Coadministration of doxorubicin with vitamin D3, Lactobacillus acidophilus, and Lactobacillus casei in the 4T1 mouse model of breast cancer: anticancer and enteroprotective effects.

The use of doxorubicin (Dox) in the treatment of breast cancer negatively affects the intestines and other tissues. Many studies have proven that probiotics and vitamin D3 have antitumor and intestinal tissue-protecting properties. To achieve effectiveness and minimize side effects, the current study aims to administer Dox together with probiotics (Lactobacillus acidophilus and Lactobacillus casei) and vitamin D3. Forty-two female BALB/c inbred mice were divided into six groups: Group 1 (Control), Group 2 (Dox), Group 3 (Dox and probiotics), Group 4 (Dox and vitamin D3), Group 5 (Dox, probiotics, and vitamin D3), and Group 6 (probiotics and vitamin D3). The 4T1 mouse carcinoma cell line was injected into the mammary fat pad of each mouse. Gene expression was examined using quantitative real-time PCR. The treated groups (except group 6) showed significantly reduced tumor volume and weight compared to the control group (P < 0.05, P < 0.01). Probiotics/vitamin D3 with Dox reduced chemotherapy toxicity and a combination of supplements had a significant protective effect against Dox (P < 0.05, 0.01, 0.001). The treated groups (except 6) had significantly higher expression of Bax/Caspase 3 genes and lower expression of Bcl-2 genes than the control group (P < 0.05, 0.01). Coadministration of Dox with probiotics and vitamin D3 showed promising results in reducing tumor size, protecting intestinal tissue and influencing gene expression, suggesting a strategy to enhance the effectiveness of breast cancer treatment while reducing side effects.

The effect of vitamin D deficiency on platelet parameters in patients with COVID-19.

Introduction: Since there is very little information about the relationship between platelet parameters and vitamin D concentration in patients with COVID-19, the aim of this study is to investigate the relationship between serum vitamin D level and platelet parameters in patients with COVID-19 and to compare these parameters in patients with COVID-19 without vitamin D deficiency and, subsequently, the prognostic value of these parameters in cases of vitamin D deficiency. Methods: Seven hundred and forty-three patients diagnosed with COVID-19 were enrolled in this study. Patients were divided into two groups: those with and without vitamin D deficiency. The associations between platelet indices and vitamin D levels were analyzed by Pearson's correlation analysis and a one-way ANOVA test. Results: Platelet count and mean platelet volume (MPV) were significantly higher in the patients with vitamin D deficiency than in the patients without vitamin D deficiency. There was a significant negative correlation between platelet count and MPV with vitamin D levels in patients with vitamin D deficiency (r = -0.835, P = 0.001 & r = -0.324, P = 0.042, respectively). Vitamin D levels in COVID-19 patients can determine the platelet count and MPV of the patients. Discussion: The aforementioned results imply that maintaining an elevated concentration of vitamin D in COVID-19 patients is important because it is associated with a decrease in MPV, which in turn reduces susceptibility to diseases such as coronary artery disease.

A State-of-the-Art Review on the Recent Advances of Mesenchymal Stem Cell Therapeutic Application in Systematic Lupus Erythematosus.

Systemic lupus erythematosus (SLE) is an autoimmune disease with an unknown etiology that has widespread clinical and immunological manifestations. Despite the increase in knowledge about the pathogenesis process and the increase in treatment options, however, the treatments fail in half of the cases. Therefore, there is still a need for research on new therapies. Mesenchymal stem cells (MSCs) are powerful regulators of the immune system and can reduce the symptoms of systemic lupus erythematosus. This study aimed to review the mechanisms of immune system modulation by MSCs and the role of these cells in the treatment of SLE. MSCs suppress T lymphocytes through various mechanisms, including the production of transforming growth factor-beta (TGF-B), prostaglandin E2 (PGE2), nitric oxide (NO), and indolamine 2 and 3-oxygenase (IDO). In addition, MSCs inhibit the production of their autoantibodies by inhibiting the differentiation of lymphocytes. The production of autoantibodies against nuclear antigens is an important feature of SLE. On the other hand, MSCs inhibit antigen delivery by antigen-presenting cells (APCs) to T lymphocytes. Studies in animal models have shown the effectiveness of these cells in treating SLE. However, few studies have been performed on the effectiveness of this treatment in humans. It can be expected that new treatment strategies for SLE will be introduced in the future, given the promising results of MSCs application.

