uti

In natural convection, the fluid motion occurs by natural means such as buoyancy. Heat transfer by natural convection happens in many physical problems and engineering applications such as geothermal systems, heat exchangers, petroleum reservoirs and nuclear waste repositories. These problems and phenomena are modeled by ordinary or partial differential equations. In most cases, experimental solutions cannot be applied to these problems, so these equations should be solved using special techniques. In this paper, natural convection of a non-Newtonian fluid flow between two vertical flat plates is investigated analytically and numerically. Collocation Method (CM) and fourth-order Runge -Kutta numerical method (NUM) are used to solve the present problem. These methods are powerful and convenient algorithms in finding the solutions for the equations. While these are capable of reducing the size of calculations. In order to compare with exact solution, velocity and temperature profiles are shown graphically. The obtained results are valid with significant accuracy.

Nanotechnology is a smart technology in the field of biomedical engineering used for the diagnosis and treatment of diseases. Nanodrugs provide better encapsulation of drug and efficiency at low dosage to kill the targeted tissue/cells. However, the chances of chronic toxicity and high cost of treatment limits its applicability [1]. To overcome these problems still, the experts of the scientific community have been working on it, to design the best one and cost-effective treatment for the human welfare.

The present report highlights our results on synthesis of NaYF4:Yb,Er@SiO2@Ag core–shell nanoparticles (CSNPs) for plasmon-enhanced upconversion luminescence (UCL). Hydrophilic surface UCL nanoparticles (UCLNPs) as cores were obtained by precipitation of Rare Earth Elements (REE) chlorides from water-alcohol solutions. The formation of a hydrophobic surface of α-NaYF4:Yb,Er NPs was achieved by thermolysis method at 280 °C and β-NaYF4:Yb,Er by precipitation method in nonpolar medium at 320 °C. Silica shell was formed by the modified Stöber method on the surfaces of UCLNPs with different polarity and phase composition. A mixture of hexane-cyclohexane-isopropyl alcohol was used as a medium for the formation of mononuclear CSNPs on hydrophobic surfaces of cores with different thicknesses of the silica shell: 5 nm and 14 nm. Formation of a predetermined thickness of silica shell was carried out by introducing a precise quantity of TEOS taking into account the size of core NPs with molar ratio TEOS: H2O equal to 1:6. The morphology and phase composition of cores and CSNPs were examined by transmission electron microscopy and selected area electron diffraction, respectively. The insertion of Ag NPs into the structure of NaYF4:Yb,Er@SiO2 was carried out in parallel at the stage of shell formation, which made this synthesis a one-step process. The control of the size of Ag NPs was implemented through the use of a colloidal solution of NPs of the cluster structure by changing the polarity of the medium. The highest intensity enhancement of 85-fold with 5 nm and 29-fold with 14 nm shell thickness was recorded, respectively. For the first time, tests on bioimaging of neutrophil cells by those CSNPs are demonstrated.

