Preparation and characterization of methylene blue nanoparticles for Alzheimer\u27s disease and other tauopathies

A delivery system of coated and uncoated nanoparticles (NP) for delivery of methylene blue (MB). The delivery system was developed using PLGA-based polymer that was repeatedly shown to be biocompatible and biodegradable. The parameters of synthesized NPs were within the suitable range for BBB permeationâspecifically, the NPs were monodispersed, with slight negative charge, and with the size within 100-150 nm range suitable for intravenous delivery and delivery to the brain. The coating on the nanoparticle did not have a significant impact on the nanoparticle size and zeta potential. Based on the immunoblotting experiments using AD cellular model, the GSH coated NPs were better in reducing tau levels compared to MB solution. In vitro BBB Transwell permeation study showed eight fold higher MB-NP permeation compared to the MB solution over 24 hours

Afobazole nanoparticles formulation for enhanced therapeutics

A novel nanoparticle drug composition and method of use thereof is presented herein. The nanoparticle drug composition is comprised of at least one nanoparticle carrier, formed from the conjugation of PLGA and PEG, which encapsulates a drug such as afobazole and its derivatives, in a pharmaceutically acceptable carrier. The nanoparticle drug composition may be used to treat various diseases of the central nervous system involving excessive neuronal activity and inflammation such as stroke, Alzheimer\u27s disease and anxiety

Afobazole nanoparticles formulation for enhanced therapeutics

A novel nanoparticle drug composition and method of use thereof is presented herein. The nanoparticle drug composition is comprised of at least one nanoparticle carrier, formed from the conjugation of PLGA and PEG, which encapsulates a drug such as afobazole and its derivatives, in a pharmaceutically acceptable carrier. The nanoparticle drug composition may be used to treat various diseases of the central nervous system involving excessive neuronal activity and inflammation such as stroke, Alzheimer\u27s disease and anxiety

Sequential Activation of Elk-1/Egr-1/GADD45α by Arsenic

Long-term exposure to arsenic, an environmental contaminant, leads to increased risks of cancers. In the present study, we investigated the sequential regulation of Elk-1 and Egr-1 on As3+-induced GADD45α, an effector of G2/M checkpoint. We found that As3+ transcriptionally induced both Elk-1 and Egr-1, and NF-κB binding site was necessary for As3+-induced Egr-1 promoter activity. However, specific inhibition of JNK, ERK, and Elk-1 inhibited Egr-1 induction. Furthermore, silencing of Egr-1 downregulated As3+-induced expression of GADD45α and ChIP assay confirmed the direct binding of Egr-1 to GADD45α promoter. Taken together, our data indicated that the increase of GADD45α in response to As3+ was mediated sequentially by Elk-1 and Egr-1

Sequential Activation of Elk-1/Egr-1/GADD45α by Arsenic

Long-term exposure to arsenic, an environmental contaminant, leads to increased risks of cancers. In the present study, we investigated the sequential regulation of Elk-1 and Egr-1 on As3+-induced GADD45α, an effector of G2/M checkpoint. We found that As3+ transcriptionally induced both Elk-1 and Egr-1, and NF-κB binding site was necessary for As3+-induced Egr-1 promoter activity. However, specific inhibition of JNK, ERK, and Elk-1 inhibited Egr-1 induction. Furthermore, silencing of Egr-1 downregulated As3+-induced expression of GADD45α and ChIP assay confirmed the direct binding of Egr-1 to GADD45α promoter. Taken together, our data indicated that the increase of GADD45α in response to As3+ was mediated sequentially by Elk-1 and Egr-1

