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1
Kitaoka, Hiroko, Shinichi Tamura, and Ryuji Takaki. "A three-dimensional model of the human pulmonary acinus." Journal of Applied Physiology 88, no. 6 (June 1, 2000): 2260–68. http://dx.doi.org/10.1152/jappl.2000.88.6.2260.
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A three-dimensional (3-D) model of the human pulmonary acinus, a gas exchange unit, is constructed with a labyrinthine algorithm generating branching ducts that fill a given space completely. Branching down to the third respiratory bronchioles is generated with the proposed algorithm. A subacinus, a region supplied by the last respiratory bronchiole, is approximated to be a set of cubic cells with a side dimension of 0.5 mm. The labyrinthine algorithm is used to determine a pathway through all cells only once, except at branching points with the smallest path lengths. In choosing each step of a pathway, random variables are used. Resulting labyrinths have equal mean path lengths and equal surface areas of inner walls. An alveolus can be generated by attaching alveolar septa, 0.25 mm long and 0.1 mm wide, to the inner walls. Total alveolar surface area and numbers of alveolar ducts, alveolar sacs, and alveoli in our 3-D acinar model are in good accordance with those reported in the literature.
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Ravaglia, Claudia, and Venerino Poletti. "Bronchiolitis and Bronchiolar Disorders." Seminars in Respiratory and Critical Care Medicine 41, no. 02 (April 2020): 311–32. http://dx.doi.org/10.1055/s-0039-3402728.
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AbstractBronchioles are noncartilaginous small airways with internal diameter of 2 mm or less, located from approximately the eighth generation of purely air conducting airways (membranous bronchioles) down to the terminal bronchioles (the smallest airways without alveoli) and respiratory bronchioles (which communicate directly with alveolar ducts and are in the range of 0.5 mm or less in diameter). Bronchiolar injury, inflammation, and fibrosis may occur in myriad disorders including connective tissue diseases, inflammatory bowel diseases, lung transplant allograft rejection, graft versus host disease in allogeneic stem cell recipients, neuroendocrine cell hyperplasia, infections, drug toxicity (e.g., penicillamine, busulfan), inhalation injury (e.g., cigarette smoke, nylon flock, mineral dusts, hard metals, Sauropus androgynous); idiopathic, common variable immunodeficiency disorder, and a host of other disorders or insults. The spectrum of bronchiolar disorders is wide, ranging from asymptomatic to fatal obliterative bronchiolitis. In this review, we discuss the salient clinical, radiographic, and histological features of these diverse bronchiolar disorders, and discuss a management approach.
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Conhaim, R. L. "Airway level at which edema liquid enters the air space of isolated dog lungs." Journal of Applied Physiology 67, no. 6 (December 1, 1989): 2234–42. http://dx.doi.org/10.1152/jappl.1989.67.6.2234.
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To identify lung units associated with liquid leakage into the air space in high-pressure pulmonary edema, we perfused air-inflated dog lung lobes with albumin solution to fill the loose peribronchovascular interstitium. Next, we perfused the lobes for 90 s with fluorescent albumin solution then froze the lobes in liquid nitrogen. This procedure confined the fluorescent perfusate to the liquid flux pathway between the circulation and the air space and eliminated the previously filled peribronchovascular cuffs as a source of the fluorescence that entered the air space. We divided each frozen lobe into three horizontal layers and prepared fluorescence-microscopic sections of each layer. In the most apical layers where alveolar flooding was minimal, 10.6 +/- 21.0% (SD) of alveolar ducts were either fluorescence filled or air filled and continuous with fluorescence-filled alveoli. In the same layers, 11.0 +/- 19.0% of respiratory bronchioles were similarly labeled. No terminal bronchioles in these layers were fluorescence labeled. This suggested that the fluorescent albumin entered the air space across the epithelium of respiratory bronchioles, alveolar ducts, or their associated alveoli. To simulate an alternative explanation, i.e., that fluorescence first entered central airways then flowed into peripheral air spaces, we prepared two additional lobes that we first partially inflated with fluorescent albumin then filled to capacity with air. This pushed the fluorescent solution along the airways into the lung periphery. In these lobes the ciliary lining of bronchi and terminal bronchioles was fluorescence coated. By comparison, cilia in fluorescence-perfused lobes were not coated. We conclude that alveolar flooding in hydrostatic pulmonary edema occurs across the epithelium of alveolar ducts, respiratory bronchioles, or their associated alveoli.(ABSTRACT TRUNCATED AT 250 WORDS)
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Tokman, Sofya, M. Frances Hahn, Hesham Abdelrazek, Tanmay S. Panchabhai, Vipul J. Patel, Rajat Walia, and Ashraf Omar. "Lung Transplant Recipient with Pulmonary Alveolar Proteinosis." Case Reports in Transplantation 2016 (2016): 1–4. http://dx.doi.org/10.1155/2016/4628354.
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Pulmonary alveolar proteinosis (PAP) is a progressive lung disease characterized by accumulated surfactant-like lipoproteinaceous material in the alveoli and distal bronchioles. This accumulation is the result of impaired clearance by alveolar macrophages. PAP has been described in 11 solid organ transplant recipients, 9 of whom were treated with mammalian target of rapamycin inhibitors. We report a case of a lung transplant recipient treated with prednisone, mycophenolate mofetil (MMF), and tacrolimus who ultimately developed PAP, which worsened when MMF was replaced with everolimus.
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Mokhtar, Doaa M., Manal T. Hussein, Marwa M. Hussein, Enas A. Abd-Elhafez, and Gamal Kamel. "New Insight into the Development of the Respiratory Acini in Rabbits: Morphological, Electron Microscopic Studies, and TUNEL Assay." Microscopy and Microanalysis 25, no. 3 (February 14, 2019): 769–85. http://dx.doi.org/10.1017/s1431927619000059.
