Influences and mechanisms of pyrolytic conditions on recycling BTX products from passenger car waste tires.

Pyrolysis is an effective method for waste tire disposal. However, it has rarely been used to recycle specific highly valuable components (such as benzene, toluene, and xylene (BTX)) from tire rubbers, owing to complicated pyrolytic reactions. This study investigated the pyrolysis process of passenger-car-waste-tires (PCWT) with the help of TG-DTG and Py-GC/MS.

Formation Mechanism of Monocyclic Aromatic Hydrocarbons during Pyrolysis of Styrene Butadiene Rubber in Waste Passenger Car Tires.

The production of aromatic hydrocarbons from the waste tire pyrolysis attracts more and more attention because of its tremendous potential. Based on styrene-butadiene rubber (SBR), which is the main rubber in the waste passenger car tires, this work studies the temperature influence on primary pyrolysis product distribution by experimental techniques (Py-GC/MS, TG-MS), and then, the formation mechanism of monocyclic aromatic hydrocarbons (MAHs) observed in the experiment was analyzed by first-principles calculations. The experimental results show that the MAHs during the pyrolysis mainly include styrene, toluene, and xylene, and subsequent calculations showed that these compounds were formed through a series of primary and secondary reactions.

Study of passenger-car-waste-tire pyrolysis: Behavior and mechanism under kinetical regime.

The pyrolysis of passenger-car-waste-tires (PCWT) has recently attracted widespread attention because it is a highly effective disposal method. However, a comprehensive understanding of real tire pyrolytic processes is limited owing to the complicated PCWT pyrolysis reaction system, particularly regarding the reaction mechanism. This study investigated the PCWT pyrolytic processes using a thermogravimetric analyzer coupled with mass spectrometry and analyzed all the pyrolytic products using pyrolysis-gas chromatography coupled with mass spectrometry.

Antitumor CD8 T cell responses in glioma patients are effectively suppressed by T follicular regulatory cells.

Regulatory T (Treg) cells are thought to contribute to tumor pathogenesis by suppressing tumor immunosurveillance and antitumor immunity. T follicular regulatory (Tfr) cells are a recently characterized Treg subset that expresses both the Treg transcription factor (TF) Foxp3 and the T follicular helper (Tfh) TF Bcl-6. The role of Tfr cells in glioma patients remains unclear.

LncRNA MACC1-AS1/MACC1 enhances the progression of glioma via regulating metabolic plasticity.

This study plans to investigate the effects of long-noncoding RNA MACC1-AS1 on glioma cells and its mechanism at metabolic plasticity angle. The MACC1-AS1 level was identified both in glioma tissues and in cells. Then the effects of MACC1-AS1 abnormal level on cell viability, apoptosis, the expression of apoptosis associated protein, glucose metabolism and redox status were measured in A172 and U251 cells by different methods.

Lowly expressed lncRNA PVT1 suppresses proliferation and advances apoptosis of glioma cells through up-regulating microRNA-128-1-5p and inhibiting PTBP1.

Background: Glioma is a primary intracranial malignancy with poor prognosis, of which the pathogenesis remains to be elucidated. Therein, the aim of this study is to discuss the impacts of lncRNA plasmacytoma variant translocation 1 (PVT1)/microRNA-128-1-5p (miR-128-1-5p)/polypyrimidine tract-binding protein 1 (PTBP1) axis on the biological characteristics of glioma cells.

Methods: Glioma tissue samples (72 cases) and normal brain tissue samples (35 cases) were harvested.

LncRNA NNT-AS1 promote glioma cell proliferation and metastases through miR-494-3p/PRMT1 axis.

Long noncoding RNAs (lncRNAs) are key players in cancer progression. However, the function of lncRNA NNT-AS1 on glioma is unclear. In the present study, a total of 73 tumor tissues and matched adjacent non-tumor tissues were collected, and glioma cell lines were cultured .

Expression of TRPC3 in cortical lesions from patients with focal cortical dysplasia.