Bone marrow mesenchymal stem cells to ameliorate experimental autoimmune encephalomyelitis via modifying expression patterns of miRNAs.

INTRODUCTION: Clinical and experimental studies highlighted the significant therapeutic role of Mesenchymal stem cells (MSCs) in neurodegenerative diseases. MSCs possess potent immunomodulatory properties by releasing exosomes, which generate a suitable microenvironment. microRNAs (miRNAs), as one of several effective bioactive molecules of exosomes, influence cellular communication and activities in recipient cells. Recent studies revealed that miRNAs could control the progression of multiple sclerosis (MS) via differentiation and function of T helper cells (Th). METHODS: Here, we investigated the therapeutic effects of syngeneic-derived BM-MSC in experimental autoimmune encephalomyelitis (EAE) mouse model of MS by evaluating expression profile of miRNAs, pro- and anti-inflammatory in serum and brain tissues. Three-time scheme groups (6th day, 6th & 12th days, and 12th day, of post-EAE induction) were applied to determine the therapeutic effects of intraperitoneally received 1*106 of BM-MSCs. RESULTS: The expression levels of mature isoforms of miR-193, miR-146a, miR-155, miR-21, and miR-326 showed that BM-MSCs treatment attenuated the EAE clinical score and reduced clinical inflammation as well as demyelination. The improved neurological functional outcome associated with enhanced expression of miR-193 and miR-146a, but decreased expression levels of miR-155, miR-21, and miR-326 were followed by suppressing effects on Th1/Th17 immune responses (reduced levels of IFN-γand IL-17 cytokine expression) and induction of Treg cells, immunoregulatory responses (increase of IL-10, TGF-ß, and IL-4) in treatment groups. CONCLUSION: Our findings suggest that BM-MSCs administration might change expression patterns of miRNAs and downstream interactions followed by immune system modulation. However, there is a need to carry out future human clinical trials and complementary experiments.

Design and manufacture of a soft robot with dual-interaction in virtual reality.

This paper examines the design and fabrication of a soft robot that can connect to a virtual reality environment. This study's primary objective is to utilize these technologies concurrently and demonstrate their applicability in various applications, particularly rehabilitation. Therefore, the process of designing and modeling the soft robot is carried out, and an applied model is created using a 3D printer and silicon material, which is then installed on gloves. Using Unity software, a virtual reality environment is created in which programs, commands, and Arduino processors control the movements of the soft robot, allowing the user to move and pick up an object in a real environment while wearing gloves, and to adjust the amount of pressure and angle of its motion based on the size of each virtual object. During the system evaluation phase, a delay in the performance and reaction time of the soft robot installed on the gloves is observed. This delay is reduced by modifying the programming structure, resulting in optimal system functionality. This capability is used to create proper mobility conditions and rehabilitation for the majority of patients with wrist injuries resulting from strokes and accidents, and it may be effective in accelerating patients' recoveries.

Curcumin's spice-infused therapeutic promise: disease severity alleviation in a mouse model of multiple sclerosis via modulation of immune responses.

