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Since late December 2019, coronavirus disease 2019 (COVID‐19) outbreak caused by severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) has been rapidly spread across the globe. The early, safe, sensitive, and accurate diagnosis of viral infection is required to decrease and control contagious infection and improve public health surveillance. The diagnosis generally is made by detecting SARS‐CoV‐2‐related agents, including a range of nucleic acid detection‐based, immunoassay‐based, radiographic‐based, and biosensor‐based methods. This review presents the progress of various detection tools for diagnosing COVID‐19 and addresses the advantages and restrictions of each detection method. Given that diagnosis of a contagious various like SARS‐COV‐2 can improve patient survival rates and break the transmission chain, there is no surprise that significant efforts should be made to reduce the limitations of tests that lead to false‐negative results and to develop a substantial test for COVID‐19 diagnosis. Significance statement: Severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) appeared in December 2019 in Wuhan, China, and spread worldwide quickly. The early and sensitive viral infection diagnosis is important for improve public health surveillance. The diagnosis generally is based on nucleic acid, immunoassay, radiographic, and biosensor methods. This review presents the various detection methods for detection of coronavirus disease 2019 with advantages and restrictions of each method. Among various available methods for SARS‐CoV‐2 laboratory diagnosis, real‐time polymerase chain reaction is the most widely used method; however, this method has several restrictions. So, a combined strategy harmonizing laboratory methods is crucial to guide patient care, prevention, and management of infection. [ABSTRACT FROM AUTHOR]

The 2019 widespread contagion of the human coronavirus novel type (SARS-CoV-2) led to a pandemic declaration by the World Health Organization. A daily increase in patient numbers has formed an urgent necessity to find suitable targets and treatment options for the novel coronavirus (COVID-19). Despite scientists' struggles to discover quick treatment solutions, few effective specific drugs are approved to control SARS-CoV-2 infections thoroughly. Drug repositioning or Drug repurposing and target-based approaches are promising strategies for facilitating the drug discovery process. Here, we review current in silico, in vitro, in vivo, and clinical updates regarding proposed drugs for prospective treatment options for COVID-19. Drug targets that can direct pharmaceutical sciences efforts to discover new drugs against SARS-CoV-2 are divided into two categories: Virus-based targets, for example, Spike glycoprotein and Nucleocapsid Protein, and host-based targets, for instance, inflammatory cytokines and cell receptors through which the virus infects the cell. A broad spectrum of drugs has been found to show anti-SARS-CoV-2 potential, including antiviral drugs and monoclonal antibodies, statins, anti-inflammatory agents, and herbal products. [ABSTRACT FROM AUTHOR]

[Display omitted] • Some Pt and Pd complexes were synthesized. • The mode of DNA binding was investigated by molecular docking simulation. • Pt/Pd complex-DNA interaction has been studied using spectroscopic methods. • Cytotoxic activities were obtained against several cancerous and normal cell lines. In this project, four new palladium (II) and platinum (II) complexes were designed and prepared to improve metallo-drugs activity in DNA binding and inhibiting cancerous cells. The complexes, 1 : [Pt(bpdca)OX], 2 : [Pd(bpdca)OX], 3 : [Pt(bpdca)(CBDC)], and 4 : [Pd(bpdca)(CBDC)] (where bpdca is 2,2′bipyridine-3,3′-dicarboxylic acid, CBDC is cis -1,1′-cyclobutyl dicarboxylato, and OX is oxalate), were structurally specified using experimental and computational analysis. Density functional theory calculations were done to evaluate the structure–activity relationship of these compounds. Also, the cytotoxicity of them was investigated on the human colorectal carcinoma (HCT116), MCF7 (breast cancer), A549 (Human Caucasian lung carcinoma), and HFF (Human Freskin Fibroblast) cell lines. According to the findings, 3 and 4 were more active than oxaliplatin and carboplatin. Because of the CBDC ligand in the designed compound, IC 50 values were obtained less than other derivatives against all mentioned cancerous cell lines. Also, regarding IC 50 values on normal HFF cell line, 4 is selectively toxic against the A549 cancer cell line with SI = 5.6. Electronic absorption, fluorescence, and CD monitoring were used to follow the binding abilities of all complexes to CT-DNA and HSA. The results indicated that they could interact with CT-DNA through groove mode and with HSA via hydrogen bond and van der Waals forces. Spectral data showed that complexes changed the way the HSA folded by modifying the proportion of a-helix. The metal complex binding with both mentioned biomolecules was predicted using docking simulation, which also verified the groove binding for the DNA-complex. The findings indicated that complex 4 had a greater negative docking energy and a higher propensity for CT-DNA and HSA interaction. So, all complexes can be suitable candidates as anticancer drugs. [ABSTRACT FROM AUTHOR]

