Insights on Protective Effect of Platelet Rich Plasma and Tadalafil on Testicular Ischemia/Reperfusion Injury in Rats Exposed to Testicular Torsion/Detorsion.

BACKGROUND/AIMS: Ischemic reperfusion (I-R) injury is greatly influenced by the testicular torsion/detorsion process (TDP). In this instance, the anti-inflammatory properties of plateletrich plasma (PRP) combined with tadalafil (Td) significantly promote tissue healing in the I-R injury model. METHODS: Five groups of rats were created: the control group, the I-R group not receiving any therapy, the I-R group receiving a single dosage of Td (0.25 mg/kg, I.P.), the I-R group receiving a single dose of PRP (80 l, intratesticular), and the I-R group receiving both Td and PRP. Sperm morphology, motility, and histology were assessed. The levels of TNF-, BAX, antioxidant status, and testosterone were measured. Additionally, E-selectin expression was done. RESULTS: PRP reduced oxidative stress, inflammation, and apoptosis while also boosting testosterone levels, which alleviated I-R injury. Otherwise, PRP reduces E-selectin expression, which modifies the pathways that control endothelial function. Td also partially demonstrated its testicular-protective activity at the same time. CONCLUSION: PRP's proven anti-inflammatory, antioxidant, and antiapoptotic potentials make it a natural treatment for testicular harm caused by tadalafil. For the first time, it was demonstrated that PRP therapy restored the functionality of the vascular endothelium, specifically the control of E-selectin expression. Combining Td and PRP therapy may be a promising strategy for improving response to PDE5 inhibitors.

Disinfection of 3D-printed surgical guides using virgin coconut oil (in vitro study).

BACKGROUND/OBJECTIVE: Disinfection of a 3D-printed surgical guide is of utmost importance as it comes into contact with hard and soft tissue during implant placement so it poses a potential risk of pathogenic transmission. Methods used for disinfection in the surgical field should be reliable, practical, and safe for the instruments and the patients. The objectives of this study were to compare the antimicrobial potential of 100% Virgin Coconut Oil, 2% Glutaraldehyde, and 70% Ethyl Alcohol used to decontaminate 3D-printed surgical guides. MATERIALS AND METHODS: Thirty identical surgical guides were printed and cut into two halves (N = 60). Both halves were then contaminated with a defined amount of human saliva samples (2 ml). The first half (n = 30) was sub-grouped into three study groups which were immersed in one of the three disinfectants for 20 min as follows; group VCO was immersed in 100% Virgin Coconut Oil, group GA was immersed in 2% Glutaraldehyde, and group EA was immersed in 70% Ethyl Alcohol. The second half (n* = 30) was sub-grouped into three control groups which were immersed in sterile distilled water as follows group VCO*, group GA*, and group EA*. The microbial count was expressed as colony-forming units per plate and the comparison of the antimicrobial potential of the three tested disinfectants between the three study and three control groups was done using the One-Way ANOVA test. RESULTS: The culture results of three study groups revealed no bacterial growth with the highest % of reduction in the mean microbial count of the oral microorganisms (about100%) and an uncountable bacterial growth was shown between the three control groups (more than 100 CFU/plate) representing the baseline of the oral microorganisms. Therefore; statistically significant differences were found between the three control and three study groups (P < .001). CONCLUSION: The antimicrobial potential of Virgin Coconut Oil was comparable and equivalent to Glutaraldehyde and Ethyl Alcohol with a significant inhibitory action against oral pathogens.

The microbiological effect of virgin coconut oil on the morphological and volumetric dimensional changes of 3D printed surgical guides (in vitro study).