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AbstractThis study investigated the histomorphological features of developing rabbit respiratory acini during the postnatal period. On the 1st day of postnatal life, the epithelium of terminal bronchiole consisted of clear cells which intercalated between few ciliated and abundant non-ciliated (Clara) cells. At this age, the rabbit lung was in the alveolar stage. The terminal bronchioles branched into several alveolar ducts, which opened into atria that communicated to alveolar sacs. All primary and secondary inter-alveolar septa were thick and showed a double-capillary network (immature septa). The primitive alveoli were lined largely by type-I pneumocytes and mature type-II pneumocytes. The type-I pneumocytes displayed an intimate contact with the endothelial cells of the blood capillaries forming the blood–air barrier (0.90 ± 0.03 µm in thickness). On the 3rd day, we observed intense septation and massive formation of new secondary septa giving the alveolar sac a crenate appearance. The mean thickness of the air–blood barrier decreased to reach 0.78 ± 0.14 µm. On the 7th day, the terminal bronchiole epithelium consisted of ciliated and non-ciliated cells. The non-ciliated cells could be identified as Clara cells and serous cells. New secondary septa were formed, meanwhile the inter-alveolar septa become much thinner and the air–blood barrier thickness was 0.66 ± 0.03 µm. On the 14th day, the terminal bronchiole expanded markedly and the pulmonary alveoli were thin-walled. Inter-alveolar septa become much thinner and single capillary layers were observed. In the 1st month, the secondary septa increased in length forming mature cup-shaped alveoli. In the 2nd month, the lung tissue grew massively to involve the terminal respiratory unit. In the 3rd month, the pulmonary parenchyma appeared morphologically mature. All inter-alveolar septa showed a single-capillary layer, and primordia of new septa were also observed. The thickness of the air–blood barrier was much thinner; 0.56 ± 0.16 µm. TUNEL assay after birth revealed that the apoptotic cells were abundant and distributed in the epithelium lining of the pulmonary alveoli and the interstitium of the thick interalveolar septa. On the 7th day, and onward, the incidence of apoptotic cells decreased markedly. This study concluded that the lung development included two phases: the first phase (from birth to the 14th days) corresponds to the period of bulk alveolarization and microvascular maturation. The second phase (from the 14th days to the full maturity) corresponds to the lung growth and late alveolarization.
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Crestani, Bruno. "Are Bronchioles Fueling Burning Alveoli in Lung Fibrosis?" Respiration 79, no. 4 (2010): 277–78. http://dx.doi.org/10.1159/000268621.
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Federspiel, W. J., and J. J. Fredberg. "Axial dispersion in respiratory bronchioles and alveolar ducts." Journal of Applied Physiology 64, no. 6 (June 1, 1988): 2614–21. http://dx.doi.org/10.1152/jappl.1988.64.6.2614.
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The mixing of gases in the pulmonary acinus was characterized by analyzing axial gas dispersion during steady flow in models of respiratory bronchioles and alveolar ducts. An analysis (method of moments) developed for addressing dispersion in porous media was used to derive an integral expression for the axial dispersion coefficient (D*). Evaluation of D* required solving the Navier-Stokes equations for the flow field and a convection-diffusion type equation arising from the analysis. D* was strongly dependent on alveolar volume per central duct volume, the aperture size through which the alveoli communicate with the central duct, and the Peclet number (Pe). At smaller Pe (flow rate) D* was substantially smaller than the molecular diffusion coefficient, whereas at larger Pe (flow rate) D* was much greater than the Taylor-Aris result for flow-enhanced dispersion in straight tubes. Also, flow-enhanced dispersion became appreciable at smaller Pe than indicated by the Taylor-Aris result. These behaviors transcend both the lower and upper limits established previously for gas mixing in the pulmonary acinus.
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Sojka, Peter A., Christina L. Ploog, Michael M. Garner, Matti Kiupel, Jane Kuypers, and Thanhthao Huynh. "Acute human orthopneumovirus infection in a captive white-handed gibbon." Journal of Veterinary Diagnostic Investigation 32, no. 3 (March 13, 2020): 450–53. http://dx.doi.org/10.1177/1040638720910521.
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We report herein a fatal case of acute human orthopneumovirus (formerly respiratory syncytial virus) infection in a captive white-handed gibbon ( Hylobates lar). Other members of the housing group had mild respiratory signs. Gross examination revealed bilateral pulmonary congestion and froth in the bronchi. Microscopically, the lungs had lymphocytic, neutrophilic infiltration of the interstitium and alveolar walls. There was necrosis of terminal bronchiolar epithelium and terminal bronchioles, and surrounding alveoli contained necrotic and exfoliated epithelial cells admixed with histiocytes and syncytial cells. Additional lesions included nonsuppurative meningoencephalitis, and epidermal hyperkeratosis and hyperplasia with syncytial cell formation. PCR screening for 12 human respiratory viruses was positive for orthopneumovirus in multiple tissues, including lung, and immunohistochemical staining for human orthopneumovirus detected viral antigen within bronchial epithelial cells. IHC and PCR for measles virus on preserved sections were negative. White-handed gibbons have not been previously reported as hosts for human orthopneumovirus, an important respiratory pathogen of both primates and humans.
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Oliveira, Diego Medeiros de, João Marcos Araújo Medeiros, Ana Lucélia de Araújo, Luciano da Anunciação Pimentel, Felipe Pierezan, Eldinê Gomes Miranda Neto, Antônio Flávio Medeiros Dantas, and Franklin Riet-Correa. "Pulmonary choristoma associated with calf meningocele." Ciência Rural 39, no. 9 (December 2009): 2652–54. http://dx.doi.org/10.1590/s0103-84782009000900045.
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Pulmonary choristoma is a rare malformation reported in different animal species defined as a mass of normal histological pulmonary tissue in an abnormal location. A case of pulmonary choristoma and meningocele is reported in a calf that presented a fluctuating subcutaneous fluid containing mass, measuring 15 x 15 x 20cm in the skull frontal region. The skin covering the sac was surgically removed. Macroscopically, subcutaneous nodules up to 2cm in diameter with irregular whitish areas mixed with red areas were observed. In the histological examination, pulmonary lobules tissue composed by alveoli, bronchi, bronchioles and cartilage were observed. Dilated blood vessels and hemorrhages were present between the lobules. In this case the pulmonary choristoma was associated with meningocele, and probably was the mechanical cause for the failure of the skull closure.