• Some Pt and Pd complexes were synthesized. • Cytotoxic activities were obtained against several cancerous cell lines. • The mode of DNA/HSA binding was investigated by molecular docking simulation. • Metal complex-DNA/HSA interaction has been studied using spectroscopic methods such as UV–vis, fluorescence, and circular dichroism. In this study, four new platinum (II) and palladium(II) complexes were synthesized to develop metallo-drugs that can attach to DNA and prevent the division of cancer cells. The complexes, 1 : [Pt(bipy)(LP)]NO 3 , 2 : [Pt(bipy)(LA)]NO 3 , 3 : [Pd(bipy)(LP)]NO 3 , and 4 : [Pd(phen)(LP)]NO 3 (where LP is propylglycine, LA is 2-heptyl glycine, bipy is 2,2-bipyridine, and phen is 1,10-phenanthroline), were structurally characterized using computational and experimental analysis. Their stability, solubility, and lipophilicity were evaluated. Single-crystal X-ray and powder X-ray crystallographic analyses were performed for [Pt(bipy)(LA)]NO 3. Density functional theory calculations were performed to investigate the reactivity, stability descriptors, and natural bond orbital analysis of these complexes. The in vitro cytotoxicity of these substances was examined against the human colorectal carcinoma (HCT116), A549 (Human Caucasian lung carcinoma), MCF7 (breast cancer), and HFF (Human Freskin Fibroblast) cell lines. According to the findings, complexes 4 and 3 had near oxaliplatin concentrations and more than carboplatin due to lipophilic ligands in their structure. Also, regarding IC 50 values on normal HFF cell line, 4 is selectively toxic against the A549 cancer cell line with SI=5.6. Fluorescence, electronic absorption spectroscopy, and CD spectroscopy were used to investigate the binding affinities of compounds to CT-DNA and HSA. The results revealed that they could interact with CT-DNA through groove mode and with HSA via hydrogen bond and van der Waals forces. Electronic absorption and CD spectra indicated that compounds changed the way the HSA folded by increasing the proportion of a-helix. The binding posture of the metal complex to both biomolecules was predicted using docking simulation, which also verified the groove binding for DNA-complex. The findings indicated that complex 4 had a greater negative docking energy and a higher propensity for CT-DNA and HSA interaction. [Display omitted] [ABSTRACT FROM AUTHOR]

