Scaling and cleaning of silica scales on reverse osmosis membrane: Effective removal and degradation mechanisms utilizing gallic acid.

Silica scaling on membranes represents one of the most important issues in industrial water systems because of its complex composition and difficulty in removal. However, there is a lack of understanding of the mechanisms for cleaning silica scales from reverse osmosis (RO) membranes. To address this research gap, this study investigated the scaling and cleaning behavior of silica on RO membrane processes, with a specific focus on the silica scale cleaning mechanism using gallic acid (GA). The membrane flux continuously decreased with operation time, even at the lowest initial silicic acid concentration, owing to silica scale blockage. The GA solution exhibited a strong efficacy in cleaning silica-scaling RO membranes. The membrane flux returned to 89.7% of the initial value by removing 81.87% of the silica scale within the first 30 min of the study period. The cleaning mechanism of GA involved its adsorption onto the surface of silica scale particles to form a surface complex and subsequently transition into a water-soluble 1:3 complex within the solution. This complex interaction facilitated the gradual decomposition of the silica scales that adhered to the membrane surface. This study has valuable implications for the development of efficient and effective silica scale cleaning solutions, providing insights into the complex interplay between GA and silica scaling mechanisms.

Removal of boron and silicon by a modified resin and their competitive adsorption mechanisms.

Boron and silicon are essential trace elements for living organisms. However, these are undesirable in excess amounts owing to the toxic effects of boron on plants, animals, and humans, and the silica scale formation by silicon in water treatment processes. Herein, a new diol-type adsorbent (T-resin) was synthesized by grafting tiron (disodium 4,5-dihydroxy-1,3-benzenedisulfonate) onto an ion-exchange resin (grafting amount is 1.2 mmol/g dry) to separate boron and silicon from a solution. The effects of pH, initial concentration, and coexisting anions, particularly, the effect of the coexistence of silicate ion on the adsorption of boron, were investigated. T-resin showed good adsorption properties for both boron and silicon in a wide pH range (pH 2-10). The adsorption of boron and silicon was effectively described by the Langmuir isotherm, and the maximum adsorption capacities of boron and silicon were 21.25 mg/g and 8.36 mg/g, respectively. In a competitive adsorption system, boron and silicon were simultaneously adsorbed on the T-resin, but the adsorption rate of boron was faster than silicon. However, silicon could replace the boron adsorbed on the resin, indicating that the adsorption of silicon was more stable than boron. 11B and 29Si solid state NMR data confirmed the different adsorption mechanisms of the two elements. Boron was adsorbed via two types of complexes, a triangular complex of [LB(OH)], as well as 1:1 tetrahedral complex of [LB(OH)2] and 1:2 tetrahedral complex of [BL2], whereas silicon was only adsorbed via a 1:3 octahedral complex of [SiL3]. Graphical abstract A new diol-type absorbent was synthesized by grafting tiron onto an ion-exchange resin to separate boron and silicon from a solution. Boron and silicon competitively adsorbed on the T-resin, and silicon could replace the boron adsorbed on the resin. 11B and 29Si solid state NMR data confirmed the different adsorption mechanisms of the two elements. Boron was adsorbed via two types of complexes, a triangular complex of [LB(OH)], as well as 1:1 tetrahedral complex of [LB(OH)2] and 1: 2 tetrahedral complex of [BL2], whereas silicon was only adsorbed via a 1:3 octahedral complex of [SiL3].

Ubiquitin ligase CHIP functions as an oncogene and activates the AKT signaling pathway in prostate cancer.