BACKGROUND: Multiple sclerosis (MS) is an autoimmune central nervous system (CNS) disorder indicated by demyelination, chronic inflammation, and neuronal destruction. Regional demyelination, inflammation responses, scar development, and various axonal damage are pathological characteristics of MS. Curcumin is a hydrophobic polyphenol extracted from the rhizome of the turmeric plant. In addition to anti-inflammatory effects, beneficial therapeutic effects such as antioxidant, anti-cancer and nerve protection have also been seen from this compound. The purpose of the current investigation was to provide light on the potential benefits of Curcumin in treating experimental autoimmune encephalomyelitis (EAE), the animal model of MS. METHODS AND RESULTS: in Female C57BL/6 mice were used to induce EAE through myelin oligodendroglial glycoprotein (MOG). Curcumin doses of 100 and 200 mg/kg were administered orally in the treatment groups starting on the first day of EAE induction. Brains and splenocytes were extracted from euthanized animals on day 25 following EAE induction. Demyelination and leukocyte infiltration, proliferation, cytokine, and gene expression profiles were assessed. Our findings demonstrate that both low and high doses of Curcumin decreased the progression of EAE. Histological analyses revealed low infiltration of leukocytes into the CNS. Curcumin therapy enhanced Th2 and Treg cell secretion of IL-4, IL-10, and TGF-ß although considerably decreasing IFN-γ and TNF-α. Curcumin-induced Th2 and Treg cell cytokine production and transcription factor gene expression (IL-13, GATA3, STAT6 and IL-35, CTLA4, Foxp3) and anti-inflammatory cytokines (IL-27, IL-33). CONCLUSION: Overall, these findings provide additional evidence that Curcumin can slow disease development and alleviate symptoms in EAE through stimulating Treg and Th2 cell polarization. They support Curcumin's potential therapeutic role in MS.

Importance of gut microbiota metabolites in the development of cardiovascular diseases (CVD).

Cardiovascular disease (CVD) remains the most common cause of death worldwide and has become a public health concern. The proven notable risk factors for CVD are atherosclerosis, hypertension, diabetes, dyslipidemia, inflammation, and some genetic defects. However, research has shown a correlation between metabolic health, gut microbiota, and dietary risk factors. The gut microbiota makes an important contribution to human functional metabolic pathways by contributing enzymes that are not encoded by the human genome, for instance, the breakdown of polysaccharides, polyphenols and vitamins synthesis. TMAO and SCFAs, human gut microbiota compounds, have respective immunomodulatory and pro-inflammatory effects. Choline and l-carnitine are abundant in high-fat diets and are transformed into TMA by gut bacteria. The liver's phase of metabolism then changes TMA into TMAO. In turn, TMAO promotes the activation of macrophages, damages vascular endothelium, and results in CVD-however, dysbiosis decreases SCFAs and bile acids, which raises intestinal permeability. Congestion in the portal vein, a drop in cardiac output, a reduction in intestinal perfusion, and intestinal leakage are all caused by heart failure. These factors induce systemic inflammation by increasing intestinal leakage. By raising CRP and pro-inflammatory reactions, human gut dysbiosis and elevated TMAO levels promote the development of arterial plaque, hasten the beginning of atherosclerosis, and raise the risk of CAD. A healthy symbiosis between the gut microbiota and host is a key factor in shaping the biochemical profile of the diet, therefore which are crucial for maintaining the intestinal epithelial barrier, growing mucosa, reducing inflammation, and controlling blood pressure.

Enhanced anti-cancer effect of artemisinin- and curcumin-loaded niosomal nanoparticles against human colon cancer cells.

Colorectal cancer (CRC) is the third broadly identified cancer in the world. The ineffectiveness of colorectal cancer treatment is redundantly reported. Natural bioactive compounds have gained popularity in reducing the drawback of conventional anti-cancer agents. Curcumin (Cur) and Artemisinin (Art) are materials of a natural source that have been utilized to treat numerous kinds of cancers. Although the benefits of bioactive materials, their utilization is limited because of poor solubility, bioavailability, and low dispersion rate in aqueous media. Nano delivery system such as niosome can improve the bioavailability and stability of bioactive compounds within the drug. In current work, we used Cur-Art co-loaded niosomal nanoparticles (Cur-Art NioNPs) as an anti-tumor factor versus colorectal cancer cell line. The synthesized formulations were characterized using dynamic light scattering, scanning electron microscopy, and FTIR. The proliferation ability of the cells and expression of apoptosis-associated gene were MTT assay and qRT-PCR, respectively. Cur-Art NioNPs exhibited well distributed with an encapsulation efficiency of 80.27% and 85.5% for Cur and Art. The NioNPs had good release and degradation properties, and had no negative effect on the survival and proliferation ability of SW480 cells. Importantly, nanoformulation form of Cur and Art significantly displayed higher toxicity effect against SW480 cells. Furthermore, Cur-Art NioNPs increased Bax, Fas, and p53 gene expressions and suppressed Bcl2, Rb, and Cyclin D 1 gene expressions. In summary, these results display the niosome NPs as a first report of nano-combinational application of the natural herbal substances with a one-step fabricated co-delivery system for effective colorectal cancer.