The morphological evolution kinetics and instabilities of alpha helical peptide 3.613, which involves large amount of stored torsional elastic deformation energy (3-40 eV/molecule), is formulated by the variational method based on the connection between the rates of internal entropy production and the changes in the global Gibbs free energy, assuming that one has isobaric irreversible processes under the isothermal conditions. The present mesoscopic nonequilibrium thermodynamic approach relies on the fact that the global Gibbs free energy of helical conformation involves not only the bulk Gibbs free energy of the amino-acid back bone structure but also the interfacial Gibbs free energy of the enclosing cylindrical shell or the cage associated with the side-wall molecular branches, and their interactions with the immediate surroundings. The proposed variational analysis applied directly on the proposed macro-model has furnished a nonlinear integral equation in terms of the normalized and scaled internal and external variables. This allows us to track down the motion of the total pitch height of the alpha polypeptide along the well-defined trajectories in the displacement-time space, dictated not only by the initial configuration of the helix but also through the gradients of the global Gibbs free energy of the strained helical conformation as the main driving force. In the negative manifold, there is a well-defined region below the dynamic instability regime, in which the helical conformation can evolve towards the nonequilibrium stationary states by expanding, or contracting, depending upon whether the interfacial free energy and/or the applied stress system are below or above the well-defined thresholds level dictated by the initial pitch height. The highest life time may be realized along that trajectory, which follows up the threshold level of the interfacial specific Gibbs free energy, which is gs = -315 erg/cm2. In the upper region of the negative manifold, the helical conformations are driven by the very large applied uniaxial tension or the negative pressure induced by the thermal expansion, in the range of p > 1GPa and/or the strong negative interfacial free energies [3-4 pH] or their combinations, they show strong kinematic instabilities, which can cause not only the accelerated unfolding phenomenon but also cause large extensions that end up with the catastrophic decimations by ruptures and fragmentations. In the positive manifold, the aging behavior of the polypeptide follows up a S-shape path having rather speedy aging behavior compared to the negative manifold, which is separated from by a well-defined boundary, which represents the isochoric path having longest relaxation times, which can be achieved with great stability. Finally, one could attempt to estimate the upper limit of the relaxation time of aging for the modern hominin, from samples of exceptional preservations, relying on the present nonequilibrium theory as well as on the very limited knowledge on the post-mortem DNA and the present pitch heights of the modern hominin, which is found to be about 25,840 yrs, with a life expectation of 451,800 yrs. These figures are very close to those calculated for Neanderthals (SH), which are found to be 31,820 yrs and 499,100 yrs, respectively.

The global virome: The viruses have a global distribution, phylogenetic diversity and host specificity. They are obligate intracellular parasites with single- or double-stranded DNA or RNA genomes, and afflict bacteria, plants, animals and human population. The viral infection begins when surface proteins bind to receptor proteins on the host cell surface, followed by internalisation, replication and lysis. Further, trans-species interactions of viruses with bacteria, small eukaryotes and host are associated with various zoonotic viral diseases and disease progression. Virome interface and transmission: The cross-species transmission from their natural reservoir, usually mammalian or avian, hosts to infect human-being is a rare probability, but occurs leading to the zoonotic human viral infection. The factors like increased human settlements and encroachments, expanded travel and trade networks, altered wildlife and livestock practices, modernised and mass-farming practices, compromised ecosystems and habitat destruction, and global climate change have impact on the interactions between virome and its hosts and other species and act as drivers of trans-species viral spill-over and human transmission. Zoonotic viral diseases and epidemics: The zoonotic viruses have caused various deadly pandemics in human history. They can be further characterized as either newly emerging or re-emerging infectious diseases, caused by pathogens that historically have infected the same host species, but continue to appear in new locations or in drug-resistant forms, or reappear after apparent control or elimination. The prevalence of zoonoses underlines importance of the animal–human–ecosystem interface in disease transmission. The present COVID-19 infection has certain distinct features which suppress the host immune response and promote the disease potential. Treatment for epidemics like covid-19: It appears that certain nutraceuticals may provide relief in clinical symptoms to patients infected with encapsulated RNA viruses such as influenza and coronavirus. These nutraceuticals appear to reduce the inflammation in the lungs and help to boost type 1 interferon response to these viral infections. The human intestinal microbiota acting in tandem with the host’s defence and immune system, is vital for homeostasis and preservation of health. The integrity and balanced activity of the gut microbes is responsible for the protection from disease states including viral infections. Certain probiotics may help in improving the sensitivity and effectivity of immune system against viral infections. Currently, antiviral therapy is available only for a limited number of zoonotic viral infections. Because viruses are intracellular parasites, antiviral drugs are not able to deactivate or destroy the virus but can reduce the viral load by inhibiting replication and facilitating the host’s innate immune mechanisms to neutralize the virus. Conclusion: Lessons from recent viral epidemics - Considering that certain nutraceuticals have demonstrated antiviral effects in both clinical and animal studies, further studies are required to establish their therapeutic efficacy. The components of nutraceuticals such as luteolin, apigenin, quercetin and chlorogenic acid may be useful for developing a combo-therapy. The use of probiotics to enhance immunity and immune response against viral infections is a novel possibility. The available antiviral therapy is inefficient in deactivating or destroying the infecting viruses, may help in reducing the viral load by inhibiting replication. The novel efficient antiviral agents are being explored.