Carboxyl terminus of Hsc-70-interacting protein (CHIP) is an E3 ubiquitin ligase that induces the ubiquitination and degradation of numerous tumor-associated proteins and serves as a suppressor or promoter in tumor progression. To date, the molecular mechanism of CHIP in prostate cancer remains unknown. Therefore, the present study investigated the biological function of CHIP in prostate cancer cells and obtained evidence that CHIP expression is upregulated in prostate cancer tissues. The CHIP vector was introduced into DU145 cancer cells and the cell biological behaviour was examined through a series of experiments, including cell growth, cell apoptosis and migration and invasion assays. The results indicated that the overexpression of CHIP in DU145 prostatic cancer cells promoted cell proliferation through activation of the protein kinase B (AKT) signaling pathway, which subsequently increased cyclin D1 protein levels and decreased p21 and p27 protein levels. The overexpression of CHIP significantly increased the migration and invasion of the DU145 cells, which is possible due to activation of the AKT signaling pathway and upregulation of vimentin. The expression level of CHIP was observed to be increased in human prostate cancer tissues compared with the adjacent normal tissue. Furthermore, the CHIP expression level exhibited a positively association with the Gleason score of the patents. These findings indicate that CHIP functions as an oncogene in prostate cancer.

miR-767-3p Inhibits Growth and Migration of Lung Adenocarcinoma Cells by Regulating CLDN18.

Claudin18 (CLDN18) is necessary for intercellular junctions and is reported to be involved in cell migration and metastasis, making it like an oncogene in various cancer types. However, the biological function and regulatory mechanisms of CLDN18 in lung adenocarcinoma are not yet clear. In this study, we found downregulation of miR-767-3p and upregulation of CLDN18 in lung adenocarcinoma tissue and cell lines. In addition, there was a negative correlation between the expression of miR-767-3p and CLDN18 in lung adenocarcinoma. Double luciferase reporter gene analysis showed that miR-767-3p modulates the expression of CLDN18 by binding its 3'-untranslated regions (3'-UTR). Knockdown of CLDN18 results in a decrease in the growth, migration, and invasion of lung adenocarcinoma cells. Although overexpression of miR-767-3p inhibits lung adenocarcinoma cell growth and migration, these effects can be rescued by reexpressing CLDN18. In summary, the data suggest that miR-767-3p inhibits tumor cell proliferation, migration, and invasion by targeting CLDN18, providing a promising therapeutic target for lung adenocarcinoma.

Lower Extremity Peripheral Arterial Disease Is an Independent Predictor of Coronary Heart Disease and Stroke Risks in Patients with Type 2 Diabetes Mellitus in China.

We aimed to determine the relationship between lower extremity peripheral arterial disease (PAD), 10-year coronary heart disease (CHD), and stroke risks in patients with type 2 diabetes (T2DM) using the UKPDS risk engine. We enrolled 1178 hospitalized T2DM patients. The patients were divided into a lower extremity PAD group (ankle-brachial index ≤ 0.9 or >1.4; 88 patients, 7.5%) and a non-PAD group (ankle-brachial index > 0.9 and ≤1.4; 1090 patients, 92.5%). Age; duration of diabetes; systolic blood pressure; the hypertension rate; the use of hypertension drugs, ACEI /ARB, statins; CHD risk; fatal CHD risk; stroke risk; and fatal stroke risk were significantly higher in the PAD group than in the non-PAD group (P < 0.05 for all). Logistic stepwise regression analysis indicated that ABI was an independent predictor of 10-year CHD and stroke risks in T2DM patients. Compared with those in the T2DM non-PAD group, the odds ratios (ORs) for CHD and stroke risk were 3.6 (95% confidence interval (CI), 2.2-6.0; P < 0.001) and 6.9 (95% CI, 4.0-11.8; P < 0.001) in those with lower extremity PAD, respectively. In conclusion, lower extremity PAD increased coronary heart disease and stroke risks in T2DM.