Recent advances in the detection of glioblastoma, from imaging-based methods to proteomics and biosensors: A narrative review.

Glioblastoma (GBM) is an aggressive type of cancer that originates in the cells called astrocytes, which support the functioning of nerve cells. It can develop in either the brain or the spinal cord and is also known as glioblastoma multiform. GBM is a highly aggressive cancer that can occur in either the brain or spinal cord. The detection of GBM in biofluids offers potential advantages over current methods for diagnosing and treatment monitoring of glial tumors. Biofluid-based detection of GBM focuses on identifying tumor-specific biomarkers in blood and cerebrospinal fluid. To date, different methods have been used to detect biomarkers of GBM, ranging from various imaging techniques to molecular approaches. Each method has its own strengths and weaknesses. The present review aims to scrutinize multiple diagnostic methods for GBM, with a focus on proteomics methods and biosensors. In other words, this study aims to provide an overview of the most significant research findings based on proteomics and biosensors for the diagnosis of GBM.

Interleukin-35 and Interleukin-37 anti-inflammatory effect on inflammatory bowel disease: Application of non-coding RNAs in IBD therapy.

Inflammatory bowel disease (IBD) is a widespread autoimmune disease that may even be life-threatening. IBD is divided into two major subtypes: ulcerative colitis and Crohn's disease. Interleukin (IL)-35 and IL-37 are anti-inflammatory cytokines that belong to IL-12 and IL-1 families, respectively. Their recruitment relieves inflammation in various autoimmune diseases, including psoriasis, multiple sclerosis, rheumatoid arthritis, and IBD. Regulatory T cells (Tregs) and regulatory B cells (Bregs) are the primary producers of IL-35/IL-37. IL-35 and IL-37 orchestrate the regulation of the immune system through two main strategies: Blocking nuclear transcription factor kappa-B (NF-kB) and mitogen-activated protein kinase (MAPK) signaling pathways or promoting the proliferation of Tregs and Bregs. Moreover, IL-35 and IL-37 can also inhibit inflammation by adjusting the T helper (Th)17/Treg ratio balance. Among the anti-inflammatory cytokines, IL-35 and IL-37 have significant potential to reduce intestinal inflammation. Therefore, administering IL-35/IL-37-based drugs or blocking their inhibitor microRNAs could be a promising approach to alleviate IBD symptoms. Overall, in this review article, we summarized the therapeutic application of IL-35 and IL-37 in both human and experimental models of IBD. Also, it is hoped that this practical information will reach beyond IBD therapy and shed some light on treating all intestinal inflammations.

Niosomes nanoparticles as a novel approach in drug delivery enhances anticancer properties of chrysin in human ovarian carcinoma cells (SKOV3): an in vitro study.

Chrysin (Chr) has drawn a lot of attention recently due to its possible anticancer properties. However, Chr's short half-life and low bioavailability restricted its utility as a medicinal agent. The purpose of this research is to design, synthesize, and test the cytotoxic effects of nano-niosomes containing chrysin (Chr-Nio) on the SKOV3 ovarian cancer cell line. Chr-Nio has a nanoparticle polydispersity index (PDI) of 0.156 and a zeta potential of - 27.4 mV, with an average diameter of 105 nm. Furthermore, Chr was encapsulated in Nio with an entrapment effectiveness of 85.5%. Chr-Nio cytotoxicity was shown to be more than free Chr in a time- and dose-dependent manner. Furthermore, as compared to free Chr-treated cells, the mRNA expression level of apoptotic genes Bcl-2, Bax, and caspase-3 in Chr-Nio-treated cells was considerably altered. According to the data, Chr may inhibit SKOV3 cell migration in vitro scratch wound experiments in a dose-dependent manner, and cells treated with Chr-Nio had the highest percentage of cell death. The findings of this study suggested that encapsulating Chr in niosome nanoparticles might be an effective medication delivery strategy for increasing Chr anticancer effects in the treatment of ovarian cancer.

