Preparation and Characterization of Carbon Nanofibers and its Composites by Chemical Vapor Deposition

Hydrocarbon gas or carbon monoxide was pyrolyzed by chemical vapor deposition (CVD), and carbon nanofiber (CNF) synthesis was performed using transition metals such as Ni, Fe, and Co as catalysts. When synthesizing carbon nanofibers using the CVD method, experimental variables are temperature, catalysts, source gas, etc. Especially, the particle size of the catalyst is the most important factor in determining the diameter of carbon nanofibers. Hydrocarbon gases, such as CH4, C2H4, benzene, and toluene are used as the carbon source, and in addition to these reaction gases, nonreactive gases such as H2, Ar, and N2 gases are used for transportation. Synthesis occurs at a synthesis temperature of 600–900°C, and catalyst metals such as Ni, Co, and Fe are definitely required when synthesizing CNFs. Therefore, it is possible to synthesize CNFs in selective areas through selective deposition of such catalyst metals. In this study, CNFs were synthesized by CVD. Ethylene gas was employed as the carbon source for synthesis of CNFs with H2 as the promoting gas and N2 as the balancing gas. Synthesized CNFs can be used in various applications, such as composite materials, electromagnetic wave shielding materials, ultrathin display devices, carbon semiconductors, and anode materials of Li secondary batteries. In particular, there is an increasing demand for light-weight, small-scale, and high-capacity batteries for portable electronic devices, such as notebook computers or smartphones along with the recent issue of fossil energy depletion. Accordingly, CNFs and their silicon-series composites are receiving attention for use as anode materials for lithium secondary batteries that are eco-friendly, light weight, and high capacity

Synthesis and Characteristics of Carbon Nanofibers/Silicon Composites and Application to Anode Materials of Li Secondary Batteries

Among the various synthesizing technologies of carbon nanofibers (CNFs), chemical vapor deposition (CVD) technology, which uses hydrocarbon gas or carbon monoxide as a carbon source gas and pyrolyzes it to grow CNFs on transition metal catalysts, such as Ni, Fe, and Co, has been regarded as the most inexpensive and convenient method to produce CNFs for industrial use. Experimental variables for CVD are source gas, catalyst layers, temperature, and reaction time. Since the particle size of metal catalysts has an influence on the diameter of CNFs, it is possible to control the diameter of CNFs by varying particle sizes of the metal. As such, it is possible to synthesize CNFs selectively through the selective deposition of catalyst metals. In this study, CNFs were grown by CVD on C-fiber textiles, which had catalysts deposited via electrophoretic deposition. The CNFs were coated with a silica layer via hydrolysis of TEOS (tetraethyl orthosilicate), and the CNFs were oxidized by nitric acid. Due to oxidation, a hydroxyl group was created on the CNFs, which was then able to be used as an activation site for the SiO2. CNFs and the CNFs/SiO2 composite can be used in various applications, such as a composite material, electromagnetic wave shielding material, ultrathin display devices, carbon semiconductors, and anode materials of Li secondary batteries. In particular, there is an increasing demand for lightweight, small-scale, and high-capacity batteries for portable electronic devices, such as laptop computers or smart phones, along with the escalating concern of fossil energy depletion. Accordingly, CNFs and CNFs/SiO2 composites are receiving attention for their use as anode materials of Li secondary batteries, which are eco-friendly, lightweight, and high capacity. Therefore, the physicochemical properties and electrochemical performance data of synthesized CNFs and CNFs/SiO2 composite are described in this chapter

Autophagy in Adipocyte Browning: Emerging Drug Target for Intervention in Obesity

Autophagy, lipophagy, and mitophagy are considered to be the major recycling processes for protein aggregates, excess fat, and damaged mitochondria in adipose tissues in response to nutrient status-associated stress, oxidative stress, and genotoxic stress in the human body. Obesity with increased body weight is often associated with white adipose tissue (WAT) hypertrophy and hyperplasia and/or beige/brown adipose tissue atrophy and aplasia, which significantly contribute to the imbalance in lipid metabolism, adipocytokine secretion, free fatty acid release, and mitochondria function. In recent studies, hyperactive autophagy in WAT was observed in obese and diabetic patients, and inhibition of adipose autophagy through targeted deletion of autophagy genes in mice improved anti-obesity phenotypes. In addition, active mitochondria clearance through activation of autophagy was required for beige/brown fat whitening – that is, conversion to white fat. However, inhibition of autophagy seemed detrimental in hypermetabolic conditions such as hepatic steatosis, atherosclerosis, thermal injury, sepsis, and cachexia through an increase in free fatty acid and glycerol release from WAT. The emerging concept of white fat browning–conversion to beige/brown fat– has been controversial in its anti-obesity effect through facilitation of weight loss and improving metabolic health. Thus, proper regulation of autophagy activity fit to an individual metabolic profile is necessary to ensure balance in adipose tissue metabolism and function, and to further prevent metabolic disorders such as obesity and diabetes. In this review, we summarize the effect of autophagy in adipose tissue browning in the context of obesity prevention and its potential as a promising target for the development of anti-obesity drugs

