The performance of image classification is highly dependent on the quality of the extracted features that are used to build a model. Designing such features usually requires prior knowledge of the domain and is often undertaken by a domain expert who, if available, is very costly to employ. Automating the process of designing such features can largely reduce the cost and efforts associated with this task. Image descriptors, such as local binary patterns, have emerged in computer vision, and aim at detecting keypoints, e.g., corners, line-segments and shapes, in an image and extracting features from those keypoints. In this paper, genetic programming (GP) is used to automatically evolve an image descriptor using only two instances per class by utilising a multi-tree program representation. The automatically evolved descriptor operates directly on the raw pixel values of an image and generates the corresponding feature vector. Seven well-known datasets were adapted to the few-shot setting and used to assess the performance of the proposed method and compared against six hand-crafted and one evolutionary computation-based image descriptor as well as three convolutional neural network (CNN) based methods. The experimental results show that the new method has significantly outperformed the competitor image descriptors and CNN-based methods. Furthermore, different patterns have been identified from analysing the evolved programs.A 12-year-old male with a family history of inflammatory bowel disease presented with sleep-disordered breathing and was found to have chronic, granulomatous swelling of the supraglottic larynx. His airway was managed with tracheostomy, regular interval laryngeal steroid injections, supraglottoplasty, and "pepper pot" CO2 laser resurfacing leading to eventual decannulation. Due to the non-necrotic nature of the granulomatous inflammation, as well as the patient's family history of inflammatory bowel disease, the leading diagnosis was Crohn disease, but isolated laryngeal sarcoidosis could not be ruled out. There are only 13 reported cases of laryngeal manifestations of Crohn disease in the literature, with only 2 cases occurring in pediatric patients. This case report adds to this body of literature and discusses strategies for managing granulomatous supraglottic edema when definitive diagnosis is not fully clear.The aryl hydrocarbon receptor (AhR) is a ligand-activated transcription factor whose physiological function is poorly understood. The AhR is highly expressed in barrier organs such as the skin, intestine, and lung. The lungs are continuously exposed to environmental pollutants such as cigarette smoke (CS) that can induce cell death mechanisms such as apoptosis, autophagy, and endoplasmic reticulum (ER) stress. CS also contains toxicants that are AhR ligands. We have previously shown that the AhR protects against apoptosis, but whether the AhR also protects against autophagy or ER stress is not known. Using cigarette smoke extract (CSE) as our in vitro surrogate of environmental tobacco exposure, we first assessed the conversion of LC3I to LC3II, a classic feature of both autophagic and ER stress-mediated cell death pathways. LC3II was elevated in CSE-exposed lung structural cells [mouse lung fibroblasts (MLFs), MLE12 and A549 cells] when AhR was absent. However, this heightened LC3II expression could not be explained by increased expression of key autophagy genes (Gabarapl1, Becn1, Map1lc3b), upregulation of upstream autophagic machinery (Atg5-12, Atg3), or impaired autophagic flux, suggesting that LC3II may be autophagy independent. This was further supported by the absence of autophagosomes in Ahr-/- lung cells. However, Ahr-/- lung cells had widespread ER dilation, elevated expression of the ER stress markers CHOP and GADD34, and an accumulation of ubiquitinated proteins.  https://www.selleckchem.com/products/ly333531.html  These findings collectively illustrate a novel role for the AhR in attenuating ER stress by a mechanism that may be autophagy independent.Chloride secretion by airway epithelial cells is primordial for water and ion homeostasis and airways surface prevention of infections. This secretion is impaired in several human diseases, including cystic fibrosis, a genetic pathology due to CFTR gene mutations leading to chloride channel defects. A potential therapeutic approach is aiming at increasing chloride secretion either by correcting the mutated CFTR itself or by stimulating non-CFTR chloride channels at the plasma membrane. Here, we studied the role of phospholipase C in regulating the transepithelial chloride secretion in human airway epithelial 16HBE14o- and CFBE cells over-expressing wild type (WT)- or F508del-CFTR. Western blot analysis shows expression of the three endogenous phospholipase C (PLC) isoforms, namely, PLCδ1, PLCγ1, and PLCβ3 in 16HBE14o- cells. In 16HBE14o- cells, we performed Ussing chamber experiments after silencing each of these PLC isoforms or using the PLC inhibitor U73122 or its inactive analogue U73343. Our results show the involvement of PLCβ3 and PLCγ1 in CFTR-dependent short-circuit current activated by forskolin, but not of PLCδ1. In CFBE-WT CFTR and corrected CFBE-F508del CFTR cells, PLCβ3 silencing also inhibits CFTR-dependent current activated by forskolin and UTP-activated calcium-dependent chloride channels (CaCC). Our study supports the importance of PLC in maintaining CFTR-dependent chloride secretion over time, getting maximal CFTR-dependent current and increasing CaCC activation in bronchial epithelial cells.The current COVID-19 pandemic is probably the worst the world has ever faced since the start of the new millennium. Although the respiratory system is the most prominent target of SARS-CoV-2 (the contagion of COVID-19), extrapulmonary involvement are emerging as important contributors of its morbidity and lethality. This article summarizes the impact of SARS-CoV and SARS-CoV-2 on the endocrine system to facilitate our understanding of the nature of coronavirus-associated endocrinopathy. Although new data are rapidly accumulating on this novel infection, many of the endocrine manifestations of COVID-19 remain incompletely elucidated. We, hereby, summarize various endocrine dysfunctions including coronavirus-induced new onset diabetes mellitus, hypocortisolism, thyroid hormone, and reproductive system aberrations so that clinicians armed with such insights can potentially benefit patients with COVID-19 at the bedside.