Due to the urgent need for water in all parts of industrial or developing societies, water supply, and transmission facilities are suitable targets for biological risks. Given that even a short interruption in water supply and water supply operations has a great impact on daily activities in the community, the deliberate contamination of urban water resources has irreparable consequences in the field of public health, and the economy of society will follow. Unfortunately, most officials in the public health control departments in our country have received limited training in detecting accidental or intentional contamination of water resources and dealing with the spread of waterborne diseases both naturally and intentionally. For this reason, there is low preparedness in the responsible agencies to deal with waterborne diseases during biological risks. In the first step of this research, a review study has been conducted on water biological risks and operational strategies to deal with them. In the following, it has studied how Escherichia coli (E. coli) bacteria spread in aqueous media. In this regard, the kinetic model of the studied microorganism was analyzed based on the implementation of (Fick Law) in polar coordinates and the combination of (Dirac Distribution) with (Legendre polynomial) distribution. Finally, after studying the factors affecting the microbial pollutant emission coefficient, the effects of all three factors of linear velocity, linear motion time period, and angle of motion on the pollutant emission flux and biofilm diffusion time in the water supply network environment were investigated. Studies have shown that the linear velocity parameter of Escherichia coli with a nonlinear relationship has the greatest effects on the release of microbial contaminants.

Background: This study aims to retrospectively investigate the comorbidity of ADHD multiple symptoms (behavioral) with alcohol addiction in a sample of adult alcohol-dependent patients and to test their current attentional skills (behavioral and cognitive). Methods: Thirty-two adult alcohol-dependent patients were examined for ADHD using a semi-structured interview and the Mini Mental State Examination to evaluate attention and inhibition functions. Brown ADD Scales were used to specifically examine ADHD syndrome. Patients were compared with thirty matched control participants selected from healthy population in few measures of attentional control and working memory. Results: 50% of patients showed evidence of primary ADHD symptoms: specifically, 28.12% showed criteria for ADHD highly probable, 12.50% for ADHD probable but not certain and 9.38% for ADHD possible but not likely. Patients also revealed several deficits in the selective visual attention, interference control and verbal working memory compared to the control group. Conclusions: These results revealed that adult alcohol-dependent patients had retrospectively high comorbidity with ADHD and significant current deficits of the executive functions. These findings suggest the importance of early diagnosis and treatment of ADHD in order to prevent the development of alcohol dependence.

The broad spectrum of heterozygous versus homozygous JAK2V617F mutated MPN consists ET, ET with early features of PV (prodromal PV), classical PV, masked PV, advanced PV and post-PV myelofibrosis. Combined use of bone marrow histology and increased erythrocyte counts above 5.8x1012/L can replace increased red cell mass at time of presentation as the pathognomonic clue for the correct diagnosis of hetero/homozygous or homozygous mutated PV. Erythrocyte counts are in the normal range below 5.8x1012/L in heterozygous JAK2V617F mutated ET and prodromal PV but above 5.8x1012/L in heterozygous-homozygous or homozygous mutated PV. The bone marrow cellularity and morphology in pre-fibrotic ET, prodromal PV and PV carrying the JAK2V617F mutation are overlapping showing clustered increase of large mature pleomorphic megakaryocytes (M) with no increase of cellularity (<60%) in ET. The bone marrow is hypercellular (60%-80%) due to increased erythropoiesis megakaryopoiesis (EM) in prodromal and classical PV and trilinear hypercellular (80%-100% due increased megakaryopoiesis, erythropoiesis and granulopoiesis (EMG) in advanced PV and masked PV. Bone marrow cellularity ranging from normal (<60%) in ET to increased erythropoiesis (EM) in prodromal PV to hypercellular (80-100%) in advanced PV and masked PV largely depends on increasing JAK2V617F mutation load from low to high on top of other biological MPN variables like constitutional symptoms during long-term follow-up. MPL515 mutated ET is featured by an increase of clustered small and giant megakaryocytes with hyper-lobulated staghorn-like nuclei in a normal cellular bone marrow. The third entity of pronounced JAK2/MPL wild type ET associated with primary megakaryocytic granulocytic myeloproliferation (PMGM) without PV features proved to be caused by calreticulin (CALR) mutation. CALR mutated thrombocythemia is characterized by dual proliferation of megakaryocytic and granulocytic bone marrow proliferation of dense clustered large to giant immature dysmorphic megakaryocytes with bulky (bulbous) hyperchromatic nuclei, which are not seen in MPL515-mutated Thrombocythemia and JAK2V617F-Thrombocythemia, prodromal PV and classical PV. 

