Development of functional composts using spent coffee grounds, poultry manure and biochar through microbial bioaugmentation.

Spent coffee grounds (SCG), poultry manure, and agricultural waste-derived biochar were used to manufacture functional composts through microbial bioaugmentation. The highest yield of tomato stalk-based biochar (40.7%) was obtained at 450°C with a surface area of 2.35 m2 g-1. Four pilot-scale composting reactors were established to perform composting for 45 days. The ratios of NH4+-N/NO3--N, which served as an indicator of compost maturity, indicate rapid, and successful composting via microbial bioaugmentation and biochar amendment. Moreover, germination indices for radish also increased by 14-34% through augmentation and biochar amendment. Microbial diversity was also enhanced in the augmented and biochar-amended composts by 7.1-8.9%, where two species of Sphingobacteriaceae were dominant (29-43%). The scavenging activities of 2,2-diphenyl-1-picrylhydrazyl (DPPH) were enhanced by 14.1% and 8.6% in the fruits of pepper plants grown in the presence of the TR-2 (augmentation applied only) and TR-3 (both augmentation and biochar amendment applied) composts, respectively. Total phenolic content was also enhanced by 68% in the fruits of the crops grown in TR-3. Moreover, the other compost, TR-L (augmentation applied only), boosted DPPH scavenging activity by 111% in leeks compared with commercial organic fertilizer, while TR-3 increased the phenolic content by 44.8%. Composting facilitated by microbial augmentation and biochar amendment shortened the composting time and enhanced the quality of the functional compost. These results indicate that functional compost has great potential to compete with commercially available organic fertilizers and that the novel composting technology could significantly contribute to the eco-friendly recycling of organic wastes such as spent coffee grounds, poultry manure, and agricultural wastes.

A Social History of Ascariasis in the 1960s Korea : From a Norm to a Shameful Disease.

Until the 1950s, Ascaris was regarded as an essential part of life which controls every aspect of human physiology among Koreans. Therefore, Ascaris should not be removed from human body. Efforts from medical professionals and the Korean government officials who wished to push forward the parasite control program, had to constantly contest with this perception of Ascaris among ordinary Koreans. In 1966, the 'Parasitic Disease Prevention Act' was promulgated and 'the Korean Association for Parasite Eradication (KAPE)' established in Korea. From the 1970s, Korea mobilized 15 million people each year to achieve the eradication goal. Such mass mobilization could not be possible without public awareness on necessity of parasite eradication. Until the early 1960s, however, Korean people were not sympathetic to the needs of eradication of parasites, especially that of Ascaris. Then, what changed the social perception towards Ascaris during the 1960s? What contributing factors allowed the mass mobilization and public involvement for that campaign? Employing newspaper articles and periodicals, this paper analyzes how social perception on Ascariasis changed during the 1960s, when the 'Parasitic Disease Prevention Act' was established. During the 1960s, Ascariasis became a shameful disease for Koreans. A series of events made Ascariasis more visible and shameful to Koreans. First event happened with Korean miners who were dispatched to Germany in 1963. When the miners turned out to have been infected with intestinal parasites, they were prohibited from work at the mines by the authorities in Germany and quarantined for several weeks. This humiliating experience of Korean expatriate people having bodies swarmed with parasites became a national shame to Koreans. The parasite infected bodies of Korean workers were revealed to the World through German newspapers. Second event happened when a child died of intestinal obstruction due to Ascariasis. The doctor retrieved 1,063 Ascaris from the bowel of the 9 year-old girl, and the photo of the 1,063 worms was published in several newspapers. It was a shocking visualization of Ascariasis in Korean society. Through these visualizations of Ascariasis, the Korean society began to perceive Ascariasis as a shame of the nation as well as that of an individual.

Dietary Aloe QDM Complex Reduces Obesity-Induced Insulin Resistance and Adipogenesis in Obese Mice Fed a High-Fat Diet.