BACKGROUND/OBJECTIVES: Disinfection of surgical guides is mandatory for intraoperative use. Virgin Coconut Oil may be a potent alternative disinfectant; however, its effect has not been fully discussed in dentistry. The objectives of this study were to compare the morphological and the volumetric dimensional changes of 3D printed surgical guides after immersion in three disinfectants: 100%Virgin Coconut Oil, 2% Glutaraldehyde, and 70% Ethyl Alcohol and to assess the antimicrobial effectiveness of the tested disinfectants. MATERIALS AND METHODS: A surgical guide was designed using open platform software to print thirty guides and then cut them into two halves (N = 60). Pre-disinfection scans of the first half of the three study groups (n = 30) were performed using Cone-beam Computed Tomography, then immersed for 20 min in three disinfectants as follows: group VCO was immersed in 100% Virgin Coconut Oil, group GA was immersed in 2% Glutaraldehyde, and group EA was immersed in 70% Ethyl Alcohol. Post-disinfection scans of the first half of the three study groups (n = 30) were performed and then compared morphologically and volumetrically using an analyzing software program The second half of the three control groups (n* = 30) were soaked for 20 min in sterile distilled water as follows: group VCO*, group GA*, and group EA* for the assessment of the antimicrobial effectiveness of the three tested disinfectants. RESULTS: At the morphological assessment of the dimensional changes, group VCO were the most accurate with the lowest mean deviation value of 0.12 ± 0.02 mm and root mean square value of 0.12 mm, group GA and group EA were less accurate with mean deviation value of = 0.22 ± 0.05 mm and = 0.19 ± 0.03 mm and root mean square value of 0.22 and 0.20 respectively (p < 0.001). At the volumetric assessment, group VCO showed lower volumetric changes with a mean deviation value of 0.17 ± 0.10 mm, root mean square value of 0.19 mm, than group GA with mean deviation value of 0.23 ± 0.10 mm, root mean square value of 0.25 mm and group EA with mean deviation value of 0.27 ± 0.11 mm, root mean square value of 0.29 mm, however, no statistically significant differences were found between the three study groups (p = 0.10). The antimicrobial effectiveness of the three tested disinfectants showed a hundred percent (100%) reduction in the total microbial count in the first half of the three study groups treated with the three disinfectants revealing no bacterial growth, however, statistically significant differences were found between the second half of the three control and the first half of the three study groups. (p < 0.001). CONCLUSIONS: Virgin Coconut Oil showed higher morphological dimensional accuracy of the tested surgical guides than Glutaraldehyde and Ethyl Alcohol without causing any volumetric dimensional changes in the 3D printed surgical guides after disinfection for 20 min and the antimicrobial effectiveness was the same between the three tested disinfectants without showing any microbial growth.

Bayesian statistical approaches to drug product variability assessment and release.

The determination of the variability of critical dosage form attributes has been a challenge in establishing the quality of pharmaceutical products. During the development process knowledge is minimal. Consequently, ad hoc statistical tools such as hypothesis or significance tests, with calibrated decision error rates are often used in an effort to vet CQAs (Critical Quality Attributes) and keep their levels "between the curbs". As progress moves towards product launch, process and mechanistic understanding grows considerably and there are opportunities to leverage that knowledge for predictive modeling. Bayesian models offer a coherent strategy for integrating prior knowledge into both experimental design as well as predictive analysis for optimal risk-based decision making. This is because the Bayesian paradigm, unlike the frequentist paradigm, can assign probabilities to underlying states of nature that directly impact safety and efficacy such as the population distribution of tablet potencies or dissolution profiles in a batch. However, there are challenges and reluctance in switching to a predictive modeling quality framework once regulatory approval has been attained. This paper offers encouragement to make this switch. In this paper, we review a joint Long Island University - Purdue University (LIU-PU) FDA funded project whose purpose was to further integrate the concepts of this adaptive approach to lot release with the rationale and methods for data generation and curation and to extend the testing of this approach. We discuss the utility of the approach in product development. We consider the regulatory compliance implications, with examples, and establish a potential way forward toward implementation of this approach for both industry and regulatory stake-holders.

Early Prediction of a Pre-Symptomatic Neurodegeneration Disorder by Measuring Macrophage Inhibitory Factor Level in Diabetic Patients.