Metabolic syndrome increases Framingham risk score of patients with type 2 diabetes mellitus / 浙江大学学报·医学版

<p><b>OBJECTIVE</b>To assess the impact of metabolic syndrome(MS) on Framingham risk score(FRS) in patients with type 2 diabetes mellitus (T2DM).</p><p><b>METHODS</b>The anthropometric and biochemical data of 1708 patients with T2DM admitted in hospital from May 2008 to April 2013 were retrospectively analyzed, including 902 males and 806 females with a mean age of 57.1±11.8 years (20-79 years). Diagnosis of MS was made according to the criteria of the Adult Treatment Panel Ⅲ Criteria modified for Asians.</p><p><b>RESULTS</b>Compared to non-MS/T2DM patients, MS/T2DM patients had higher waist circumference, body weight, body mass index, systolic and diastolic blood pressure, fasting C peptide, total cholesterol, triglyceride, and LDL-C (P<0.05), while lower HDL-C (P<0.01). Both FRS [13.0(10.0, 15.0) vs 11.0(9.0, 13.0) in male,15.0(12.0, 18.0) vs 12.0(6.0, 14.8) in female,P<0.01)] and 10-year cardiovascular risk [12.0%(6.0%, 20.0%) vs 8.0%(5.0%,12.0%) in male,3.0%(1.0%, 6.0%) vs 1.0%(0.0%, 2.8%) in female,P<0.01] were higher in MS/T2DM patients than those in non-MS/T2DM patients.Both FRS and 10-year cardiovascular risk were increased with the components of MS.</p><p><b>CONCLUSION</b>T2DM patients with MS have more cardiovascular risk factors, higher FRS and 10-year cardiovascular risk.</p>

Genetic variation among four bred populations of two tilapia strains, based on mitochondrial D-loop sequences.

The hybrid between Nile tilapia (Oreochromis niloticus,♀) and blue tilapia (O. aureus,♂) is an important strain in Chinese aquaculture industry. Two populations named AF (O. aureus, 29 samples) and NF (O. niloticus, 22 samples) were gathered from Freshwater Fisheries Research Center (FFRC). The other two named AG (O. aureus, 29 samples) and NG (O. niloticus, 28 samples) from Guangxi Fisheries Research Institute (GFRI). GFRI introduced AG and NG from AF and NF. The mitochondrial DNA D-loop was sequenced to assess the genetic diversity among four populations. A 580 bp fragment was sequenced. The 93 variable sites defined 39 haplotypes and three were shared. As a result, the genetic diversity of O. aureus AF and AG was much lower (H=0.497-0.532, K=0.69-0.714, π=0.0012-0.00124) than that of O. niloticus (H=0.849-0.866, K=24.286-24.807, π=0.04246-0.04337). Furthermore, the indices (H, K, π and D) was a slight increase between AF and AG, so did NF and NG. These results indicated that as the male parent, the AF and AG population was purebred and sustainable. And as the female parent, NF and NG had high genetic diversity. The conclusions might give reference to keep the germplasm diversity of tilapia and other introduced fishes.

Effects of hydroxysafflor yellow A on the experimental traumatic brain injury in rats.

This paper explores the effects of hydroxysafflor yellow A (HSYA) on traumatic brain injury (TBI). Rats were divided into four groups: control, TBI, TBI combined with HSYA, and TBI combined with nimodipine. Saline, HSYA, or nimodipine was i.v. injected at 30 min before and 6 h after the onset of TBI. The contusion volume of brain, mitochondrial ATPase activity, brain malondialdehyde (MDA) content, and the concentrations of tissue plasminogen activator (t-PA) and plasminogen activator inhibitor-1 (PAI-1) in the blood plasma were investigated. The results showed that the inhibitory rate of HSYA at a dose of 4 mg/kg was 59.2% compared with the TBI group. After the insult by TBI for 48 h, the activity of Na(+), K(+)-ATPase, Ca(2+)-ATPase, and Mg(2+)-ATPase decreased to 31, 35, and 38% of control group. HSYA increased these ATPase activities by 162, 96, and 131% of TBI group. HSYA also increased superoxide dismutase activity and decreased MDA content in the right parietal lobe adjacent to contusion foci in TBI rats. HSYA enhanced the t-PA activity by 64.64%, decreased the PAI-1 activity by 71.88%, and decreased the MMP-9 expression to 49.11% in the hippocampus of the TBI group at 12 h. In conclusion, HSYA may exert a potential therapeutic strategy to improve the outcome following TBI injury.