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Khaleel, Hadeel Kamil. "Investigating the Histological Changes in Heart, Lung, Liver and Kidney of Male Albino Mice Treated with Ivabradine." Baghdad Science Journal 16, no. 3(Suppl.) (September 22, 2019): 0719. http://dx.doi.org/10.21123/bsj.2019.16.3(suppl.).0719.
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The present study aimed to investigate the histological changes of heart, lung, liver and kidney which caused by different concentrations (10, 20 and 40 mg/kg) of Ivabradine. Results of the study revealed some histological changes represented by aggregation of the lymphocytes around respiratory bronchioles of the lung. In the liver, the drug caused hepatocyte necrosis and infiltration of the lymphocytes. In Kidney, there are no histopathological modifications in the tissue after the animals treated with 10 mg\kg of Ivabradine. When the animals treated with Ivabradine drug at 20mg/kg of bw, dose showed vascular congestion between myocardial fibers of heart. Emphysematous changes of the alveoli and infiltration of lymphocytes around respiratory bronchioles of lung. In the liver there were dilated blood sinusoids. Also, there are vascular congestion and congestion of capillaries in the glomerular of kidney. Male mice treated with Ivabradine drug at 40 mg/kg of bw cause increase spaces between myocardial fibers, cardiac atrophy and myocardial degeneration in the heart. In addition, there are infiltration of lymphocytes around respiratory bronchioles, pulmonary congestion and emphysematous changes of the alveoli in lung. In the liver, the drug cause amyloid deposition and degeneration of hepatocytes. Furthermore, the drug caused vascular congestion in the kidney. Conclusion: From the current study, we conclude that the different concentrations of Ivabradine caused tissue changes in the heart, lung, liver and kidneys. The study should continue using different drugs and concentrations.
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Minenkova, T. A., Yu L. Mizernitsky, N. S. Razinkova, A. V. Serezhkina, and M. V. Kostyuchenko. "Hamman–Rich syndrome in a young child." Rossiyskiy Vestnik Perinatologii i Pediatrii (Russian Bulletin of Perinatology and Pediatrics) 64, no. 4 (September 15, 2019): 83–87. http://dx.doi.org/10.21508/1027-4065-2019-64-4-83-87.
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Hamman–Rich syndrome (idiopathic fibrosing alveolitis) is a lung disease of unknown nature, characterized by non-infectious inflammation of the interstitium, alveoli and terminal bronchioles with an outcome in progressive pulmonary fibrosis. Idiopathic fibrosing alveolitis in young children, despite the timely verification of the diagnosis and therapy, is characterized by an unfavorable prognosis and rapidly progressive course. The article describes the clinical case of Hamman–Rich syndrome in a child of 8 months, its main clinical manifestations and diagnostic features.
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Vezzosi, Tommaso, Stefania Perrucci, Francesca Parisi, Simone Morelli, Michela Maestrini, Giulia Mennuni, Donato Traversa, and Alessandro Poli. "Fatal Pulmonary Hypertension and Right-Sided Congestive Heart Failure in a Kitten Infected with Aelurostrongylus abstrusus." Animals 10, no. 12 (December 1, 2020): 2263. http://dx.doi.org/10.3390/ani10122263.
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Aelurostrongylus abstrusus is considered the most important respiratory nematode of domestic cats worldwide. This parasite inhabits the alveoli, alveolar ducts, and bronchioles and causes a subacute to chronic respiratory clinical disease. Clinical signs may occur in domestic cats of any age, though they are more often described in young animals. Physical examination, echocardiography, thoracic radiography, pulmonary and cardiac pathological findings, classical, and molecular parasitological analysis of a six-month-old kitten referred at the Veterinary Teaching Hospital of the University of Pisa (Italy) led to a diagnosis of parasitic bronchopneumonia caused by A. abstrusus, which was complicated by severe pulmonary hypertension (PH) and right-sided congestive heart failure (R-CHF) that caused the death of the animal. Cases of reversible PH associated with A. abstrusus infection have been seldom reported in cats. This is the first report of fatal PH and R-CHF in a kitten with clinical aelurostrongylosis.
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Hainis, K. D., J. I. Sznajder, and D. E. Schraufnagel. "Lung lymphatics cast from the airspace." American Journal of Physiology-Lung Cellular and Molecular Physiology 267, no. 2 (August 1, 1994): L199—L205. http://dx.doi.org/10.1152/ajplung.1994.267.2.l199.
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Lymphatics are important in the resolution of pulmonary edema, but which lymphatics drain alveolar fluid and how they change during lung injury and edema is uncertain. To study this question 16 rats were exposed to 85% O2 for 7 days. At 0, 3, 7, and 14 days after removal from the hyperoxic chamber, the lungs of the rats were cast by instilling methyl methacrylate into the trachea. The lungs of four similar room-air breathing rats served as controls. Tissue was taken for light microscopy and the casts were examined for lymphatic filling with a scanning electron microscope. Rats exposed to hyperoxia had diffuse damage and extensive edema. On removal from hyperoxia (day 0), 29% of the rat bronchioles had saccular lymphatic casts around them and 6% of bronchioles were surrounded by these lymphatics. Twenty-five percent of bronchioles had conduit lymphatic casts. Fourteen percent of arteries had lymphatic casts around them. All were different from the rats kept in room air (P < 0.0001). Rats exposed to hyperoxia had lymphatics on the pleural surface, near alveoli and alveolar ducts, and around veins. The peribronchial and periarterial saccular lymphatics formed separate groups with communicating conduit lymphatics. The perivenous lymphatics had their own separate conduit lymphatics. Fourteen days after returning to ambient air, the lymphatics were similar to those of control animals. In this model, airway casting allows three-dimensional analysis of the lung lymphatics. It shows that lymphatic compartments expand during hyperoxic lung injury and that peribronchial and perivascular saccular lymphatics connect to conduit lymphatics of the bronchoalveolar bundle.
