In order to make this discovery, they conducted the experiment in three steps. First, they injected the lung protein alone inside frog eggs to measure its function. Second, they injected both the M2 protein from H1N1 virus and the lung protein inside frog eggs and found that the H1N1 virus M2 protein caused the lung protein function to decrease significantly. By means of molecular biology techniques, scientists isolated the segment of the H1N1 virus M2 protein responsible for the damage to the lung protein and were able to demonstrate that without this segment, the H1N1 virus was unable to damage the lung protein. Third, an intact, full H1N1 virus M2 protein and the lung protein were then re-injected into frog eggs along with antioxidant drugs. This also prevented H1N1 virus M2 protein from damaging the lung protein. When these experiments were repeated using human lung cells, the results were exactly the same ...
TY - JOUR. T1 - IL-33 mediates inflammatory responses in human lung tissue cells. AU - Yagami, Akiko. AU - Orihara, Kanami. AU - Morita, Hideaki. AU - Futamura, Kyoko. AU - Hashimoto, Noriko. AU - Matsumoto, Kenji. AU - Saito, Hirohisa. AU - Matsuda, Akio. PY - 2010/11/15. Y1 - 2010/11/15. N2 - IL-33 is a member of the IL-1 family and mediates its biological effects via the ST2 receptor, which is selectively expressed on Th2 cells and mast cells. Although polymorphic variation in ST2 is strongly associated with asthma, it is currently unclear whether IL-33 acts directly on lung tissue cells at sites of airway remodeling. Therefore, we aimed to identify the IL-33-responsive cells among primary human lung tissue cells. ST2 mRNA was expressed in both endothelial and epithelial cells but not in fibroblasts or smooth muscle cells. Correspondingly, IL-33 promoted IL-8 production by both endothelial and epithelial cells but not by fibroblasts or smooth muscle cells. Transfection of ST2 small ...
In recent years, significant progress has been made in dissecting the genetic control of mammalian lung development. Many transcription factors, peptide growth factors and their receptors, as well as extracellular matrix components have been identified as important regulators of lung morphogenesis in reverse genetics approaches (Warburton et al. 2000; Groenman et al. 2004; Kumar and Ryan 2004). Chemical mutagenesis using the potent germline mutagen ENU represents a powerful means to complement these gene-driven approaches by phenotype-based screens in mice (De Angelis et al. 2000; Nolan et al. 2000; Kile et al. 2003). This report describes the positional cloning of the perinatal lethal, ENU-induced l7Rn64234SB allele and identifies a pivotal role for the previously hypothetical gene NM_026304 in Clara cell function during mouse lung development. The ENU-induced nonsense mutation truncated the carboxy-terminal 17 aa, rendering the l7Rn64234SB protein unstable. However, detection of residual ...
TY - JOUR. T1 - Low-dose of ionizing radiation enhances cell proliferation via transient ERK1/2 and p38 activation in normal human lung fibroblasts. AU - Kim, Cha Soon. AU - Kim, Jin Mo. AU - Nam, Seon Young. AU - Yang, Kwang Hee. AU - Jeong, Meeseon. AU - Kim, Hee Sun. AU - Lim, Young Khi. AU - Kim, Chong Soon. AU - Jin, Young Woo. AU - Kim, Joon. PY - 2007/9/27. Y1 - 2007/9/27. N2 - This study shows the human cellular responses and the mechanism of low-dose ionizing radiation in CCD 18 Lu cells, which are derived from normal human lung fibroblasts. Cell proliferation and viability assay were measured for the cells following γ-irradiation using trypan blue, BrdU incorporation, and Wst-1 assay. We also examined genotoxicity using a micronuclei formation assay. The activation of the MAPKs pathway was determined by Western blot analysis, and the siRNA system was used to inhibit the expression of ERK1/2 and p38. We found that 0.05 Gy of ionizing radiation stimulated cell proliferation and did not ...