Primary myelofibrosis (PMF) is a distinct clinicopathological myeloproliferatve disease (MPD) not preceded by any other MPD ET, PV, CML,... Combined use of bone marrow histology and increased erythrocyte counts above 5.8x1012/L can replace increased red cell mass at time of presentation as the pathognomonic clue for the correct diagnosis of hetero/homozygous or homozygous mutated PV. Erythrocyte counts are in the normal range below 5.8x1012/L in heterozygous JAK2V617F mutated ET and prodromal PV but above 5.8x1012/L in heterozygous-homozygous or homozygous mutated PV. The bone marrow cellularity and morphology in pre-fibrotic ET, prodromal PV and PV carrying the JAK2V617F mutation are overlapping showing clustered increase of large mature pleomorphic megakaryocytes (M) with no increase of cellularity (<60%) in ET. The bone marrow is hypercellular (60%-80%) due to increased erythropoiesis megakaryopoiesis (EM) in prodromal and classical PV and trilinear hypercellular (80%-100% due increased megakaryopoiesis, erythropoiesis and granulopoiesis (EMG) in advanced PV and masked PV. Bone marrow cellularity ranging from normal (<60%) in ET to increased erythropoiesis (EM) in prodromal PV to hypercellular (80-100%) in advanced PV and masked PV largely depends on increasing JAK2V617F mutation load from low to high on top of other biological MPN variables like constitutional symptoms during long-term follow-up. MPL515 mutated ET is featured by an increase of clustered small and giant megakaryocytes with hyper-lobulated staghorn-like nuclei in a normal cellular bone marrow. The third entity of pronounced JAK2/MPL wild type ET associated with primary megakaryocytic granulocytic myeloproliferation (PMGM) without PV features proved to be caused by calreticulin (CALR) mutation. CALR mutated thrombocythemia is characterized by dual proliferation of megakaryocytic and granulocytic bone marrow proliferation of dense clustered large to giant immature dysmorphic megakaryocytes with bulky (bulbous) hyperchromatic nuclei, which are not seen in MPL515-mutated Thrombocythemia and JAK2V617F-Thrombocythemia, prodromal PV and classical PV. 

