SARM1 participates in axonal degeneration and mitochondrial dysfunction in prion disease.

Prion disease represents a group of fatal neurogenerative diseases in humans and animals that are associated with energy loss, axonal degeneration, and mitochondrial dysfunction. Axonal degeneration is an early hallmark of neurodegeneration and is triggered by SARM1. We found that depletion or dysfunctional mutation of SARM1 protected against NAD loss, axonal degeneration, and mitochondrial functional disorder induced by the neurotoxic peptide PrP.

Association of Gene rs4245739 Polymorphism with the Risk and Clinical Characteristics of Colorectal Cancer in a Chinese Han Population.

Background: Studies show that MDM4 may play a pivotal role in colorectal cancer (CRC). Recently, a host of studies suggest that MDM4 gene rs4245739 polymorphism may modify the risk of different cancers.

Methods: In this study, we were interested whether MDM4 gene rs4245739 polymorphism correlated with the risk and clinical characteristics of CRC.

Optomechanical transistor: controlling the optical bistability in a photonic molecule.

We theoretically investigate the optical bistability in a composite photonic molecule cavity optomechanical system consisting of two whispering gallery mode microcavities, where one of the optical cavities is optomechanical with a high quality factor, and the other optical cavity is an auxiliary cavity with high cavity dissipation. By controlling the coupling strength between the two cavities determined by their distance, the decay rate ratio of the two cavities, and the pump power , the optical bistability can be controlled. Further, the transmission spectrum of the signal field can be efficiently attenuated or amplified, depending on the power of a second "gating" (pump) field , and other parameters.

PRAS40 alleviates neurotoxic prion peptide-induced apoptosis via mTOR-AKT signaling.

Aims: The proline-rich Akt substrate of 40-kDa (PRAS40) protein is a direct inhibitor of mTORC1 and an interactive linker between the Akt and mTOR pathways. The mammalian target of rapamycin (mTOR) is considered to be a central regulator of cell growth and metabolism. Several investigations have demonstrated that abnormal mTOR activity may contribute to the pathogenesis of several neurodegenerative disorders and lead to cognitive deficits.

Overexpression of BAT3 alleviates prion protein fragment PrP106-126-induced neuronal apoptosis.

Backgrounds And Aims: Prion diseases are a group of infectious neurodegenerative diseases characterized by neuronal death and degeneration. Human leukocyte antigen-B-associated transcript 3 (BAT3) is an important apoptosis regulator. We therefore investigated the interactions between BAT3 and prion protein and the potential role of BAT3 in PrP106-126-induced apoptosis.

PrP106-126 and Aβ 1-42 peptides induce BV-2 microglia chemotaxis and proliferation.

Transmissible spongiform encephalopathies (TSEs) and Alzheimer's disease (AD) belong to a growing family of neurodegenerative disorders that is characterized by the generation of toxic protein aggregates in affected brains (PrP(Sc) and Aβ in TSEs and AD, respectively). To better understand how protein aggregates can modulate microglial processes in these diseases, we treated BV-2 microglia with PrP(106-126) or Aβ1-42 peptides individually at three different concentrations (25-100 μM PrP(106-12) and 2.5-10 μM Aβ1-42) or with a mixture of PrP(106-126) and Aβ1-42 peptides at specified concentrations for 6-24 h.

Using protein misfolding cyclic amplification generates a highly neurotoxic PrP dimer causing neurodegeneration.

Under the "protein-only" hypothesis, prion-based diseases are proposed to result from an infectious agent that is an abnormal isoform of the prion protein in the scrapie form, PrP(Sc). However, since PrP(Sc) is highly insoluble and easily aggregates in vivo, this view appears to be overly simplistic, implying that the presence of PrP(Sc) may indirectly cause neurodegeneration through its intermediate soluble form. We generated a neurotoxic PrP dimer with partial pathogenic characteristics of PrP(Sc) by protein misfolding cyclic amplification in the presence of 1-palmitoyl-2-oleoylphosphatidylglycerol consisting of recombinant hamster PrP (23-231).