Human, Mouse, Rat - Lung Tissue Array (5 slides/pk) Cell/Tissue Protein Lysate TAS-1003 Human, Mouse, Rat - Lung Tissue Array (5 slides/pk) Cell/Tissue Protein Lysate TAS-1003
Image: by Phil Schatz License: CC BY 4.0. Basically, a distinction is made between right and left lung. The left lung consists of two cloth (Lobi superior and inferior pulmonis sinistri), which are separated from each other by the fissura obliqua. The right lung, in turn, consists of three lobes (lobi superior, medius and inferior pulmonis dextri). The subdivision is done by the Fissura obliqua and the Fisura horizontalis pulmonis dextri. These fissures extend deep into the lung tissue and are, like the surface of the lung, lined with the visceral pleura.. The further structure is identical in both lungs. One distinguishes between the lung tip (Apex pulmonis), the lung base (Base pulmonis), the lung surfaces and the lung margins. The lung surface is covered by a serous skin, the visceral pleura, and appears pale pink in the healthy to gray. Depending on the position and the relationship to the thorax one differentiates with the lung surfaces (Facies pulmonis) between the facies costalis, ...
TY - JOUR. T1 - Foxf1 haploinsufficiency reduces Notch-2 signaling during mouse lung development. AU - Kalinichenko, Vladimir V.. AU - Gusarova, Galina A.. AU - Kim, Il-man. AU - Shin, Brian. AU - Yoder, Helena M.. AU - Clark, Jean. AU - Sapozhnikov, Alexander M.. AU - Whitsett, Jeffrey A.. AU - Costa, Robert H.. PY - 2004/3/1. Y1 - 2004/3/1. N2 - The forkhead box (Fox) f1 transcription factor is expressed in the mouse splanchnic (visceral) mesoderm, which contributes to development of the liver, gallbladder, lung, and intestinal tract. Pulmonary hemorrhage and peripheral microvascular defects were found in approximately half of the newborn Foxf1(+/-) mice, which expressed low levels of lung Foxf1 mRNA [low-Foxf1(+/-) mice]. Microvascular development was normal in the surviving newborn high-Foxf1(+/-) mice, which compensated for pulmonary Foxf1 haploinsufficiency and expressed wild-type Foxf1 levels. To identify expression of genes regulated by Foxf1, we used Affymetrix microarrays to determine ...
Matched Pair (Normal and Carcinoma) Human Lung Tissue Array (5 slides/pk) Cell/Tissue Protein Lysate TAS-1002 Matched Pair (Normal and Carcinoma) Human Lung Tissue Array (5 slides/pk) Cell/Tissue Protein Lysate TAS-1002
The development of lungs and the process that enables respiration is still not well understood at the molecular level. To fill the knowledge gaps, PNNL scientists are systematically characterizing normal lung development in mice and humans.
While the adult murine lung utilizes multiple restricted progenitor cells during homeostasis and fix compartmentally, very much less is known about the progenitor cells from the human lung. fix utilizing murine versions have got provided essential ideas into both lung regeneration and homeostasis. These research have got proven that the adult mouse lung epithelium can be fairly quiescent and will not really adhere to the traditional control cell model [1]. Rather, the lung shows up to conform to a maintenance structure identical to that of various other tissue with gradual turnover prices, such as the pancreas [2], [3]. During regular tissues homeostasis, abundant facultative progenitor cells located throughout the lung epithelium mediate any 1420477-60-6 manufacture required maintenance. These facultative progenitor cells, Clara cells and Type II pneumocytes, are quiescent and function as differentiated cells of the mature lung epithelium, but keep the capability to differentiate and self-renew ...
Bronchopulmonary dysplasia (BPD) remains a major respiratory illness in extremely premature infants. The biological mechanisms leading to BPD are not fully understood, although an arrest in lung development has been implicated. The current study aimed to investigate the occurrence of autophagy in the developing mouse lung and its regulatory role in airway branching and terminal sacculi formation. We found 2 windows of epithelial autophagy activation in the developing mouse lung, both resulting from AMPK activation. Inhibition of AMPK-mediated autophagy led to reduced lung branching in vitro. Conditional deletion of beclin 1 (Becn1) in mouse lung epithelial cells (Becn1Epi-KO), either at early (E10.5) or late (E16.5) gestation, resulted in lethal respiratory distress at birth or shortly after. E10.5 Becn1Epi-KO lungs displayed reduced airway branching and sacculi formation accompanied by impaired vascularization, excessive epithelial cell death, reduced mesenchymal thinning of the interstitial ...