The role of non-coding RNAs in the diagnosis of different stages (HCC, CHB, OBI) of hepatitis B infection.

Despite the availability of an effective hepatitis B virus (HBV) vaccine and universal immunization schedules, HBV has remained a health problem in various stages such as occult hepatitis B infection (OBI), chronic hepatitis B (CHB), and hepatocellular carcinoma (HCC), which is considered one of the possible phases during chronic HBV infection. OBI is defined as the persistence of HBV genomes in hepatocytes of patients with a negative HBV surface antigen (HBsAg) test and detectable or undetectable HBV DNA in the blood. OBI is occasionally associated with infection caused by mutant viruses that produce a modified HBsAg that is undetected by diagnostic procedures or with replication-defective variations. Many aspects of HBV (OBI more than any other stage) including prevalence, pathobiology, and clinical implications has remained controversial. According to a growing body of research, non-coding RNAs (lncRNAs) and microRNAs (miRNAs) have been linked to the development and progression of a number of illnesses, including viral infectious disorders. Despite a shortage of knowledge regarding the expression and biological activities of lncRNAs and miRNAs in HBV infection, Hepatitis B remains a major global public health concern. This review summarizes the role of lncRNAs in the diagnosis and treatment of different stages of hepatitis B infection.

Comprehensive Investigations Relationship Between Viral Infections and Multiple Sclerosis Pathogenesis.

Multiple sclerosis (MS) is a chronic autoimmune disease that affects the central nervous system (CNS). Compared to other types of self-limiting myelin disorders, MS compartmentalizes and maintains chronic inflammation in the CNS. Even though the exact cause of MS is unclear, it is assumed that genetic and environmental factors play an important role in susceptibility to this disease. The progression of MS is triggered by certain environmental factors, such as viral infections. The most important viruses that affect MS are Epstein-Barr virus (EBV), human herpes virus 6 (HHV-6), human endogenous retrovirus (HERV), cytomegalovirus (CMV), and varicella zoster virus (VZV). These viruses all have latent stages that allow them to escape immune detection and reactivate after exposure to various stimuli. Furthermore, their tropism for CNS and immune system cells explains their possible deleterious function in neuroinflammation. In this study, the effect of viral infections on MS disease focuses on the details of viruses that can change the risk of the disease. Paying attention to the most recent articles on the role of SARS-CoV-2 in MS disease, laboratory indicators show the interaction of the immune system with the virus. Also, strategies to prevent viruses that play a role in triggering MS are discussed, such as EBV, which is one of the most important.

New insight into GARP striking role in cancer progression: application for cancer therapy.

T regulatory cells play a crucial role in antitumor immunity suppression. Glycoprotein-A repetitions predominant (GARP), transmembrane cell surface marker, is mostly expressed on Tregs and mediates intracellular organization of transforming growth factor-beta (TGF-ß). The physiological role of GARP is immune system homeostasis, while it may cause tumor development by upregulating TGF-ß secretion. Despite the vast application of anti- programmed cell death protein-1 (PD-1)/programmed death-ligand 1 (PD-L1) and anti-cytotoxic T-lymphocyte Antigen-4 (CTLA-4) antibodies in immunotherapy, anti-GARP antibodies have the advantage of better response in patients who has resistance to anti-PD-1/PD-L1. Furthermore, simultaneous administration of anti-GARP antibody and anti-PD-1/PD-L1 antibody is much more effective than anti-PD-1/PD-L1 alone. It is worth mentioning that the GARP-mTGF-ß complex is more potent than secretory TGF-ß to induce T helper 17 cells differentiation in HIV + patients. On the other hand, TGF-ß is an effective cytokine in cancer development, and some microRNAs could control its secretion by regulating GARP. In the present review, some information is provided about the undeniable role of GARP in cancer progression and its probable importance as a novel prognostic biomarker. Anti-GARP antibodies are also suggested for cancer immunotherapy.