• Some Pt and Pd complexes were synthesized. • Cytotoxic activities were obtained against several cancerous cell lines. • The mode of DNA/HSA binding was investigated by molecular docking simulation. • Metal complex-DNA/HSA interaction has been studied using spectroscopic methods such as UV–vis, fluorescence, and circular dichroism. In this study, four new platinum (II) and palladium(II) complexes were synthesized to develop metallo-drugs that can attach to DNA and prevent the division of cancer cells. The complexes, 1 : [Pt(bipy)(LP)]NO 3 , 2 : [Pt(bipy)(LA)]NO 3 , 3 : [Pd(bipy)(LP)]NO 3 , and 4 : [Pd(phen)(LP)]NO 3 (where LP is propylglycine, LA is 2-heptyl glycine, bipy is 2,2-bipyridine, and phen is 1,10-phenanthroline), were structurally characterized using computational and experimental analysis. Their stability, solubility, and lipophilicity were evaluated. Single-crystal X-ray and powder X-ray crystallographic analyses were performed for [Pt(bipy)(LA)]NO 3. Density functional theory calculations were performed to investigate the reactivity, stability descriptors, and natural bond orbital analysis of these complexes. The in vitro cytotoxicity of these substances was examined against the human colorectal carcinoma (HCT116), A549 (Human Caucasian lung carcinoma), MCF7 (breast cancer), and HFF (Human Freskin Fibroblast) cell lines. According to the findings, complexes 4 and 3 had near oxaliplatin concentrations and more than carboplatin due to lipophilic ligands in their structure. Also, regarding IC 50 values on normal HFF cell line, 4 is selectively toxic against the A549 cancer cell line with SI=5.6. Fluorescence, electronic absorption spectroscopy, and CD spectroscopy were used to investigate the binding affinities of compounds to CT-DNA and HSA. The results revealed that they could interact with CT-DNA through groove mode and with HSA via hydrogen bond and van der Waals forces. Electronic absorption and CD spectra indicated that compounds changed the way the HSA folded by increasing the proportion of a-helix. The binding posture of the metal complex to both biomolecules was predicted using docking simulation, which also verified the groove binding for DNA-complex. The findings indicated that complex 4 had a greater negative docking energy and a higher propensity for CT-DNA and HSA interaction. [Display omitted] [ABSTRACT FROM AUTHOR]

For investigating reduction of side effects of commercial anticancer drugs, such as cisplatin, three new platinum complexes with glycine derivatives and the formula of [Pt(R-amine)2(R-gly)]NO3 were synthesized where R-amine is propylamine, isopentylamine, and tertpentylamine and R-gly is propylglycine, isopentylglycine, and tertpentylglycine, which were characterized by spectroscopic methods, such as ultraviolet–visible, infrared, and proton nuclear magnetic resonance (1H-NMR) spectroscopy. The in-vitro cytotoxicity of these water-soluble complexes and cisplatin as a controller was assessed against MCF-7 cell line by MTT assay. The 50% inhibitory concentration values showed that the inhibitory effect of propyl derivative was better than the other systems. According to solubility of these compounds in water and also comparing the results of assessing adsorption, distribution, metabolism, and excretion, these compounds can be considered as drug-like molecules and oral medication. Given the density functional theory data, such as electronegativity, nucleophilicity, additional electronic charges, and global softness, anticancer properties of the synthesized complexes were almost similar and predominantly more than the cisplatin. DNA binding modes were evaluated by experimental circular dichroism (CD) spectroscopy, and also theoretical study of molecular docking. CD spectra showed a decrease in the intensity of the positive band and an increase in the negative band indicating formation of DNA-complex electrostatic interaction for positively charged synthesized complexes. CD spectra indicated conversion of B-DNA into A-DNA form via electrostatic interaction for positively charged propyl complex at high concentration. Results of studying molecular docking showed that hydrogen bonding is more effective than other interactions, such as electrostatic and covalent interactions, especially for bulky systems. In this regard, glycine derivatives may reduce the side effects of Pt-drugs in treatment of cancer. Three new anticancer Pt(II) complexes were synthesized with glycine derivatives. In vitro cytotoxicity effects were tested against the human breast cancer cell line of MCF-7. Moreover, the modes of DNA binding with synthesized compounds were investigated using Circular dichroism spectra, ADME prediction, DFT, MEP, and molecular docking. [ABSTRACT FROM AUTHOR]

