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Nanotechnology in Stem Cell Regenerative Therapy and Its Applications
Published in Harishkumar Madhyastha, Durgesh Nandini Chauhan, Nanopharmaceuticals in Regenerative Medicine, 2022
Layered photoreceptor nuclei formed from NPCs restores visual activity; therefore, iPSCs-derived NPCs’ transplantation can be utilised in the cure of age-related macular degeneration (ARMD) and other eye-related defects (Yang et al. 2016a). The molecular signature of telencephalic INs from GABAergic-INs (interneurons) (iGABA-INs) cells releases GABA, which inhibits to host granule neuronal activity (Pasca et al. 2015). When these cells are transplanted in the growing embryo, it helps cure seizures and related neurodegenerative disorders. Also, it heals genetic and acquired seizures by transplanting INs in developing embryos. A1AD (α-1 antitrypsin deficiency) is a condition that increases the risk for liver and lung diseases. The mutated gene SERPINA1 results in this deficiency. This gene guides the protein α-1 antitrypsin, which is responsible for guarding the lungs against the enzyme neutrophils elastase that is powerful in damaging the lung connective tissues. The known fact is that a single base-pair mutation of gene SERPINA1 causes A1AD, which can be rectified by transplanted A1AD mutation corrected iPSCs (Wilson et al. 2015).
Gene Therapy for Acute Diseases of the Lungs
Published in Kenneth L. Brigham, Gene Therapy for Diseases of the Lung, 2020
In mice, we initially demonstrated delivery of a chloramphenicol acetyltransferase reporter gene (8) to the lungs using a plasmid/cationic liposome delivery system; those data are summarized in Table 1. Subsequently, this technology has been shown capable of delivering other reporter genes (11), the human growth hormone gene (9), the CFTR gene (12), the alpha-1 antitrypsin gene (10), and the prostaglandin synthase gene (13) to the lungs of experimental animals. The CFTR gene has also been effectively delivered to the nasal mucosa of patients with cystic fibrosis using this delivery system (14). We have begun initial clinical investigations with this system in patients with alpha-1 antitrypsin deficiency.
Paediatrics
Published in Seema Khan, Get Through, 2020
This is an inherited disorder. (α1-Antitrypsin is an enzyme produced by the liver and stops the degeneration of lung tissue by the enzyme neutrophil elastase. A deficiency of (α1-antitrypsin results in destruction of lung tissue and consequently emphysema develops. In some patients a nominal amount of the enzyme is produced but this is usually defective and accumulates in the liver causing liver damage.
Acute inhalation toxicity of aerosolized electrochemically generated solution of sodium hypochlorite
Published in Inhalation Toxicology, 2022
Bohdan Murashevych, Dmitry Girenko, Hanna Maslak, Dmytro Stepanskyi, Olha Abraimova, Olha Netronina, Petro Zhminko
Proteinase inhibitor α1-antitrypsin is an acute-phase protein that is predominantly produced by hepatocytes and secreted into the blood (Stockley 2014). In addition to antiprotease activity, α1-AT has other biological effects: antioxidant and antimicrobial action participates in the local immune response and prevent apoptosis (Mitchell and Khan 2017). Reactive oxygen species, in particular hypochlorous acid, reduce the activity of this enzyme by sulfoxidation of methionine in its active center (Schönberg et al. 2012; Siddiqui et al. 2016). In our study, on the contrary, an increase in the activity of α1-AT in experimental animals has been found both on the 1st (by 17%) and on the 14th (by 24.6%) days after sodium hypochlorite inhalation relative to the control group. On the one hand, this indicates the absence of an inhibitory effect of such concentrations of active chlorine, on the other hand, it may be a signal of the occurrence of unclear hepatocellular disorders. At the same time, there was an increase in the activity of α1-AT in the blood serum of animals of the control group during the period of their observation. This aspect requires further consideration.
Alveolar hemorrhage due to marijuana smoking using water pipe made with plastic bottle: case report and narrative review of the literature
Published in Inhalation Toxicology, 2021
Ségolène Toquet, Joël Cousson, Nathalie Choiselle, Claire Gozalo, Delphine Giusti, Firouze Bani-Sadr, Yohan N’Guyen
Besides supplemental oxygen administered at 6 l/min in intensive care unit, a treatment by prednisone 1 mg/kg/d was prescribed in association with levofloxacin. This latter was withdrawn 4 d later, once negative results were obtained from bacteriological analyses (see below). Supplemental oxygen requirements decreased rapidly (Figure 1(D)). Bronchoalveolar lavage (BAL) performed the third day yielded fluid becoming progressively bloody suggestive of AH (Golde score 34). Neither virus, bacteria, fungi nor malignant cells were detected in BAL fluid. Antineutrophils cytoplasmic, anti-glomerular basement membrane and anti-transglutaminase antibodies were all negative. Serum alpha-1 antitrypsin levels were 270 mg/dL. Congestive heart failure was ruled out by transthoracic echocardiography and the diagnosis of AH due to inhaled toxic compound was presumed. Screening for drugs and their metabolites in urine samples using gas chromatography/mass spectrometry evidenced only THC-COOH (degradation product of tetrahydrocannabinol [THC]) and para-methoxyphenylpiperazine metabolite but it ruled out the presence of benzylecgonine (cocaine degradation product). No other exposure to environmental toxic compound was evidenced after careful questioning of the patient.
Obstructive lung diseases and risk of rheumatoid arthritis
Published in Expert Review of Clinical Immunology, 2020
H. Maura Friedlander, Julia A. Ford, Alessandra Zaccardelli, Alexsandra V. Terrio, Michael H. Cho, Jeffrey A. Sparks
COPD is defined by the presence of chronic, irreversible airflow limitation in the presence of risk factors and absent other etiologies of [88]. COPD includes chronic bronchitis and emphysema. Heavy smoking is a well-established risk factor for COPD, but up to 25% may have relatively low smoking history or never smoked [89]. Other inhalants such as pollution and occupational exposures may also contribute to COPD risk. Patients with COPD may also experience heterogeneous disease severity, some with relatively mild shortness of breath or cough and some that progress to respiratory failure and death [90]. A small minority of patients may have alpha-1 antitrypsin deficiency [91]. Patients may also have asthma-COPD overlap syndrome, which presents as clinical symptoms of both asthma and COPD [92]. The pathogenesis of COPD involves neutrophil and macrophage infiltration with smoking as a strong environmental factor [93]. It has been shown that there are higher levels of citrullination in COPD patient lung samples compared to patients with no airway disease [94]. Patients with COPD are also more likely to produce autoantibodies to a broad spectrum of self-antigens, which may increase susceptibility to RA [95]. Prior research has also found RA to be significantly associated with subsequent risk of developing COPD [96]. A phenome-wide association study found an association between HLA-C and autoimmune diseases and bronchiectasis, suggesting a genetic link between autoimmune disorders and obstructive lung disease [29].