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Matsushita, K., P. B. McCray, R. D. Sigmund, M. J. Welsh, and J. B. Stokes. "Localization of epithelial sodium channel subunit mRNAs in adult rat lung by in situ hybridization." American Journal of Physiology-Lung Cellular and Molecular Physiology 271, no. 2 (August 1, 1996): L332—L339. http://dx.doi.org/10.1152/ajplung.1996.271.2.l332.
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The transport of Na+ through amiloride-sensitive sodium channels (ENaC) plays a major role in the absorption of fluid across the pulmonary epithelium. The proteins forming the ENaC channel are encoded by three genes in the rat (alpha-, beta-, and gamma-rENaC). According to Northern blot, all three subunit mRNAs were expressed in adult rat lung. Each subunit was expressed as a single transcript of approximately 3.7, 2.2, and 3.2 kb for alpha-, beta-, and gamma-rENaC, respectively. To localize the alpha-, beta-, and gamma-rENaC subunit mRNAs, we used in situ hybridization. Frozen and paraffin-embedded tissues were hybridized with sense and antisense 35S-labeled riboprobes. The alpha-rENaC mRNA was most abundant and was expressed diffusely in epithelia of the trachea, bronchi, bronchioles, and alveoli. At the alveolar level, alpha-rENaC was expressed in type II cells. The beta- and gamma-rENaC mRNAs were most abundant in the bronchial and bronchiolar epithelia. All three subunits were expressed in the renal cortical collecting duct in a pattern similar to that previously reported by other investigators. Thus the rENaC subunit mRNAs are expressed in regions of the lung where functional Na+ absorption is found. These results are consistent with an important role for ENaC in the absorption of Na+ and fluid across the pulmonary epithelium in all regions of the lung.
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M, Devesh Raj, Naveen Kumar V.S, Raghul S, Raja Selvan R.P, and Santhosh Rajah S. "Electrical Modeling and Analysis of Human Respiratory System." Bulletin of Scientific Research 2, no. 1 (May 30, 2020): 43–48. http://dx.doi.org/10.34256/bsr2017.
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The human respiratory system mainly consists of four parts namely trachea, main bronchi, bronchioles and alveoli respectively. The alveoli in the lungs are responsible for the transfer of oxygen and carbon-dioxide through capillaries blood vessels leading to the pulmonary vein. A person cannot breathe properly during Chronic Obstructive Pulmonary Disease (COPD) due to abnormal transfer of oxygen and carbon-dioxide. Artificial ventilation is recommended for a person who suffers from COPD with no breathing or abnormal breathing, to manually preserve intact brain function. So, the blood oxygen level required for the person should be continuously monitored using pulse oximeter and controlled automatically using artificial ventilation. Hence, in this paper human respiratory system is modelled as analogies electrical model by using RLC parameters. The analogous electrical model parameters are represented as resistance, inheritance and compliance respectively. Using this analogous electrical model of human respiratory system, time domain and stability analysis are performed to identify COPD condition.
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Ichikawa, S., S. P. Sreedharan, R. L. Owen, and E. J. Goetzl. "Immunochemical localization of type I VIP receptor and NK-1-type substance P receptor in rat lung." American Journal of Physiology-Lung Cellular and Molecular Physiology 268, no. 4 (April 1, 1995): L584—L588. http://dx.doi.org/10.1152/ajplung.1995.268.4.l584.
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Peptidergic nerves in the respiratory tract release vasoactive intestinal peptide (VIP) and substance P (SP), which mediate physiological and immune functions. Antipeptide antibodies to type I VIP receptor (VIPR) and NK-1-type SP receptor (SPR) were used to identify these receptors in normal rat lungs. VIPRs and SPRs were detected on airway epithelium from the trachea to the respiratory bronchioles but not in alveoli, submucosal glands, or pulmonary smooth muscle, except for that of some pulmonary veins. VIPRs also were expressed on macrophages around capillaries, in tracheal and bronchial connective tissue, in alveolar walls, and in the subintima of pulmonary veins and some arterioles. The absence of receptors from airway smooth muscle and submucosal glands implies that mediation of some known effects of SP and VIP may be epithelial or macrophage dependent. Other types of VIPRs and SPRs on airway glands and smooth muscle may transduce direct effects. The similar localization of VIPRs and SPRs in rat lung suggests that VIP and SP may coordinately regulate some pulmonary functions.
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Hales, C. A., P. Barkin, W. Jung, D. Quinn, D. Lamborghini, and J. Burke. "Bronchial artery ligation modifies pulmonary edema after exposure to smoke with acrolein." Journal of Applied Physiology 67, no. 3 (September 1, 1989): 1001–6. http://dx.doi.org/10.1152/jappl.1989.67.3.1001.
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Pulmonary edema can follow smoke inhalation and is believed to be due to the multiple chemical toxins in smoke, not the heat. We have developed a synthetic smoke composed of aerosolized charcoal particles to which one toxin at a time can be added to determine whether it produces pulmonary edema. Acrolein, a common component of smoke, when added to the synthetic smoke, produced a delayed-onset pulmonary edema in dogs in which the extravascular lung water (EVLW) as detected by a double-indicator technique began to rise after 42 +/- 2 (SE) min from 148 +/- 16 to 376 +/- 60 ml at 165 min after smoke exposure. The resulting pulmonary edema was widespread macroscopically but appeared focal microscopically with fibrin deposits in alveoli adjacent to small bronchi and bronchioles. Bronchial vessels were markedly dilated and congested. Monastral blue B when injected intravenously leaked into the walls of the bronchial vessels down to the region of the small bronchioles (less than or equal to 0.5 mm ID) of acrolein-smoke-exposed dogs but not into the pulmonary vessels. Furthermore, ligation of the bronchial arteries delayed the onset of pulmonary edema (87 +/- 3 min, P less than 0.05) and lessened the magnitude (232 +/- 30 ml, P less than 0.05) at 166 +/- 3 min after acrolein-smoke exposure.(ABSTRACT TRUNCATED AT 250 WORDS)
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Zeman, Kirby L., and William D. Bennett. "Growth of the small airways and alveoli from childhood to the adult lung measured by aerosol-derived airway morphometry." Journal of Applied Physiology 100, no. 3 (March 2006): 965–71. http://dx.doi.org/10.1152/japplphysiol.00409.2005.
