Nitrogen removal performance and microbial characteristics during simultaneous chemical phosphorus removal process using Fe3.

To evaluate the effect of Fe3+ on nitrogen (N) removal and associated microbial characteristics during simultaneous chemical phosphorus (P) removal, a sequencing batch reactor was used to analyze the changes in the microbial community and metabolic pathways caused by Fe3+ addition. Results demonstrated that Fe3+ promoted ammonia nitrogen (NH4+-N) removal and inhibited denitrification process, and increased the sludge particles (D50) and the biomass per sludge particle size. Furthermore, the abundances of denitrifying bacteria (Haliangium and Terrimonas) and biological phosphorus removing bacteria (Halaingium, norank_f_Saprospiraceae and SM1A02) were decreased. On the contrary, the increase of nitrifying bacteria abundance and the coding genes of nitrification-related enzymes confirmed the promotion for nitrification with Fe3+ addition. Besides, Fe3+ inhibited the interspecific relationship between denitrifying bacteria genera and other genera to reduce denitrification efficiency.

α-Carotene: a valuable carotenoid in biological and medical research.

α-Carotene, one of the C40 carotenes, is a natural lipid-soluble terpene. The chemical structure of α-carotene is based on the unsaturated polyene chain skeleton, with an ε-ring and a ß-ring on each side of the skeleton. α-Carotene is widely found in dietary fruits and vegetables, and the concentration depends on the plant species. In addition, processing methods and storage conditions used in the food and medical industries can alter the concentration of α-carotene in raw materials. This review of α-carotene summarizes the major studies on chemical structure, source, extraction, detection, biosynthesis, processing effect, bioactivity, medicine, and biotechnology. Whether α-carotene supplementation or a diet rich in fruits and vegetables has a positive effect on the prevention of cancer, cardiovascular disease, and other diseases is the focus of this study. © 2022 Society of Chemical Industry.

Deoxypodophyllotoxin inhibits cell viability and invasion by blocking the PI3K/Akt signaling pathway in human glioblastoma cells.

Deoxypodophyllotoxin (DPT) is a natural chemical that has been demonstrated to inhibit cellular viability and motility in various cancer cell types. Although previous studies have indicated that programmed cell death and cell cycle arrest are involved in the suppression of glioma development by DPT, the underlying mechanism has not been fully explored. Different methods were used to the elucidate the mechanisms of DPT that inhibit the malignant behavior of glioma cells. Cellular viability was assessed by MTT assay. Relative protein and mRNA expression levels were detected by western blot analysis and reverse transcription­quantitative polymerase chain reaction analyses, respectively. Cell cycle distribution and the apoptosis rate were detected by flow cytometry. Hochest 33258 staining was also performed to detect apoptosis. Transwell assays without and with Matrigel were used to assess migration and invasion abilities, respectively. It was determined that DPT suppressed cellular viability by inducing cell cycle arrest at the G1/S phase by targeting the phosphatidylinositol 4,5­bisphosphate 3­kinase (PI3K)/RAC­α serine/threonine­protein kinase (Akt)­cyclin­dependent kinase inhibitor 1­cyclin­dependent kinase 2/cyclin E signaling cascades. Additionally, DPT significantly enhanced apoptosis by attenuating the PI3K/Akt­mediated suppression of Bcl­2­associated agonist of cell death expression, which was accompanied by an increased apoptosis regulator BAX/apoptosis regulator Bcl­2 ratio. Furthermore, DPT downregulated the invasiveness of glioma cells by hindering PI3K/Akt­matrix metalloproteinase (MMP)9/MMP2 signaling pathways. In conclusion, DPT effectively inhibited the expression of PI3K and downregulated PI3K/Akt­mediated signaling pathways to prevent glioblastoma progression.

Simultaneous decomplexation in blended Cu(II)/Ni(II)-EDTA systems by electro-Fenton process using iron sacrificing electrodes.