Neurotoxic effect of the complex of the ovine prion protein (OvPrP(C)) and RNA on the cultured rat cortical neurons.

Prion diseases are conformational diseases, many factors are involved in altering the conformation of prion, such as RNA, DNA, pH, and copper etc. However the neurotoxic mechanism of prion diseases is not clear yet. The aim of this study is to investigate the effect of the nucleoprotein complex of RNA and recombinant ovine prion protein (OvPrP(C)) on the cultured rat cortical neurons in vitro.

PrP 106-126 altered PrP mRNA gene expression in mouse microglia BV-2 cells.

Prion diseases are infectious and fatal neurodegenerative diseases. The pathogenic agent is an abnormal prion protein aggregate. Microglial activation in the centre nervous system is a characteristic feature of prion disease.

Polymorphism of prion protein gene in sheep of Inner Mongolian, China.

Susceptibility to natural scrapie in sheep is associated with polymorphisms at codons 136, 154 and 171 of the prion protein (PrP) gene. To assess the risk of scrapie in sheep raised in China, DNA from 30 sheep of two breeds was isolated, amplified and sequenced for the PrP gene. The ovine PrP gene was found to be highly homogenous.

Variable levels of 37-kDa/67-kDa laminin receptor (RPSA) mRNA in ovine tissues: potential contribution to the regulatory processes of PrPSc propagation?

The 37-kDa laminin receptor precursor/67-kDa laminin receptor (LRP/LR, also known as ribosomal protein SA, RPSA) has been reported to be involved in cancer development and prion internalization. Previous studies have shown that the LRP/LR is expressed in a wide variety of tissues. In particular, expression of LRP/LR mRNA may be closely related to the degree of PrP(Sc) propagation.

[Study on testing methods of Al content of polyimide hybrid films with Al2O3].

The inorganic particles hybrid polyimide films are newly emerging advanced materials with excellent corona-resistant and have been widely used in frequency control motor. The Al2O3/PI hybrid films with different Al2O3 contents were prepared by superfine aluminum power treated by coupling agent and polyamide acid (PAA). Qualitative analysis and quantitative analysis on the inorganic content to it were conducted using Fourier Transform Infrared Spectroscope (FTIR), X-ray photoelectron spectroscopy (XPS), Inductively coupled plasma spectrometry (ICP), Gravimetric method, Thermogravimetric Analysis (TG/air atmosphere).

[Characterization of inorganic nano-alundum composite film of polyimide].

The key to the study on the regularity about the mechanical, thermology and electricities property of the inorganic nano-mingled organic composition thin film is to understand the incorporated quantity, the particle size and distribution of nano-inorganic matter in the membrane quickly and accurately. In the present paper, the chemical structure, surface morphology and the actual content of nano-Al2O3 of the nano Al2O3-composite film of polyimide were characterized by X-ray atomic fluorescent spectroscopy (XRF), Fourier transform infrared spectroscopy (FTIR), scanning electron microscopy (SEM) and atomic forced microscope (AFM). The results are that the organic phase of PI and the inorganic phase of Al2O3 formed a complex composite hybrid system of bond-to-bond pattern, the nano-Al2O3 particles in the film of PI are dispersed homogeneously, and the diameter of the particle is smaller than 50 nm; the weight content of Al2O3 is 7.

Copper(II) inhibits in vitro conformational conversion of ovine prion protein triggered by low pH.

To gain insight into the conformational conversion of ovine prion protein (OvPrP(C)) at different pH values and/or in the presence of CuCl(2), the secondary structure of OvPrP(C) was analysed by circular dichroism (CD) spectroscopy. Copper treatment of OvPrP(C) under moderately acidic conditions (pH approximately 5.0-6.

The quantification of prion gene expression in sheep using real-time RT-PCR.

