Two Spectrophotometric Assays for Dopamine Derivatives in Pharmaceutical Products and in Biological Samples of Schizophrenic Patients Using Copper Tetramine Complex and Triiodide Reagent

Two simple, rapid, and sensitive spectrophotometric methods are proposed for the determination of levodopa (LD). The first method is based on coupling of 4-aminoantipyrine (4-AAP) with one of the dopamine derivatives (LD, CD) to give a new ligand that reacts with copper tetramine complex to give intensely colored chelates. The colored products are quantified spectrophotometrically at 525 and 520 nm for LD and CD, respectively. The optimization of the experimental conditions is described. The method has been used for the determination of 19.7–69.0 and 18.1–54.3 μg mL(−1) of LD and CD, respectively. The accuracy of the method is achieved by the values of recovery (100 ± 0.2%) and the precision is supported by the low standard deviation (SD = 0.17–0.59) and relative standard deviation (CV = 0.4%–1.54%) values. The second method is based on the formation of ion-pair iodinated inner sphere or outer sphere colored complexes between the LD and triiodide ions at pH 5 and room temperature (23 ± 3(°)C). This method has been used for the determination of LD within the concentration range 39.44–78.88 μg mL(−1) with SD = 0.22–0.24 and recovery percent = 100 ± 0.3%. The sensitivity of the two methods is indicated by Sandell's sensitivity of 0.014–0.019 g cm(−2). The results of the two methods are compared with those of the official method. The interference of common drug additives, degradation products, and excipients was also studied. The proposed methods were applied successfully to the determination of the LD-CD synthetic mixture and Levocare drug. The determination of LD in urine of some schizophrenic patients was applied with good precision and accuracy. The reliability of the methods was established by parallel determinations against the official British pharmacopoeia method

Cow’s milk protein elimination in autistic children: language, cognitive and behavioral outcome

Background: Behavioral modification and structured education are necessary in autism but rather insufficient. Various dietary restrictions have been suggested as important prerequisites to benefit from other interventions in this disorder. Objective: This study was designed to highlight the degree of benefit in various aspects of development of autistic children upon elimination of cow's milk protein (CMP) from their diet and assess the level of specific IgE for CMP in their sera. Methods: The current study was conducted on 22 autistic children who were compared to 30 age and sex matched healthy children. Enrolled autistic children were randomly assigned to one of two groups. The parents of first group were instructed to eliminate cow milk (CM) from the diet of their children throughout the study period while patients of the second group were allowed to eat without restrictions. Each enrolled child was subjected to complete dietetic history taking, clinical examination and measurement of IgE for CM antigen in their sera by enzyme immunoassay. Autistic patients underwent a Childhood Autism Rating Scale (CARS) test. The patients were also subjected to language and intelligent quotient (IQ) testing, social and mental age assessment and child psychiatric evaluation. The autistic children received an interventional program for six months and were then re-evaluated using the previous clinical parameters. Results: The first group achieved significantly lower CARS test results (p < 0.01), significantly higher language age (p < 0.05) and significantly higher rate of change of CARS, language, social age, mental age and IQ (p < 0.001, <0.05, <0.05, <0.01 and <0.05 respectively) compared to the second group after 6 months of follow up. There was also a significantly higher mean specific IgE level to CMP in the autistic patients as compared to the controls. Additionally, 45.5% of patients who were on CM elimination diet went one CARS category down compared to only 36.4% of the second group. Conclusion: We report improvement in language, cognition and behavioral capabilities upon CM elimination in a group of autistic children. The higher CM specific IgE in these children may suggest that such adverse reaction to CM may have an allergic basis. Wider scale studies are needed to justify this adjuvant therapeutic option in autistic children hoping for better achievement from the current interventional programs. Keywords: Allergy – Autism – CARS – Cow milk – IgE – IQEgypt J Pediatr Allergy Immunol 2006; 4(1): 15-2

Assignment of PCR markers to river buffalo chromosomes

International audienc

Pomegranate (Punica graantum) Peels as an Agricultural Waste for Removing of CD(II), CR(VI), CU(II), NI(II), PB(II) and ZN(II) from Their Aqueous Solutions