The clinical phenotypes in 268 JAK2V617F mutated MPN patients in the Seoul study were PV in 101, ET in 95 and MF in 78 and 56 CALR mutated MPN consisted of PV in none, ET in 40 and MF in 16 cases. CALR mutated MPN patients were younger than JAK2V617F mutated MPN patients (mean ages 57.5 and 66 years), had lower values for values for leukocytes (8.6 vs 11.9x109/L) and higher values for platelets (898 vs 643x109/L respectively). Bone marrow histopathology in 268 JAK2V617F mutated MPN patients in the Seoul study was featured by an increased erythropoiesis and megakaryopoiesis (EM) in 13.5%, an increased erythropoiesis, megakaryopoiesis and granulopoiesis (EMG) in 31.3%, a normocellular megakaryocytic (M) proliferation in 29,1%, a megakaryocytic and granulocytic (MG) proliferation with a relative reduction of erythropoiesis in post-ET and Post-PV myelofibrosis in 26.2%. The bone marrow histology in 56 cases of CALR mutated MPN show a predominantly increased megakaryopoiesis (M) in two thirds and an increased megakaryopoiesis and granulopoiesis (MG) with a decreased erythropoiesis in one third. Thirteen consecutive CALR MPN patients in the Belgian & Dutch cross sectional study presented with thrombocythemia associated with a typical PMGM bone marrow histology in 11 and myelofibrosis in 2 cases. All 11 thrombocythemia and 2 myelofibrosis CALR mutated MPN patients did not have constitutional symptoms and did not suffer from microvascular erythromelalgic disturbances, major thrombosis at platelet counts between 400 and 1000x109/L. There was an occurrence of hemorrhages at platelet counts above 1000x109/L in two CALR thrombocythemia cases. Bone marrow histology of CALR mutated thrombocythemia in the Seoul and Belgian/Dutch study showed loose clusters of large megakaryocytes (M) with bulky, cloud-like nuclei with a normal or a minor reduction of erythropoiesis and no increase in reticulin fibers grade 0 or 1 (RF 0 or 1). CALR thrombocythemia patients show various degrees of increased bone marrow cellularity due to dual megakaryocytic and granulocytic (MG) proliferation featured by large megakaryocytes with roundish bulky nuclear forms and cloud-like clumsy nuclei, which are almost never seen in JAK2V617F ET and PV. Assessment of allele burden is an independent and most important factor for all molecular variants MPN disease burden. Overt myelofibrosis with advanced post PV and or ET myelofibrosis at the bone marrow level occurred in one third (30%) of 208 evaluable JAK2 MPN patients and in 8 (14%) of 56 CALR MPN patients in the Seoul study.

Ailment repairing regiments has turn out to be arduous, despite a plenty of understanding and knowledge acquired in the past relating to the molecular underpinnings of Alzheimer’s disease (AD. Umpteen clinical experiments targeting the fabrication and accumulation have been turned fruitless to fit potency standards. The tests aiming beta-amyloid hypothesis also turned futile making it exigent for further handling tactics. The new emanation of a comparably candid, economical, and punctilious system known as gene editing have showed light in path of cure for AD by CRISPR/Cas9 gene editing. Being a straight approach this procedure has already shown assurance in other neurological disorders too such as Huntington’s disease. This review standpoint the immanent service of CRISPR/Cas9 as a remedial option for AD by aiming on specific genes inclusive of those that induce early-onset AD, as well as those that are substantial risk components for late-onset AD such as the apolipoprotein E4 (APOE4) gene.

Allogeneic hematopoietic stem cell transplant (alloHSCT) is a curative treatment for many hematologic malignancies. Unfortunately, about 30-50% of all recipients undergoing alloHSCT develop acute graft-versus-host-disease (aGVHD), which is associated with high morbidity and mortality [1,2]. Treatment of aGVHD involves the use of immune suppressive drugs such as high dose of steroids that leads to further immunosuppression and risk for opportunistic infections. Often patients are refractory to steroids therapy making the prognosis dismal. Thus, it is critical to identify robust biomarkers to detect aGVHD before onset of clinical symptoms so that therapeutic strategies can be implemented that may result in better treatment responses and less toxicity. 

In this work is analyzed scientific literature involved in human evolution to be used as an archeological Pathway to link different sciences in an overall new discipline. A rational classification of single evidence make possible to better understand under new light some Physiological process. The archeological instrument to be applied in other field like biology or other sciences.