Focal cortical dysplasia (FCD) is one of the main causes of medically intractable epilepsy. Some studies have reported that transient receptor potential canonical channel 3 (TRPC3) may play an important role in the occurrence of seizures. In this study, we investigated the expression patterns of TRPC3 in different types of FCD.

Galangin inhibits epithelial-mesenchymal transition and angiogenesis by downregulating CD44 in glioma.

Galangin (3,5,7‑trihydroxyflavone), a natural flavonoid present in plants, has been reported to possess anticancer properties in various types of cancers comprising glioma. The underlying mechanism, however, has not been fully elucidated. CD44, a hall marker in glioma, has been reported to be associated with epithelial-mesenchymal transition (EMT) and angiogenesis, which play important roles in glioma progression.

Culture and Differentiation of Lung Bronchiolar Epithelial Cells In Vitro.

Club cells are a major bronchiolar epithelial cell type in the lung. Using genetic lineage tracing in mice and in vitro culture of purified cells, we have shown that club cells can differentiate into alveolar type I and II cells. Here we describe the detailed protocol for culturing and differentiating club cells in 3-dimensional culture.

Intrahepatic CD206 macrophages contribute to inflammation in advanced viral-related liver disease.

Background & Aims: Liver inflammation is key in the progression of chronic viral hepatitis to cirrhosis and hepatocellular carcinoma. The magnitude of viral replication and the specific anti-viral immune responses should govern the degree of inflammation, but a direct correlation is not consistently found in chronic viral hepatitis patients. We aim to better define the mechanisms that contribute to chronic liver inflammation.

Differentiation of Club Cells to Alveolar Epithelial Cells In Vitro.

Club cells are known to function as regional progenitor cells to repair the bronchiolar epithelium in response to lung damage. By lineage tracing in mice, we have shown recently that club cells also give rise to alveolar type 2 cells (AT2s) and alveolar type 1 cells (AT1s) during the repair of the damaged alveolar epithelium. Here, we show that when highly purified, anatomically and phenotypically confirmed club cells are seeded in 3-dimensional culture either in bulk or individually, they proliferate and differentiate into both AT2- and AT1-like cells and form alveolar-like structures.

Expression of TRPC6 and BDNF in Cortical Lesions From Patients With Focal Cortical Dysplasia.

Focal cortical dysplasia (FCD) likely results from abnormal migration of neural progenitor cells originating from the subventricular zone. To elucidate the roles in molecules that are involved in neural migration pathway abnormalities in FCDs, we investigated the expression patterns of transient receptor potential canonical channel 6 (TRPC6) and brain-derived neurotrophic factor (BDNF) in cortical lesions from FCD patients and in samples of normal control cortex. TRPC6 and BDNF mRNA and protein levels were increased in FCD lesions.

Metabolomics Investigation Reveals Metabolite Mediators Associated with Acute Lung Injury and Repair in a Murine Model of Influenza Pneumonia.

Influenza virus infection (IVI) can cause primary viral pneumonia, which may progress to acute lung injury (ALI) and respiratory failure with a potentially fatal outcome. At present, the interactions between host and influenza virus at molecular levels and the underlying mechanisms that give rise to IVI-induced ALI are poorly understood. We conducted a comprehensive mass spectrometry-based metabolic profiling of serum, lung tissue and bronchoalveolar lavage fluid (BALF) from a non-lethal mouse model with influenza A virus at 0, 6, 10, 14, 21 and 28 days post infection (dpi), representing the major stages of IVI.

Increased Expression and Cellular Localization of P2X7R in Cortical Lesions of Patients With Focal Cortical Dysplasia.

Focal cortical dysplasias (FCDs) are major brain malformations that commonly lead to medically intractable epilepsy. The purinergic ionotropic P2X7 receptor (P2X7R) is an atypical P2X subtype that gates calcium and sodium ions. Previous animal studies have suggested that P2X7R is a contributing factor in epileptogenesis.

Expression Patterns of TRPC1 in Cortical Lesions from Patients with Focal Cortical Dysplasia.

