Role of BDNF in the taste system

Neurotrophins are a family of proteins that regulate neural survival, development, function and plasticity in the central and the peripheral nervous system. There are four neurotrophins： NGF, BDNF, NT-3 and NT-4. Among them, BDNF is mostly studied in the taste system due to its high expression. Recent studies have shown BDNF play an important role in the developmental and mature taste system, by regulating survival of taste cells and geniculate ganglion neurons, and maintaining and guiding taste nerve innervations. These studies imply BDNF has great potentialities for therapeutic usage to enhance sensory regeneration following nerve injury, with aging, and in some neurodegenerative diseases.     

Ectopic Osteogenesis and Scaffold Biodegradation of Nano-Hydroxyapatite-Chitosan in a Rat Model

The bone-formation and scaffold-biodegradation processes have not been fully characterized. This study aimed to determine the osteogenic ability of nHA-CS osteo-induced bone marrow mesenchymal stem cell (BMSC) composites and to explore the relationship between bone formation and scaffold biodegradation. The nHA-CS osteo-induced BMSC composites (nHA-CS+cells group) and the nHA-CS scaffolds (nHA-CS group) were implanted into the femoral spatium intermusculare of SD rats. At 2, 4, 6, 8, and 12 weeks post-implantation, the rat femurs were scanned using computerized tomography (CT), and the CT values of the implants were measured and comparatively analyzed. The implants were then harvested and subjected to hematoxylin and eosin (HE) and Masson''s trichrome staining, and the percentages of bone area, scaffold area and collagen area were compared between the two groups. The CT values of the implants were higher in the nHA-CS+cells group than the nHA-CS group at the same time points (P < 0.05). Histological analysis revealed that de novo bone and collagen formation in the pores of the scaffolds gradually increased from 2 weeks post-implantation in both groups and that the scaffold gradually degraded as bone formation proceeded. However, more de novo bone and collagen formation and scaffold degradation occurred in the nHA-CS+cells group than in the nHA-CS group at the same time points (P < 0.05). In conclusion, nHA-CS osteo-induced BMSC composites are promising bone tissue engineering substitutes, and osteo-induced BMSCs can significantly enhance the osteogenic ability and play an active role in the degradation of nHA-CS scaffolds on par with bone formation.     

Blockade of TREM-1 prevents vitreoretinal neovascularization in mice with oxygen-induced retinopathy

In pathological retinal neovascularization (RNV) disorders, the retina is infiltrated by activated leukocytes and macrophages. Triggering receptor expressed on myeloid cells 1 (TREM-1), an inflammation amplifier, activates monocytes and macrophages and plays an important role in cancer, autoimmune and other inflammation-associated disorders. Hypoxia-inducible TREM-1 is involved in cancer angiogenesis but its role in RNV remains unclear. Here, to close this gap, we evaluated the role of TREM-1 in RNV using a mouse model of oxygen-induced retinopathy (OIR). We found that hypoxia induced overexpression of TREM-1 in the OIR retinas compared to that of the room air group. TREM-1 was observed specifically in areas of pathological RNV, largely colocalizing with macrophage colony-stimulating factor (M-CSF) and CD45- and Iba-1-positive cells. TREM-1 blockade using systemically administered first-in-class ligand-independent TREM-1 inhibitory peptides rationally designed using the signaling chain homooligomerization (SCHOOL) strategy significantly (up to 95%) reduced vitreoretinal neovascularization. The peptides were well-tolerated when formulated into lipopeptide complexes for peptide half-life extension and targeted delivery. TREM-1 inhibition substantially downregulated retinal protein levels of TREM-1 and M-CSF suggesting that TREM-1-dependent suppression of pathological angiogenesis involves M-CSF. Targeting TREM-1 using TREM-1-specific SCHOOL peptide inhibitors represents a novel strategy to treat retinal diseases that are accompanied by neovascularization including retinopathy of prematurity.     

