Influence of Effective Microorganisms on Qualities of Tomatoes (Lycopersicon esculentum) Grown on Tropical Loam Soil

The use of Effective Microorganism (EM) consortium along with compost may overcome the harmful effects caused by chemical fertilizer while improving the nutritional quality of crops. The study aimed to determining the influence of compost inoculated with EM on the nutritional qualities of tomatoes (Lycopersicon esculentum) grown in tropical loam soil.  Four sets of treated loamy soils was experimented. The treatments were the compost without EM (C); compost containing effective microorganisms (EM); compost containing effective microorganisms with chicken manure (CEM) and urea as mineral fertilizer (M). Tomatoes were harvested randomly after matured and kept in plastic bag and immediately transferred to the laboratory for analysis of beta-carotene, vitamin C and brix contents.  The results shows that tomatoes planted with EM inoculated compost have relatively higher level of β-Carotene (7.76µg/100g), Brix (4.9%), and vitamin C (77.55mg/100g) compared with those from mineral 4.01µg/100g, 4.8%, and 3.83mg/100g respectively. This is likely reflect the efficiency of organic nature decomposition of EM compost over mineral fertilizers. We may therefore conclude that EM compost can be applied to supersede chemical fertilizer to promote sustainable and environmentally friendly tomatoes agriculture. Keywords: Beta-carotene, Brix, Compost, Effective microorganisms, Vitamin C

Assessment of Monthly Variation of Two Water Bodies in Erbil Governorate.

The present study was conducted on Erbil wastewater channel and Greater Zab River. Seven sites were selected, three of them from polluted channel and four from the Greater Zab River. Water samples for chemical and biological analysis were collected monthly from May 2006 to April 2007. Factor analysis (Principal component analysis) revealed six significant main components which represented by more than 64.5% of the total variance, in which explained by 26.13%, 15.73%, 11.92%, 8.33%, 7.36% and 5.85% respectively, it revealed that sewagewater from Erbil city and agricultural activities a round polluted channel were the major source of pollutant in the channel, whereas, for the Greater Zab river the seven PCs, of the total variance, were 23%, 14.63%, 10%, 8.96%, 7.73%, 6.55%, and 6.24% respectively, with 77.14% of a cumulative variance, in which Greater Zab river was polluted by effluent of polluted channel, agricultural activities and mineral erosion through rainfall

Silymarin-albumin nanoplex: preparation and its potential application as an antioxidant in nervous system in vitro and in vivo

In this study, we formulated silymarin-HSA nanoplex and assayed its ability to reduce LPSinduced toxicity in vitro and in vivo. Silymarin molecules were encapsulated into HSA nanoplex and the loading efficiency and characterization of fabricated nanoplex were performed by using HPLC, TEM, SEM, DLS, FTIR analysis, and theoretical studies. Afterwards, their protective effect against LPS (20 µg/ml) -induced toxicity in SH-SY5Y cells was investigated by MTT, ROS, and apoptosis assays. For in vivo experiments, rats were pre-treated with either silymarin or silymarin -HSA nanoplex (200 mg/kg) orally for 3 days and at third day received LPS by IP at a dose of 0.5 mg/kg, 150 min before scarification followed by SOD and CAT activity assay. The formulation of silymarin-HSA nanoplex showed a spherical shape with an average diameter between 50 nm to 150 nm, hydrodynamic radius of 188.3 nm, zeta potential of -26.6 mV, and a drug loading of 97.3%. In LPS-treated cells, pretreatments with silymarin-HSA noncomplex recovered the cell viability and decreased the ROS level and corresponding apoptosis more significantly than free silymarin. In rats, it was also depicted that, silymarin-HSA noncomplex can increase the SOD and CAT activity in brain tissue at LPS-triggered oxidative stress model more significantly than free counterpart. Nanoformulation of silymarin improved its capability to reduce LPS-induced oxidative stress by restoring cell viability and elevation of SOD and CAT activity in vitro and in vivo, respectively. Therefore, formulation of silymarin may hold a great promise in the field of antioxidant agent development