BACKGROUND: The relationship between diabetes mellitus and neurodegenerative disorders has been of great interest. Macrophage migration inhibitory factor (MIF) is a pro-inflammatory cytokine in which a variety of signaling cascades are activated through it. MIF has been involved in the pathogenesis of several diseases and can predict early pre-symptomatic stages of neurodegeneration in diabetic patients. OBJECTIVE: To investigate whether serum MIF could predict brain neurodegeneration at the early pre-symptomatic stages in diabetic patients. METHODS: We examined adults with type 2 diabetes mellitus and compared with normal control adults using a short form of the IQCODE and biochemical examination, including assessment of HA1C, fasting blood glucose, lipid profile, and MIF which was measured by ELISA technique. Correlations between parameters were studied. Computational PathLinker bioinformatic tool was used to search for potential pathway reconstructions for the insulin/amyloid-ß/MIF signaling. RESULTS: We demonstrated that MIF level was increased in the serum at the early pre-symptomatic stages of neurodegenerative disorder in diabetic patients. In addition, network analysis demonstrates that insulin receptor substrate 1 can ameliorate amyloid-ß protein precursor through COP9 signalosome complex subunit 5 that enhances MIF elevation. CONCLUSION: Diagnosis processes could not be used as routine examinations for still pre-symptomatic neurodegenerative disorders. This may be due to the time constraints and the heavy dependence on the physician's experience. Therefore, serum MIF level could predict brain neurodegeneration at the early pre-symptomatic stages in diabetic patients which may support its potential utility as a clinically useful biomarker.

Bedside testing of CYP2C19 vs. conventional clopidogrel treatment to guide antiplatelet therapy in ST-segment elevation myocardial infarction patients.

BACKGROUND: ST-segment elevation myocardial infarction (STEMI) patients are treated with dual antiplatelet therapy comprising aspirin and a P2Y12 inhibitor. Clopidogrel is widely used in these patients in several areas worldwide, such as Middle East, but is associated to sub-optimal platelet inhibition in up to 1/3 of treated patients. We investigated a CYP2C19 genotype-guided strategy to select the optimal P2Y12 inhibitor. METHODS: This prospective randomized clinical trial included STEMI patients. The standard-treatment group received clopidogrel, while the genotype-guided group were genotyped for CYP2C19 loss-of-function alleles and carriers were prescribed ticagrelor and noncarriers were prescribed clopidogrel. Primary outcome was a combined ischemic and bleeding outcome, comprising myocardial infarction, non-fatal stroke, cardiovascular death, or Platelet Inhibition and Patient Outcomes major bleeding one year after STEMI. RESULTS: STEMI patients (755) were randomized into a genotype-guided- (383) and standard-treatment group (372). In the genotype-guided group, 31 patients carrying a loss-of-function allele were treated with ticagrelor, while all other patients in both groups were treated with clopidogrel. Patients in the genotype-guided group had a significantly lower risk of primary outcome (odds ratio (OR) 0.34, 95% confidence interval (CI) 0.20-0.59,), recurrent myocardial infarction (OR 0.25, 95%CI 0.11-0.53), cardiovascular death (OR 0.16, 95%CI0.06-0.42) and major bleeding (OR 0.49, 95%CI 0.32-0.74). There was no significant difference in the rate of stent thrombosis (OR 0.85, 95%CI 0.43-1.71). CONCLUSION: A genotype-guided escalation of P2Y12 inhibitor strategy is feasible in STEMI patients treated with clopidogrel and undergoing PCI and is associated with a reduction of primary outcomes compared to conventional antiplatelet therapy.

Protein networks linking Warburg and reverse Warburg effects to cancer cell metabolism.

It was 80 years after the Otto Warburg discovery of aerobic glycolysis, a major hallmark in the understanding of cancer. The Warburg effect is the preference of cancer cell for glycolysis that produces lactate even when sufficient oxygen is provided. "reverse Warburg effect" refers to the interstitial tissue communications with adjacent epithelium, that in the process of carcinogenesis, is needed to be explored. Among these cell-cell communications, the contact between epithelial cells; between epithelial cells and matrix; and between fibroblasts and inflammatory cells in the underlying matrix. Cancer involves dysregulation of Warburg and reverse Warburg cellular metabolic pathways. How these gene and protein-based regulatory mechanisms have functioned has been the basis for this review. The importance of the Warburg in oxidative phosphorylation suppression, with increased glycolysis in cancer growth and proliferation is emphasized. Studies that are directed at pathways that would be expected to shift cell metabolism to an increased oxidation and to a decrease in glycolysis are emphasized. Key enzymes required for oxidative phosphorylation, and affect the inhibition of fatty acid metabolism and glutamine dependence are conferred. The findings are of special interest to cancer pharmacotherapy. Studies described in this review are concerned with the effects of therapeutic modalities that are intimately related to the Warburg effect. These interactions described may be helpful as adjuvant therapy in controlling the process of proliferation and metastasis.

