Green Preparation of Lightweight, High-Strength Cellulose-Based Foam and Evaluation of Its Adsorption Properties.

In recent years, the application scope of most cellulose-based foams is limited due to their low adsorbability and poor recyclability. In this study, a green solvent is used to extract and dissolve cellulose, and the structural stability of the solid foam is enhanced by adding a secondary liquid via the capillary foam technology, and the strength of the solid foam is improved. In addition, the effects of the addition of different gelatin concentrations on the micro-morphology, crystal structure, mechanical properties, adsorption, and recyclability of the cellulose-based foam are investigated.

Clinical and genomic analysis of a large Chinese family with familial cortical myoclonic tremor with epilepsy and intronic repeat expansion.

Objective: Our goal was to perform detailed clinical and genomic analysis of a large multigenerational Chinese family with 21 individuals showing symptoms of Familial Cortical Myoclonic Tremor with Epilepsy (FCMTE) that we have followed for over 20 years.

Methods: Patients were subjected to clinical evaluation, routine EEG, and structural magnetic resonance imaging. Whole exome sequencing, repeat-primed PCR, long-range PCR, and PacBio sequencing were performed to characterize the disease-causing mutation in this family.

Intronic (TTTGA) insertion in SAMD12 also causes familial cortical myoclonic tremor with epilepsy.

Background: Intronic (TTTCA) insertions in the SAMD12, TNRC6A, and RAPGEF2 genes have been identified as causes of familial cortical myoclonic tremor with epilepsy.

Objective: To identify the cause of familial cortical myoclonic tremor with epilepsy pedigrees without (TTTCA) insertions in SAMD12, TNRC6A, and RAPGEF2.

Methods: Repeat-primed polymerase chain reaction, long-range polymerase chain reaction, and Sanger sequencing were performed to identify the existence of a novel (TTTGA) insertion.

Artery of Percheron Infarction as an Unusual Cause of Korsakoff's Syndrome.

The Korsakoff syndrome is defined as "an abnormal mental state in which memory and learning are affected out of all proportion to other cognitive functions in an otherwise alert and responsive patient." Confabulation refers to false or erroneous memories arising, not deliberately, in the context of a neurological amnesia and is often thought of as pathognomonic of the Korsakoff syndrome. Although the exact pathophysiology is unknown, various studies have identified brain lesions in the thalami, mammillary bodies, and frontal cortex.

Competitive binding between miR-122 and p68 onto hepatitis C viral RNA.

Background: Liver-specific microRNA (miR)-122 has been shown to be involved in regulating translation of hepatitis C viral (HCV) RNA. This study aimed to explore the molecular mechanism of miR-122 in regulating HCV RNA translation initiation.

Material/methods: In human liver hepatocellular carcinoma cell line HepG2, UV cross-link assay was performed on a large scale to identify RNA-binding proteins with gradient concentrations of miR-122.

Role of A20 in interferon-α-mediated functional restoration of myeloid dendritic cells in patients with chronic hepatitis C.

Hepatitis C virus (HCV) infection is a global health problem characterized by a high rate of chronic infection, which may in part be due to a defect in myeloid dendritic cells (mDCs). This defect appears to be remedied by treatment with interferon-α (IFN-α) -based antiviral therapies; however, the molecular mechanisms underlying mDC dysfunction in HCV infection and restoration by IFN-α treatment are unclear. The ubiquitin-editing protein A20 plays a crucial role in controlling the maturation, cytokine production and immunostimulatory function of mDCs.

FGF2 and FGFR1 signaling regulate functional recovery following cuprizone demyelination.

In demyelinating diseases, such as multiple sclerosis, remyelination offers the potential to recover function of viable denuded axons by restoring saltatory conduction and/or protecting from further damage. Mice with genetic reduction of fibroblast growth factor 2 (Fgf2) or Fgf receptor 1 (Fgfr1) exhibit dramatically improved remyelination following experimental demyelination with cuprizone. The current studies are the first to test neurobehavioral outcomes with these gene deletions that improved remyelination.

Primary results of chest wall reconstruction with polydioxanone mesh on animals.