This research explored the application of electro-Fenton (E-Fenton) technique for the simultaneous decomplexation in blended Cu(II)/Ni(II)-EDTA systems by using iron sacrificing electrodes. Standard discharge (0.3 mg L-1 for Cu and 0.1 mg L-1 for Ni in China) could be achieved after 30 min reaction under the optimum conditions (i.e. initial solution pH of 2.0, H2O2 dosage of 6 mL L-1 h-1, current density of 20 mA/cm2, inter-electrode distance of 2 cm, and sulfate electrolyte concentration of 2000 mg L-1). The distinct differences in apparent kinetic rate constants (kapp) and intermediate removal efficiencies corresponding to mere and blended systems indicated the mutual promotion effect toward the decomplexation between Cu(II) and Ni(II). Massive accumulation of Fe(Ⅲ) favored the further removal of Cu(II) and Ni(II) by metal ion substitution. Species distribution results demonstrated that the decomplexation of metal-EDTA in E-Fenton process was mainly contributed to the combination of various reactions, including Fenton reaction together with the anodic oxidation, electro-coagulation (E-coagulation) and electrodeposition. Unlike hypophosphite and citrate, the presence of chlorine ion displayed favorable effects on the removal efficiencies of Cu(II) and Ni(II) at low dosage, but facilitated the ammonia nitrogen (NH4+-N) removal only at high dosage.

Smart Human-Serum-Albumin-As2 O3 Nanodrug with Self-Amplified Folate Receptor-Targeting Ability for Chronic Myeloid Leukemia Treatment.

Arsenic trioxide (ATO, As2 O3 ) is currently used to treat acute promyelocytic leukemia. However, expanding its use to include high-dose treatment of other cancers is severely hampered by serious side effects on healthy organs. To address these limitations, we loaded ATO onto folate (FA)-labeled human serum albumin (HSA) pretreated with glutathione (GSH) based on the low pH- and GSH-sensitive arsenic-sulfur bond, and we termed the resulting smart nanodrug as FA-HSA-ATO. FA-HSA-ATO could specifically recognize folate receptor-ß-positive (FRß+) chronic myeloid leukemia (CML) cells, resulting in more intracellular accumulation of ATO. Furthermore, the nanodrug could upregulate FRß expression in CML cancer cells and xenograft tumor model, facilitating even more recruitment and uptake of FRß-targeting drugs. In vitro and in vivo experiments indicate that the nanodrug significantly alleviates side effects and improves therapeutic efficacy of ATO on CML and xenograft tumor model.

ARISTOLOCHIA BRACTEOLATE RETZ. ATTENUATES HYPERURICEMIA IN A METABOLIC ARTHRITIS RAT MODEL.

BACKGROUND: The leaves of Aristolochia bracteolata Retz. has been documented in the folk medicine literature for its anti-arthritic activity. The target of the research envisaged was to elucidate the activity of A. bracteolata extract on hyperuricemic condition in arthritis rat model. MATERIALS AND METHODS: Dried and powdered plant leaves were extracted using ether and chloroform. Potassium oxonate was injected intra-articularly to produce arthritis. The hyperuricemic effect, of A. bracteolate was analyzed by studying levels of uric acid in serum as well as in urine of arthritis induced rats. Effects of plant extracts were also studied on BUN (blood urea nitrogen) levels and fraction of uric acid excreted. RESULTS: Results indicate that administration of A. bracteolata presented substantial change in uric acid concentration, augmented by potassium oxonate administration in rats. The reduction in levels of uric acid levels was nearly same as allopurinol. The investigation also revealed that the primary plant extract has nephroprotective effect by enhancing the production of Prostaglandin E2 and Interleukin-1. Histological studies of rat kidney slices indicated the safety of the present plant extract. CONCLUSION: The crude extract of A. bracteolate can be used to reduce hyperuricemia in metabolic arthritis produced in rat model, without inducing any potential damaging effects.

Atorvastatin enhances angiogenesis to reduce subdural hematoma in a rat model.