Bronchopulmonary dysplasia (BPD) remains a major respiratory illness in extremely premature infants. The biological mechanisms leading to BPD are not fully understood, although an arrest in lung development has been implicated. The current study aimed to investigate the occurrence of autophagy in the developing mouse lung and its regulatory role in airway branching and terminal sacculi formation. We found 2 windows of epithelial autophagy activation in the developing mouse lung, both resulting from AMPK activation. Inhibition of AMPK-mediated autophagy led to reduced lung branching in vitro. Conditional deletion of beclin 1 (Becn1) in mouse lung epithelial cells (Becn1Epi-KO), either at early (E10.5) or late (E16.5) gestation, resulted in lethal respiratory distress at birth or shortly after. E10.5 Becn1Epi-KO lungs displayed reduced airway branching and sacculi formation accompanied by impaired vascularization, excessive epithelial cell death, reduced mesenchymal thinning of the interstitial ...
Carlon, Marianne ; Toelen, Jaan ; Himmelreich, Uwe ; Debyser, Zeger ; Deprest, Jan. Combined non-invasive bioluminiscence and magnetic resonance imaging improves detection after pulmonary gene transfer in a fetal mouse model.30th Annual Meeting of the Society-for-Maternal-Fetal-Medicine (Chicago(Il), Feb 01-06, 2010). In: American Journal of Obstetrics and Gynecology, Vol. 201, no. 6, p. S261 (2009 ...
Biology Assignment Help, Mammalian lungs - respiration, Mammalian Lungs - Respiration In this we will study mainly mammalian lungs as it is the best representative of a respiratory surface adapted for terrestrial respiration. For this purpose, human lung can be taken as a model as shown in Figure. Wh
Optimal lung health from embryo through adulthood requires the complex interaction of pulmonary airspaces, interstitial and vasculature, beginning with organ development and culminating in programmed senescence. Technological advances have fostered a growing appreciation for the impact of cellular plasticity and the importance of cellular niche both during development and in response to both injury and repair. In addition to expanding the role of reactivation of developmental pathways lung repair, recent discoveries have demonstrated unique aging programs that will provide novel treatment strategies for chronic lung disease. The 5th Gordon Research Conference on Lung Development, Injury and Repair in August of 2019 seeks to attract cutting edge science to drive forward the field of lung development, injury, and repair toward the goal of facilitating novel therapeutic approaches to maximize lung health across the lifespan. This conference will strive to highlight new concepts behind the interactions
The lung is the main organ in the respiratory system and doesnt develop till about week 4 in the embryo. This stage of development is known as the Embryonic stage that covers the period of week 4-5 of the developing embryo. In this stage the 2 lung buds would have formed and lung lobes and the bronchopulmonary segments. The stem diverticulum will have differentiated into trachea and larynx. The Pseudoglandular stage is the period from 6 weeks to 16 weeks in the growing fetus. The events that occur in this stage include the formation of extensive airway branching of about 14 or more generations of branching resulting in terminal bronchioles. The conducting epithelium tubes are formed and are surrounded by thick mesenchyme. At 2 months all of the segmental bronchi would have formed. The distal structures at this stage are lined with cuboidal epithelium. The next stage is the Canalicular stage, from the period of week 16 to 25. The terminal bronchioles divide into two or more respiratory ...
If you are not aware of the lung problems then see here. There is a healthy lung month that will aware you about the various lungs problems.
