Vitamins

This chapter is going to explain a part of the nutrients the human body needs. They are organic compounds called vitamins. Those compounds will be clarified, as well as their benefits, deficiencies, chemical structure, and why the body needs them crucially. Vitamins is an exceptionally vital recognized name required in certain amounts in the body, some of them exist as a complicated natural compounds found in herbal meals. It plays a key function in regular metabolism, the absence of which in the diet causes deficiency and several diseases. Vitamins are differentiated from the trace elements, also found in the weight-reduction plan in small quantities for health, growth, replica, and other crucial metabolism

Frequency-Doubling of Femtosecond Pulses in “Thick” Nonlinear Crystals With Different Temporal and Spatial Walk-Off Parameters

We present a comparative study on frequency-doubling characteristics of femtosecond laser pulses in thick nonlinear crystals with different temporal and spatial walk-off parameters. Using single-pass second harmonic generation (SHG) of 260 fs pulses at 1064 nm from a high-average-power femtosecond Yb-fiber laser in 5-mm-long crystals of β-BaB2O4 (BBO) and BiB3O6 (BIBO), we find that for comparable values of temporal and spatial walk-off parameters in each crystal, the optimum focusing condition for SHG is more strongly influenced by spatial walk-off than temporal walk-off. It is also observed that under such conditions, the Boyd and Kleinman theory commonly used to define the optimum focusing condition for frequency-doubling of cw and long-pulse lasers is also valid for SHG of ultrafast lasers. We also investigate the effect of focusing on the spectral, temporal, and spatial characteristics of the second harmonic (SH) radiation, as well as angular acceptance bandwidth for the SHG process, under different temporal and spatial walk-off conditions in the two crystalsPeer ReviewedPostprint (author's final draft

Antioxidant activity of Linalool

In recent years, Essential oils from their various aromatic plants hadbeen reported to be used in treating of many types of cancer due to their antitumoractivity. In addition, numerous studies had investigated the highest capability ofchemopreventive phytochemicals compound to act as anticancer drugs. In thepresent research, the antioxidant activity of Linalool on free radicals compoundswas studied. The Antioxidant activity was performed using two methods, DPPHand Hydrogen Peroxide (H2O2) Scavenging Capacity. The DPPH scavengingactivity demonstrated that Linalool had antioxidant activity comparing withascorbic acid. Linalool demonstrated moderate antioxidant activity with50.57471% compared with ascorbic acid that showed 86%. Meanwhile, H2O2scavenging capacity methods investigated that Linalool exhibited moderatescavenging activity 56.36% comparing with ascorbic acid that showed 65%. Theresults of this study investigated that the Linalool can be used as easily accessiblesource of natural antioxidants. It can able to be used in the treating several typesof cancers as a result of antioxidant activity of it

Toxicity of Porous Silicon Nanoparticles on Liver of Mice

Nanoparticles are a special group of materials with unique features and extensive application in diverse fields. The present work demonstrates the toxicity impact of porous silicon nanoparticles (PSNPs) on kidney parameter which is prepared by electrochemical etching method. the synthesis of porous silicon nanoparticles are conformed by using structural and optical properties from through scanning electron microscope and atomic force microscopy techniques. The effect of toxicity of these nanoparticles on the liver parameters in laboratory animals use four groups each groups involve three duplicities was studied. Injected of porous silicon nanoparticles in the intraperitoneal at concentration of 1mg/kg. The results of biochemical assay Aspartate Amino-Transferase (GOT), Alanine Amino-Transferase (GPT), Alkaline Phosphatase (ALP) were compared with the control groups, for four weeks and then confirm a result was made with Histological study for section of liver. Results show no significant differences in levels (GOT, GPT, ALT) among the test groups via comparison with controls groups. This Result indicates no toxic effect of porous silicon nanoparticles' on kidney parameters

IL-33 promotes ST2-dependent lung fibrosis by the induction of alternatively activated macrophages and innate lymphoid cells in mice

Background<p></p> The initiation and regulation of pulmonary fibrosis are not well understood. IL-33, an important cytokine for respiratory diseases, is overexpressed in the lungs of patients with idiopathic pulmonary fibrosis.<p></p> Objectives<p></p> We aimed to determine the effects and mechanism of IL-33 on the development and severity of pulmonary fibrosis in murine bleomycin-induced fibrosis.<p></p> Methods<p></p> Lung fibrosis was induced by bleomycin in wild-type or Il33r (St2)−/− C57BL/6 mice treated with the recombinant mature form of IL-33 or anti–IL-33 antibody or transferred with type 2 innate lymphoid cells (ILC2s). The development and severity of fibrosis was evaluated based on lung histology, collagen levels, and lavage cytology. Cytokine and chemokine levels were quantified by using quantitative PCR, ELISA, and cytometry.<p></p> Results<p></p> IL-33 is constitutively expressed in lung epithelial cells but is induced in macrophages by bleomycin. Bleomycin enhanced the production of the mature but reduced full-length form of IL-33 in lung tissue. ST2 deficiency, anti–IL-33 antibody treatment, or alveolar macrophage depletion attenuated and exogenous IL-33 or adoptive transfer of ILC2s enhanced bleomycin-induced lung inflammation and fibrosis. These pathologic changes were accompanied, respectively, by reduced or increased IL-33, IL-13, TGF-β1, and inflammatory chemokine production in the lung. Furthermore, IL-33 polarized M2 macrophages to produce IL-13 and TGF-β1 and induced the expansion of ILC2s to produce IL-13 in vitro and in vivo.<p></p> Conclusions<p></p> IL-33 is a novel profibrogenic cytokine that signals through ST2 to promote the initiation and progression of pulmonary fibrosis by recruiting and directing inflammatory cell function and enhancing profibrogenic cytokine production in an ST2- and macrophage-dependent manner

The role of statins in amyotrophic lateral sclerosis: protective or not?

Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disease of motor neurons characterized by muscle weakness, muscle twitching, and muscle wasting. ALS is regarded as the third-most frequent neurodegenerative disease, subsequent to Alzheimer's disease (AD) and Parkinson's disease (PD). The World Health Organization (WHO) in 2007 declared that prolonged use of statins may induce development of ALS-like syndrome and may increase ALS risk. Subsequently, different studies have implicated statins in the pathogenesis of ALS. In contrast, results from preclinical and clinical studies highlighted the protective role of statins against ALS neuropathology. Recently, meta-analyses and systematic reviews illustrated no association between long-term use of statins and ALS risk. These findings highlighted controversial points regarding the effects of statins on ALS pathogenesis and risk. The neuroprotective effects of statins against the development and progression of ALS may be mediated by regulating dyslipidemia and inflammatory changes. However, the mechanism for induction of ALS neuropathology by statins may be related to the dysregulation of liver X receptor signaling (LXR) signaling in the motor neurons and reduction of cholesterol, which has a neuroprotective effect against ALS neuropathology. Nevertheless, the exact role of statins on the pathogenesis of ALS was not fully elucidated. Therefore, this narrative review aims to discuss the role of statins in ALS neuropathology

Gold and silica gold nanoparticles enhances macrophages kill tumor cells via granzyme-perforin pathway

The goal of the study was to see if gold nanoparticles (GNPs) and silica gold nanoparticles (Si-GNPs) could help cancer cells phagocytes.  Scanning electron microscopy (SEM) and Ultraviolet-visible spectroscopy (UV-VIS) absorptions were used to characterize the nanomaterial's. In both in vitro and in vivo conditions, the GNPs and Si-GNPs enhanced macrophage phagocytosis capabilities, resulting in the annihilation of cancer cells. The effect of GNPs and Si-GNPs in Tumor necrosis factor alpha (TNF-α) and Interleukin-8 (IL-8) levels was investigated in Ehrlich tumor cells using Enzyme linked immunosorbent assay (ELISA) assay. The results shows the ability of GNPs and Si-GNPs to increase TNF-α and IL-8 in treated Ehrlich Ascites Carcinoma (EAC).  It was found that the most effect was in Si-GNPs group. GNPs and Si-GNPs enhance phagocytic cells for increased granzyme and perforin-mediated cancer cell death on a regular basis. Overall, the findings showed that GNPs and Si-GNPs improved phagocytic cell activation, which might be employed as a promising technique for managing cancer cells by enhancing cell death via a Granzyme-perforin dependent mechanism

Effects of metformin on fibroblast growth factor 21 in patients with type 2 diabetes mellitus: faraway but so close

Abstract Type 2 diabetes mellitus (T2DM) is a chronic metabolic disorder characterized by insulin resistance (IR) and hyperglycemia. The development of inflammatory disorders in T2DM triggers the activation of different growth factors as a compensatory mechanism to reduce IR and adipose tissue dysfunction in T2DM. Fibroblast growth factor 21 (FGF21) which is involved in the regulation of glucose homeostasis is attractive to be a novel therapeutic target in the management of T2DM. FGF21 has poor pharmacokinetic profile as it rapidly degraded; therefore, FGF21 analogs which are more stable can be used in T2DM patients. However, FGF21 analogs are tested pre-clinically but not approved in clinical settings. Therefore, searching for anti-diabetic agents who enhance FGF21 expression is mandatory. It has been shown that metformin which used as a first-line in the management of T2DM can positively affect the expression of FGF21, though the underlying mechanisms for metformin-induced FGF21 expression are not fully elucidated. Therefore, this review from published studies aimed to find how metformin improves insulin sensitivity through FGF21-dependent pathway in T2DM. In conclusion, metformin improves FGF21 signaling in T2DM, and this could be a novel mechanism for metformin in the amelioration of glucose homeostasis and metabolic disorders in T2DM patients

Galangin/β-Cyclodextrin Inclusion Complex as a Drug-Delivery System for Improved Solubility and Biocompatibility in Breast Cancer Treatment

The purpose of this study was to evaluate the potential of a newly modified cyclodextrin derivative, water-soluble β-cyclodextrin–epichlorohydrin (β-CD), as an effective drug carrier to enhance the poor solubility and bioavailability of galangin (GAL), a poorly water-soluble model drug. In this regard, inclusion complexes of GAL/β-CDP were prepared. UV-VIS spectrophotometry, Fourier-transform infrared spectroscopy (FTIR), X-ray crystallography (XRD), zeta potential analysis, particle size analysis, field emission scanning electron microscopy (FESEM), and transmission electron microscopy (TEM) were applied to characterize the synthesized GAL/β-CD. Michigan Cancer Foundation-7 (MCF-7; human breast cancer cells) and rat embryo fibroblast (REF; normal cells) were employed to examine the in vitro cytotoxic effects of GAL/β-CD using various parameters. The dye-based tests of MTT and crystal violet clearly exhibited that GAL/β-CD-treated cells had a reduced proliferation rate, an influence that was not found in the normal cell line. The cells’ death was found to follow apoptotic mechanisms, as revealed by the dye-based test of acridine orange/ethidium bromide (AO/EtBr), with the involvement of the mitochondria via caspase-3-mediated events, as manifested by the Rh 123 test. We also included a mouse model to examine possible in vivo toxic effects of GAL/β-CD. It appears that the inclusion complex does not have a significant influence on normal cells, as indicated by serum levels of kidney and liver enzymatic markers, as well as thymic and splenic mass indices. A similar conclusion was reached on the histological level, as manifested by the absence of pathological alterations in the liver, kidney, thymus, spleen, heart, and lung