Obesity-induced disorders contribute to the development of metabolic diseases such as insulin resistance, fatty liver diseases, and type 2 diabetes (T2D). In this study, we evaluated whether the Aloe QDM complex could improve metabolic disorders related to blood glucose levels and insulin resistance. Male C57BL/6 obese mice fed a high-fat diet for 54 days received a supplement of Aloe QDM complex or pioglitazone (PGZ) or metformin (Met) and were compared with unsupplemented controls (high-fat diet; HFD) or mice fed a regular diet (RD). RT-PCR and western blot analysis were used to quantify the expression of obesity-induced inflammation. Dietary Aloe QDM complex lowered body weight, fasting blood glucose, plasma insulin, and leptin levels, and markedly reduced the impairment of glucose tolerance in obese mice. Also, Aloe QDM complex significantly enhanced plasma adiponectin levels and insulin sensitivity via AMPK activity in muscles. At the same time, Aloe QDM decreased the mRNA and protein of PPARγ/LXRα and scavenger receptors in white adipose tissue (WAT). Dietary Aloe QDM complex reduces obesity-induced glucose tolerance not only by suppressing PPARγ/LXRα but also by enhancing AMPK activity in the WAT and muscles, both of which are important peripheral tissues affecting insulin resistance. The Aloe QDM complex could be used as a nutritional intervention against T2D.

Dietary Aloe Reduces Adipogenesis via the Activation of AMPK and Suppresses Obesity-related Inflammation in Obese Mice.

BACKGROUND: Metabolic disorders, including type II diabetes and obesity, present major health risks in industrialized countries. AMP-activated protein kinase (AMPK) has become the focus of a great deal of attention as a novel therapeutic target for the treatment of metabolic syndromes. In this study, we evaluated whether dietary aloe could reduce obesity-induced inflammation and adipogenesis. METHODS: Male C57BL/6 obese mice fed a high-fat diet for 54 days received a supplement of aloe formula (PAG, ALS, Aloe QDM, and Aloe QDM complex) or pioglitazone (PGZ) and were compared with unsupplemented controls (high-fat diet; HFD) or mice fed a regular diet (RD). RT-PCR and western blot analysis were used to quantify the expression of obesity-induced inflammation. RESULTS: Aloe QDM complex down-regulated fat size through suppressed expression of scavenger receptors on adipose tissue macrophages (ATMs) compared with HFD. Both white adipose tissue (WATs) and muscle exhibited increased AMPK activation through aloe supplementation, and in particular, the Aloe QDM complex. Obesity-induced inflammatory cytokines (IL-1ß and -6) and HIF1α mRNA and protein were decreased markedly, as was macrophage infiltration by the Aloe QDM complex. Further, the Aloe QDM complex decreased the translocation of NF-κB p65 from the cytosol in the WAT. CONCLUSION: Dietary aloe formula reduced obesity-induced inflammatory responses by activation of AMPK in muscle and suppression of proinflammatory cytokines in the WAT. Additionally, the expression of scavenger receptors in the ATM and activation of AMPK in WAT led to reduction in the percent of body fat. Thus, we suggest that the effect of the Aloe QDM complex in the WAT and muscle are related to activation of AMPK and its use as a nutritional intervention against T2D and obesity-related inflammation.

Dietary Aloe Improves Insulin Sensitivity via the Suppression of Obesity-induced Inflammation in Obese Mice.

BACKGROUND: Insulin resistance is an integral feature of metabolic syndromes, including obesity, hyperglycemia, and hyperlipidemia. In this study, we evaluated whether the aloe component could reduce obesity-induced inflammation and the occurrence of metabolic disorders such as blood glucose and insulin resistance. METHODS: Male C57BL/6 obese mice fed a high-fat diet for 54 days received a supplement of aloe formula (PAG, ALS, Aloe QDM, and Aloe QDM complex) or pioglitazone (PGZ) and were compared with unsupplemented controls (high-fat diet; HFD) or mice fed a regular diet (RD). RT-PCR and western blot analysis were used to quantify the expression of obesity-induced inflammation. RESULTS: Aloe QDM lowered fasting blood glucose and plasma insulin compared with HFD. Obesity-induced inflammatory cytokine (IL-1ß, -6, -12, TNF-α) and chemokine (CX3CL1, CCL5) mRNA and protein were decreased markedly, as was macrophage infiltration and hepatic triglycerides by Aloe QDM. At the same time, Aloe QDM decreased the mRNA and protein of PPARγ/LXRα and 11ß-HSD1 both in the liver and WAT. CONCLUSION: Dietary aloe formula reduces obesity-induced glucose tolerance not only by suppressing inflammatory responses but also by inducing anti-inflammatory cytokines in the WAT and liver, both of which are important peripheral tissues affecting insulin resistance. The effect of Aloe QDM complex in the WAT and liver are related to its dual action on PPARγ and 11ß-HSD1 expression and its use as a nutritional intervention against T2D and obesity-related inflammation is suggested.