Determination of the transcription level of cellular prion protein (PrP(C)) is essential for understanding its poorly explained role in organisms. Scrapie in sheep is the prototype of all prion diseases. However, the expression of prion protein (PrP) mRNA in sheep has not been quantified in great detail.

Development of a rapid real-time PCR assay for detection and quantification of four familiar species of Chlamydiaceae.

Chlamydiae are one of the causative agents of various diseases in animals and human beings, which include abortion, pneumonia, gastroenteritis, encephalomyelitis, conjunctivitis, arthritis and sexually transmitted diseases. Much work has been carried out to attempt to develop an efficient pathogen detection strategy. Here, we presented a Chlamydiaceae-specific 23S rRNA-based real-time PCR assay for simultaneous detection and quantification of four members of Chlamydiaceae family, C.

Altered expression of the prion gene in rat astrocyte and neuron cultures treated with prion peptide 106-126.

Neuronal degeneration and astrogliosis are hallmarks of prion disease. Synthetic prion protein (PrP) peptide 106-126 (PrP106-126) can induce death of neurons and proliferation of astrocytes in vitro and this neurotoxic effect depends on the expression of cellular PrP (PrPC) and is hence believed to be PrP(C) -mediated. To further elucidate the involvement of PrPC in PrP106-126-induced neurotoxicity, we determined the expression of PrP mRNA in primary culture of rat cortical neuron cells, cerebellar granule cells, and astrocytes following treatment with 50 microM of PrP106-126 scrambled PrP106-126 by quantitative real-time RT-PCR.

Quantification of prion gene expression in brain and peripheral organs of golden hamster by real-time RT-PCR.

Determination of tissue-specific expression of cellular prion protein (PrPc) is essential for understanding its poorly explained role in organisms. Herein we report on quantification of PrP mRNA in golden hamsters, a popular experimental model for studying mechanisms of transmissible spongiform encephalopathies (TSE), by real-time RT-PCR. Total RNA was isolated from four different regions of the brain and six peripheral organs of eight golden hamsters.

[A study on pathological changes of brain after high +Gx exposure in rhesus monkey].

Objective: To study the pathological morphological changes of cerebral cortex and hippocampi in rhesus monkey caused by +Gx exposure, and to explore the relation between +Gx level and pathological changes.

Method: Healthy rhesus monkeys were randomly divided into one control group and three experimental groups (+15 Gx, +18 Gx, +21 Gx). Monkeys in each group were exposed to the corresponding level of +Gx, after that, the required tissue was qualitatively studied on the basis of pathological morphology.

Comparative analysis of the prion protein open reading frame nucleotide sequences in peacock and parakeet.

The open reading frame of peacock and parakeet prion protein (PrP) genes was cloned and sequenced. The peacock and parakeet PrP genes consisted of 833 and 866 nucleotides encoding 266 and 277 amino acids, respectively (GenBank Accession numbers AY365065 and AY365066). Sequence analysis showed that the peacock and parakeet PrP genes had 93.

[Effect of extremely low frequency magnetic field on the focal brain injury in rats].

Objective: To examine the effect of extremely low frequency magnetic field (ELMF) on the brain trauma in rats.

Method: Using the focal left-brain cortex contusion model, rats were divided into two groups, ELMF group (3 d and 8 d) and control group (3 d and 8 d), ELMF stimulations were given after the brain trauma provided by a coil (phi 10 cm) which was driven by 15 Hz sinusoidal signals so that ELMF strength of 18 mT at the midpoint was obtained. The morphologic changes were observed in these groups.

[Effects of three different immunosuppressive drugs on SD rat islet cell viability].

Objective: To investigate the effect of immunosuppressive drugs on the viability of pancreatic islet cells cultured in vitro, and to explore their effects on the outcome of islet transplantation.

Methods: Pancreatic islet cells from SD rats were cultured in vitro, and the changes in their viability determined by MTT assay after incubation with immunosuppressive drugs at different concentrations.

Results: The viability of the islet cells was reduced after exposure to rapamycin at higher concentrations (>or= 1 ng/ml), but not at lower concentrations.