The Myeloproliferative Neoplasms (MPN) of trilinear polycythemia vera (PV) and megakaryocytic leukemia (ML = primary megakaryocytic granulocytic myeloproliferation: PMGM) and Essential Thrombocythemia (ET) in the studies of Dameshek and Michiels are caused by the MPN driver mutations JAK2V617F, JAK2exon12, CALR and MPL515 discovered by Constantinescu-Vainchenker, Green and Kralovics. The JAK2V617F mutated trilinear myeloproliferative neoplasms (MPN) include a broad spectrum of clinical laboratory and bone marrow features in essential thrombocythemia (ET), prodromal PV and erythrocythemic PV, classical PV and advanced stages of masked PV and PV complicated by splenomegaly and secondary myelofibrosis (MF). Heterozygous JAK2V617F mutated ET is associated with low JAK2 allele and MPN disease burden and normal life expectance. In combined heterozygous and homozygous or homozygous JAK2V617F mutated trilinear PV, the JAK2 mutation load increases from less than 50% in prodromal PV and classical PV to above 50% up to 100% in hypercellular PV, advanced PV and PV with MF. Bone marrow histology show diagnostic features of eryhrocytic, megakaryocytic and granulocytic (EMG) myeloproliferation in JAK2V617F mutated trilinear MPN, which clearly differs from monolinear megakaryocytic (M) myelproliferation in MPL and CALR thrombocythemia and dual megakaryocytic granulocytic (MG) myeloproliferation in CALR mutated thrombocythemia. The morphology of clustered large pleomorphic megakaryocytes with hyperlobulated nuclei are similar in JAK2V617F thrombocythemia, prodromal PV and classical PV patients. Monolinear megakaryocytic (M) myeloproliferation of large to giant megakaryocytes with hyperlobulated staghorn-like nuclei is the hallmark of MPL515 mutated normocellular thrombocythemia. CALR mutated thrombocythemia usually presents with high platelet count around 1000x109/l and normocellular megakaryocytic (M) proliferation of immature megakaryocytes with cloud-like hyperchromatic nuclei followed by dual megakaryocytic granulocytic (MG) myeloproliferation followed by various degrees of bone marrow fibrosis. Natural history and life expectancy of MPN patients are related to the response to treatment and the degree of anemia, splenomegaly, myelofibrosis and constitutional symptoms. The acquisition of epigenetic mutations at increasing age on top of MPN disease burden independently predict unfavorable outcome in JAK2V617F, MPL515 and CALR mutated myeloproliferative neoplasms (MPNs, which mutually exclude each other).

Aim of this work is to verify the effect of some neurotoxins, physical factors and geography in presentation of some Relevant Neurological disorder like some form of ASL, PD, AD. The geographic diffusion of the ASL/PD in west pacific (GUAM foci), and mutation of SOD 1 and other mutations are interesting facts to verify the recent literature about the neurotoxic process. Related to the references presented a global conclusion about the pathogenetic progression of some neurological disease will be produced as instrument for new hypothesis and for the introduction of new innovative therapeutic strategies.

Aim:The work was to perform a comparative study of the neuroprotective and nootropic activities of two pharmaceutical substances, the HLDF-6 peptide and its amide form (HLDF-6-NH2). Materials and Methods: We used in the study healthy adult male Wistar rats aged 180–200 days weighing 280–300 g. We modelled ischemic stroke in rats by chronical occlusion of carotid arteries. Solutions of the HLDF-6-NH2 and HLDF-6 peptides were administered intranasally. Cognitive functions we assessed with Novel object recognition test and Morris maze. Results: The amide form of HLDF-6 peptide is more efficient: the neuroprotective activity of HLDF-6-NH2, evaluated by improvement of cognitive functions in animals, surpassed that of the native HLDF-6 peptide. A dose of 250 µg/kg of HLDF-6-NH2 peptide resulted in practically complete restoration of the disturbed functions. In the model of ischemic stroke, the amide form of the peptide significantly excelled the reference substance mexidol both in the effective dose and biological activity. Conclusion: The results of study of the agent allow hoping for its success in further clinical investigation. In view of high demand for the agent and in case of successful clinical trials, it will surely become widely used in clinical practice in treatment of IS.

Aim of this work is to produce a general theory related an new depurative strategy to be devalued for reduce or delay some spinal cord and brain degenerative and inflammatory chronic disease or acute traumatic condition. It is used and informatics approach in order to set correct the problem and the process. Scope of this project is to submit to the researcher a new therapeutic strategy (under a depurative- toxicological-pharmacological) in this complex kind of disease. A Turing machine theory say us a method to TRASLATE the need of a strategy in a practical hypotesys of work. A global conceptual map can help in this field.