Gastrointestinal Tract, Microbiota and Multiple Sclerosis (MS) and the Link Between Gut Microbiota and CNS.

Multiple sclerosis (MS) is a chronic inflammatory disease characterized by central nervous system (CNS) lesions that can lead to severe neurological defects. Evidence is mounting that immune function is crucial in neuroinflammatory illnesses like MS. Through its impact on systemic immunological reactions, the large microbial population known as the gut microbiota has been linked to both human health and disease. The gut-brain axis (GBA) therefore encompasses neurological, immunological, and hormonal pathways, and microbiota can have a number of effects on the immune system, influencing MS. Recent research revealed a bidirectional relationship between metabolites originating from the gut microbiota, namely short-chain fatty acids (SCFAs). Intestinal epithelial cells are influenced by SCFAs, which also boosts the secretion of -Defensins and regenerating islet-derived III (REGIII) proteins. These proteins reduce intestinal pathogens, induce T-reg differentiation, and modulate immune responses by reducing IL-1 and IL-6 expression and increasing IL-10. Nutrition and psychological stress are two of the most significant elements that can directly and indirectly change the microbiota compositions along with other environmental influencing factors. An important regulator of intestinal physiology in the gut-brain-microbiota axis is butyrate, a well-known SCFA. Intestinal dysbiosis, altered intestinal barrier function, behavioral abnormalities, and activation of the hypothalamic-pituitary-adrenal (HPA) axis are all brought on by exposure. Probiotics, bacterial metabolite supplementation, fecal matter transplantation, defined microbial communities, and dietary intervention are some methods for modifying the composition of the gut microbiota that may be used to affect disease-related immune dysfunction and serve as the foundation for a new class of therapeutics.

Oral Administration of Myelin Oligodendrocyte Glycoprotein Attenuates Experimental Autoimmune Encephalomyelitis through Induction of Th2/Treg Cells and Suppression of Th1/Th17 Immune Responses.

Multiple Sclerosis (MS) is a demyelinating autoimmune disorder of the central nervous system (CNS). Experimental autoimmune encephalomyelitis (EAE) has been widely used to determine the pathogenesis of the disease and evaluate new treatment strategies for MS. Therefore, we investigated the efficacy of oral administration of a Myelin Oligodendrocyte Glycoprotein (MOG) in the treatment of EAE. Female C57BL/6 mice were utilized in three groups (Control group, received PBS orally; prevention group, oral administration of MOG35-55 two weeks before EAE induction; treatment group, oral administration of MOG35-55 after EAE induction). MOG administration, both as prevention and treatment, significantly controlled clinical score, weight loss, CNS inflammation, and demyelination, mainly through the modulation of T cell proliferation, and reduction in pro-inflammatory cytokines and transcription factors, including TNF-α, IFN-γ, IL-17, T-bet, and ROR-γt. MOG administration, both as prevention and treatment, also induced anti-inflammatory cytokines and transcription factors, including IL-4, TGF-ß, GATA-3, and Foxp3. The results showed that oral administration of MOG, both as prevention and treatment, could efficiently control EAE development. Immunomodulatory mechanisms include the induction of Th2 and Treg cells and the suppression of pro-inflammatory Th1 and Th17 cells.

Recent advances in treatment Crimean-Congo hemorrhagic fever virus: A concise overview.

The Crimean Congo Hemorrhagic Fever Virus (CCHFV) is widespread in Africa, Asia, and Europe, among other places. The disease was initially discovered in the Crimean cities of the Soviet Union and the Congo, and it was given the name Crimean Congo because it induces hemorrhagic fever. According to studies, when the virus enters the body, it settles in immune cells such as macrophages and dendritic cells, causing them to malfunction and secrete inflammatory cytokines such as TNF-alpha, IL1, and IL6, resulting in cytokine storms that induces shock via endothelial activation and vascular leakage, while on the other hand, clots and disseminated intravascular coagulation (DIC) formation causes massive defects in various organs such as the liver and kidneys, as well as fatal bleeding. Disease prevention and treatment are crucial since no other effective vaccination against the disease has yet been developed. Immunotherapy is utilized as a consequence. One of the most effective treatments, when combined with compensatory therapies such as blood and platelet replacement, water, electrolytes, Fresh Frozen Plasma (FFP) replacement, and other compensatory therapies, is one of the most effective treatments. Studies; show that immunotherapy using IVIG and neutralizing and non-neutralizing monoclonal antibodies; cytokine therapy, and anti-inflammatory therapy using corticosteroids are effective ways to treat the disease.