Pomegranate (Punica graantum) peels as an agricultural waste was used as an adsorbent for removal of Cd, Cr, Cu, Ni, Pb and Zn ions from simulated aqueous solutions. The adsorption process was carried out using the batch method. Various effective parameters such as pH, initial metal ion concentration, and adsorbent dose, shaking time, particle size and temperature were investigated. Fourier Transform Infrared (FTIR) and Scanning Electron Microscopy (SEM) of Punica graantum peels were done. The efficiency of Punica graantum peels toward removal of metal ions was ordered as Pb2+ \u3c Cr6+ \u3c Cu2+ \u3c Cd2+ \u3c Zn2+ \u3c Ni2+, with the corresponding values of 92.8%, 84.6%, 52.8%, 38%, 25.4% and 22.8%, respectively

Acetylsalicylic Acid Suppresses Alcoholism-Induced Cognitive Impairment Associated with Atorvastatin Intake by Targeting Cerebral miRNA155 and NLRP3: In Vivo, and In Silico Study

Alcoholism is one of the most common diseases that can lead to the development of several chronic diseases including steatosis, and cognitive dysfunction. Statins are lipid-lowering drugs that are commonly prescribed for patients with fatty liver diseases; however, the exact effect of statins on cognitive function is still not fully understood. In the present study, we have investigated the molecular and microscopic basis of cognitive impairment induced by alcohol and/or Atorvastatin (ATOR) administration to male Wistar albino rats and explored the possible protective effect of acetylsalicylic acid (ASA). The biochemical analysis indicated that either alcohol or ATOR or together in combination produced a significant increase in the nucleotide-binding domain–like receptor 3 (NLRP3), interleukin-1β (IL-1β) miRNA155 expression levels in the frontal cortex of the brain tissue. The histological and morphometric analysis showed signs of degeneration in the neurons and the glial cells with aggregations of inflammatory cells and a decrease in the mean thickness of the frontal cortex. Immunohistochemical analysis showed a significant increase in the caspase-8 immunoreaction in the neurons and glial cells of the frontal cortex. Interestingly, administration of ASA reversed the deleterious effect of the alcohol and ATOR intake and improved the cognitive function as indicated by biochemical and histological analysis. ASA significantly decreased the expression levels of miRNA155, NLRP3, and IL1B, and produced a significant decrease in caspase-8 immunoreaction in the neurons and glial cells of the frontal cortex with a reduction in the process of neuroinflammation and neuronal damage. To further investigate these findings, we have performed an extensive molecular docking study to investigate the binding affinity of ASA to the binding pockets of the NLRP3 protein. Our results indicated that ASA has high binding scores toward the active sites of the NLRP3 NACHT domain with the ability to bind to the NLRP3 pockets by a set of hydrophilic and hydrophobic interactions. Taken together, the present study highlights the protective pharmacological effect of ASA to attenuate the deleterious effect of alcohol intake and long term ATOR therapy on the cognitive function via targeting miRNA155 and NLRP3 proteins.Peer Reviewe

Acetylsalicylic Acid Suppresses Alcoholism-Induced Cognitive Impairment Associated with Atorvastatin Intake by Targeting Cerebral miRNA155 and NLRP3: In Vivo, and In Silico Study

Alcoholism is one of the most common diseases that can lead to the development of several chronic diseases including steatosis, and cognitive dysfunction. Statins are lipid-lowering drugs that are commonly prescribed for patients with fatty liver diseases; however, the exact effect of statins on cognitive function is still not fully understood. In the present study, we have investigated the molecular and microscopic basis of cognitive impairment induced by alcohol and/or Atorvastatin (ATOR) administration to male Wistar albino rats and explored the possible protective effect of acetylsalicylic acid (ASA). The biochemical analysis indicated that either alcohol or ATOR or together in combination produced a significant increase in the nucleotide-binding domain–like receptor 3 (NLRP3), interleukin-1β (IL-1β) miRNA155 expression levels in the frontal cortex of the brain tissue. The histological and morphometric analysis showed signs of degeneration in the neurons and the glial cells with aggregations of inflammatory cells and a decrease in the mean thickness of the frontal cortex. Immunohistochemical analysis showed a significant increase in the caspase-8 immunoreaction in the neurons and glial cells of the frontal cortex. Interestingly, administration of ASA reversed the deleterious effect of the alcohol and ATOR intake and improved the cognitive function as indicated by biochemical and histological analysis. ASA significantly decreased the expression levels of miRNA155, NLRP3, and IL1B, and produced a significant decrease in caspase-8 immunoreaction in the neurons and glial cells of the frontal cortex with a reduction in the process of neuroinflammation and neuronal damage. To further investigate these findings, we have performed an extensive molecular docking study to investigate the binding affinity of ASA to the binding pockets of the NLRP3 protein. Our results indicated that ASA has high binding scores toward the active sites of the NLRP3 NACHT domain with the ability to bind to the NLRP3 pockets by a set of hydrophilic and hydrophobic interactions. Taken together, the present study highlights the protective pharmacological effect of ASA to attenuate the deleterious effect of alcohol intake and long term ATOR therapy on the cognitive function via targeting miRNA155 and NLRP3 proteins

