Interactive Simulation System for Artificial Ventilation on the Internet: Virtual Ventilator

Objective. To develop an interactive simulation system “virtual ventilator” that demonstrates the dynamics of pressure and flow in the respiratory system under the combination of spontaneous breathing, ventilation modes, and ventilator options. The simulation system was designed to be used by unexperienced health care professionals as a self-training tool. Methods. The system consists of a simulation controller and three modules: respiratory, spontaneous breath, and ventilator. The respiratory module models the respiratory system by three resistances representing the main airway, the right and left lungs, and two compliances also representing the right and left lungs. The spontaneous breath module generates inspiratory negative pressure produced by a patient. The ventilator module generates driving force of pressure or flow according to the combination of the ventilation mode and options. These forces are given to the respiratory module through the simulation controller. Results. The simulation system was developed using HTML, VBScript (3000 lines, 100 kB) and ActiveX control (120 kB), and runs on Internet Explorer (5.5 or higher). The spontaneous breath is defined by a frequency, amplitude and inspiratory patterns in the spontaneous breath module. The user can construct a ventilation mode by setting a control variable, phase variables (trigger, limit, and cycle), and options. Available ventilation modes are: controlled mechanical ventilation (CMV), continuous positive airway pressure, synchronized intermittent mandatory ventilation (SIMV), pressure support ventilation (PSV), SIMV + PSV, pressure-controlled ventilation (PCV), pressure-regulated volume control (PRVC), proportional assisted ventilation, mandatory minute ventilation (MMV), bilevel positive airway pressure (BiPAP). The simulation system demonstrates in a graph and animation the airway pressure, flow, and volume of the respiratory system during mechanical ventilation both with and without spontaneous breathing. Conclusions. We developed a web application that demonstrated the respiratory mechanics and the basic theory of ventilation mode.     

Laryngopharyngeal reflux

Laryngopharyngeal reflux (LPR) or reflux laryngitis refers to the backflow of stomach contents into the larynx and hypopharynx. LPR is increasingly cited as the cause of laryngeal signs and symptoms such as globus sensation, hoarseness, chronic cough, chronic throat clearing, and throat pain. The diagnosis of LPR is often based on the presenting symptoms and associated laryngeal signs. An empiric trial of double-dose proton pump inhibitors (PPIs) has been recommended as a first line therapy in patients with suspected LPR. However, recent systemic review has shown no benefit of PPIs over placebo in the treatment of LPR. Clearly, more well designed, prospective large scale trials are warranted in the future.     

Transient receptor potential 1 regulates capacitative Ca(2+) entry and Ca(2+) release from endoplasmic reticulum in B lymphocytes

Capacitative Ca(2+) entry (CCE) activated by release/depletion of Ca(2+) from internal stores represents a major Ca(2+) influx mechanism in lymphocytes and other nonexcitable cells. Despite the importance of CCE in antigen-mediated lymphocyte activation, molecular components constituting this mechanism remain elusive. Here we demonstrate that genetic disruption of transient receptor potential (TRP)1 significantly attenuates both Ca(2+) release-activated Ca(2+) currents and inositol 1,4,5-trisphosphate (IP(3))-mediated Ca(2+) release from endoplasmic reticulum (ER) in DT40 B cells. As a consequence, B cell antigen receptor-mediated Ca(2+) oscillations and NF-AT activation are reduced in TRP1-deficient cells. Thus, our results suggest that CCE channels, whose formation involves TRP1 as an important component, modulate IP(3) receptor function, thereby enhancing functional coupling between the ER and plasma membrane in transduction of intracellular Ca(2+) signaling in B lymphocytes.     

Study on local immune response in Escherichia coli-induced experimental urinary tract infection in mice--infiltration of Ia-positive cells, macrophages, neutrophils, T cells and B cells]

We studied the local immune response in a mouse experiment with acute ascending cystitis and pyelonephritis. The experimental infections were induced in BALB/c female mice by transurethral instillation of Escherichia coli O6. Immune response cells were stained, including Ia-positive cells, macrophages, neutrophils, T cells (CD4+ and CD8+) and B cells (IgA, IgM, IgG-positive B cell). They were stained by the immunohistochemical method (ABC method) using monoclonal antibodies against lineage specific antigens except for neutrophils that were readily identified by the standard hematoxylin-eosin. Even in the control mice having no evidence of the infection, mucosa associated lymphoid tissue (MALT) consisted of macrophages, Ia-positive cells and T cells that were sparingly found in the urinary tract tissue and renal parenchyma. Ia-positive cells, macrophages, neutrophils, T cells (CD4+, CD8+) and IgA positive B cells were significantly infiltrated in the bladder submucosa from 6 hours after bacterial inoculation. The infiltration of similar immune response cells was found in the submucosa of the renal pelvis, except for IgA positive B cells that appeared one day after the induction of the infection. In renal parenchyma, Ia-positive cells appeared at 6 hours after introduction of the infection, followed by an infiltration of neutrophils, macrophages and T cells (CD4+, CD8+) at the first day, and IgA positive B cells at the third day. These results are summarized as follows. When microbes invaded the urinary tract tissue, a significant number of Ia-positive cells infiltrated, which were initially present in normal urinary tract tissue. Subsequently, neutrophils, macrophages and T cells (CD4+, CD8+) appeared in the lesion followed by a delayed occurrence of IgA positive B cells.