Arsenite exposure suppresses adipogenesis, mitochondrial biogenesis and thermogenesis via autophagy inhibition in brown adipose tissue

Arsenite, a trivalent form of arsenic, is an element that occurs naturally in the environment. Humans are exposed to high dose of arsenite through consuming arsenite-contaminated drinking water and food, and the arsenite can accumulate in the human tissues. Arsenite induces oxidative stress, which is linked to metabolic disorders such as obesity and diabetes. Brown adipocytes dissipating energy as heat have emerging roles for obesity treatment and prevention. therefore, understanding the pathophysiological role of brown adipocytes can provide effective strategies delineating the link between arsenite exposure and metabolic disorders. Our study revealed that arsenite significantly reduced differentiation of murine brown adipocytes and mitochondrial biogenesis and respiration, leading to attenuated thermogenesis via decreasing UCP1 expression. Oral administration of arsenite in mice resulted in heavy accumulation in brown adipose tissue and suppression of lipogenesis, mitochondrial biogenesis and thermogenesis.Mechanistically, arsenite exposure significantly inhibited autophagy necessary for homeostasis of brown adipose tissue through suppression of Sestrin2 and ULK1. These results clearly confirm the emerging mechanisms underlying the implications of arsenite exposure in metabolic disorders

Autophagy in Adipocyte Browning: Emerging Drug Target for Intervention in Obesity

Autophagy, lipophagy, and mitophagy are considered to be the major recycling processes for protein aggregates, excess fat, and damaged mitochondria in adipose tissues in response to nutrient status-associated stress, oxidative stress, and genotoxic stress in the human body. Obesity with increased body weight is often associated with white adipose tissue (WAT) hypertrophy and hyperplasia and/or beige/brown adipose tissue atrophy and aplasia, which significantly contribute to the imbalance in lipid metabolism, adipocytokine secretion, free fatty acid release, and mitochondria function. In recent studies, hyperactive autophagy in WAT was observed in obese and diabetic patients, and inhibition of adipose autophagy through targeted deletion of autophagy genes in mice improved anti-obesity phenotypes. In addition, active mitochondria clearance through activation of autophagy was required for beige/brown fat whitening – that is, conversion to white fat. However, inhibition of autophagy seemed detrimental in hypermetabolic conditions such as hepatic steatosis, atherosclerosis, thermal injury, sepsis, and cachexia through an increase in free fatty acid and glycerol release from WAT. The emerging concept of white fat browning–conversion to beige/brown fat–has been controversial in its anti-obesity effect through facilitation of weight loss and improving metabolic health. Thus, proper regulation of autophagy activity fit to an individual metabolic profile is necessary to ensure balance in adipose tissue metabolism and function, and to further prevent metabolic disorders such as obesity and diabetes. In this review, we summarize the effect of autophagy in adipose tissue browning in the context of obesity prevention and its potential as a promising target for the development of anti-obesity drugs

Arsenic Toxicity on Metabolism and Autophagy in Adipose and Muscle Tissues

Arsenic, a naturally occurring metalloid derived from the environment, has been studied worldwide for its causative effects in various cancers. However, the effects of arsenic toxicity on the development and progression of metabolic syndrome, including obesity and diabetes, has received less attention. Many studies suggest that metabolic dysfunction and autophagy dysregulation of adipose and muscle tissues are closely related to the development of metabolic disease. In the USA, arsenic contamination has been reported in some ground water, soil and grain samples in major agricultural regions, but the effects on adipose and muscle tissue metabolism and autophagy have not been investigated much. Here, we highlight arsenic toxicity according to the species, dose and exposure time and the effects on adipose and muscle tissue metabolism and autophagy. Historically, arsenic was used as both a poison and medicine, depending on the dose and treatment time. In the modern era, arsenic intoxication has significantly increased due to exposure from water, soil and food, which could be a contributing factor in the development and progression of metabolic disease. From this review, a better understanding of the pathogenic mechanisms by which arsenic alters metabolism and autophagy regulation could become a cornerstone leading to the development of therapeutic strategies against arsenic-induced toxicity and metabolic disease

Mycophenolate mofetil as an alternative treatment for autoimmune hepatitis

Autoimmune hepatitis (AIH) is an immune-mediated chronic liver disease characterized by hepatocellular inflammation, necrosis, and fibrosis, which can progress to cirrhosis and fulminant hepatic failure. The standard treatment for AIH includes corticosteroids alone or in combination with azathioprine. Although most patients achieve remission using the standard regimen, some patients do not respond due to either drug intolerance or refractory disease; in such cases alternative immunosuppressive agents should be explored. The second-line therapies are cyclophilin inhibitors such as cyclosporine A or tacrolimus, and nowadays mycophenolate mofetil (MMF) is widely used if azathioprine-based therapies are not tolerated. Although these are recommended as an alternative to the first-line regimen, there is insufficient evidence for the efficacy of second-line therapies, with the evidence based mainly on expert opinion. Therefore, we report an AIH patient receiving the standard regimen in whom remission did not occur due to side effects to azathioprine, but was successfully treated with MMF in combination with corticosteroids as an alternative to the standard regimen