectrometry analysis demonstrates a gradual increase in sodium and potassium ion concentrations within the silicon as immersion days progress. This outcome is ascribed to the nanobelt's exposure to the buffer solution during the biosensing period, enabling ion penetration from the buffer into the silicon. This study emphasizes the critical need to address buffer-solution-induced degradation to ensure the long-term stability and performance of FET-based biosensors in practical applications.

CSC-3436 sensitizes triple negative breast cancer cells to TRAIL-induced apoptosis through ROS-mediated p38/CHOP/death receptor 5 signaling pathways.

Tumor necrosis factor-related apoptosis-induced ligand (TRAIL) shows little or no toxicity in most normal cells and preferentially induces apoptosis in a variety of malignant cells. However, patients develop resistance to TRAIL, therefore, sensitizing agents that can sensitize the tumor cells to TRAIL-mediated apoptosis are necessary. In this study, we investigated the effect of 2-(3-hydroxyphenyl)-5-methylnaphthyridin-4-one (CSC-3436), an useful flavonoid, to overcome the TRAIL-resistant triple negative breast cancer (TNBC) cells. We found that CSC-3436 potentiated TRAIL-induced apoptosis in TRAIL-resistant TNBC cells and this correlated with the upregulation of death receptors (DR)-5 and down-regulation of decreased decoy receptor (DcR)-1 expression. When examined for its mechanism, we found that the decreased expression of anti-apoptotic proteins c-FLIPS/L, Bcl-Xl, Bcl-2, Survivin, and XIAP. CSC-3436 would increase the expression of Bax and promoted the cleavage of bid. In addition, the induction of DR5 by CSC-3436 was found to be dependent on the modulation of reactive oxygen species (ROS)/p38/C/EBP-homologous protein (CHOP) signaling pathways. Overall, our results indicated that CSC-3436 could potentiate the apoptotic effects of TRAIL through down-regulation of cell survival proteins and upregulation of DR5 via the ROS-mediated upregulation of CHOP protein.

Demethoxycurcumin induces apoptosis in HER2 overexpressing bladder cancer cells through degradation of HER2 and inhibiting the PI3K/Akt pathway.

Bladder cancer is the most common malignancy of the urinary tract and arising from the epithelial lining of the urinary bladder. Resistance to cytotoxic therapies is associated with overexpression of oncogenic proteins; including HER2, and Akt in chemotherapy resistance of bladder cancer. Various studies demonstrated that curcuminoids, the most important active phenolic compounds of turmeric (Curcuma longa), have anti-tumor activities in a wide range of human malignant cell lines. The aim of this study is to evaluate whether curcuminoids (curcumin, demethoxycurcumin (DMC), and bisdemethoxycurcumin) could repress the expression of HER2 in HER2-overexpressing bladder cancer cells. Among the test compounds, DMC significantly suppressed the expression of HER2, and preferentially inhibited cell proliferation and induced apoptosis in HER2-overexpressing bladder cancer cells. DMC decreases HER2 level through inhibiting the interaction of HER2 and Hsp90. Our study also indicated that DMC showed additive activity in combination with chemotherapeutic agents, including paclitaxel and cisplatin. These findings show that DMC should be developed further as a new antitumor drug candidate for treatment of HER2-overexpressing bladder cancer.

Tetrandrine Enhances H2O2-Induced Apoptotic Cell Death Through Caspase-dependent Pathway in Human Keratinocytes.

BACKGROUND: Tetrandrine, a bis-benzylisoquinoline alkaloid, induces apoptosis of many types of human cancer cell. Hydrogen peroxide (H2O2) is a reactive oxygen species inducer; however, there are no reports to show whether pre-treatment of tetrandrine with H2O2 induces more cell apoptosis than H2O2 alone. Thus, the present study investigated the effects of tetrandrine on H2O2-induced cell apoptosis of human keratinocytes, HaCaT, in vitro. MATERIALS AND METHODS: HaCaT cells were pre-treated with and without tetrandrine for 1 h, and then treated with H2O2 for examining cell morphological changes and cell viability using contrast-phase microscopy and propidium iodide (PI) exclusion assay, respectively. Cells were measured apoptotic cell death by using annexin V/PI double staining and further analyzed by flow cytometer. Cells were further assessed for DNA condensation using 2-(4-amidinophenyl)-6-indolecarbamidine staining. Western blotting was used to measure expression of apoptosis-associated proteins and confocal laser microscopy was used to measure the protein expression and nuclear translocation from the cytoplasm to nuclei. RESULTS: Pre-treatment of tetrandrine for 1 h and treatment with H2O2 enhanced H2O2-induced cell morphological changes and reduced cell viability, whilst increasing apoptotic cell death and DNA condensation. Furthermore, tetrandrine significantly increased expression of reactive oxygen species-associated proteins such as superoxide dismutase (Cu/Zn) and superoxide dismutase (Mn) but significantly reduced the level of catalase, which was also confirmed by confocal laser microscopy. It also increased expression of DNA repair-associated proteins ataxia telangiectasia mutated, ataxia-telangectasia and Rad3-related, phospho-P53, P53 and phosphorylated histone H2AX, and of pro-apoptotic proteins BCL2 apoptosis regulator-associated X-protein, caspase-3, caspase-8, caspase-9 and poly ADP ribose polymerase in HaCaT cells. CONCLUSION: These are the first and novel findings showing tetrandrine enhances H2O2-induced apoptotic cell death of HaCaT cells and may provide a potent approach for the treatment of proliferated malignant keratinocytes.