Multiple sclerosis (MS) is an autoimmune inflammatory disorder of the central nervous system (CNS) resulting in demyelination and axonal loss in the brain and spinal cord. The precise pathogenesis and etiology of this complex disease are still a mystery. Despite many studies that have been aimed to identify biomarkers, no protein marker has yet been approved for MS. There is urgently needed for biomarkers, which could clarify pathology, monitor disease progression, response to treatment, and prognosis in MS. Proteomics and metabolomics analysis are powerful tools to identify putative and novel candidate biomarkers. Different human compartments analysis using proteomics, metabolomics, and bioinformatics approaches has generated new information for further clarification of MS pathology, elucidating the mechanisms of the disease, finding new targets, and monitoring treatment response. Overall, omics approaches can develop different therapeutic and diagnostic aspects of complex disorders such as multiple sclerosis, from biomarker discovery to personalized medicine. [ABSTRACT FROM AUTHOR]

Cancer is a leading cause of death in both developed and developing countries, and because of population growth and aging, it is a growing medical burden worldwide. With robust development in medicine, the use of stem cells has opened new treatment modalities in cancer therapy. In adult stem cells, mesenchymal stem cells (MSCs) are showing rising promise in cancer treatment due to their unique properties. Among different sources of MSCs, human amniotic fluid/membrane is an attractive and suitable reservoir. There are conflicting opinions about the role of human amniotic membrane/fluid mesenchymal stem cells (hAMSCS/hAFMSCs) in cancer, as some studies demonstrating the anticancer effects of these cells and others suggesting their progressive effects on cancer. This review focuses on recent findings about the role of hAMSCs/hAFMSCs in cancer treatment and summarizes the suppressing as well as promoting effects of these cells on cancer progression and underling mechanisms. [ABSTRACT FROM AUTHOR]

Multiple sclerosis (MS) is an autoimmune inflammatory disorder of the central nervous system (CNS) resulting in demyelination and axonal loss in the brain and spinal cord. The precise pathogenesis and etiology of this complex disease are still a mystery. Despite many studies that have been aimed to identify biomarkers, no protein marker has yet been approved for MS. There is urgently needed for biomarkers, which could clarify pathology, monitor disease progression, response to treatment, and prognosis in MS. Proteomics and metabolomics analysis are powerful tools to identify putative and novel candidate biomarkers. Different human compartments analysis using proteomics, metabolomics, and bioinformatics approaches has generated new information for further clarification of MS pathology, elucidating the mechanisms of the disease, finding new targets, and monitoring treatment response. Overall, omics approaches can develop different therapeutic and diagnostic aspects of complex disorders such as multiple sclerosis, from biomarker discovery to personalized medicine. [ABSTRACT FROM AUTHOR]

Heat shock protein 90 (HSP90), a highly and unique chaperone, presents as a double-edged sword. It plays an essential role in many physiological and pathological processes, including tumor development. The current review highlights a recent understanding of the roles of HSP90 in molecular mechanisms underlying cancer survival and progression. HSP90 and its client proteins through the regulation of oncoproteins including signaling proteins, receptors, and transcriptional factors involved in tumorigenesis. It also has potential clinical application as diagnostic and prognostic biomarkers for assessing cancer progression. In this way, using HSP90 to develop new anticancer therapeutic agents including HSP90 inhibitors, anti-HSP90 antibody, and HSP90-based vaccines has been promising. [ABSTRACT FROM AUTHOR]