Research in the Cardoso lab focuses on the mechanisms that regulate lung progenitor cell fate during lung development and on the contribution of developmental mechanisms to disease pathogenesis and regeneration-repair of the adult lung. We are investigating how progenitor cells generate the wide diversity of cell types of the mature respiratory system. In this context, we have been identifying early markers of cell fate and characterizing the genetic programs associated with acquisition of the various airway epithelial cell phenotypes as the lung forms. These studies have provided insights into the role of specific pathways, including retinoids, Fgf, Tgf beta and Notch in controlling the specification and expansion of lung progenitors, airway branching and differentiation of the various lung epithelial cell lineages. Over these years Our studies continue to explore the basic mechanisms of lung development, using this knowledge to understand the role of stem/progenitor cells in lung ...
Epithelia from lung rudiments in which secondary bronchial buds are already established (14th and 13th gestational day for rat and mouse respectively) are able to undergo branching morphogenesis and cytodifferentiation in submandibular mesenchyme in vitro, whereas lung epithelium from one day younger foetuses rarely gives a morphogenetic response to submandibular mesenchyme and usually differentiates into primary (non-budding) bronchial epithelium.. The failure of 13-day rat lung epithelium to respond to submandibular mesenchyme can be prevented by peeling off the submandibular mesenchyme from the lung epithelium after 2½ days culture and replacing the same mesenchyme, or renewing it with fresh salivary mesenchyme ex vivo. Changes in the epithelial contour are visible by 10 h and buds form within 24 h; this is followed by branching morphogenesis in more than 66% of the samples.. The number of cells in S-phase in the epithelium is doubled within 3 to 5 h after the operation and the number of ...
Publikations-Datenbank der Fraunhofer Wissenschaftler und Institute: Aufsätze, Studien, Forschungsberichte, Konferenzbeiträge, Tagungsbände, Patente und Gebrauchsmuster
Aim: Chronic exposure to indoxacarb and pulmonary expression of toll-like receptor 9 (TLR-9) in mice.. Materials and Methods: In this study, healthy male Swiss albino mice (n=30) aging 8-10 weeks were used to evaluate TLR-9 expression in lungs of mice following indoxacarb exposure with and without lipopolysaccharide (LPS). Indoxacarb was administered orally dissolved in groundnut oil at 4 and 2 mg/kg/day for 90 days. On day 91, five animals from each group were challenged with LPS/normal saline solution at 80 μg/animal. The lung tissues were processed for real time and immunohistochemical studies.. Results: LPS resulted increase in fold change m-RNA expression level of TLR-9 as compare to control, while indoxacarb (4 mg/kg) alone and in combination with LPS resulted 16.21-fold change and 29.4-fold change increase in expression of TLR-9 m-RNA, respectively, as compared to control. Similarly, indoxacarb (2 mg/kg) alone or in combination with LPS also altered TLR-9 expression. Further at protein ...
When lung cells are injured, there seems to be a cross talk between the damaged cells, the lung endothelial cells and the stem cells," explains Lee.. Lee and Kim are still trying to eavesdrop on this cross-talk, but one key factor produced by endothelial cells is a protein called thrombospondin (TSP-1). By adding it to 3-D cultures exposed to the air, mimicking the lung environment, Kim and Lee were able to prod even a single lung stem cell to start churning out alveolar cells. And by simply taking the TSP-1-rich liquid surrounding cultured endothelial cells and injecting it into the mice, they were able to reverse the lung damage caused by pulmonary fibrosis.. Conversely, when the researchers engineered lung endothelial cells to lack TSP-1 and added them to the 3-D cultures, the stem cells went down a different pathway, producing more airway cells. And in live mice unable to make TSP-1, airway repair was enhanced after injury.. TSP-1 is clearly a potential target for manipulation in patients ...
Illustration of Human lungs. Respiratory system. Healthy lungs. Light in the form of a tree. Line art. Drawing by hand. Medicine. vector art, clipart and stock vectors. Image 90830878.