Pre-Treatment of Pterostilbene Enhances H2O2-induced Cell Apoptosis Through Caspase-dependent Pathway in Human Keratinocyte Cells.

BACKGROUND/AIM: Hydrogen peroxide (H2O2) is one of the reactive oxygen species (ROS), which can induce apoptotic cell death in numerous cancer cells. Pterostilbene (PTE), a natural polyphenolic compound, induces cell apoptosis in many human cancer cells. MATERIALS AND METHODS: We investigated whether PTE could enhance H2O2-induced cell apoptosis in human keratinocyte HaCaT cells in vitro. The morphological change of HaCaT cells was observed and photographed under a contrast-phase microscope. The percentage of cell viability was measured by propidium iodide exclusion assay. Cell apoptosis was performed by Annexin V/PI double staining and assayed by flow cytometer. DNA condensation was measured by DAPI staining. The protein expression was determined by western blotting. ROS production-associated proteins were also assayed by confocal laser scanning microscopy. RESULTS: PTE pre-treatment enhanced H2O2 (600 µM)-induced cell morphological changes and reduced the total cell number (cell viability). The decreased cell viability in HaCaT cells was through induction of apoptotic cell death, which was confirmed by Annexin V/PI double staining and DAPI staining. Western blotting studies indicated that HaCaT cells which were pre-treated with PTE (100 µM) and then co-treated with H2O2 (600 µM) for 12 h showed significantly increased levels of SOD (Cu/Zn), SOD (Mn), Bax, caspase-3, caspase-8, caspase-9, PARP, p53, p-p53, and p-H2A.X but decreased levels Bcl-2 and catalase. Results also showed that HaCaT cells pre-treated with PTE and then co-treated with H2O2 had increased expression of SOD (Cu/Zn) and glutathione but decreased catalase. CONCLUSION: These observations suggest that PTE pre-treatment can enhance the H2O2-induced apoptotic cell death in keratinocyte cells and may be an effective candidate for the treatment of proliferative keratinocytes.

Friction and Wear Performance of Staple Carbon Fabric-Reinforced Composites: Effects of Surface Topography.

Here, staple carbon fiber fabric-reinforced polycarbonate (PC)- and epoxy (EP)-based composites with different impregnating resin levels were fabricated using a modified film stacking process. The effects of surface topographies and resin types on the tribological properties of stable carbon fabric composites (sCFC) were investigated. Friction and wear tests on the carbon composites were conducted under unlubricated sliding using a disk-on-disk wear test machine. Experimental results showed that the coefficient of friction (COF) of the sCFC was dominated by matrix type, followed by peak material portion (Smr1) values, and finalized with core height (Sk) values. The COF of composites decreased by increasing the sliding speed and applied pressure. This also relied on surface topography and temperature generated at the worn surface. However, the specific wear rate was strongly affected by resin impregnation. Partially-impregnated composites showed lower specific wear rate, whereas fully-impregnated composites showed a higher wear rate. This substantially increased by increasing the sliding speed and applied pressure. Scanning electron microscopy observations of the worn surfaces revealed that the primary wear mechanisms were abrasion, adhesion, and fatigue for PC-based composites. For EP-based composites, this was primarily abrasion and fatigue. Results proved that partially-impregnated composites exhibited better tribological properties under severe conditions.

Evaluating the Far-Infrared Radiation Bioeffects on Micro Vascular Dysfunction, Nervous System, and Plantar Pressure in Diabetes Mellitus.

The most frequent clinical complication is diabetes. Diabetes is characterized by elevated blood glucose levels resulting in sensory nerve damage or lesions. Diabetic foot wounds are often slow to heal and require medical attention and monitoring. This study evaluates the effect of far-infrared radiation on the microcirculation and plantar pressure in the diabetic foot. Ten diabetics and 4 nondiabetics were recruited in this study. The diabetic group was examined before and after the intervention in each month for 3 consecutive months. Four nondiabetic groups were also measured before and after the intervention for 2 weeks in each month. The surface temperature and blood flow in the diabetic foot was significantly improved (temperature: 32.1 ± 2.3°C vs 33.5 ± 2.2°C, P < .05; blood flow image: 118.3 ± 58.1 PU [perfusion unit] vs 50.4 ± 4.3 PU, P < .05). The sympathetic nerve activity index LF also increased from 40.8 ± 18.6% to 61.8 ± 13.5% (P = .07) in the second month. Plantar pressure tended to increase in the third month. This might indicate that far-infrared radiation could affect the mechanical properties of the plantar foot soft tissue. These results indicated that the effects of far-infrared radiation would improve blood circulation and change the soft tissue properties in the diabetic foot.