Currently, there is a growing trend of replacing synthetic antioxidants with natural alternatives to prevent the oxidation of edible oils. Herein, we assessed the phenolic compounds and antioxidant properties of ethanolic extracts that are obtained from Cydonia oblonga (SQ). Furthermore, we incorporated SQ at two different concentrations (1% and 2%) into cold-pressed sesame oil, storing it for 30 days under ambient conditions. We then assessed the peroxide value (PV), acid value (AV), oxidative stability using the Rancimat apparatus, and the fatty acid (FA) composition. Additionally, we performed the molecular docking analyses to explore the interaction between trans fatty acids (TFAs; C18:1 and C18:2) and key proinflammatory cytokines such as tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and C-reactive protein (CRP). The total phenol, flavonoid content, and antioxidant activity of SQ were found to be 95.33 ± 5.03 mg GAE/g, 343.67 ± 16.44 mg QE/g, and 465.67 ± 5.51 mmol Fe2+/g, respectively. The presence of SQ exhibited a significant impact on reducing PV and AV when compared to the control group. Furthermore, the addition of SQ resulted in a significant increase in the induction period (IP) compared to the control. The predominant FAs in the samples were 18:2n-6, 18:1n-9, 16:0, and 18:0, respectively. The levels of TFAs in all samples at 30 days were higher than those at 0 day. TNF-α and IL-6 showed a higher binding affinity for the trans-C18:1 ligand, with a docking score of -6.81 and -5.82, respectively, compared to the trans-C18:2 ligand. In this context, SQ can be proposed as a natural antioxidant to enhance the oxidative stability of sesame oil. Additionally, the binding preferences and specific interactions of TFAs with these proinflammatory cytokines indicate their potential role in modulating inflammation. [ABSTRACT FROM AUTHOR]

[Display omitted] • The infection of host cells by COVID-19 mediated by the binding of its RBD from SARS-CoV-2 to the ACE2 receptor. • Rational drug design applied on over 100 million compounds to discover potential inhibitor against SARS-CoV-2 Spike RBD. • PubChem 84,280,085 compound is suggested as a potential PPIs inhibitor to demolish SARS-CoV-2 RBD/ACE2 interactions. The lack of effective treatment remains a bottleneck in combating the current coronavirus family pandemic, particularly coronavirus 2019 (COVID-19), which is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The infection of host cells by SARS-CoV-2 is mediated by the binding of its receptor-binding domain (RBD) on the spike (S) glycoprotein to the host angiotensin-converting enzyme (ACE2) receptor. As all developed and available vaccines against COVID-19 do not provide long-term immunity, the creation of an effective drug for the treatment of COVID-19 is necessary and cannot be ignored. Therefore, the aim of this study is to present a computational screening method to identify potential inhibitor candidates with a high probability of blocking the binding of RBD to the ACE2 receptor. Pharmacophore mapping, molecular docking, molecular dynamics (MD) simulations, and binding free-energy analyses were performed to identify potential inhibitor candidates against ACE2/SARS-CoV-2. In conclusion, we propose the compound PubChem-84280085 as a potential inhibitor of protein–protein interactions to disrupt the binding of the SARS-CoV-2-RBD to the ACE2 receptor. [ABSTRACT FROM AUTHOR]

Urine has been in the center of attention among scientists of clinical proteomics in the past decade, because it is valuable source of proteins and peptides with a relative stable composition and easy to collect in large and repeated quantities with a noninvasive procedure. In this review, we discuss technical aspects of urinary proteomics in detail, including sample preparation, proteomic technologies, and their advantage and disadvantages. Several recent experiments are presented which applied urinary proteome for biomarker discovery in renal diseases including diabetic nephropathy, immunoglobulin A (IgA) nephropathy, focal segmental glomerulosclerosis, lupus nephritis, membranous nephropathy, and acute kidney injury. In addition, several available databases in urinary proteomics are also briefly introduced. [ABSTRACT FROM AUTHOR]