BACKGROUND AND PURPOSE: Statins are active in reducing plasma lipids, suppressing inflammation and promoting angiogenesis. Because angiogenesis is critical for the absorbance of subdural hematoma (SDH), we hypothesize that atorvastatin promotes angiogenesis to enhance hematoma absorption. METHODS: SDH was induced in adult Wistar rats and treated with 3mg/kg, 8mg/kg of atorvastatin, or vehicle saline daily for 7days. The treated rats were examined for the level of CD34+/CD133+ endothelial progenitor cells (EPCs) in the circulation by flow cytometry, hematoma volumes by magnetic resonance imaging (MRI), and changes in cognitive functions. We also examined angiogenesis in the hematoma wall by transmission electronic microscopy and immunohistochemistry for the expression of vascular endothelial growth factor (VEGF), matrix metalloprotease 9 (MMP 9) and angiopoietin. RESULTS: SDH volume was significantly reduced and neurological deficits improved in rats receiving the low dose atorvastatin compared to those receiving either the high dose of atorvastatin or saline. Consistent with these outcome measures, the low dose atorvastatin increased the expression of angiopoient-1 and VEGF and reduced MMP9 expression in the connective tissue of the SDH wall, resulting in an increased vascular density and enhanced vascular maturation. CONCLUSIONS: The low-dose atorvastatin is effective in reducing SDH and improving neurological deficits in a rat model, primarily by promoting angiogenesis and vascular maturation.

[Chemical constituents from flowers of Scabiosa tschilliensis].

Twenty-two compounds were isolated from the flowers of Scabiosa tschilliensis. Their structures were identified by spectroscopic methods as octacosanol (1), stearic acid (2), ß-sitosterol (3), oleanolic acid (4), apigenin (5), luteolin (6), daucosterol (7), kaempferol-3-O-ß-D-6-O-(p-hydroxycinnamoyl) -glucopyranoside (8), kaempferol-3-O-ß-D- (3, 6-di-p-(hydroxycinnamoyl) -glucopyranoside (9), apigenin-7-O-ß-D-glucopyranoside (10), luteolin-4'-O-ß-D-glucopyranoside (11), apigenin-7-O-rutinoside (12), luteolin-7-O-ß-D-glucopyranoside (13), apigenin-4'-O-ß-D-glucopyranoside (14), caffeic acid methyl ester (15), loganin (16), adenosine (17), luteolin-6-C-ß-D-glycopyranosyl (18), sweroside (19), sylvestrosides I (20), sylvestrosides II (21), urceolide (22). Among them, compounds 1, 2, 7-9, 12, 15, 17-18, 20-22 were isolated from the genus Scabiosa for the first time, and compounds 1-4, 6-9, 11-12, 14-22 were isolated from this plant for the first time. 13C-NMR data of 22 were reported for the first time.

Stress-dose hydrocortisone reduces critical illness-related corticosteroid insufficiency associated with severe traumatic brain injury in rats.

INTRODUCTION: The spectrum of critical illness-related corticosteroid insufficiency (CIRCI) in severe traumatic brain injury (TBI) is not fully defined and no effective treatments for TBI-induced CIRCI are available to date. Despite growing interest in the use of stress-dose hydrocortisone as a potential therapy for CIRCI, there remains a paucity of data regarding its benefits following severe TBI. This study was designed to investigate the effects of stress-dose hydrocortisone on CIRCI development and neurological outcomes in a rat model of severe traumatic brain injury. METHODS: Rats were subjected to lateral fluid percussion injury of 3.2-3.5 atmosphere. These rats were then treated with either a stress-dose hydrocortisone (HC, 3 mg/kg/d for 5 days, 1.5 mg/kg on day 6, and 0.75 mg on day 7), a low-dose methylprednisolone (MP, 1 mg/kg/d for 5 days, 0.5 mg/kg on day 6, and 0.25 mg on day 7) or control saline solution intraperitoneally daily for 7 days after injury. RESULTS: We investigated the effects of stress-dose HC on the mortality, CIRCI occurrence, and neurological deficits using an electrical stimulation test to assess corticosteroid response and modified neurological severity score (mNSS). We also studied pathological changes in the hypothalamus, especially in the paraventricular nuclei (PVN), after stress-dose HC or a low dose of MP was administered, including apoptosis detected by a TUNEL assay, blood-brain barrier (BBB) permeability assessed by brain water content and Evans Blue extravasation into the cerebral parenchyma, and BBB integrity evaluated by CD31 and claudin-5 expression. We made the following observations. First, 70% injured rats developed CIRCI, with a peak incidence on post-injury day 7. The TBI-associated CIRCI was closely correlated with an increased mortality and delayed neurological recovery. Second, post-injury administration of stress-dose HC, but not MP or saline increased corticosteroid response, prevented CIRCI, reduced mortality, and improved neurological function during the first 14 days post injury dosing. Thirdly, these beneficial effects were closely related to improved vascular function by the preservation of tight junctions in surviving endothelial cells, and reduced neural apoptosis in the PVN of hypothalamus. CONCLUSIONS: Our findings indicate that post-injury administration of stress-dose HC, but not MP reduces CIRCI and improves neurological recovery. These improvements are associated with reducing the damage to the tight junction of vascular endothelial cells and blocking neuronal apoptosis in the PVN of the hypothalamus.