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Understanding the human development of pulmonary air spaces is important for calculating the dose from exposure to inhaled materials as a function of age. We have measured, in vivo, the air space caliber of the small airways and alveoli at their natural full distension [total lung capacity (TLC)] by aerosol-derived airway morphometry in 53 children of age 6–22 yr and 59 adults of age 23–80 yr. Aerosol-derived airway morphometry utilizes the gravitational settling time of inhaled inert particles to infer the vertical distance necessary to produce the observed loss of particles to the airway surfaces at sequential depths into the lung. Previously, we identified anatomical features of the lung: the caliber of the transitional bronchioles [transitional effective air space dimension (EADtrans)]; the mean linear dimension of the alveoli (EADmin); and a measure of conducting airway volume [volumetric lung depth (VLDtrans)]. In the present study, we found that EADmin increased with age, from 184 μm at age 6 to 231 μm at age 22, generally accounting for the increase in TLC observed over this age range. EADtrans did not increase with TLC, averaging 572 μm, but increased with subject age and height when the entire age range of 6–80 yr is included {EADtrans (μm) = 0.012[height (cm)] × [age (yr)] + 508; P = 0.007}. VLDtrans scaled linearly with lung volume, but VLDtrans relative to TLC did not change with age, averaging 7.04 ± 1.55% of TLC. The data indicate that from childhood (age of 6 yr) to adulthood a constant number of respiratory units is maintained while both the smallest bronchioles and alveoli expand in size to produce the increased lung volume with increased age and height.
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Mantell, Lin L., Thomas H. Shaffer, Stuart Horowitz, Ray Foust, Marla R. Wolfson, Cindy Cox, Poonam Khullar, et al. "Distinct patterns of apoptosis in the lung during liquid ventilation compared with gas ventilation." American Journal of Physiology-Lung Cellular and Molecular Physiology 283, no. 1 (July 1, 2002): L31—L41. http://dx.doi.org/10.1152/ajplung.00037.2001.
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To determine whether liquid ventilation (LV) causes less cell injury and improves lung function compared with conventional gas ventilation (GV), we analyzed pulmonary physiological profiles, lung histology, and cell death in 110- and 120-day preterm lambs, which were randomized to receive either ventilation modality on Fi O2 = 1. LV lungs were well expanded with adequate pulmonary function, whereas GV animals exhibited marked atelectasis, poor pulmonary function, and increased mortality. Both ventilatory strategies induced marked lung cell apoptosis, but with distinct patterns of distribution. Although GV induced apoptosis of epithelium primarily in the lining and within the lumina of bronchioles, LV induced significant apoptosis much more homogeneously throughout lung parenchyma including alveoli and interstitial spaces. These studies suggest that although both forms of ventilation cause regional apoptosis, LV more effectively delivers oxygen and recruits the lung more homogeneously than GV.
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Muntean, Petru-Emil. "Clinical Aspects and Evolution under Current Treatments on Pulmonary Alveolar Phospholipoproteinosis Patients." Folia Medica 61, no. 1 (March 1, 2019): 148–51. http://dx.doi.org/10.2478/folmed-2018-0048.
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Abstract A 34-year-old female smoker (4 packs a year), with the following symptoms: dry cough, moderate dyspnea, fatigue, night sweats and no exposure to respiratory poisoning or contact with tuberculosis. Clinical findings at admission: normal temperature, Hippocratic fingers and cyanosis, diminished bilateral breath sounds, fine bilateral rattling respiratory sounds, rhythmic cardiac noises, oxygen saturation 95%, pulse 87, blood pressure 125/80 mm Hg. Chest computed tomography describes infiltration images of intra-alveolar and intra-bronchial with matte glass pattern, confluent and stretched across all lung segments. Pulmonary biopsy: preserved pulmonary architecture, thick alveolar septs and terminal bronchioles, alveoli and macrophages loaded with lipoprotein material. Bronchial aspirate: negative BAAR, no tumor cells. Bronchoalveolar lavage: opalescent, abundant PAS + appearance. total cell numbers – 4.3 million, macrophages – 34.1%, lymphocytes – 56.9%, neutrophils – 10%, eosinophils – 0.4%, epithelial cells – 33%.The treatment option chosen for this case was total bronchoalveolar lavage for therapeutic purposes. The patient had a rapid favourable evolution and at discharge was recommended a periodic imaging and functional control. Key Messages: Bronchoalveolar lavage is the optimal diagnostic method. Moderate/severe forms, total bronchoalveolar lavage is recommended. Systemic corticotherapy or immunosuppression is not indicated. GM-CSF administered subcutaneously or by nebulization. Rituximab/plasmapheresis are under evaluation. Pulmonary transplantation is indicated in patients who do not respond to therapeutic bronchoalveolar lavage repeated 6-12 months.
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Ewing, Ruth Y., and Antonio A. Mignucci-Giannoni. "A Poorly Differentiated Pulmonary Squamous Cell Carcinoma in a Free-Ranging Atlantic Bottlenose Dolphin (Tursiops Truncatus)." Journal of Veterinary Diagnostic Investigation 15, no. 2 (March 2003): 162–65. http://dx.doi.org/10.1177/104063870301500211.
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A free-ranging, adult, female offshore bottlenose dolphin ( Tursiops truncatus) was found freshly dead in 1999 on Ocean Park Beach in San Juan, Puerto Rico. The left-lung and right-lung pleura had multiple white, firm-to-hard nodules with coagulative necrosis. Histologically, the neoplasms were characterized by multiple well-circumscribed, nonencapsulated expansile masses consisting mostly of polygonal cells with fewer circumferential flattened basaloid cells that compressed alveoli, bronchioles, and bronchi. Neoplastic cells stained positive for cytokeratin, with sporadic vimentin staining, and were negative for epithelial membrane antigen, thyroid transcription factor-1, calretinin, and human mesothelial cell antigen. A diagnosis of poorly differentiated pulmonary squamous cell carcinoma with lymph node and renal metastases was made on the basis of histomorphology and immunohistochemical staining. This is the first documentation of pulmonary squamous cell carcinoma in a dolphin.