Natural product compounds have lately attracted interest in the scientific community as a possible treatment for gastrointestinal (GI) cancer, due to their anti-inflammatory and anticancer properties. There are many preclinical, clinical, and epidemiological studies, suggesting that the consumption of polyphenol compounds, which are abundant in vegetables, grains, fruits, and pulses, may help to prevent various illnesses and disorders from developing, including several GI cancers. The development of GI malignancies follows a well-known path, in which normal gastrointestinal cells acquire abnormalities in their genetic composition, causing the cells to continuously proliferate, and metastasize to other sites, especially the brain and liver. Natural compounds with the ability to affect oncogenic pathways might be possible treatments for GI malignancies, and could easily be tested in clinical trials. Resveratrol is a non-flavonoid polyphenol and a natural stilbene, acting as a phytoestrogen with anti-cancer, cardioprotective, anti-oxidant, and anti-inflammatory properties. Resveratrol has been shown to overcome resistance mechanisms in cancer cells, and when combined with conventional anticancer drugs, could sensitize cancer cells to chemotherapy. Several new resveratrol analogs and nanostructured delivery vehicles with improved anti-GI cancer efficacy, absorption, and pharmacokinetic profiles have already been developed. This present review focuses on the in vitro and in vivo effects of resveratrol on GI cancers, as well as the underlying molecular mechanisms of action. [ABSTRACT FROM AUTHOR]

Cancer is one of the most serious human health issues. Drug therapy is the major common way to treat cancer. There is a growing interest in using natural compounds to overcome drug resistance, adverse reactions, and target specificity of certain types of drugs that may affect several targets with fewer side effects and be beneficial against various types of cancer. In this regard, the use of herbal medicines alone or in combination with the main anticancer drugs is commonly available. Berberine (BBR), a nature‐driven phytochemical component, is a well‐known nutraceutical due to its wide variety of pharmacological activities, including antioxidant, anti‐inflammatory, antibacterial, antifungal, antiparasitic, antidiabetic, antihypertensive, and hypolipidemic. In addition, BBR exerts anticancer activities. In present article, we summarized the information available on the therapeutic effects of BBR and its mechanisms on five types of the most prevalent gastrointestinal cancers, including esophageal, gastric, colorectal, hepatocarcinoma, and pancreatic cancers. [ABSTRACT FROM AUTHOR]

Cancer remains a leading cause of death worldwide, necessitating the development of innovative and more effective treatment strategies. Conventional cancer treatments often suffer from limitations such as systemic toxicity, poor pharmacokinetics, and drug resistance. Recently, there has been growing attention to utilizing natural compounds derived from various sources as possible cancer therapeutics. Natural compounds have demonstrated diverse bioactive properties, including antioxidant, anti‐inflammatory, and antitumor effects, making them attractive candidates for cancer treatment. However, their limited solubility and bioavailability present challenges for effective delivery to cancer cells. To overcome these limitations, researchers have turned to nanotechnology‐based drug delivery systems. Nanoparticles, with their small size and unique properties, can encapsulate therapeutic agents and offer benefits such as improved solubility, prolonged drug release, enhanced cellular uptake, and targeted delivery. Functionalizing nanoparticles with specific ligands further enhances their precision in recognizing and binding to cancer cells. Combining natural compounds with nanotechnology holds great promise in achieving efficient and safe cancer treatments by enhancing bioavailability, pharmacokinetics, and selectivity toward cancer cells. This review article provides an overview of the advancements in utilizing natural substances and nanotechnology‐based drug delivery systems for cancer treatment. It discusses the benefits and drawbacks of various types of nanoparticles, as well as the characteristics of natural compounds that make them appealing for cancer therapy. Additionally, current research on natural substances and nanoparticles in preclinical and clinical settings is highlighted. Finally, the challenges and future perspectives in developing natural compound‐nanoparticle‐based cancer therapies are discussed. [ABSTRACT FROM AUTHOR]