Echinacoside ameliorates hepatic fibrosis and tumor invasion in rats with thioacetamide-induced hepatocellular carcinoma

Hepatocellular carcinoma (HCC) affects approximately 800,000 individuals globally each year. Despite advancements in HCC treatments, there is still a pressing need to identify new drugs that can combat resistance. One potential option is echinacoside, a natural caffeic acid glycoside with antioxidant, anti-inflammatory, antidepressant, and antidiabetic properties. Therefore, we aimed to investigate the ability of echinacoside to exhibit antitumor activity against HCC in rats through ameliorating hepatic fibrosis and tumor invasion. Rats were given thioacetamide to induce HCC, and some were given 30 mg/kg of echinacoside twice a week for 16 weeks. The liver impairment was assessed by measuring serum α-fetoprotein (AFP) and examining liver sections stained with Masson trichrome or anti-transforming growth factor (TGF)-β1 antibodies. The hepatic expression of mRNA and protein levels of TGF-β1, β-catenin, SMAD4, matrix metalloproteinase-9 (MMP9), phosphoinositide 3-kinases (PI3K), mammalian target of rapamycin (mTOR), connective tissue growth factor 2 (CCN2), E-Cadherin, platelets derived growth factor (PDGF)-B and fascin were also analyzed. Echinacoside improved the survival rate of rats by decreasing serum AFP and the number of hepatic nodules. Examination of micro-images indicated that echinacoside can reduce fibrosis. It also significantly decreased the expression of TGF-β1, β-catenin, SMAD4, MMP9, PI3K, mTOR, CCN2, PDGF-B, and fascin while enhancing the expression of E-Cadherin. In conclusion, echinacoside exhibits a protective effect against HCC by increasing survival rates and decreasing tumor growth. It also acts as an inhibitor of the hepatic tissue fibrosis pathway by reducing the expression of TGF-β1, β-catenin, SMAD4, PI3K, CCN2, PDGF-B and mTOR. Additionally, it prevents tumor invasion by suppressing MMP9 and fascin, and increasing the expression of E-Cadherin

Metformin restores prohormone processing enzymes and normalizes aberrations in secretion of proinsulin and insulin in palmitate‐exposed human islets

Aim: To elucidate how proinsulin synthesis and insulin was affected by metformin under conditions of nutrient overstimulation. Materials and methods: Isolated human pancreatic islets from seven donors were cultured at 5.5 mmol/L glucose and 0.5 mmol/L palmitate for 12, 24 or 72 h. Metformin (25 μmol/L) was introduced after initial 12 h with palmitate. Proinsulin and insulin were measured. Expression of prohormone convertase 1/3 (PC1/3) and carboxypeptidase E (CPE), was determined by western blot. Adolescents with obesity, treated with metformin and with normal glucose tolerance (n = 5), prediabetes (n = 14), or type 2 diabetes (T2DM; n = 7) were included. Fasting proinsulin, insulin, glucose, 2-h glucose and glycated haemoglobin were measured. Proinsulin/insulin ratio (PI/I) was calculated. Results: In human islets, palmitate treatment for 12 and 24 h increased proinsulin and insulin proportionally. After 72 h, proinsulin but not insulin continued to increase which was coupled with reduced expression of PC1/3 and CPE. Metformin normalized expression of PC1/3 and CPE, and proinsulin and insulin secretion. In adolescents with obesity, before treatment, fasting proinsulin and insulin concentrations were higher in subjects with T2DM than with normal glucose tolerance. PI/I was reduced after metformin treatment in subjects with T2DM as well as in subjects with prediabetes, coupled with reduced 2-h glucose and glycated haemoglobin. Conclusions: Metformin normalized proinsulin and insulin secretion after prolonged nutrient-overstimulation, coupled with normalization of the converting enzymes, in isolated islets. In adolescents with obesity, metformin treatment was associated with improved PI/I, which was coupled with improved glycaemic control

AR loss in prostate cancer stroma mediated by NF-κB and p38-MAPK signaling disrupts stromal morphogen production