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Skerrett, Shawn J., H. Denny Liggitt, Adeline M. Hajjar, Robert K. Ernst, Samuel I. Miller, and Christopher B. Wilson. "Respiratory epithelial cells regulate lung inflammation in response to inhaled endotoxin." American Journal of Physiology-Lung Cellular and Molecular Physiology 287, no. 1 (July 2004): L143—L152. http://dx.doi.org/10.1152/ajplung.00030.2004.
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To determine the role of respiratory epithelial cells in the inflammatory response to inhaled endotoxin, we selectively inhibited NF-κB activation in the respiratory epithelium using a mutant IκB-α construct that functioned as a dominant negative inhibitor of NF-κB translocation (dnIκB-α). We developed two lines of transgenic mice in which expression of dnIκB-α was targeted to the distal airway epithelium using the human surfactant apoprotein C promoter. Transgene expression was localized to the epithelium of the terminal bronchioles and alveoli. After inhalation of LPS, nuclear translocation of NF-κB was evident in bronchiolar epithelium of nontransgenic but not of transgenic mice. This defect was associated with impaired neutrophilic lung inflammation 4 h after LPS challenge and diminished levels of TNF-α, IL-1β, macrophage inflammatory protein-2, and KC in lung homogenates. Expression of TNF-α within bronchiolar epithelial cells and of VCAM-1 within peribronchiolar endothelial cells was reduced in transgenic animals. Thus targeted inhibition of NF-κB activation in distal airway epithelial cells impaired the inflammatory response to inhaled LPS. These data provide causal evidence that distal airway epithelial cells and the signals they transduce play a physiological role in lung inflammation in vivo.
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De Felice, Claudio, Marcello Rossi, Silvia Leoncini, Glauco Chisci, Cinzia Signorini, Giuseppina Lonetti, Laura Vannuccini, et al. "Inflammatory Lung Disease in Rett Syndrome." Mediators of Inflammation 2014 (2014): 1–15. http://dx.doi.org/10.1155/2014/560120.
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Rett syndrome (RTT) is a pervasive neurodevelopmental disorder mainly linked to mutations in the gene encoding the methyl-CpG-binding protein 2 (MeCP2). Respiratory dysfunction, historically credited to brainstem immaturity, represents a major challenge in RTT. Our aim was to characterize the relationships between pulmonary gas exchange abnormality (GEA), upper airway obstruction, and redox status in patients with typical RTT (n= 228) and to examine lung histology in aMecp2-null mouse model of the disease. GEA was detectable in ~80% (184/228) of patients versus ~18% of healthy controls, with “high” (39.8%) and “low” (34.8%) patterns dominating over “mixed” (19.6%) and “simple mismatch” (5.9%) types. Increased plasma levels of non-protein-bound iron (NPBI), F2-isoprostanes (F2-IsoPs), intraerythrocyte NPBI (IE-NPBI), and reduced and oxidized glutathione (i.e., GSH and GSSG) were evidenced in RTT with consequently decreased GSH/GSSG ratios. Apnea frequency/severity was positively correlated with IE-NPBI, F2-IsoPs, and GSSG and negatively with GSH/GSSG ratio. A diffuse inflammatory infiltrate of the terminal bronchioles and alveoli was evidenced in half of the examinedMecp2-mutant mice, well fitting with the radiological findings previously observed in RTT patients. Our findings indicate that GEA is a key feature of RTT and that terminal bronchioles are a likely major target of the disease.
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Geigel, Edgar J., Richard W. Hyde, Irene B. Perillo, Alfonso Torres, Peter T. Perkins, Anthony P. Pietropaoli, Lauren M. Frasier, Mark W. Frampton, and Mark J. Utell. "Rate of nitric oxide production by lower alveolar airways of human lungs." Journal of Applied Physiology 86, no. 1 (January 1, 1999): 211–21. http://dx.doi.org/10.1152/jappl.1999.86.1.211.
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This report describes methods for measuring nitric oxide production by the lungs’ lower alveolar airways (V˙no), defined as those alveoli and bronchioles well perfused by the pulmonary circulation. Breath holding or vigorous rebreathing for 15–20 s minimizes removal of NO from the lower airways and results in a constant partial pressure of NO in the lower airways (Pl). Then the amount of NO diffusing into the perfusing blood will be the pulmonary diffusing capacity for NO (Dno) multiplied by Pl and by mass balance equalsV˙no, or V˙no = Dno(Pl). To measure Pl, 10 normal subjects breath held for 20 s followed by exhalation at a constant flow rate of 0.83 ± 0.14 (SD) l/s or rebreathed at 59 ± 15 l/min for 20 s while NO was continuously measured at the mouth. Dno was estimated to equal five times the single-breath carbon monoxide diffusing capacity. By using breath holding, Pl equaled 2.9 ± 0.8 mmHg × 10−6and V˙noequaled 0.39 ± 0.12 μl/min. During rebreathing Pl equaled 2.3 ± 0.6 mmHg × 10−6 andV˙no equaled 0.29 ± 0.11 μl/min. Measurements of NO at the mouth during rapid, constant exhalation after breath holding for 20 s or during rebreathing provide reproducible methods for measuringV˙no in humans.
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Massaro, G. D., J. Olivier, C. Dzikowski, and D. Massaro. "Postnatal development of lung alveoli: suppression by 13% O2 and a critical period." American Journal of Physiology-Lung Cellular and Molecular Physiology 258, no. 6 (June 1, 1990): L321—L327. http://dx.doi.org/10.1152/ajplung.1990.258.6.l321.