Role of Nutritional Factors in Pathogenesis of Cancer

Diet and nutrition are crucial factors throughout the complete life course in the promotion and upholding of good health. It has always been accepted that our defencelessness to infection and disease was influenced by diet and environmental as well as genetic factors. Nutrition is coming to the front position as a principle modifiable determinant of chronic disease, with scientific confirmation with time more supporting the view that alterations in diet have strong effects, equally positive as well as negative, on health throughout life. For the most part notably, nutritional adjustments may not only influence present health but also determine whether or not an individual will develop chronic non-communicable diseases like cancer. Diet is a blend of protective, mutagenic, and carcinogenic agents; the majority of them are metabolized by the enzymes of biotransformation process. Genetic polymorphisms that alter protein expression or else the function of these enzymes can change the risk of developing cancer. The scientific community has identified numerous naturally occurring materials in plant food with the power to resolve possible carcinogens. A few of these nutrients and natural phytochemicals look for toxins and usher them from the body before they can cause cell damage that may lead to cancer. Others give the impression to make it easier for the body to make repairs at the cellular level. At a standstill, others may help bring to an end cancer cells from reproducing. Even after a cell begins to experience damage that can lead to cancer, what you eat and drink, and how you live can still help short-circuit the cancer process. It is thought that a diet containing defensive micronutrients as well as carcinogens and mutagens may adapt the risk of cancer development, particularly in genetically susceptible individuals

Role of Nutritional Factors in Pathogenesis of Cancer

Diet and nutrition are crucial factors throughout the complete life course in the promotion and upholding of good health. It has always been accepted that our defencelessness to infection and disease was influenced by diet and environmental as well as genetic factors. Nutrition is coming to the front position as a principle modifiable determinant of chronic disease, with scientific confirmation with time more supporting the view that alterations in diet have strong effects, equally positive as well as negative, on health throughout life. For the most part notably, nutritional adjustments may not only influence present health but also determine whether or not an individual will develop chronic non-communicable diseases like cancer. Diet is a blend of protective, mutagenic, and carcinogenic agents; the majority of them are metabolized by the enzymes of biotransformation process. Genetic polymorphisms that alter protein expression or else the function of these enzymes can change the risk of developing cancer. The scientific community has identified numerous naturally occurring materials in plant food with the power to resolve possible carcinogens. A few of these nutrients and natural phytochemicals look for toxins and usher them from the body before they can cause cell damage that may lead to cancer. Others give the impression to make it easier for the body to make repairs at the cellular level. At a standstill, others may help bring to an end cancer cells from reproducing. Even after a cell begins to experience damage that can lead to cancer, what you eat and drink, and how you live can still help short-circuit the cancer process. It is thought that a diet containing defensive micronutrients as well as carcinogens and mutagens may adapt the risk of cancer development, particularly in genetically susceptible individuals

Loteprednol etabonate nanoparticles in thermoreversible gels for enhanced therapeutics

The present invention provides a sustained drug delivery system for the treatment of age-related macular degeneration (AMD), comprising corticosteroid encapsulated nanoparticles incorporated into a thermoreversible hydrogel. The corticosteroid may be triamcinolone acetate (TA), dexamethasone, or loteprednol etabonate (LE). The proposed drug delivery system is nontoxic to ARPE-19 (retinal pigment epithelium) cells and significantly reduces VEGF (vascular endothelial growth factor) expression as compared to solutions of the coticosteroids. The present invention provides sustained delivery of the corticosteroid to the posterior segment of the eye, reducing the frequency of intraocular injections necessary to maintain therapeutic concentrations

Nanoparticles in thermoreversible gels for enhanced therapeutics

The present invention provides a sustained drug delivery system for the treatment of age-related macular degeneration (AMD), comprising corticosteroid encapsulated nanoparticles incorporated into a thermoreversible hydrogel. The corticosteroid may be triamcinolone acetate (TA), dexamethasone, or loteprednol etabonate (LE). The proposed drug delivery system is nontoxic to ARPE-19 (retinal pigment epithelium) cells and significantly reduces VEGF (vascular endothelial growth factor) expression as compared to solutions of the coticosteroids. The present invention provides sustained delivery of the corticosteroid to the posterior segment of the eye, reducing the frequency of intraocular injections necessary to maintain therapeutic concentrations

Nanoparticles for treatment of posterior segment ocular diseases and conditions

The present invention concerns nanoparticles useful for treating posterior segment ocular diseases or conditions, such as macular degeneration and diabetic retinopathy; compositions comprising the nanoparticles; methods for producing the nanoparticles; and methods for treating posterior segment ocular diseases or conditions, comprising administering the nanoparticles or compositions to the ocular posterior segment of an afflicted eye