Vildagliptin, a DPP-4 inhibitor, attenuates carbon tetrachloride-induced liver fibrosis by targeting ERK1/2, p38α, and NF-κB signaling.

Mitogen-activated protein kinases (MAPKs) and nuclear factor (NF)-ĸB signaling have been recognized for their causal connection with liver fibrosis. Hence, it is encouraging to discover drugs that can modify the interactions between these signaling cascades. It has been suggested that glucagon-like peptide-1 receptors (GLP-1Rs) might have a role in the observed hepatoprotection of dipeptidyl peptidase-4 inhibitors other than vildagliptin (VLD). Consequently, we aimed to elucidate the mechanisms underlying its potential antifibrotic activity in a CCl4-intoxicated mouse model. VLD increased the percentage of viable CCl4-intoxicated primary rat hepatocytes in vitro. It also attenuated hepatic fibrosis, improved liver function, and prolonged survival of CCl4-intoxicated mice in a dose-dependent manner. This hepatoprotection might be mediated mainly through interference with extracellular signal-regulated protein kinase 1/2 phosphorylation, the most downstream signal of the MAPK pathway. In addition, VLD hepatoprotective activity could be partially mediated through inhibition of p38α phosphorylation and phosphorylation-induced NF-ĸB activation. As a result, VLD downregulated profibrogenic mediators, such as tumor necrosis factor α, transforming growth factor ß, tissue inhibitor of metalloproteinase 1 and platelet-derived growth factor BB. Consequently, decreased expression levels of fibrosis markers, such as hydroxyproline and α smooth muscle actin, were confirmed. VLD showed a strong trend toward increasing the antioxidant defense machinery of fibrotic tissue, and we confirmed that GLP-1Rs were not implicated in the observed hepatoprotection. Since VLD poses little risk of hypoglycemia and is a safe drug for patients with liver injury, it may be a hopeful candidate for adjuvant treatment of liver fibrosis in humans.

Bedside testing of CYP2C19 gene for treatment of patients with PCI with antiplatelet therapy.

BACKGROUND: To mitigate the risk of stent thrombosis, patients treated by percutaneous coronary intervention (PCI) are administered dual anti-platelet therapy comprising aspirin and a platelet P2Y12 receptor inhibitor. Clopidogrel is a prodrug requiring activation by the cytochrome P450 enzyme, CYP2C19. In Saudi Arabia, it has been reported that approximately 26% of the population carries CYP2C19*2 and/or *3 loss-of-function polymorphisms in addition to a high prevalence of CVD. METHODS: This prospective (April 2013-December 2020) parallel assignment clinical trial focuses on ST-Elevation Myocardial Infarction (STEMI) patient outcomes. The clinical trial includes 1500 STEMI patients from two hospitals in the Eastern Province of Saudi Arabia. Patients are assigned to one of two groups; the control arm receives conventional therapy with clopidogrel, while in the active arm the Spartan RX CYP2C19 assay is used to determine the *2 genotype. Carriers of a CYP2C19*2 loss-of-function allele receive prasugrel or ticagrelor, while non-carriers are treated with clopidogrel. Follow-up is one year after primary PCI. The primary end point is the number of patients who develop an adverse major cardiovascular event, including recurrent MI, non-fatal stroke, cardiovascular death, or major bleeding one year after PCI. DISCUSSION: The risk of stent thrombosis in PCI patients is usually reduced by dual anti-platelet therapy, comprising aspirin and a P2Y12 inhibitor, such as clopidogrel. However, clopidogrel requires activation by the cytochrome P450 enzyme, CYP2C19. Approximately 20% of the population are unable to activate clopidogrel as they possess the CYP2C19*2 loss-of function (LoF) allele. The primary goal of this trial is to study the benefits of treating only those patients that cannot activate clopidogrel with an alternative that has shown to be a more effective platelet inhibitor and does not require bioactivation by the cytochrome P450 enzyme. We expect an improvement in net clinical benefit outcome in the active arm patients, thus supporting pharmacogenetic testing in PCI patients post STEMI. TRIAL REGISTRATION: Trial registration name is "Bedside Testing of CYP2C19 Gene for Treatment of Patients with PCI with Antiplatelet Therapy" (number NCT01823185) retrospectively registered with clinicaltrials.gov on April 4, 2013. This trial is currently at the patient recruitment stage.