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We studied the effect of 13% O2 on the development of the lung's gas-exchange region. Rats, acclimatized to 13% O2, remained in 13% O2 while pregnant, and were kept with their pups in 13% O2 until the pups were killed or were placed in air at age 15 days; other rats were always in air. Pups kept in 13% O2, unlike air pups, did not decrease mean chord length (Lm) or increase surface-to-volume ratio (S/V) of gas-exchange air spaces between age 2 and 14 days or by age 40 days. Rats placed in air at age 15 days did not change Lm or S/V even in air. Rats kept in 13% O2, and rats placed in air at age 15 days had fewer alveolar attachments to bronchioles than air rats. Gas-exchange air volume (VA) in 13% O2 rats was equal to or greater than in air rats; VA/kg was larger in 13% O2 than air rats. We conclude that maintenance of rats in 13% O2 during gestation and during the period alveoli are formed by septation blocks septation in a seemingly irrevocable manner. We suggest diminished septation decreases radial traction on conducting airways leading to increased VA/kg.
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Mitchell, G. B., M. E. Clark, R. Lu, and J. L. Caswell. "Localization and Functional Characterization of Pulmonary Bovine Odorant-Binding Protein." Veterinary Pathology 48, no. 6 (September 8, 2010): 1054–60. http://dx.doi.org/10.1177/0300985810381907.
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Bovine odorant-binding protein (OBP) may function in olfaction and defense against oxidative injury, but its role in inflammation and defense against bacterial infection has not been investigated. Expression of OBP was discovered in the bovine lung and found to undergo changes in abundance during glucocorticoid administration and stress. OBP was localized to nasal, tracheal, and bronchial mucosal glands with immunohistochemistry, with faint expression in airway surface epithelium and none in bronchioles or alveoli. Two isoforms of OBP were identified, appearing to be differentially regulated during lipopolysaccharide-induced pulmonary inflammation, but differences between these isoforms were not revealed by matrix-assisted laser desorption/ionization–time of flight mass spectrometry. Functional studies showed no effect of OBP on in vitro growth of Escherichia coli or Mannheimia haemolytica under iron-replete or iron-depleted conditions, nor did OBP opsonize bacteria for an enhanced neutrophil oxidative burst. However, OBP did reduce the ability of supernatants from lipopolysaccharide-stimulated macrophages to induce neutrophil chemotaxis. These findings indicate that OBP may inhibit neutrophil recruitment by inflammatory mediators, and they suggest an ability to bind macrophage-derived inflammatory mediators within the airways.
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Di Teodoro, Giovanni, Giuseppe Marruchella, Andrea Di Provvido, Anna Rita D’Angelo, Gianluca Orsini, Paola Di Giuseppe, Flavio Sacchini, and Massimo Scacchia. "Contagious Bovine Pleuropneumonia: A Comprehensive Overview." Veterinary Pathology 57, no. 4 (May 11, 2020): 476–89. http://dx.doi.org/10.1177/0300985820921818.
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Contagious bovine pleuropneumonia (CBPP) is a respiratory disease of cattle that is listed as notifiable by the World Organization for Animal Health. It is endemic in sub-Saharan Africa and causes important productivity losses due to the high mortality and morbidity rates. CBPP is caused by Mycoplasma mycoides subsp. mycoides ( Mmm) and is characterized by severe fibrinous bronchopneumonia and pleural effusion during the acute to subacute stages and by pulmonary sequestra in chronic cases. Additional lesions can be detected in the kidneys and in the carpal and tarsal joints of calves. Mmm infection occurs through the inhalation of infected aerosol droplets. After the colonization of bronchioles and alveoli, Mmm invades blood and lymphatic vessels and causes vasculitis. Moreover, Mmm can be occasionally demonstrated in blood and in a variety of other tissues. In the lung, Mmm antigen is commonly detected on bronchiolar and alveolar epithelial cells, in lung phagocytic cells, within the wall of blood and lymphatic vessels, inside necrotic areas, and within tertiary lymphoid follicles. Mmm antigen can also be present in the cytoplasm of macrophages within lymph node sinuses, in the germinal center of lymphoid follicles, in glomerular endothelial cells, and in renal tubules. A complete pathological examination is of great value for a rapid presumptive diagnosis, but laboratory investigations are mandatory for definitive diagnosis. The purpose of this review is to describe the main features of CBPP including the causative agent, history, geographic distribution, epidemiology, clinical course, diagnosis, and control. A special focus is placed on gross and microscopic lesions in order to familiarize veterinarians with the pathology and pathogenesis of CBPP.
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Trejo, Eduardo Lening, Christian T. Le, Gary Weinstein, Patrick Barr, and Mark Feldman. "Swyer-James-MacLeod Syndrome: A case report in an adult and review of the literature." Case Reports in Internal Medicine 5, no. 4 (October 29, 2018): 23. http://dx.doi.org/10.5430/crim.v5n4p23.
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Swyer-James-MacLeod Syndrome (SJMS) is a rare, unilateral lung disease represented by radiographic translucency of the lung parenchyma secondary to the diminution of the pulmonary vasculature and to the overdistention of the alveoli. It is an uncommon sequela of post-infectious bronchiolitis obliterans (BO) in childhood. Patients with SJMS are often diagnosed in childhood and typically present with recurrent respiratory tract infections. Symptoms during childhood can be mild or absent, leading to a delayed diagnosis in adulthood. SJMS is characterized by the destruction of the small bronchioles and agenesis or hypoplasia of the pulmonary arteries leading to hypoperfusion of the pulmonary parenchyma, resulting in characteristic chest imaging findings of unilateral hyperlucency or translucence.Swyer and James first described this syndrome in 1953. It is a rare disease that can be can be caused by an infection with adenoviruses (types 3, 7, or 21) or Bordetella pertussis, a foreign body in the airway and hydrocarbon inhalation. We present a case of SJMS in whom the adult patient had been misdiagnosed with chronic obstructive pulmonary disease (COPD). She was eventually diagnosed with SJMS based on chest x-ray and chest CT findings of unilateral lung hyperlucency, as well as with scintigraphic findings showing virtually absent perfusion to the left lower lobe of the lung.
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Beresneva, E. A., T. G. Spiridonova, E. A. Zhirkova, M. V. Barinova, T. I. Semenova, P. A. Brygin, O. A. Zabavskaya, E. P. Sokolova, E. A. Lapshina, and A. S. Orlov. "The Importance of X-Ray in Examination of Lungs in Patients with Inhalation Trauma." Russian Sklifosovsky Journal "Emergency Medical Care" 8, no. 3 (November 6, 2019): 279–87. http://dx.doi.org/10.23934/2223-9022-2019-8-3-279-287.