Major comorbidities lead to the risk of adverse cardiovascular events in chronic obstructive pulmonary disease patients using inhaled long-acting bronchodilators: a case-control study.

BACKGROUND: While inhaled bronchodilators reduce symptoms and acute exacerbations of chronic obstructive pulmonary disease (COPD), their use is associated with increased cardiovascular events in some studies. This study investigates the risk of adverse events associated with the use of inhaled bronchodilators in COPD patients with multimorbidity. METHODS: A case-control study was conducted between January 2015 and December 2017, and patients with spirometry-confirmed diagnosis of COPD (N = 1565) using inhaled long-acting bronchodilators were enrolled. Medical records were reviewed and clinical data, including age, gender, smoking status, major comorbidities, lung function stage, history of exacerbations, bronchodilator regimens, and treatment duration were analyzed. Major adverse cardiovascular events occurring during long-acting bronchodilator use were recorded. RESULTS: The most common comorbidities were cardiovascular disease (CVD) (53.6%) and chronic kidney disease (CKD) (25.8%). We observed that CVD (odds ratio [OR], 5.77), CKD (OR, 2.02) and history of frequent exacerbations (OR, 2.37) were independent risk factors for cardiovascular events, regardless of the type of bronchodilators use. Moreover, COPD patients with both CKD and CVD had higher risk (6.32-fold) of adverse cardiovascular effects than those with neither comorbidity. Eighty-seven of 1565 (5.56%) COPD patients died during this study period. Of them, 21.8% (19/87) were cardiovascular-related and 73.6% (64/87) patients were respiratory-related mortality. Among COPD patients using long-acting bronchodilators, CKD was the only risk factor to predict cardiovascular events and cardiovascular-related mortality (OR, 4.87; 95% confidence interval [CI], 1.75-13.55]. CONCLUSIONS: COPD patients had higher risk of cardiovascular events were associated with their CVD and/or CKD comorbidities and history of frequent exacerbations, rather than associated with their use of inhaled bronchodilators.

Using the entrapped bioprocess as the pretreatment method for the drinking water treatment receiving eutrophic source water.

Control of organic matter, nutrients and disinfection byproduct formation is a major challenge for the drinking water treatment plants on Matsu Islands, Taiwan, receiving source water from the eutrophic reservoirs. A pilot entrapped biomass reactor (EBR) system was installed as the pretreatment process to reduce organic and nitrogen contents into the drinking water treatment plant. The effects of hydraulic retention time (HRT) and combination of preceding physical treatment (ultraviolet and ultrasound) on the treatment performance were further evaluated. The results showed that the EBR system achieved higher than 81%, 35%, 12% and 46% of reduction in chlorophyll a (Chl a), total COD (TCOD), dissolved organic carbon (DOC) and total nitrogen (TN), respectively under varied influent concentrations. The treatment performance was not significantly influenced by HRT and presence/absence of physical pretreatment and the effluent water quality was stable; however, removal efficiencies and removal rates of Chl a, TCOD and DOC showed strong correlation with their influent concentrations. Excitation-emission matrix (EEM) fluorescence spectroscopy identified fulvic-like and humic-like substances as the two major components of dissolved organic matter (DOM) in the reservoir, and decreased intensity of the major peaks in effluent EEM fluorescence spectra suggested the effective removal of DOM without production of additional amount of soluble microbial products in the EBR. Through the treatment by EBR, about 10% of reduction of total trihalomethane formation potential for the effluent could also be achieved. Therefore, the overall results of this study demonstrate that EBR can be a potential pretreatment process for drinking water treatment plants receiving eutrophic source water.

Involvement of iron in biofilm formation by Staphylococcus aureus.

Staphylococcus aureus is a human pathogen that forms biofilm on catheters and medical implants. The authors' earlier study established that 1,2,3,4,6-penta-O-galloyl-ß-D-glucopyranose (PGG) inhibits biofilm formation by S. aureus by preventing the initial attachment of the cells to a solid surface and reducing the production of polysaccharide intercellular adhesin (PIA). Our cDNA microarray and MALDI-TOF mass spectrometric studies demonstrate that PGG treatment causes the expression of genes and proteins that are normally expressed under iron-limiting conditions. A chemical assay using ferrozine verifies that PGG is a strong iron chelator that depletes iron from the culture medium. This study finds that adding FeSO(4) to a medium that contains PGG restores the biofilm formation and the production of PIA by S. aureus SA113. The requirement of iron for biofilm formation by S. aureus SA113 can also be verified using a semi-defined medium, BM, that contains an iron chelating agent, 2, 2'-dipyridyl (2-DP). Similar to the effect of PGG, the addition of 2-DP to BM medium inhibits biofilm formation and adding FeSO(4) to BM medium that contains 2-DP restores biofilm formation. This study reveals an important mechanism of biofilm formation by S. aureus SA113.