High-dose glucocorticoid aggravates TBI-associated corticosteroid insufficiency by inducing hypothalamic neuronal apoptosis.

Emerging experimental and clinical data suggest that severe illness, such as traumatic brain injury (TBI), can induce critical illness-related corticosteroid insufficiency (CIRCI). However, underlying mechanisms of this TBI-associated CIRCI remain poorly understood. We hypothesized that dexamethasone (DXM), a synthetic glucocorticoid, which was widely used to treat TBI, induces hypothalamic neuronal apoptosis to aggravate CIRCI. To test this hypothesis, we have evaluated the dose effect of DXM (1 or 10mg/kg) on the development of acute CIRCI in rats with fluid percussion injury-induced TBI and on cultured rat hypothalamic neurons in vitro (DXM, 10(-5)-10(-8)mol/L). Corticosterone Increase Index was recorded as the marker for CIRCI. In addition, MTT and TUNEL assays were used to measure the viability and apoptosis of hypothalamic neurons in primary culture. Moreover, high-resolution hopping probe ion conductance microscopy (HPICM) was used to monitor the DXM-induced morphological changes in neurons. The incidence of acute CIRCI was significantly higher in the high-dose DXM group on post-injury day 7. Cellular viability was significantly decreased from 12h to 24h after the treatment with a high-dose of DXM. A significantly increase in TUNEL positive cells were detected in cultured cells treated with a high-dose of DXM after 18h. Neurites of hypothalamic neuron were dramatically thinner and the numbers of dendritic beadings increased in neurons treated with the high dose of DXM for 12h. In conclusion, high-dose DXM induced hypothalamic neurons to undergo apoptosis in vivo and in vitro, which may aggravate TBI-associated CIRCI.

Aptamer-conjugated nanorods for targeted photothermal therapy of prostate cancer stem cells.

Prostate cancer results in about 30,000 deaths annually in the United States, making it the second leading cause of cancer mortality in men in the Western world. Therefore, it is of great significance to capture and kill prostate cancer cells. It is well known that cancer stem cells are responsible for the maintenance and metastasis of tumors. This concept offers the possibility of developing a selective therapeutic approach in which cancer stem cells are directly targeted and killed. In this work, aptamers selected against DU145 prostate cancer cells (aptamer CSC1) and their subpopulation of cancer stem cells (aptamer CSC13) were linked to the surfaces of gold nanorods (AuNRs), and the resulting conjugates were successfully used to target and kill both cancer cells and cancer stem cells by near-infrared (NIR) laser irradiation. Even though cancer stem cells represent only a small population among all cancer cells, the entire cell viability was very low after laser irradiation, suggesting that tumorigenesis could be successfully controlled by this aptamer-based method, thus paving the way for early diagnosis and targeted therapy.

Photon-manipulated drug release from a mesoporous nanocontainer controlled by azobenzene-modified nucleic acid.

Herein a photon-manipulated mesoporous release system was constructed based on azobenzene-modified nucleic acids. In this system, the azobenzene-incorporated DNA double strands were immobilized at the pore mouth of mesoporous silica nanoparticles. The photoisomerization of azobenzene induced dehybridization/hybridization switch of complementary DNA, causing uncapping/capping of pore gates of mesoporous silica. This nanoplatform permits holding of guest molecules within the nanopores under visible light but releases them when light wavelength turns to the UV range. These DNA/mesoporous silica hybrid nanostructures were exploited as carriers for the cancer cell chemotherapy drug doxorubicin (DOX) due to its stimuli-responsive property as well as good biocompatibility via MTT assay. It is found that the drug release behavior is light-wavelength-sensitive. Switching of the light from visible to the UV range uncapped the pores, causing the release of DOX from the mesoporous silica nanospheres and an obvious cytotoxic effect on cancer cells. We envision that this photocontrolled drug release system could find potential applications in cancer therapy.