With the increasing prevalence of more infective and/or virulent strains of influenza, understanding the impact of virus on the host epithelium and the processes involved in lung repair are of great importance," says John F. Alcorn, PhD, an immunologist affiliated with the department of pediatrics at the Childrens Hospital of Pittsburgh of UPMC. He notes that the findings open up new possibilities for developing therapeutic agents that promote recovery of normal lung function and architecture after influenza infection and lessen the likelihood of secondary infections. "A key finding is that even after the resolution of infection, influenza results in lung parenchymal remodeling that may be critical to susceptibility to further injury," says Dr. Alcorn. This series of experiments used 6- to 8-week-old wild-type (WT) mice (C57BL/6 strain) as well as IL-22-deficient mice, infected with influenza A PR/8/34 H1N1 or control vehicle. To determine the distribution of IL-22 in the lung, they used ...
You know that smoking is bad for your lungs, but what does that mean? Heres what you need to know about the smokers lung vs. healthy lung discussion.
Stress is defined as the force applied to a material, while strain is the consequent deformation. In the whole lung, stress can be roughly approximated by the transpulmonary pressure, whereas the approximation of the average strain is the change in volume relative to the lung resting volume. The same tidal volume per kilogram may result in completely different strain according to the size of the baby lung (the V0 of the previous equation). For example, a 70-kg man with ARDS may have, according to the severity of the lung injury, a residual baby lung equal to 60%, 40%, or 20% of his normal lung size. If the ventilator is set to deliver 10 mL/kg, the actual delivered tidal volume would generate an alveolar strain, which would result from the application, in normal lung, of a tidal volume equal to 17 mL/kg, 25 mL/kg, and 50 mL/kg, values associated with a significant lung injury in laboratory studies. Recently we attempted to quantify the relationship between stress-strain and VILI in healthy ...
NIH Funding Opportunities and Notices in the NIH Guide for Grants and Contracts: Lymphatics in Health and Disease in the Digestive, Urinary, Cardiovascular and Pulmonary Systems (R01) PAR-12-259. NIDDK
NIH Funding Opportunities and Notices in the NIH Guide for Grants and Contracts: Lymphatics in Health and Disease in the Digestive, Cardiovascular and Pulmonary Systems (R21) PAR-12-260. NIDDK
Work in the Robert H. Brown Lab explores several topics within pulmonary physiology, with a long-term goal of understanding the structural changes in the lungs that lead to the pathophysiology of lung disease. Our core studies examine the structure-function relationship of pulmonary airways and vessels as well as their role in chronic obstructive pulmonary disease (COPD) and reactive airway disease. Recent research has involved studying the mechanisms and treatment of COPD progression, new methods for treating asthma, and lung inflation and airway hyperresponsiveness. We are also exploring the impact of HIV infection on the etiology of lung disease and the pathophysiologic consequences of lung distention.. Research Areas: asthma, HIV, pulmonary physiology, lung disease, COPD, reactive airway disease ...
The NF-kappaB pathway has been shown to play a critical role in both adaptive and innate immunity and has been implicated as a focal point for induction of lung inflammation by a variety of inflammatory stimuli; however, the role of NF-kappaB in specific lung cell types remains unclear. We hypothesized that individual cell types in the lungs make important and unique contributions to the NF-kappaB dependent innate immune response. To determine the temporal and cell specific activation of NF-kappaB in vivo, an NF-kappaB reporter mouse in which expression of an enhanced green fluorescent protein (eGFP)/luciferase fusion protein cDNA driven by an NF-kappaB inducible promoter (NGL mouse) was generated. NF-kappaB activity was detected in intact, anesthetized animals by bioluminescence imaging and at the cellular level by detection of GFP on lung tissue sections. Using Eschericia coli lipopolysaccharide (LPS) and Pseudomonas aeruginosa models of lung inflammation, the timing and duration of NF-kappaB ...
To understand lung cancer, we must first understand the lungs. The lungs are two sponge-like organs in the chest. The right lung has three sections, called lobes. The left lung has two lobes. It is smaller because the heart takes up more room on that side of the body. The lungs bring air in and out, taking in oxygen and getting rid of carbon dioxide gas, which is a waste product of the body.. The lining which surrounds the lungs is called the pleura. The pleura protects the lungs. The windpipe, or trachea, brings air down into the lungs, and divides into tubes called bronchi, which divide into smaller branches called bronchioles. At the end of these small branches are tiny air sacs known as alveoli.. Most lung cancers start in the lining of the bronchi. But lung cancer can also begin in other areas such as the trachea, bronchioles, or alveoli. Lung cancer usually takes many years to develop.. ...