Cubically cage-shaped mesoporous ordered silica for simultaneous visual detection and removal of uranium ions from contaminated seawater

A dual-function organic-inorganic mesoporous structure is reported for naked-eye detection and removal of uranyl ions from an aqueous environment. The mesoporous sensor/adsorbent is fabricated via direct template synthesis of highly ordered silica monolith (HOM) starting from a quaternary microemulsion liquid crystalline phase. The produced HOM is subjected to further modifications through growing an organic probe, omega chrome black blue G (OCBBG), in the cavities and on the outer surface of the silica structure. The spectral response for [HOM-OCBBG → U(VI)] complex shows a maximum reflectance at λmax = 548 nm within 1 min response time (tR); the LOD is close to 9.1 μg/L while the LOQ approaches 30.4 μg/L, and this corresponds to the range of concentration where the signal is linear against U(VI) concentration (i.e., 5-1000 μg/L) at pH 3.4 with standard deviation (SD) of 0.079 (RSD% = 11.7 at n = 10). Experiments and DFT calculations indicate the existence of strong binding energy between the organic probe and uranyl ions forming a complex with blue color that can be detected by naked eyes even at low uranium concentrations. With regard to the radioactive remediation, the new mesoporous sensor/captor is able to reach a maximum capacity of 95 mg/g within a few minutes of the sorption process. The synthesized material can be regenerated using simple leaching and re-used several times without a significant decrease in capacity. Graphical abstract: [Figure not available: see fulltext.

Hepatoprotective Role of Carvedilol against Ischemic Hepatitis Associated with Acute Heart Failure via Targeting miRNA-17 and Mitochondrial Dynamics-Related Proteins: An In Vivo and In Silico Study

Acute heart failure (AHF) is one of the most common diseases in old age that can lead to mortality. Systemic hypoperfusion is associated with hepatic ischemia–reperfusion injury, which may be irreversible. Ischemic hepatitis due to AHF has been linked to the pathogenesis of liver damage. In the present study, we extensively investigated the role of mitochondrial dynamics-related proteins and their epigenetic regulation in ischemic liver injury following AHF and explored the possible hepatoprotective role of carvedilol. The biochemical analysis revealed that the ischemic liver injury following AHF significantly elevated the activity of alanine aminotransferase (ALT), aspartate aminotransferase (AST), and alkaline phosphatase (ALP) enzymes, the level of total and direct bilirubin, and the expression of hepatic mitogen-activated protein kinase (MAPK), dynamin-1-like protein (DNM1L), and hepatic miRNA-17. At the same time, it significantly reduced the serum albumin level, the activity of hepatic superoxide dismutase (SOD), and the expression of mitochondrial peroxisome proliferator-activated receptor-1α (PGC-1α), and mitofusin 2 (Mtf2). The histological examination of the liver tissue revealed degenerated hepatocytes. Interestingly, administration of carvedilol either prior to or after isoprenaline-induced AHF significantly improved the liver function and reversed the deterioration effect of AHF-induced ischemic hepatitis, as demonstrated by biochemical, immunohistochemical, and histological analysis. Our results indicated that the hepatoprotective effect of carvedilol in ameliorating hepatic ischemic damage could be attributed to its ability to target the mitochondrial dynamics-related proteins (Mtf2, DNM1L and PGC-1α), but also their epigenetic regulator miRNA-17. To further explore the mode of action of carvedilol, we have investigated, in silico, the ability of carvedilol to target dynamin-1-like protein and mitochondrial dynamics protein (MID51). Our results revealed that carvedilol has a high binding affinity (−14.83 kcal/mol) toward the binding pocket of DNM1L protein. In conclusion, our study highlights the hepatoprotective pharmacological application of carvedilol to attenuate ischemic hepatitis associated with AHF.Faculty of Medicine, and Faculty of Science, Ain Shams UniversityPrincess Nourah bint Abdulrahman Universit