Background: Drosophila models of amyotrophic lateral sclerosis (ALS) have been widely used in understanding molecular mechanisms of ALS pathogenesis as well as discovering potential targets for therapeutic drugs. Mutations in the copper/zinc superoxide dismutase (SOD1) cause ALS by gain of toxic functions and induce toxicity in fly motor neurons. Results: In this study, we have determined that human carbonic anhydrase I (CA1) can alleviate mutant SOD1-induced motor neuron toxicity in the transgenic fly model of ALS. Interestingly, we found that motor neuron expression of CA1 could independently induce locomotion defect as well as decreasing the survival rate. In addition, CA1-induced toxicity in motor neurons is anhydrase activity-dependent. Mechanistically, we identified that both SOD1- and CA1-induced toxicity involve the activation of eIF2α in the ER stress response pathway. Downstream activation of the JNK pathway has also been implicated in the induced toxicity. Conclusion: Our results have confirmed that SOD1-induced toxicity in fly motor neuron also involves endoplasmic reticulum (ER) stress pathway. More importantly, we have discovered a new cellular role that CA1 plays by antagonizing mutant SOD1-induced toxicity in motor neurons involving the ER stress pathway. Such information can be potentially useful for further understanding disease mechanisms and developing therapeutic targets for ALS. 

The biological changes caused by oxidative stress (OS) are known to be involved in the etiology of neurodegenerative disorders, including Alzheimer’s disease, amyotrophic lateral sclerosis, Huntington’s disease, and Parkinson’s disease. The brain is particularly vulnerable to OS due to its high lipid content and extensive consumption of oxygen. OS processes, particularly the excessive production of reactive oxygen species (ROS), play a critical role in how neurodegenerative disorders develop. This is evidenced by in vivo studies investigating various biomolecules related to OS, such as products of lipid and DNA oxidation. Accordingly, ROS can also cause oxidative-related damage in neurodegenerative disorders, including dopamine auto-oxidation, mitochondrial dysfunction, glial cell activation, α-synuclein aggregation, excessive free iron, and changes in calcium signaling. Furthermore, excessive levels of cellular oxidants reduce antioxidant defenses, which in turn propagate the cycle of OS. As such, it is increasingly important to determine the linkage between a high intake of antioxidants through dietary interventions and a lower risk of developing neurodegenerative diseases. Indeed, in addition to modulating the immune system, optimal nutritional status is capable of changing various processes of neuroinflammation known to be involved in the pathogenesis of neurodegeneration. Accordingly, a better understanding of the role ROS plays in the etiology of neurodegeneration is needed, along with the identification of dietary interventions that may lead to improved therapeutic strategies for both the treatment and prevention of neurodegenerative disorders. Therefore, this review presents a comprehensive summary of the role of ROS in the pathogenesis of neurodegenerative disorders. In addition, nutrients believed to be useful for mitigating and counteracting ROS are discussed. 

Background: Gliomas represent the most frequent primary tumors of central nervous system (CNS), contributing to more than half of the incidence of brain tumors. Cancer stem cell markers (CSC) identify a group of patients at high risk for progression. Nestin is an intermediate filament (IF) protein was first described as a neural stem cell/progenitor cell marker. Nestin-positive neuroepithelial stem cells are detected in the subventricular zone of the human adult brain and they remain mitotically active throughout adulthood. The expression of Nestin in gliomas has been suggested to be related to dedifferentiation, improved cell motility, invasive potential and increased malignancy. This study aims to investigate Nestin immunohistochemical expression in different types of glioma and its correlation with different clinicopathological parameters. Materials and Methods: Nestin immunostaining was studied in 60 specimens of glioma using avidin-biotin peroxidase method. Results: Nestin was strongly expressed in 11/60 (18.33%), moderately expressed in 29/60 (48.33%) and weekly expressed in 15/60 (25%) of studied gliomas. A significant positive correlation was found between Nestin expression and histologic type (p < 0.001) and increasing grade of gliomas (p < 0.001). Conclusion: Increased Nestin expression is correlated with tumor progression, increasing grade and poor prognostic parameter of glioma. Nestin is a useful marker for detection of CSC in high-grade glioma which is responsible for resistance to chemo-radiotherapy and may serve as a predictor for patient outcomes.