Dendritic cells (DCs) residing in the lung are known to acquire inhaled Ag and, after migration to the draining bronchial lymph node (brLN), to present it to naive T cells in an either tolerogenic or immunogenic context. To visualize endogenous lung-derived DCs, we applied fluorescent latex beads (LXs) intratracheally, thereby in vivo labeling the majority of phagocytic cells within the lung. Of note, LX-bearing cells subsequently arriving in the draining brLN were found to represent lung-derived migratory DCs. Imaging explanted brLN by two-photon laser-scanning microscopy, we quantitatively analyzed the migration and interaction behavior of naive CD4+ T cells and endogenous, lung-derived DC presenting airway-delivered Ag under inflammatory or noninflammatory conditions. Ag-specific naive CD4+ T cells engaged in stable as well as transient contacts with LX-bearing DCs in both situations and displayed similar overall motility kinetics, including a pronounced decrease in motility at 16-20 h after ...
The use of the porcine lung to demonstrate recruitment maneuvers stimulated us to consider the possibility of using the ASL 5000 to investigate ways to improve protocols for the handling of ex-vivo perfused lungs. We believe this would provide interesting research projects for students and faculty. Many of the current ex-vivo perfusion protocols involve using positive pressure and high concentrations of oxygen to maintain isolated perfused lungs. The longest time that perfused lungs have been kept viable ex-vivo is about 10 hours. Using the ASL 5000 to model breathing, we would like to explore the possibility of extending survival time of ex-vivo perfused lungs. We believe that lowering the FiO2 and avoiding positive pressure ventilation could improve viability. Further development of this model could lead to advances in therapeutics related to airway clearance, mechanical ventilation, and airway pharmacology.. In the video below, the porcine lungs are attached to an Avea ventilator in the CPAP ...
Goal of the present study is to investigate the specific cellular responses to nCeO2 and nFe2O3 in various lung cell types and develop an in vitro chronic exposure model to predict the potential fibrogenic and carcinogenic effects. Primary human lung fibroblasts were treated with nCeO2 (size dXRD = 17 nm, SSA = 61 m2/g) and direct stimulation of collagen production (a hallmark of fibrosis) was evaluated. In separate experiments, primary human small airway epithelial cells were exposed to a sub-lethal concentration (0.625 µg/cm2) of nCeO2 and nFe2O3 (size dXRD = 20 nm, SSA = 50 m2/g) for 6 weeks and their effects on cell transformation and invasion were evaluated. Our results showed new data that nCeO2 can induce a dose-dependent increase in collagen production by lung fibroblasts; nCeO2 can induce proliferation of lung epithelial cells as compared to vehicle-treated control and nFe2O3 induced neoplastic transformation of epithelial cells as determined by soft-agar colony formation assay and transwell
Intestinal bacteria transferred at birth affect lung development, bacterial resistance and susceptibility to inflammatory conditions in newborns, according to a new mouse study.
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YALE (US)-Scientists have achieved an important first step in regenerating fully functional lung tissue that can exchange gas-the key role of the lungs.. Details appear in the June 24 issue of Science Express.. Lung disease accounts for around 400,000 deaths each year in the United States. Lung tissue is difficult to regenerate because it does not generally repair or regenerate beyond the microscopic level.. The only current way to replace damaged adult lung tissue is to perform lung transplantation, which is highly susceptible to organ rejection and infection and achieves only 10 percent to 20 percent survival at 10 years.. The researchers goal was to see if it was possible to successfully implant tissue-engineered lungs, cultured in vitro, that could serve the lungs primary function of exchanging oxygen and carbon dioxide.. They took adult rat lungs and first removed their existing cellular components, preserving the extracellular matrix and hierarchical branching structures of the airways ...