A state-of-the-art review on the recent advances of niosomes as a targeted drug delivery system.

The buildup of nonionic surfactants in the aqueous environment produces niosomes. The usage of niosomes is becoming increasingly frequent due to their sustainability, low cost of components and assembly, large-scale manufacture, and, finally, easy maintenance of the niosomes to the other. Because of their nonionic characteristics, niosomes play a critical role in medication delivery systems. Controlled release and targeted distribution of niosomes to treat cancer, infectious illnesses, and other disorders are one of their most important properties. Niosomes can also be injected by ocular and transdermal routes, which are less common than oral and parenteral administration. Using niosomes to manufacture biotechnology goods and novel vaccines is one of the most exciting research fields today. The molecular structure of niosomes, the physicochemical characteristics of nonionic surfactants in their formulation, the influence of external stimuli on niosomes, the many methods of niosomes administration, and their diverse therapeutic qualities are all explored in this study.

Akkermansia muciniphila as a novel powerful bacterial player in the treatment of metabolic disorders.

Akkermansia muciniphila (A. muciniphila) is a mucin-degrading bacterium that commonly lives in the intestinal mucus layer. It is normally detected in human faecal specimens and is one of the few bacteria potentially associated to obesity development. In this narrative review, possible mechanisms that support how A. muciniphila is implicated in the pathogenesis of obesity and metabolic-associated disease are described with the evaluation of its role as an intermediary or independent agent whose manipulation could be useful in the management of metabolic disorders. The ampleness of A. muciniphila is notably diminished in obesity, type 2 diabetes (T2D), non-alcoholic fatty liver disease (NAFLD), cardiometabolic diseases and low-grade inflammation. Furthermore, an inverse relationship between A. muciniphila, body weight and insulin sensitivity has been observed in both humans and animals. Antidiabetic drugs, gastric bypass surgery, prebiotics and biologically active compounds, such as polyphenols or saponins, have been shown to be associated with A. muciniphila relative abundance and thus could have favourable effects on metabolic disorders. Furthermore, A. muciniphila supplementation alone has been correlated with weight reduction and improvement of metabolic disorders, including fat mass gain, adipose tissue inflammation, metabolic endotoxaemia, and insulin resistance. Nevertheless, since the primary beneficial impacts of this bacterium have been predominantly investigated in various preclinical models, these results need to be confirmed in randomized clinical trials.

The role of the host microbiome in autism and neurodegenerative disorders and effect of epigenetic procedures in the brain functions.

Autism Spectrum Disorder (ASD) is a severe neurological/neurodegenerative syndrome that results in cognitive and communication disorders. The degree of dysbiosis is related to the severity of ASD signs. The gut is conferred with a variety of sensory receptors that cooperate with effector systems including the endocrine, nervous and gut immune systems of the intestine. Gut dysbiosis causes amplified inflammation, the launch of the HPA axis, changed levels of neurotransmitters and bacterial metabolites; these may donate to abnormal signaling throughout the Vagus nerve in ASD. Decreased integrity of the gastrointestinal barrier led to extreme leakage of substances as of the intestine in early life and inflammation followed by disruption of BBB integrity maybe increase the risk of ASD. Microbiota, by controlling the barrier permeability, regulate the quantity and types of bioactive materials that are transferred from the intestine to the brain. Exposure to metabolites and microbial products regulate significant procedures in the CNS, including glial cell role, myelination, synaptic pruning, and play a role in neurobehavioral, neurodegenerative, psychiatric, and metabolic syndrome.