Background: With the development of surgical techniques and biomedical material, increasing synthetic materials are applied to the chest wall reconstruction, such as autologous rib, muscle flap, bovine pericardium and sheet metal.

Aim: To detect the safety and efficiency of synthetic material Polydioxanone (PDO) in chest wall reconstruction.

Materials And Methods: Healthy adult mongrel dogs operated with PDO, and then some clinical data were collected.

Fibroblast growth factor 1 (FGFR1) modulation regulates repair capacity of oligodendrocyte progenitor cells following chronic demyelination.

The adult mammalian brain contains multiple populations of endogenous progenitor cell types. However, following CNS trauma or disease, the regenerative capacity of progenitor populations is typically insufficient and may actually be limited by non-permissive or inhibitory signals in the damaged parenchyma. Remyelination is the most effective and simplest regenerative process in the adult CNS yet is still insufficient following repeated or chronic demyelination.

Musashi1 RNA-binding protein regulates oligodendrocyte lineage cell differentiation and survival.

Expression of Musashi1 (Msi1), an evolutionarily conserved RNA-binding protein, in neural stem cells of the subventricular zone in the postnatal and adult CNS indicates a potential role in the generation of oligodendrocytes. We now show Msi1 expression in a subset of oligodendrocyte progenitor (OP) cells in white matter areas temporally and spatially associated with oligodendrogenesis in the postnatal CNS. Msi1 function was evaluated by infection of OP cells with retroviral transduction of Msi1 or knockdown of endogenous Msi1.

Interaction of fibroblast growth factor 2 (FGF2) and notch signaling components in inhibition of oligodendrocyte progenitor (OP) differentiation.

Oligodendrocyte progenitor (OP) cell differentiation is a critical process of developmental myelination, tumor formation, and remyelination in the CNS. Activation of the fibroblast growth factor 2 (FGF2) or notch pathway can inhibit differentiation of OP cells. The current study examines the interaction of FGF2 and notch signaling components in regulating OP differentiation.

Fibroblast growth factor receptor-1 is required for long-term potentiation, memory consolidation, and neurogenesis.

Background: Although substantial evidence supports the view that adult neurogenesis is involved in learning and memory, how newly generated neurons contribute to the cognitive process remains unknown. Fibroblast growth factor 2 (FGF-2) is known to stimulate the proliferation of neuronal progenitor cells (NPCs) in adult brain. Using conditional knockout mice that lack brain expression of FGFR1, a major receptor for FGF-2, we have investigated the role of adult neurogenesis in hippocampal synaptic plasticity and learning and memory.

Retroviral lineage analysis of fibroblast growth factor receptor signaling in FGF2 inhibition of oligodendrocyte progenitor differentiation.

Fibroblast growth factor 2 (FGF2) inhibits oligodendrocyte progenitor cell (OPC) differentiation during development and limits remyelination following chronic demyelination. The current study examines the mechanism underlying this effect of FGF2 expression on OPC differentiation. Retroviral lineage tracing demonstrates a direct in vivo effect of FGF receptor (FGFR) signaling on OPC differentiation.

Correlation between TIMP-1 expression and liver fibrosis in two rat liver fibrosis models.

Aim: To evaluate serum TIMP-1 level and the correlation between TIMP-1 expression and liver fibrosis in immune-induced and CCL4-induced liver fibrosis models in rats.

Methods: Immune-induced and CCL4-induced liver fibrosis models were established by dexamethasone (0.01 mg) and CCL4 respectively.

Endogenous cell repair of chronic demyelination.

In multiple sclerosis lesions, remyelination typically fails with repeated or chronic demyelinating episodes and results in neurologic disability. Acute demyelination models in rodents typically exhibit robust spontaneous remyelination that prevents appropriate evaluation of strategies for improving conditions of insufficient remyelination. In the current study, we used a mouse model of chronic demyelination induced by continuous ingestion of 0.

PDGF and FGF2 pathways regulate distinct oligodendrocyte lineage responses in experimental demyelination with spontaneous remyelination.