Kidney injury molecule-1: A potential marker of renal recovery after laparoscopic sleeve gastrectomy.

BACKGROUND: Bariatric surgeries were reported to improve diabetes and hypertension; however, the effect on renal recovery has not been fully explored. The aim of this study was to evaluate the effect of laparoscopic sleeve gastrectomy (LSG) in morbidly obese patients on renal function, degree of albuminuria, and kidney injury molecule-1 (KIM-1) level. METHODS: This was a prospective observational study conducted at Mansoura University Hospitals from January to June 2017. Forty-four morbidly obese patients (29 females and 15 males) who met the 1991 WHO criteria for obesity surgery were included. Patients underwent surgical LSG for treatment of morbid obesity, and all were followed for 6 months after surgery. Demographic, clinical, and laboratory data were collected and compared before and after surgery. Primary endpoints were the differences of albuminuria, estimated glomerular filtration rate (eGFR) and serum KIM-1 between baseline (pre-surgery) and 6-month post-surgery values. RESULTS: Six-month post-surgery data showed significant reduction of body mass index, HbA1c, microalbuminuria, and serum KIM-1, and a significant increase in eGFR (all, P < 0.001). The serum KIM-1 level positively correlated with microalbuminuria and serum creatinine (r = 0.596, P = 0.001 and r = 0.402, P = 0.034, respectively). Postoperative data showed that patients with microalbuminuria had significantly lower eGFR and higher KIM-1 values than those without microalbuminuria (P = 0.003 and 0.049, respectively). CONCLUSION: We showed potential benefits of LSG against obesity-associated kidney damage. This is evidenced by improving eGFR and reducing levels of both KIM-1 and microalbuminuria. The serum level of KIM-1 may be a potential marker for renal recovery after LSG.

Omega-3 offers better hypothalamus protection by decreasing POMC expression and elevating ghrelin hormone: a prospective trial to overcome methotrexate-induced anorexia.

PURPOSE: Methotrexate (MTX) therapy is widely used in treatment of different types of diseases including inflammatory diseases, autoimmune disorders, and cancer. However, most of patients respond well to MTX, they suffer from multiple side effects including severe anorexia. Omega-3 fatty acid possesses many beneficial biological activities. Therefore, the objective of our study is to explore the effect of the combined modality of omega-3 (400 mg/kg/day) in MTX-induced anorexia in rats. METHODS: The effect of MTX alone and in combination with omega-3 on the body weight, ghrelin hormone level, histopathological findings of taste buds and hypothalamus and POMC gene expression were investigated. RESULTS: Interestingly, the capability of omega-3 to overcome the anorexic effect of MTX could be manifested by controlling weight loss, increasing serum HDL, elevating the ghrelin level as well as reducing both lesions within taste buds and hypothalamus and hypothalamic POMC gene expression. CONCLUSIONS: our findings revealed that the omega-3 might be used as a complementary supplement during the MTX therapy to ameliorate its anorexic effect.

Evaluation of acinetobacter baumannii pneumonia among critically ill patients in a tertiary care hospital in Saudi Arabia.

Microbiology; Bacteria; Antimicrobial; Infectious disease; Medical microbiology; Pharmacology; Pneumonia; Acinetobacter baumannii; Colistin.

