We aimed to determine (1) the test-retest reliability of a newly developed portable fixed dynamometer (PFD) as compared to the hand-held dynamometer (HHD) in patients with motor neuron disease (MND) and (2) the PFD's ability to reduce possible examiner-induced ceiling effects.
 
  Test-retest reliability of isometric muscle strength of the quadriceps was measured in patients with MND and non-neurological controls using the HHD and PFD. Reliability was estimated by the intraclass correlation coefficient (ICC) and standard error of measurement (SEM) using linear mixed effects models, and the Bland-Altman method of agreement.
 
  In total, 45 patients with MND and 43 healthy controls were enrolled in this study. The ICC of the PFD was excellent and similar in both patients and controls (ICC 
  99.5% vs. ICC 
  98.6%) with a SEM of 6.2%. A strong examiner-induced ceiling effect in HHD was found when the participant's strength exceeded that of examiner. Employing the PFD increased the range of muscle strength measurements across individuals nearly twofold from 414 to 783N.
 
  Portable fixed dynamometry may significantly reduce examiner-induced ceiling effects, optimize the standardization of muscle strength testing, and maximize reliability. Ultimately, PFD may improve the delivery of care due to its potential for unsupervised, home-based assessments and reduce the burden to the patient of participating in clinical trials for MND or other neuromuscular diseases.
 Portable fixed dynamometry may significantly reduce examiner-induced ceiling effects, optimize the standardization of muscle strength testing, and maximize reliability. Ultimately, PFD may improve the delivery of care due to its potential for unsupervised, home-based assessments and reduce the burden to the patient of participating in clinical trials for MND or other neuromuscular diseases.The cell membrane, which is lipid-rich, is not only a simple mechanical barrier but also an important and complex component of the cell. It also communicates with the external environment. Sphingomyelin is an important class of phospholipids in the membrane that performs many functions. Interest in sphingomyelin-based liposomes, which are a critical component of cell membranes, have become the focus of intense study in recent years. Through additional research, the function of sphingomyelin and its derivatives in diseases can be gradually elucidated. Sphingomyelin consists of ceramide and its derivatives including ceramide-1-phosphate glucosylceramide and sphingosine-1-phosphate. The metabolism of glucosylceramide is regulated by glucosylceramide synthase (EC 2.4.1.80) which is the key enzyme in the glycosylation of ceramide. The activity of glucosylceramide synthase directly affects the level of glucosylceramide in cells which in turn affects the function of cells and may eventually lead to diseases. Recently, the relationship between glucosylceramide and its metabolic enzymes, with diseases has become a relatively new area of study.  https://www.selleckchem.com/ATM.html  The purpose of this paper is to address the relationship between glucosylceramide, glucosylceramide synthase, and their possible association with liver diseases at the theoretical level.
  To study the features of the bronchial mucosa lesion in relation to centrally growing lung cancer (LC) according to diagnostic fibrobronchoscopy in comparison with the results of cytomorphological data to determine the possible origin of tumor growth (histogenesis).
 
  The data of fibrobronchoscopy and cytological findings based on the materials of 75patients with a clinical diagnosis of LC were studied and compared. By the sum of the numerous cytomorphological features of epithelial cells and their components, the cells of the cylindrical epithelium and LC of various histological types were identified. The cells in bronchial smears and bronchial lavage were stained by Pappenheim and Papanicolau. Diagnostic material was examined by light microscopy.
 
  We have found that in a part of the patients (49%), the tumors with exophytic growth in the bronchus are covered with a cylindrical epithelium, which indirectly indicates the origin of cancer growth under the epithelial layer. In cytological preparations of 51% patients, cancer cells were found, which confirms the tumor invasion into the bronchial mucosa. In 48 (64%) patients, fibrobronchoscopy revealed that the examined bronchus was compressed from 50% to pinpoint width, evidencing that tumor growth develops from the outside, peribronchially.
 
  The obtained data indirectly confirm the development of central LC from type II pneumocytes, which are found in the glands of the submucous membrane of the bronchus. However, it does not exlude the development of this type of LC from the basal cell of the bronchial epithelium.
 The obtained data indirectly confirm the development of central LC from type II pneumocytes, which are found in the glands of the submucous membrane of the bronchus. However, it does not exlude the development of this type of LC from the basal cell of the bronchial epithelium.Pericellular plasmin generation triggers apoptosis/anoikis in normal adherent cells. However, cancer cells are notoriously resistant to anoikis, enabling metastasis and new tumor growth beyond their original environment. Autophagy can be a major contributor to anoikis resistance in cancer.
  To investigate if protective autophagy can be induced in lung adenocarcinoma cells in response to plasminogen treatment.
 
  Human lung adenocarcinoma A549cells were incubated with Glu-plasminogen (0.1-1.0µM) for 24h. Pericellular plasmin activity was monitored spectrophotometrically by a cleavage of the specific chromogenic- substrate S-2251. Cell survival was assessed by 3-[4,5-dimethyl thiazol-2-yl]-2,5-diphenyl tetrazolium bromide (MTT)-test. Degradation of fibronectin, levels of autophagy markers (beclin-1and light chain 3 (LC3)) and glycolysis regulator (TIGAR) were evaluated by western blot. Intracellular localization of LC-3was visualized by immunocytochemistry.
 
  It was shown that plasminogen is converted into plasmI conversion in plasminogen-treated A549cells are the hallmarks of autophagy induction. According to immunocytochemistry data, increased LC3puncta and autophagosome formation after exposure to plasminogen could reflect autophagy activation.
 
  Therefore, we showed stimulation of prosurvival signals and induction of autophagy in plasminogen-treated adenocarcinoma cells rendering them resistant to apoptosis/anoikis. Based on the obtained data, autophagy has a great potential for novel targets that affect cancer cell death, in addition to the current cytotoxic agents.
 Therefore, we showed stimulation of prosurvival signals and induction of autophagy in plasminogen-treated adenocarcinoma cells rendering them resistant to apoptosis/anoikis. Based on the obtained data, autophagy has a great potential for novel targets that affect cancer cell death, in addition to the current cytotoxic agents.