Androgen Receptor (AR) activity in prostate stroma is required to maintain prostate homeostasis. This is mediated through androgen-dependent induction and secretion of morphogenic factors that drive epithelial cell differentiation. However, stromal AR expression is lost in aggressive prostate cancer. The mechanisms leading to stromal AR loss and morphogen production are unknown. We identified TGFβ1 and TNFα as tumor-secreted factors capable of suppressing AR mRNA and protein expression in prostate stromal fibroblasts. Pharmacological and RNAi approaches identified NF-κB as the major signaling pathway involved in suppressing AR expression by TNFα. In addition, p38α- and p38δ-MAPK were identified as suppressors of AR expression independent of TNFα. Two regions of the AR promoter were responsible for AR suppression through TNFα. FGF10 and Wnt16 were identified as androgen-induced morphogens, whose expression was lost upon TNFα treatment and enhanced upon p38-MAPK inhibition. Wnt16, through non-canonical Jnk signaling, was required for prostate basal epithelial cell survival. These findings indicate that stromal AR loss is mediated by secreted factors within the TME. We identified TNFα/TGFβ as two possible factors, with TNFα mediating its effects through NF-κB or p38-MAPK to suppress AR mRNA transcription. This leads to loss of androgen-regulated stromal morphogens necessary to maintain normal epithelial homeostasis.U.S. Department of Health & Human Services | NIH | National Cancer Institute6 month embargo; first published 20 May 2024This item from the UA Faculty Publications collection is made available by the University of Arizona with support from the University of Arizona Libraries. If you have questions, please contact us at [email protected]

Antioxidant properties of gold nanozyme: A review

AuNPs with enzyme-like features have received strong attention in different areas, although limited data is available in literature on their biological/industrial functions. NPs especially Au counterparts have been shown to functionally mimic the activity of antioxidant enzyme. Indeed, due to low cytotoxicity and SPR characteristics of AuNPs, there are a great number of reports in which Au nanozymes yield promising responses in biomedical applications. In this review, we aim to overview the enzymatic activity of Au nanozymes along with their regulatory and controlling mechanisms. We have reviewed the effect of various factors such as dimension, morphology, functionalization and presence of hybrid materials on the catalytic activity of Au nanozymes as well as a detail survey on the oxidase, peroxidase, SOD, and CAT-like activities of Au nanozyme. Finally, the significance of Au nanozymes in mitigating oxidative stress followed by conclusion and challenges were reported. Based on this paper, we envision that Au nanozymes can be used as a promising material to prevent oxidative stress-stimulated disorders.Scopu

Hydrogen sulfide-evoked intracellular ca2+ signals in primary cultures of metastatic colorectal cancer cells

Exogenous administration of hydrogen sulfide (H2S) is emerging as an alternative anticancer treatment. H2S-releasing compounds have been shown to exert a strong anticancer effect by suppressing proliferation and/or inducing apoptosis in several cancer cell types, including colorectal carcinoma (CRC). The mechanism whereby exogenous H2S affects CRC cell proliferation is yet to be clearly elucidated, but it could involve an increase in intracellular Ca2+ concentration ([Ca2+]i). Herein, we sought to assess for the first time whether (and how) sodium hydrosulfide (NaHS), one of the most widely employed H2S donors, induced intracellular Ca2+ signals in primary cultures of human metastatic CRC (mCRC) cells. We provided the evidence that NaHS induced extracellular Ca2+ entry in mCRC cells by activating the Ca2+-permeable channel Transient Receptor Potential Vanilloid 1 (TRPV1) followed by the Na+-dependent recruitment of the reverse-mode of the Na+/Ca2+ (NCX) exchanger. In agreement with these observations, TRPV1 protein was expressed and capsaicin, a selective TRPV1 agonist, induced Ca2+ influx by engaging both TRPV1 and NCX in mCRC cells. Finally, NaHS reduced mCRC cell proliferation, but did not promote apoptosis or aberrant mitochondrial depolarization. These data support the notion that exogenous administration of H2S may prevent mCRC cell proliferation through an increase in [Ca2+]i, which is triggered by TRPV1