The Lung Scan provides a detailed visualization of the lungs. The Advanced Lung Analysis software allows highly accurate volume measurement of lung nodules. With its 3D volume measurement, we are better able to determine changes in nodule volume and to quantify growth rate and doubling time for lesions, allowing earlier and more accurate identification of small lung cancers. This enables our radiologists to detect lung cancer at its earliest stage, usually undetectable by an ordinary chest x-ray.. The Lung Scan can also detect other lung damage such as emphysema from smoking or lung scarring from prior infection. ...
Small airways are abnormal in asthma [1]. One measurement of small airway function is Sacin, derived from the multiple-breath nitrogen washout (MBNW) test. Sacin reflects ventilation heterogeneity in diffusion-dependent airways, and is correlated with airway hyperresponsiveness [2] and asthma control [3]. Theoretically, heterogeneity of diffusion-dependent ventilation can arise due to the heterogeneity of cross-sectional areas of airway openings in terminal airways and the acini [4]. Therefore, Sacin may be affected by structural changes in those airways. The elastic properties of the lung may also affect Sacin, as the phase III slope, a marker of ventilation heterogeneity derived from the single-breath nitrogen washout, correlates with lung compliance in explanted lungs of smokers and in healthy lungs [5]. ...
Among adults in the United States, the prevalence of reduced lung function including obstructive and restrictive lung disease is about 20%, representing an over 40 million adults. Persons with reduced lung function often demonstrate chronic systemic inflammation, such as from elevated levels of C-reactive protein. Substantial data suggests that inflammation may have a significant role in the association between reduced lung function and cardiovascular disease (CVD); however, how reduced lung function predicts CVD as risk modification remains largely unknown. Poor lung function has been shown to be a better predictor of all-cause and cardiac-specific mortality than established risk factors such as serum cholesterol, and CVD is the leading cause of mortality among those with impaired lung function. The exact mechanism of atherosclerosis is not clear, but persistent low grade inflammation is considered as one of the culprits in clot formation. The initial presentation of coronary heart disease is either
The lung is an organ constantly exposed to microbiota either through inhalation or subclinical microaspiration from birth. Historically, medical texts allude to a sterile lung environment, and this dogma has persisted in contemporary medicine. In the last decade, a revolution of sorts has taken place in our understanding of how the lung and microbiota interact and exist. This revolution stems from new knowledge that the lung is not sterile (10) and, in fact, harbors an abundance of diverse interacting microbiota. As mentioned above, the gut microbiome modulates host mucosal defense (11, 12); however, there is a paucity of information regarding the potential role of lung microbiota to regulate immunity and homeostasis.. The lung is not sterile, contrary to centuries of dogma asserting the same. Throughout the 1900s this inference was reinforced by respiratory culture-based protocols that sought only to identify clinically significant pathogens and by a spurious conclusion that upper respiratory ...
Primary human lung cells or cell lines were cultured on a stretchable silastic membrane forming the bottom of a 12-well plexiglas® box. The box was connected to an adult ventilator and "ventilated" for up to 36 hours at 20 cycles/min with a pressure-volume regimen resembling that of MV. Several lung cell types were tested in this model. The alveolar macrophage was identified as the main cellular source of key inflammatory mediators, such as tumor necrosis factor, the chemokine interleukin (IL)-8, and matrix metalloproteinase-9, produced during mechanical ventilation. Mechanical ventilation also induced low levels of IL-8 secretion by human alveolar epithelial type II-like cells. Other lung cell types such as endothelial cells, bronchial cells, and fibroblasts failed to produce IL-8 in response to mechanical ventilation (1,2). Conclusions and Relevance for 3R ...
By Claire Mulvihill, Lung Cancer Support Nurse, Lung Foundation Australia. There are a number of symptoms and side effects which you may experience when living with lung cancer and other lung diseases in addition to various treatments. Lung cancer and its treatment can affect people in different ways depending on the type, location and size of your lung cancer. You may have general symptoms and not feel well, or have very specific symptoms relating to your lungs or other parts of the body that have been affected by the cancer. Whilst there are a number of side effects which you may experience, in this edition we feature breathlessness and some tips to managing this. We will highlight other common symptoms in such as weight loss and fatigue in future editions.. Shortness of breath is the most common challenge people living with lung cancer and other lung diseases have. It can be uncomfortable and scary and you may feel like you cant get enough air into your lungs. The common causes of ...