Glioblastoma (GBM) is the most frequent malignancy among primary brain tumors in adults and one of the worst 5-year survival rates (< 7%) among all human cancers. Till now, treatments that target particular cell or intracellular metabolism have not improved patients' survival. GBM recruits healthy brain cells and subverts their processes to create a microenvironment that contributes to supporting tumor progression. This microenvironment encompasses a complex network in which malignant cells interact with each other and with normal and immune cells to promote tumor proliferation, angiogenesis, metastasis, immune suppression, and treatment resistance. Communication can be direct via cell-to-cell contact, mainly through adhesion molecules, tunneling nanotubes, gap junctions, or indirect by conventional paracrine signaling by cytokine, neurotransmitter, and extracellular vesicles. Understanding these communication routes could open up new avenues for the treatment of this lethal tumor. Hence, therapeutic approaches based on glioma cells' communication have recently drawn attention. This review summarizes recent findings on the crosstalk between glioblastoma cells and their tumor microenvironment, and the impact of this conversation on glioblastoma progression. We also discuss the mechanism of communication of glioma cells and their importance as therapeutic targets and diagnostic and prognostic biomarkers. Overall, understanding the biological mechanism of specific interactions in the tumor microenvironment may help in predicting patient prognosis and developing novel therapeutic strategies to target GBM. [ABSTRACT FROM AUTHOR]

Background: Currently, the efficient production of chimeric mice and their survival are still challenging. Recent researches have indicated that preimplantation embryo culture media and manipulation lead to abnormal methylation of histone in the H19/Igf2 promotor region and consequently alter their gene expression pattern. This investigation was designed to evaluate the relationship between the methylation state of histone H3 and H19/Igf2 expression in mice chimeric blastocysts. Methods: Mouse 129/Sv embryonic stem cells (mESCs) expressing the green fluorescent protein (mESCs-GFP) were injected into the perivitelline space of 2.5 days post-coitis (dpc) embryos (C57BL/6) using a micromanipulator. H3K4 and H3K9 methylation, and H19 and Igf2 expression was measured by immunocytochemistry and q-PCR, respectively, in blastocysts. Results: Histone H3 trimethylation in H3K4 and H3K9 in chimeric blastocysts was significantly less and greater, respectively (p< 0.05), than in controls. H19 expression was significantly less (p< 0.05), while Igf2 expression was less, but not significantly so, in chimeric than in control blastocysts. Conclusions: Our results showed, that the alteration ofH3K4me3 and H3K9me3 methylation, change H19/Igf2 expression in chimeric blastocysts. [ABSTRACT FROM AUTHOR]

Objective (s): Several methods have been proposed for repairing defects and damages, one of which is cell therapy. Bone marrow stromal cells seem to be suitable for this purpose. On the other hand, many biometric materials are used to improve and correct the defects in the body. Nanofibers are widely used in the medical industry, especially in tissue engineering, as scaffolds in wound healing and wound dressing. Chitosan/ polyethylene oxide nanofibers can be a suitable replacement for routine wound coverages. Hence, this study was conducted to present a combination of these methods. Materials and Methods: Chitosan/polyethylene oxide nanofibers and thin films of chitosan were produced and optimized by electron microscopy, on which the bone marrow stromal cells were then cultivated. Interactions between the cells and these biomaterials were investigated through viability, morphology, immunocytochemistry and electron microscopy of cells after 6 days. All data were analyzed using Student's t-test and one-way ANOVA tests in SPSS version 16. P<0.05 was considered significant. Results: It seems that the high viscosity of chitosan prevents the formation of nanofibers, while chitosan/polyethylene oxide solutions with 80/20 and 90/10 ratios produce perfect, regular, bead free and non-toxic nanofibers with average diameter of 240±10 and 220±10 nm, respectively. The results of immunocytochemistry and viability showed that the cells had relatively high proliferation on the thin chitosan membranes, while the results of the electron microscopy showed that the morphology of cells was better on the nanofibers than on the thin membrane of chitosan. Conclusion: Since bone marrow stromal cells were grown well on chitosan-nanofibers, each of them alone was used in the therapeutic methods. It is better to consider a combination of two methods as the treatment method, especially in tissue engineering and cell therapy. [ABSTRACT FROM AUTHOR]

