The effect of Hericium erinaceum on the prevention of chemically induced experimental colitis in rats.

BACKGROUND/AIMS: The aim of this study is to investigate the effects of the Hericium erinaceum on an experimental colitis model. METHODS: Twenty-four Wistar albino were included in this study. Rats were divided into three groups. Group 1 (n = 8) was sham group. Group 2 is the group of chemically induced by intrarectal administration of trinitrobenzene sulfonic acid (TNBS) resulting in colitis. Group 3 (n = 8) is the group that was treated 7 days before and 7 days after with H. erinaceum resulting in colitis. The activity of colitis was evaluated macroscopically and microscopically in rats. In other words, nitric oxide (NO) levels, malondialdehyde (MDA), interleukin 6 (IL-6), nuclear factor-kappa B (NF-κB) and, tumor necrosis factor-α (TNF-α) in addition to the myeloperoxidasem (MPO) activities was determined. RESULTS: The rate of TNBS-induced colitis caused to increase the level of MDA activities meaningfully in the colitis group than the control group. The results indicated that MDA (p = 0.001), NO (p = 0.001), IL-6 (p = 0.001), MPO (p = 0.878), TNF-α (p = 0.001), and NF-κB levels of treatment group decreased in the blood and colon tissues because of the H. erinaceum treatment when compared to the colitis group. H. erinaceum treatment was related to the declining of MDA, NF-κB, NO, IL-6, and TNF-α levels. CONCLUSION: H. erinaceum had a positive effect on the colitis by reducing oxidative damage in blood and tissue.

A Toll-receptor map underlies structural brain plasticity.

Experience alters brain structure, but the underlying mechanism remained unknown. Structural plasticity reveals that brain function is encoded in generative changes to cells that compete with destructive processes driving neurodegeneration. At an adult critical period, experience increases fiber number and brain size in Drosophila. Here, we asked if Toll receptors are involved. Tolls demarcate a map of brain anatomical domains. Focusing on Toll-2, loss of function caused apoptosis, neurite atrophy and impaired behaviour. Toll-2 gain of function and neuronal activity at the critical period increased cell number. Toll-2 induced cycling of adult progenitor cells via a novel pathway, that antagonized MyD88-dependent quiescence, and engaged Weckle and Yorkie downstream. Constant knock-down of multiple Tolls synergistically reduced brain size. Conditional over-expression of Toll-2 and wek at the adult critical period increased brain size. Through their topographic distribution, Toll receptors regulate neuronal number and brain size, modulating structural plasticity in the adult brain.

Everything that you experience leaves its mark on your brain. When you learn something new, the neurons involved in the learning episode grow new projections and form new connections. Your brain may even produce new neurons. Physical exercise can induce similar changes, as can taking antidepressants. By contrast, stress, depression, ageing and disease can have the opposite effect, triggering neurons to break down and even die. The ability of the brain to change in response to experience is known as structural plasticity, and it is in a tug-of-war with processes that drive neurodegeneration. Structural plasticity occurs in other species too: for example, it was described in the fruit fly more than a quarter of a century ago. Yet, the molecular mechanisms underlying structural plasticity remain unclear. Li et al. now show that, in fruit flies, this plasticity involves Toll receptors, a family of proteins present in the brain but best known for their role in the immune system. Fruit flies have nine different Toll receptors, the most abundant being Toll-2. When activated, these proteins can trigger a series of molecular events in a cell. Li et al. show that increasing the amount of Toll-2 in the fly brain makes the brain produce new neurons. Activating neurons in a brain region has the same effect, and this increase in neuron number also depends on Toll-2. By contrast, reducing the amount of Toll-2 causes neurons to lose their projections and connections, and to die, and impairs fly behaviour. Li et al. also show that each Toll receptor has a unique distribution across the fly brain. Different types of experiences activate different brain regions, and therefore different Toll receptors. These go on to trigger a common molecular cascade, but they modulate it such as to result in distinct outcomes. By working together in different combinations, Toll receptors can promote either the death or survival of neurons, and they can also drive specific brain cells to remain dormant or to produce new neurons. By revealing how experience changes the brain, Li et al. provide clues to the way neurons work and form; these findings may also help to find new treatments for disorders that change brain structure, such as certain psychiatric conditions. Toll-like receptors in humans could thus represent a promising new target for drug discovery.

Effect of Resected Gastric Fundus Fat on Ghrelin Tissue Levels: A Prospective Study.

Introduction: Obesity is currently an important health problem that is rapidly increasing worldwide. In recent years, the number of obesity-related surgeries has increased. The most common type of obesity-related surgery is laparoscopic sleeve gastrectomy (LSG). The aim of this study was to compare the genetic expression of the hormone ghrelin in different parts of the stomach. Materials and Methods: Nineteen obese patients who underwent LSG were examined in this study. Fat tissue from two different parts of the stomach, the fundus and the upper part of the fundus, were analysed by enzyme-linked immunosorbent assay (ELISA). The ribonucleic acid (RNA) isolation, complementary DNA (cDNA) and real-time quantitative polymerase chain reaction (RQ-PCR) techniques were applied. Additionally, a human ghrelin ELISA kit was used to measure ghrelin in obese patients. The ghrelin levels of fat tissue from the fundus and upper part of the fundus were statistically compared. Results: In all 19 patients, the average ghrelin level in the fundus was greater than 30. The average ghrelin level of the fat pad, which is located in the upper part of the fundus, was greater than 30 for 4 patients; the average level was approximately 5 in the remaining patients. A statistically significant difference in the ghrelin level was found between the fundus and the fundus fat tissue. CONCLUSION: Collection of fundus fat tissue is not routinely performed during LSG. However, ghrelin hormone elevation in this tissue may require collection of fundus tissue during surgery.