This unique didactic/hands-on workshop provides a comprehensive overview of respiratory biology and the use of mice as model systems of human lung diseases.
1 Segmental bronchial branches. Rami bronchiales segmentorum. Branches of individual segmental bronchi.. 2 Tunica muscularis. Muscle layer in the wall of the bronchus.. 3 Tela submucosa. Connective tissue layer beneath the bronchial mucosa.. 4 Tunica mucosa. Mucous membrane of the bronchi lined by ciliated columnar epithelium.. 5 Bronchial glands. Gll. bronchiales. Mixed glands located below the mucosa.. 6 LUNGS. Pulmones. They occupy the greater portion of the thoracic space. A B C D. 7 RIGHT/LEFT LUNGS. Pulmo dexter/sinister. Right lobes are larger; left lobes smaller (10%). A B C D. 8 Base of lung. Basis pulmonis (pulmonalis). Lower lung segment bordering on the diaphragm. A BCD. 9 Apex of lung. Apex pulmonis (pulmonalis). Apical portion of the lung partially occupying the superior thoracic aperture. A B C D. Costal surface. [[Facies costalis]]. Lung surface bordering the ribs. AC. Medial surface. [[Facies medialis]]. Medial lung surface facing the mediastinum. B D Vertebral part. Pars ...
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Time sequenced regional lung parenchymal analysis is dependent upon the successful registration of lung data sets that corrects for local distortions. An elastic model based image registration scheme is proposed and developed in 2D. It models the registration as a deformation process of an elastic material. An example of real lung image registration is given to show the process. The performance of the registration method is assessed by generating a pair of synthetic images with known matching points and comparing the actual matching points with the ones from our method. Three types of geometric transformation are applied to simulate different effects of distortions and the results show good promise to register images with both global and local distortions ...
Mutational activation of the K-ras oncogene often occurs in human and mouse lung adenocarcinomas. Since K-ras p21 functions in trans-membrane signaling, we have investigated whether the amount of this protein in lung cell membranes is a variable that could influence lung tumorigenesis, either due to genetic differences or in response to tumor promoters. The six mouse strains assessed showed little difference in the total lung K-ras p21 after immunoprecipitation and immunoblotting. However, amount of ras p21 in the membrane fraction showed significant differences, with C57BL/6 and BALB/c having 3-5-fold more than NIH Swiss, AKR and DBA mice. Interestingly, a congenic AKR strain having the Ahr(b-1) Ah receptor allele from C57BL/6 mice (designated AKR.B6Ah) had high lung membrane K-ras p21 similar to that of C57BL/6. To test for possible changes related to lung tumor promotion, mice were treated with a promotional dose of TCDD (5 nmol/kg). After 48 h C57BL/6 lungs showed an increase in p21 in both ...
Free Online Library: Smoking inhibits lungs immune cells. (Biomedicine) by Science News; Science and technology, general Immune response Analysis Respiratory tract diseases Development and progression Tobacco Physiological aspects
The study of formation of defensive mechanisms in the human fetal lung at different stages of embryogenesis is of great interest, in particular, because of the high frequency of pathology of the respiratory organs in neonates. Several structural components of the lungs are involved in the development of local reactions of cellular and humoral immunity: broncho-associated lymphoid tissue (the BALT system), lymphoid ceils of the lung parenchyma, and also the alveolar macrophages. The formation of the material substrate of local cellular immunity has been studied experimentally [5-7]. The results of an investigation of the subpopulation composition of lymphoid cells in the parenchyma of the adult human lung have been obtained [4]. No information on phenotypic characteristics of the lymphoid cells of the embryonic human lung could be found in the literature. This paper describes a study of the subpopulation composition of lymphoid cells in the parenchyma of the human fetal Iung at different stages of