Jordanmelchiorsen8751

Fish silage (FS) has been confirmed as a high-quality feed ingredient because of its balanced nutrition, low cost, and environmental friendliness. In the present study, we evaluated the performance of replacing fishmeal by FS in the diet of white shrimp, Litopenaeus vannamei. Five isonitrogenous (410 g kg-1) and isolipidic (75 g kg-1) diets were formulated with replacement of fishmeal by 0% (FM), 25% (FS25%), 50% (FS50%), 75% (FS75%), and 100% (FS100%) FS. After an 8-week trial, shrimps fed low FS diets (FM and FS25%) had significantly higher final weight (FW), weight gain (WG), and specific growth ratio (SGR) (P 0.05). Compared to high FS groups (FS75% and FS100%), low FS replacement levels (0 and 25%) had enhanced trypsin activity. And trypsin transcriptional level presented a similar trend with trypsin activity. In terms of intestinal histopathology, no obvious histological damage was observed in the intestine of all groups. tor and s6k of low replacement level groups (FM and FS25%) were significantly upregulated (P less then 0.05), which indicated activation of mammalian target of rapamycin (mTOR) signaling pathway in low FS groups at transcriptional level. The enhanced performances of growth and mTOR signaling pathway in low FS groups (FM and FS25%) provided us some insights into the regulation mechanism of nutrient signal on growth. Based on the above, dietary FS could influence the growth of shrimp by regulating mTOR at the transcriptional level, and FS is a potential substitute of fishmeal in shrimp feed.Depression is considered a widespread neuropsychiatric disease associated with neuronal injury within specific brain regions. Etomoxir in vitro Fluoxetine, a selective serotonin reuptake inhibitor, has been widely used in depressed patients. Recently, fluoxetine has demonstrated neuroprotective effects apart from the effect on serotonin. However, the underlying mechanism involved in this neuroprotection remains unclear, in particular, whether fluoxetine exerts antidepressant effects via protecting against neuronal injury. Here, we found that treatment with fluoxetine (10 mg/kg, i.p.) for 2 weeks ameliorated depression-like behaviors in a chronic unpredictable mild stress (CUMS)-induced rat model of depression and was accompanied with an alleviation of glia activation and inhibition of interleukin-1β (IL-1β), interferon gamma (IFN-γ), and tumor necrosis factor-α (TNF-α) expression in the hippocampal dentate gyrus (DG) region. Meanwhile, CUMS rats treated with fluoxetine showed reductions in neuronal apoptosis and a downregulation of the apoptotic protein Bax, cleaved caspase 3, and caspase 9 levels. These effects appear to involve a downregulation of p38 mitogen-activated protein kinase (MAPK) signaling within the DG hippocampus as the specific inhibitor of p38 MAPK, SB203580, significantly suppressed apoptosis, as well as ameliorated depressive behaviors resulting from CUMS exposure. Moreover, fluoxetine could rescue neuronal deterioration and depression-like phenotypes caused by overexpression of p38 in DG. This finding extends our knowledge on the antidepressant-like effects of fluoxetine, which appear to at least partially profit from neuroprotection against inflammation and neuronal apoptosis via downregulation of the p38 MAPK pathway. The neuroprotective mechanisms of fluoxetine may provide some novel therapeutic avenues for stress-related neurological diseases.Screening and surveillance for gastrointestinal (GI) cancers by endoscope guided biopsy is invasive, time consuming, and has the potential for sampling error. Tissue endogenous fluorescence spectra contain biochemical and physiological information, which may enable real-time, objective diagnosis. We first briefly reviewed optical biopsy modalities for GI cancer diagnosis with a focus on fluorescence-based techniques. In an ex vivo pilot clinical study, we measured fluorescence spectra and lifetime on fresh biopsy specimens obtained during routine upper GI screening procedures. Our results demonstrated the feasibility of rapid acquisition of time-resolved fluorescence (TRF) spectra from fresh GI mucosal specimens. We also identified spectroscopic signatures that can differentiate between normal mucosal samples obtained from the esophagus, stomach, and duodenum.There are three members of the endogenous gas transmitter family. The first two are nitric oxide and carbon monoxide, and the third newly added member is hydrogen sulfide (H2S). They all have similar functions relaxing blood vessels, smoothing muscles, and getting involved in the regulation of neuronal excitation, learning, and memory. The cystathionine β-synthase (CBS), 3-mercaptopyruvate sulfur transferase acts together with cysteine aminotransferase (3-MST/CAT), cystathionine γ-lyase (CSE), and 3-mercaptopyruvate sulfur transferase with D-amino acid oxidase (3-MST/DAO) pathways are involved in the enzymatic production of H2S. More and more researches focus on the role of H2S in the central nervous system (CNS), and H2S plays a significant function in neuroprotection processes, regulating the function of the nervous system as a signaling molecule in the CNS. Endoplasmic reticulum stress (ERS) and protein misfolding in its mechanism are related to neurodegenerative diseases. H2S exhibits a wide variety of cytoprotective and physiological functions in the CNS degenerative diseases by regulating ERS. This review summarized on the neuroprotective effect of H2S for ERS played in several CNS diseases including Alzheimer's disease, Parkinson's disease, and depression disorder, and discussed the corresponding possible signaling pathways or mechanisms as well.Postmenopausal osteoporosis is a worldwide disease characterized by reduced bone mineral density and increased fracture risk. Inflammatory bone loss due to excessive osteoclast bone resorption is significant in the pathogenesis and development of osteoporosis. Punicalagin (PUN) is a pomegranate fruit derivative and has potential anti-inflammatory effects. However, the effect of PUN on osteoporotic bone loss has yet to be clarified. In this study, we investigated the effect of PUN on RANKL-induced osteoclast formation and bone resorption in vitro, as well as its potential therapeutic effect on ovariectomized-induced bone loss in vivo. PUN was demonstrated to suppress osteoclast formation and bone resorptive function dose-dependently, while osteoclast-specific genes were also downregulated by PUN. In vivo micro-CT and histopathological staining showed that the OVX procedure led to significant bone loss characterized by decreased bone parameters and increased osteoclast numbers, while PUN treatment dramatically prevented these changes.