Focal cortical dysplasia (FCD) is known as a common cause of chronic refractory epilepsy, but the underlying mechanisms of the factors that lead to FCD-related epilepsy are unclear. Previous studies have shown that canonical transient receptor potential channels (TRPCs) might be involved in the process of epileptogenesis. Canonical transient receptor potential channel 1 (TRPC1), which is ubiquitously expressed in the brain, has been shown to be involved in epileptiform bust firing in knockout mice.

Characterisation of liver pathogenesis, human immune responses and drug testing in a humanised mouse model of HCV infection.

Objective: HCV infection affects millions of people worldwide, and many patients develop chronic infection leading to liver cancers. For decades, the lack of a small animal model that can recapitulate HCV infection, its immunopathogenesis and disease progression has impeded the development of an effective vaccine and therapeutics. We aim to provide a humanised mouse model for the understanding of HCV-specific human immune responses and HCV-associated disease pathologies.

Aging exacerbates damage and delays repair of alveolar epithelia following influenza viral pneumonia.

Background: Influenza virus infection causes significantly higher levels of morbidity and mortality in the elderly. Studies have shown that impaired immunity in the elderly contributes to the increased susceptibility to influenza virus infection, however, how aging affects the lung tissue damage and repair has not been completely elucidated.

Methods: Aged (16-18 months old) and young (2-3 months old) mice were infected with influenza virus intratracheally.

Increased expression of TRPC5 in cortical lesions of the focal cortical dysplasia.

Focal cortical dysplasias (FCDs) are frequently associated with the medical refractory epilepsy in both children and adults. Transient receptor potential canonical channel 5 (TRPC5), a receptor-operated cation channel, has been well recognized as a regulator in the central nervous system. Here, we examined the expression and cellular distribution of TRPC5 in the specimens from patients with FCDIa (n = 14), FCDIIa (n = 12), and FCDIIb (n = 12) compared with the age-matched control cortex (CTX).

Expression and cellular distribution of the interleukin 2 signaling system in cortical lesions from patients with focal cortical dysplasia.

Focal cortical dysplasia (FCD) is a well-known cause of medically intractable epilepsy. To understand the potential role of the inflammatory cytokine interleukin 2 (IL-2) in the pathogenesis of FCD, we investigated the expression patterns of IL-2 and its receptors (IL-2Rs) in FCD and control samples that included epileptic neocortex from mesial temporal lobe epilepsy patients and nonepileptic normal cortex (CTX). Greater mRNA and protein levels of IL-2 and IL-2Rs were observed in FCD versus CTX samples.

Evidence for Scgb1a1(+) cells in the generation of p63(+) cells in the damaged lung parenchyma.

Transformation-related protein 63-expressing (p63(+)) basal cells are confined to the trachea in the mouse lung. However, after influenza virus infection or bleomycin treatment, patches of p63(+) cells were observed in the damaged lung parenchyma. To address whether the newly induced p63(+) cells are derived from the p63(+) basal cells, we performed lineage tracing.

Endogenous subventricular zone neural progenitors contribute to the formation and hyperexcitability of experimental model of focal microgyria.

Microgyria is associated with epilepsy and due to developmental disruption of neuronal migration. However, the role of endogenous subventricular zone-derived neural progenitors (SDNPs) in formation and hyperexcitability has not been fully elucidated. Here, we establish a neonatal cortex freeze-lesion (FL) model, which was considered as a model for focal microgyria, and simultaneously label SDNPs by CM-DiI.

A cellular pathway involved in Clara cell to alveolar type II cell differentiation after severe lung injury.

Regeneration of alveolar epithelia following severe pulmonary damage is critical for lung function. We and others have previously shown that Scgb1a1-expressing cells, most likely Clara cells, can give rise to newly generated alveolar type 2 cells (AT2s) in response to severe lung damage induced by either influenza virus infection or bleomycin treatment. In this study, we have investigated cellular pathway underlying the Clara cell to AT2 differentiation.