One of the main goals of tissue engineering and regenerative medicine is to develop skin substitutes for treating deep dermal and full thickness wounds. In this regard, both scaffold and cell source have a fundamental role to achieve exactly the same histological and physiological analog of skin. Amnion epithelial and mesenchymal cells possess the characteristics of pluripotent stem cells which have the capability to differentiate into all three germ layers and can be obtained without any ethical concern. Amniotic cells also produce different growth factors, angio-modulatory cytokines, anti-bacterial peptides and a wide range of anti-inflammatory agents which eventually cause acceleration in wound healing. In addition, amniotic membrane matrix exhibits characteristics of an ideal scaffold and skin substitute through various types of extracellular proteins such as collagens, laminins and fibronectins which serve as an anchor for cell attachment and proliferation, a bed for cell delivery and a reservoir of drugs and growth factors involved in wound healing process. Recently, isolation of amniotic cells exosomes, surface modification and cross-linking approaches, construction of amnion based nanocomposites and impregnation of amnion with nanoparticles, construction of amnion hydrogel and micronizing process promoted its properties for tissue engineering. In this manuscript, the recent progress was reviewed which approve that amnion-derived cells and matrix have potential to be involved in skin substitutes; an enriched cell containing scaffold which has a great capability to be translated into the clinic. [ABSTRACT FROM AUTHOR]

Gastrointestinal (GI) carcinomas are a group of cancers affecting the GI tract and digestive organs, such as the gastric, liver, bile ducts, pancreas, small intestine, esophagus, colon, and rectum. MicroRNAs (miRNAs) are small functional non-coding RNAs (ncRNAs) which are involved in regulating the expression of multiple target genes; mainly at the post-transcriptional level, via complementary binding to their 3′‐untranslated region (3′‐UTR). Increasing evidence has shown that miRNAs have critical roles in modulating of various physiological and pathological cellular processes and regulating the occurrence and development of human malignancies. Among them, miR-145 is recognized for its anti-oncogenic properties in various cancers, including GI cancers. MiR-145 has been implicated in diverse biological processes of cancers through the regulation of target genes or signaling, including, proliferation, differentiation, tumorigenesis, angiogenesis, apoptosis, metastasis, and therapy resistance. In this review, we have summarized the role of miR-145 in selected GI cancers and also its downstream molecules and cellular processes targets, which could lead to a better understanding of the miR-145 in these cancers. In conclusion, we reveal the potential diagnostic, prognostic, and therapeutic value of miR-145 in GI cancer, and hope to provide new ideas for its application as a biomarker as well as a therapeutic target for the treatment of these cancer. [ABSTRACT FROM AUTHOR]

Glioblastoma (GBM) remains the most lethal brain tumor without any curative treatment. Exosomes can mediate cell-to-cell communication, and may function as a new type of targeted therapy. In this study, the therapeutic benefits of exosomes generated by U87 cells treated with curcumin and/or temozolomide were investigated. The cells were cultured and treated with temozolomide (TMZ), curcumin (Cur), or their combination (TMZ+Cur). Exosomes were isolated with a centrifugation kit and characterized using DLS, SEM, TEM, and Western blotting. The levels of exosomal BDNF and TNF-α were measured. Naïve U87 cells were treated with the isolated exosomes, and the effects on apoptosis-related proteins HSP27, HSP70, HSP90, and P53 were assessed. All exosomes, Cur-Exo, TMZ-Exo, and TMZ+Cur-Exo increased cleaved caspase 3, Bax, and P53 proteins, while reducing HSP27, HSP70, HSP90, and Bcl2 proteins. Moreover all treatment groups increased apoptosis in naïve U87 recipient cells. Exosomes released from treated U87 cells had less BDNF and more TNF-α compared to exosomes released from naive U87 cells. In conclusion, we showed for the first time that exosomes released from drug-treated U87 cells could be a new therapeutic approach in glioblastoma, and could reduce the side effects produced by drugs alone. This concept needs to be further examined in animal models before clinical trials could be considered. [ABSTRACT FROM AUTHOR]