Cryptosporidiosis: Pathogenesis and immunology

Cryptosporidium parvum is an increasingly recognized agent of intestinal infection in normal and immunocompromised humans, and in many other animals. The intraepithelial cell infection results in villous atrophy, mild submucosal inflammation, reduction of brush-border enzymes and a characteristic persistent watery diarrhea. The infection is self-limiting in immunocompetent hosts, probably because of specific acquired immunity; specific serum and secretory antibody responses develop that may be required for clearance and protection against reinfection. Passive milk antibody, especially i f in high titers, may be partially protective but severe, persistent infection in athymic rodents and humans with AIDS demonstrate that T cells are essential for controlling the infection. Specific anti-bodies and lymphocyte extracts have been tested in cases of cryptosporidiosis but the interpretation of the results remains controversial. Here, Shu-Xian Zu, Guo-Dong Fang, Ronald Foyer and Richard Guerrant emphasize that effective treatment and prevention remain dependent on advances in our understanding of the host cell-parasite relationship.     

Stress‐Relieved Nanowires by Silicon Substitution for High‐Capacity and Stable Lithium Storage

Silicon is promising as a high energy anode for next‐generation lithium‐ion batteries. However, severe capacity fading upon cycling associated with huge volume change is still an obstacle for silicon toward practical applications. Herein, the authors report that Si‐substituted Zn₂(GeO₄)_0.8(SiO₄)_0.2 nanowires can effectively suppress volume expansion effect, exhibiting high specific capacity (1274 mA h g^?1 at 0.2 A g^?1 after 700 cycles) and ultralong cycling stability (2000 cycles at 5 A g^?1 with a capacity decay rate of 0.008% per cycle), which represents outstanding comprehensive performance. The superior performance is ascribed to the substitution of Si atom that imparts to the nanowires not only high reactivity and reversibility, but also the unique stress‐relieved property upon lithiation which is further confirmed by detailed density‐functional theory computation. This work provides a new guideline for designing high‐performance Si‐based materials toward practical energy storage applications.     

Thermal inactivation of immobilized penicillin acylase in the presence of substrate and products

Inactivation of immobilized penicillin acylase has been studied in the presence of substrate (penicillin G) and products (phenylacetic acid and 6-aminopenicillanic acid), under the hypothesis that substances which interact with the enzyme molecule during catalysis will have an effect on enzyme stability. The kinetics of immobilized penicillin acylase inactivation was a multistage process, decay constants being evaluated for the free-enzyme and enzyme complexes, from whose values modulation factors were determined for the effectors in each enzyme complex at each stage. 6-Aminopenicillanic acid and penicillin G stabilized the enzyme in the first stage of decay. Modulation factors in that stage were 0.96 for penicillin G and 0.98 for 6-aminopenicillanic acid. Phenylacetic acid increased the rate of inactivation in both stages, modulating factors being -2.31 and -2.23, respectively. Modulation factors influence enzyme performance in a reactor and are useful parameters for a proper evaluation. (c) 1996 John Wiley & Sons, Inc.     

中国音天牛属二新种记述（鞘翅目：天牛总科）

本文记述了中国音天牛属２新种－－细点音天牛和齿胫音天牛,模式标本保存于西南农业大学昆虫标本馆。     

Resveratrol suppresses the epithelial-to-mesenchymal transition in PC-3 cells by down-regulating the PI3K/AKT signaling pathway

Resveratrol possesses a wide spectrum of pharmacological properties and has been an ideal alternative drug for the treatment of different cancers, including prostate cancer. However, the mechanisms by which resveratrol inhibits the growth of prostate cancer are still not fully elucidated. To understand the effect of resveratrol on the apoptosis and the epithelial-to-mesenchymal transition (EMT) of prostate cancer as well as its related mechanism, we investigated the potential use of resveratrol in PC-3 prostate cancer cells in vitro using real-time PCR, fluorescence-activated cell sorting, Western blotting, etc. Resveratrol suppresses the PC-3 prostate cancer cell growth and induces apoptosis. Resveratrol also influences the expression of EMT-related proteins (increased E-cadherin and decreased Vimentin expression). Finally, resveratrol also suppressed Akt phosphorylation in PC-3 cells. This study indicates that resveratrol may be a potential anti-cancer treatment for prostate cancer; moreover, it provides new evidence that resveratrol suppresses prostate cancer growth and metastasis.