Neuroprotective effects of Eucommia ulmoides Oliv. Bark on amyloid beta(25-35)-induced learning and memory impairments in mice.

In the present study, we examined whether aqueous extract of Eucommia ulmoides Oliv. Bark (EUE) with graded doses exerted its neuroprotective effects on amyloid beta(25-35) (Aß(25-35))-induced learning and memory impairments in mice. Mice received a single intracerebroventricular (i.c.v.) injection of Aß(25-35) 6 nmol as the critical factor in Alzheimer's disease (AD), cognition was evaluated using Y-maze, passive avoidance, and Morris water maze tests. EUE significantly improved the Aß(25-35)-induced memory deficit in the Y-maze test. Also, EUE increased step-through latency time with Aß(25-35)-induced learning and memory deficits in the passive avoidance test. In addition, EUE decreased the escape latencies with Aß(25-35)-induced cognitive impairments in the Morris water maze test. In the probe trial session, EUE increased time spent in the target quadrant. In the in vitro study, EUE was found to inhibit acetylcholinesterase (AChE) activity in a dose-dependent manner (IC50 value; 172 µg/ml). Ex vivo study, EUE significantly inhibited AChE activity in the hippocampus and frontal cortex. These results demonstrate that EUE possesses potent neuroprotective effects and that its beneficial effects are mediated, in part, by AChE inhibition, and therefore, might be a potential candidate in neurodegenerative diseases such as AD.

Neuroprotective effects of chlorogenic acid on scopolamine-induced amnesia via anti-acetylcholinesterase and anti-oxidative activities in mice.

Chlorogenic acid is a major polyphenolic component of many plants and beverages, and is particularly abundant in coffee. We evaluated the neuroprotective effects of chlorogenic acid on learning and memory impairment induced by scopolamine (0.5 mg/kg, i.p.), a muscarinic antagonist, using the Y-maze, passive avoidance, and Morris water maze tests. The chlorogenic acid significantly improved the impairment of short-term or working memory induced by scopolamine in the Y-maze test, and significantly reversed cognitive impairments in mice as measured by the passive avoidance test. In addition, chlorogenic acid decreased escape latencies in the Morris water maze test. In a probe trial session, chlorogenic acid increased the latency time in the target quadrant in a dose-dependent manner. Ex vivo, chlorogenic acid inhibited acetylcholinesterase activity in the hippocampus and frontal cortex. Chlorogenic acid also decreased malondialdehyde levels in the hippocampus and frontal cortex. In vitro, chlorogenic acid was found to inhibit acetylcholinesterase activity (IC50=98.17 µg/ml) and free radical scavenging activity (IC50=3.09 µg/ml) in a dose-dependent manner. These results indicate that chlorogenic acid may exert anti-amnesic activity via inhibition of acetylcholinesterase and malondialdehyde in the hippocampus and frontal cortex.

Angiogenic activity of beta-sitosterol in the ischaemia/reperfusion-damaged brain of Mongolian gerbil.

Aloe vera continues to be used for wound healing as a folk medicine. We previously reported that A. vera gel has angiogenic activity. In this study, we report upon the isolation of an angiogenic component beta-sitosterol from A. vera and examination of its effect upon damaged blood vessels of the Mongolian gerbil. In a chick embryo chorioallantoic membrane assay, beta-sitosterol was found to have an angiogenic effect. It enhanced new vessel formation in gerbil brains damaged by ischaemia/reperfusion, especially in the cingulated cortex and septal regions, in a dose-dependent fashion (up to 500 microg/kg, p < 0.05, n = 34 - 40). beta-Sitosterol also enhanced the expressions of proteins related to angiogenesis, namely von Willebrand factors, vascular endothelial growth factor (VEGF), VEGF receptor Flk-1, and blood vessel matrix laminin (p < 0.05, n = 6). In addition, the intraperitoneal administration of beta-sitosterol at 500 microg/kg/day for a period of 19 days significantly improved the motion recovery of ischaemia/reperfusion-damaged gerbils as assessed by rota-rod testing (p < 0.001, n = 10). Our results suggest that beta-sitosterol has therapeutic angiogenic effects on damaged blood vessels.