Novel Exopolysaccharide from Marine Bacillus subtilis with Broad Potential Biological Activities: Insights into Antioxidant, Anti-Inflammatory, Cytotoxicity, and Anti-Alzheimer Activity

In the presented study, Bacillus subtilis strain AG4 isolated from marine was identified based on morphological, physiological, phylogenetic characteristics and an examination of 16S rRNA sequences. Novel exopolysaccharide (EPSR4) was extracted and isolated from the Bacillus subtilis strain as a major fraction of exopolysaccharide (EPS). The analysis of structural characterization indicated that EPSR4 is a β-glycosidic sulphated heteropolysaccharide (48.2%) with a molecular weight (Mw) of 1.48 × 104 g/mole and has no uronic acid. Analysis of monosaccharide content revealed that EPSR4 consists of glucose, rhamnose and arabinose monosaccharide in a molar ratio of 5:1:3, respectively. Morphological analysis revealed that EPSR4 possess a high crystallinity degree with a significant degree of porosity, and its aggregation and conformation in the lipid phase might have a significant impact on the bioactivity of EPSR4. The biological activity of EPSR4 was screened and evaluated by investigating its antioxidant, cytotoxicity, anti-inflammatory, and anti-Alzheimer activities. The antioxidant activity results showed that EPSR4 has 97.6% scavenging activity toward DPPH free radicals at 1500 µg/mL, with an IC50 value of 300 µg/mL, and 64.8% at 1500 µg/mL toward hydrogen peroxide free radicals (IC50 = 1500 µg/mL, 30 min). Furthermore, EPSR4 exhibited considerable inhibitory activity towards the proliferation of T-24 (bladder carcinoma), A-549 (lung cancer) and HepG-2 (hepatocellular carcinoma) cancer cell lines with IC50 of 244 µg/mL, 148 µg/mL and 123 µg/mL, respectively. An evaluation of anti-inflammatory activity revealed that EPSR4 has potent lipoxygenase (LOX) inhibitory activity (IC50 of 54.3 µg/mL) and a considerable effect on membrane stabilization (IC50 = 112.2 ± 1.2 µg/mL), while it showed cyclooxygenase (COX2) inhibitory activity up to 125 µg/mL. Finally, EPSR4 showed considerable inhibitory activity towards acetylcholine esterase activity. Taken together, this study reveals that Bacillus subtilis strain AG4 could be considered as a potential natural source of novel EPS with potent biological activities that would be useful for the healthcare system.Faculty of Science, Suez Canal UniversityPrincess Nourah bint Abdulrahman UniversityTaif UniversityPeer Reviewe

Preventing type 2 diabetes mellitus in Qatar by reducing obesity, smoking, and physical inactivity: mathematical modeling analyses.

BACKGROUND: The aim of this study was to estimate the impact of reducing the prevalence of obesity, smoking, and physical inactivity, and introducing physical activity as an explicit intervention, on the burden of type 2 diabetes mellitus (T2DM), using Qatar as an example. METHODS: A population-level mathematical model was adapted and expanded. The model was stratified by sex, age group, risk factor status, T2DM status, and intervention status, and parameterized by nationally representative data. Modeled interventions were introduced in 2016, reached targeted level by 2031, and then maintained up to 2050. Diverse intervention scenarios were assessed and compared with a counter-factual no intervention baseline scenario. RESULTS: T2DM prevalence increased from 16.7% in 2016 to 24.0% in 2050 in the baseline scenario. By 2050, through halting the rise or reducing obesity prevalence by 10-50%, T2DM prevalence was reduced by 7.8-33.7%, incidence by 8.4-38.9%, and related deaths by 2.1-13.2%. For smoking, through halting the rise or reducing smoking prevalence by 10-50%, T2DM prevalence was reduced by 0.5-2.8%, incidence by 0.5-3.2%, and related deaths by 0.1-0.7%. For physical inactivity, through halting the rise or reducing physical inactivity prevalence by 10-50%, T2DM prevalence was reduced by 0.5-6.9%, incidence by 0.5-7.9%, and related deaths by 0.2-2.8%. Introduction of physical activity with varying intensity at 25% coverage reduced T2DM prevalence by 3.3-9.2%, incidence by 4.2-11.5%, and related deaths by 1.9-5.2%. CONCLUSIONS: Major reductions in T2DM incidence could be accomplished by reducing obesity, while modest reductions could be accomplished by reducing smoking and physical inactivity, or by introducing physical activity as an intervention