New insights into weight management by orlistat in comparison with cinnamon as a natural lipase inhibitor.

BACKGROUND AND OBJECTIVES: Orlistat which is taken by obese patients may present some therapeutic assistance through its inhibition of lipase activity. Otherwise, a natural lipase inhibitor as cinnamon is widely used traditional medicine to decrease cholesterol and body weight. The current study aimed to investigate the weight management of orlistat in comparison with cinnamon through different obesity related targets. METHODS: Subjects were divided into: Group 1: subjects received cinnamon capsules for 60 days. Group 2: subjects were received orlistat twice daily for 30 days, then once daily for another 30 days. Blood samples were collected at baseline and after 2 months. RESULTS: Both orlistat and cinnamon groups showed a significant reduction in BMI, lipid profile, and lipase activity compared with baseline. Orlistat group showed significant elevation (p < 0.001) in glucagon, insulin-degrading enzyme (IDE) and dopamine level concomitant with the decrease of serum glutamate compared with baseline level of the same group and cinnamon group. However, cinnamon reduced serum insulin level and insulin resistance (IR) compared with baseline level of the same group and orlistat group. CONCLUSIONS: Orlistat can be used in weight management not only for its pancreatic lipase inhibition but also, due to its indirect appetite reduction effect through elevated glucagon, IDE and dopamine levels and its inhibitory effect on glutamate neurotransmitter, whereas, cinnamon improves BMI and glycaemic targets.

Olmesartan ameliorates chemically-induced ulcerative colitis in rats via modulating NFκB and Nrf-2/HO-1 signaling crosstalk.

Alteration in the expression pattern of Nrf-2 and NFκB has been reported in ulcerative colitis (UC) in which functional crosstalk between these two critical pathways has been suggested. The ameliorative potential of the AT1R blocker olmesartan (OLM) on oxidative stress and inflammatory cytokines has received considerable attention in recent years. Acetic acid (AA)-induced UC demonstrates close resemblance to human UC regarding histopathological features and cytokine profile and is associated with local intense immune response, oxidative stress and release of inflammatory cytokines. Therefore, The effect of OLM (1, 5 and 10 mg/kg) administered orally to rats subjected to intra-rectal instillation of 2 ml of 3% AA in saline solution is investigated. The study revealed that OLM ameliorated colon injury and inflammatory signs as visualized by histopathological examination. Levels of colon IL-6, TNF-α, IL-1ß, TGF-ß, and serum CRP were down-regulated, while the level of colon IL-10 was up-regulated. In a dose-dependent manner, OLM suppressed AA-induced neutrophils accumulation and improved colon anti-oxidant defense machinery. Also, OLM repressed the Bax:BCL-2 ratio and caspase3 expression. The mechanism of these protective effects was found to lay behind its ability to down-regulate gene expression and inhibit phosphorylation and nuclear translocation of p65 subunits. On the other hand, OLM up-regulated gene expression of Nrf-2 and HO-1. In conclusion, our data show that OLM is an Nrf2 activator, NFkB inhibitor and apoptosis inhibitor in an experimental model of ulcerative colitis. Overall, the study indicates that OLM shows promise as a potential therapy for the treatment of human inflammatory bowel diseases.

Ubiquitin-Proteasome Pathway and Muscle Atrophy.

Many systemic diseases are featured by muscle atrophy. Cellular proteins are modified by covalent attachment to a small protein known as ubiquitin (Ub) through ubiquitination. This ubiquitination process serves as signal for protein turnover that leads to rapid muscle mass lack. This process is carried out through an enzymatic cascade, which includes three groups of enzymes termed ubiquitin E1 (activating enzyme), ubiquitin E2 (conjugating enzyme), and ubiquitin E3 (ligase). There are several ways of ubiquitin conjugation driving to ubiquitination of specific proteins through ubiquitin-proteasome system (UPS). A lot of UPS genes stated to be included in skeletal muscle atrophy. These genes do their effects by modifying different processes which affect muscle mass including myofibrillar protein degradation, myogenesis inhibition, and even modulation of autophagy as well as upstream regulatory pathways.