Repair of myelin damage in the adult CNS requires oligodendrocyte progenitor (OP) proliferation and subsequent differentiation into remyelinating oligodendrocytes. Platelet-derived growth factor (PDGF) and fibroblast growth factor-2 (FGF2) have been predicted to act individually and/or cooperatively to generate remyelinating oligodendrocytes. Analysis of PDGF alpha receptor (PDGF alpha R) heterozygous (+/-) mice indicates that PDGF alpha R expression modulates oligodendrocyte density in non-lesioned adult CNS.

Induction of hepatitis C virus-specific cytotoxic T and B cell responses by dendritic cells expressing a modified antigen targeting receptor.

Aim: To find a novel antigen (Ag) presentation strategy to improve the immune responses induced by dendritic cell (DC) vaccine expressing hepatitis C virus (HCV) core antigen (pcDNA3HCV C-Fc) in Balb/c mice (H-2d).

Methods: pcDNA3HCV C-Fc plasmid and eukaryotic expression vector pcDNA3 were injected into mice sc. Immune responses to pcDNA3HCV C-Fc were studied.

In vivo analysis of oligodendrocyte lineage development in postnatal FGF2 null mice.

Analysis of fibroblast growth factor 2 null (FGF2-/-) and wild-type (FGF2+/+) mice was used to interpret the potential in vivo role of endogenous FGF2 on oligodendrocyte lineage cell (OLC) responses during oligodendrogenesis and myelination. In wild-type mouse spinal cord, FGF2 levels increased approximately threefold between the first and second postnatal weeks, a period corresponding with the peak of oligodendrogenesis. Absence of this developmental FGF2 elevation in FGF2-/- mice eliminated the transient overproduction of oligodendrocytes that is known to occur at the peak of oligodendrogenesis in wild-type mice.

DC-SIGN: binding receptors for hepatitis C virus.

Objective: To review the recent developments in and research into binding receptors of hepatitis C virus (HCV) and especially the role of dendritic cell-specific adhesion receptor (DC-SIGN) in HCV.

Data Sources: Both Chinese- and English-language literature was searched using MEDLINE (2000 - 2003) and the databank of Chinese-language literature (2000 - 2003).

Study Selection: Relevant articles on DC-SIGN and HCV binding receptors in recent domestic and foreign literature were selected.

The shortest expanded allele of the MJD1 gene in a Chinese MJD kindred with autonomic dysfunction.

Machado-Joseph disease (MJD) is the most common type of autosomal dominant spinocerebellar ataxia caused by an expanded CAG repeat in the MJD1 gene. Intermediate CAG alleles have been previously described, and they tend to be associated with unusual manifestations of the nervous system. Here we describe a Chinese kindred with hereditary spinocerebellar ataxia, in which the proband presented with autonomic dysfunction besides the typical features of MJD.

Promoting hepatic growth factor in the treatment of heavy type hepatitis and severe chronic hepatitis: a multicenter clinical study.

Background: The mortality rate of heavy type hepatitis is high. No special treatment is available except general treatment. This multicenter clinical study was designed to observe the safety and efficacy of promoting hepatic growth factor (PHGF) in the treatment of heavy type hepatitis and severe chronic hepatitis.

[Acceleration of mixed lymphocyte reaction by HCV C-Fc gene-transferred murine dendritic cells].

Aim: To observe the metergasis of murine dendritic cells (DCs) transfected with HCV C-Fc gene through electroporation.

Methods: Mononucleocytes isolated from murine bone marrow were co-cultured with rmGM-CSF and rm-IL-4 for 7 days. Morphological characteristics of the cultured cells were observed under scan electron-microscope (SEM) and the expression of DEC205 on the cells was detected by FACS.

[The mechanism for up-regulation of HLA-I expression on HepG2 cells by HBV].

Aim: To explore the mechanism of up-regulation of HLA-I expression on HepG2 cells by wild type (WT) and nucleocapsid mutants(L97 and V60) of hepatitis B virus (HBV).

Methods: The HBV-stable expression vectors EBO-WT, EBO-L97 and EBO-V60 were transfected into HepG2 cells via the liposome mediation, respectively. The cells were assayed by semi-quantitative RT-PCR for HLA-A gene and antigen presentation-related genes LMP2, TAP1, and tapasin mRNA expression.