Muscle proteolytic system modulation through the effect of taurine on mice bearing muscular atrophy.

Skeletal muscle atrophy occurs in different catabolic conditions and mostly accompanied with upregulation of Muscle ring finger 1 (MuRF1) gene which is one of the master regulatory genes in muscle atrophy. Taurine amino acid is widely distributed in different tissues and has anti-inflammatory and antioxidant effects. This study aimed to investigate the potential influence of taurine on muscle atrophy induced by reduced mechanical loading. Twenty-eight Albino mice were used, and divided equally into four groups: group I (control); group II (immobilization); group III (immobilization + taurine); and group IV (taurine). Quadriceps muscle sections were taken for histopathology, immunohistochemical analysis of caspase 3 expression, and qRT-PCR of MuRF1 gene. Our data revealed Zenker necrosis associated with axonal injury of the nerve trunk of the immobilized muscle together with increase of caspase 3 expression and upregulation of MuRF1 gene. While, taurine supplementation alleviated the muscular and neural tissues damage associated with disuse skeletal muscle atrophy through downregulation of MuRF1 gene and decrease of tissue caspase 3 expression. In conclusion, taurine may be helpful to counteract apoptosis and up-regulated MuRF1 gene expression related to muscle atrophy, which might be hopeful for a large number of patients.

A shape tailored gold-conductive polymer nanocomposite as a transparent electrode with extraordinary insensitivity to volatile organic compounds (VOCs).

In this study, the transparent conducting polymer of poly (3,4-ethylenendioxythiophene): poly(styrene sulphonate) (PEDOT:PSS) was nanohybridized via inclusion of gold nanofillers including nanospheres (NSs) and nanorods (NRs). Such nanocomposite thin films offer not only more optimum conductivity than the pristine polymer but also excellent resistivity against volatile organic compounds (VOCs). Interestingly, such amazing properties are achieved in the diluted regimes of the nanofillers and depend on the characteristics of the interfacial region of the polymer and nanofillers, i.e. the aspect ratio of the latter component. Accordingly, a shape dependent response is made that is more desirable in case of using the Au nanorods with a much larger aspect ratio than their nanosphere counterparts. This transparent nanocomposite thin film with an optimized conductivity and very low sensitivity to organic gases is undoubtedly a promising candidate material for the touch screen panel production industry. Considering PEDOT as a known material for integrated electrodes in energy saving applications, we believe that our strategy might be an important progress in the field.

Curcumin Protects against Monosodium Glutamate Neurotoxicity and Decreasing NMDA2B and mGluR5 Expression in Rat Hippocampus.

BACKGROUND: Monosodium glutamate (MSG) is a flavor enhancer used in food industries. MSG is well documented to induce neurotoxicity. Curcumin (CUR) reportedly possesses beneficial effects against various neurotoxic insults. Hence, this present study has been designed to evaluate the neuroprotective effect of curcumin on MSG-induced neurotoxicity in rats. METHODS: Thirty-two male Wister rats were divided into four groups (n=8): Control group, MSG group, CUR group and MSG + CUR group. CUR (Curcumin 150 mg/kg, orally) was given day after day for four weeks along with MSG (4 mg/kg, orally). After 4 weeks, rats were sacrificed and brain hippocampus was isolated immediately on ice. Inflammatory marker TNFα and acetylcholinesterase (AChE) activity (marker for cholinergic function) were estimated. Gene expressions of metabotropic glutamate receptor 5 (mGluR5) and N-methyl-D-aspartate receptor 2B (NMDA2B) along with glutamate concentration were assessed. RESULTS: Treatment with CUR significantly attenuated AChE activity and TNFα in MSG-treated animals. The anti-inflammatory properties of CUR may be responsible for this observed neuroprotective action. A possible role of CUR to attenuate both glutamate level and gene expression of NMDA2B and mGLUR5 in brain hippocampus was established when compared to MSG group. CONCLUSION: We concluded that CUR as flavor enhancer protects against MSG-induced neurotoxicity in rats.