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Relevance Inhalation trauma (IT) is a combined injury of the respiratory tract, lung parenchyma and the central nervous system. Alterations of a mucous membrane during thermochemical airway burn as a result of inhalation of combustion products is most fully described in the literature, while the lesion of pulmonary parenchyma hasn’t been studied. The aim of the study To determine the capabilities and significance of the X-ray method in the study of lungs in patients with IT.Material and methods We examined 184 victims with IT, of which 53 patients had airways burn of the 1st degree, 92 patients had airways burn of the 2nd degree, and 39 patients had airways burn of the 3rd degree. Methods used: X-ray, chest X-ray computed tomography, ultrasound of the chest, study of the function of external respiration, morphological examination of lungs, statistical methods.Results X-ray studies in patients with IT revealed changes in peripheral parts of both lungs like network deformation of pulmonary pattern to forms resembling “mulberries” or “a bunch of grapes”. A study of the function of external respiration revealed signs of decreased lung ventilation and obstructive changes in bronchioles. The X-ray computed tomography of peripheral regions of the lungs in some patients revealed multiple local areas of reduced density with no visible walls corresponding to alveoli holding the air. Histological examination of the peripheral parts of the lungs found round air formations and significantly expanded alveoli. These changes are associated with exhalation disorders due to the constriction of respiratory bronchioles.Conclusion The X-ray method allows to detect signs of damage to the pulmonary parenchyma in patients with IT. Using a statistical evaluation, we showed that the presence of network deformation of the pulmonary pattern under the conditions of IT is an objective feature, confirmed with Cohen’s kappa coefficient (0.6±0.14; 95% CI [0.32–0.88]).
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Mohamed, Marwa T., Sawsan A. Zaitone, Amal Ahmed, Eman T. Mehanna, and Norhan M. El-Sayed. "Raspberry Ketones Attenuate Cyclophosphamide-Induced Pulmonary Toxicity in Mice through Inhibition of Oxidative Stress and NF-ΚB Pathway." Antioxidants 9, no. 11 (November 23, 2020): 1168. http://dx.doi.org/10.3390/antiox9111168.
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Cyclophosphamide (CP) was found to have a potential toxic effect on lung tissues. Raspberry ketones (RKs) are natural antioxidant chemicals isolated from red raspberries (Rubus ideaus). They are commonly used for weight loss and obesity. The current study aimed to evaluate the possible protective effects of RKs against lung toxicity induced by CP. Mice were allocated into six groups: (1) control group; (2) CP group: received a single intraperitoneal dose of CP (150 mg/kg, i.p.); and (3–6) mice were pre-treated orally with different doses of RKs (25, 50, 100, and 200 mg/kg) for 14 consecutive days, respectively, before the administration of an intraperitoneal dose of CP (150 mg/kg, i.p.). Mice were then sacrificed under anesthesia, then lungs were removed for histopathological and biochemical investigations. A single dose of CP markedly altered the levels of some oxidative stress biomarkers and resulted in the fragmentation of DNA in lung homogenates. Histological examination of CP-treated mice demonstrated diffuse alveolar damage that involved apparent hyalinization of membranes, thickening of inter alveolar septa, and proliferation of type II pneumocytes. The immunohistochemical results of CP-treated mice revealed strongly positive Bax and weakly positive proliferating cell nuclear antigen (PCNA) staining reactivity of the nuclei of the lining epithelium of the bronchioles and alveoli. CP activated the cyclooxygenase-2/nuclear factor-kappa B pathway. However, pre-treatment with RKs significantly attenuated CP-evoked alterations in the previously mentioned parameters, highlighting their antioxidant, anti-inflammatory, and anti-apoptotic potential. RKs may be suggested to be a potential candidate to ameliorate CP-induced pulmonary toxicity.
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Grothausmann, Roman, Lars Knudsen, Matthias Ochs, and Christian Mühlfeld. "Digital 3D reconstructions using histological serial sections of lung tissue including the alveolar capillary network." American Journal of Physiology-Lung Cellular and Molecular Physiology 312, no. 2 (February 1, 2017): L243—L257. http://dx.doi.org/10.1152/ajplung.00326.2016.
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Grothausmann R, Knudsen L, Ochs M, Mühlfeld C. Digital 3D reconstructions using histological serial sections of lung tissue including the alveolar capillary network. Am J Physiol Lung Cell Mol Physiol 312: L243–L257, 2017. First published December 2, 2016; doi: 10.1152/ajplung.00326.2016 .—The alveolar capillary network (ACN) provides an enormously large surface area that is necessary for pulmonary gas exchange. Changes of the ACN during normal or pathological development or in pulmonary diseases are of great functional impact and warrant further analysis. Due to the complexity of the three-dimensional (3D) architecture of the ACN, 2D approaches are limited in providing a comprehensive impression of the characteristics of the normal ACN or the nature of its alterations. Stereological methods offer a quantitative way to assess the ACN in 3D in terms of capillary volume, surface area, or number but lack a 3D visualization to interpret the data. Hence, the necessity to visualize the ACN in 3D and to correlate this with data from the same set of data arises. Such an approach requires a large sample volume combined with a high resolution. Here, we present a technically simple and cost-efficient approach to create 3D representations of lung tissue ranging from bronchioles over alveolar ducts and alveoli up to the ACN from more than 1 mm sample extent to a resolution of less than 1 μm. The method is based on automated image acquisition of serially sectioned epoxy resin-embedded lung tissue fixed by vascular perfusion and subsequent automated digital reconstruction and analysis of the 3D data. This efficient method may help to better understand mechanisms of vascular development and pathology of the lung.
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Lemarchand, P., M. Jones, C. Danel, I. Yamada, A. Mastrangeli, and R. G. Crystal. "In vivo adenovirus-mediated gene transfer to lungs via pulmonary artery." Journal of Applied Physiology 76, no. 6 (June 1, 1994): 2840–45. http://dx.doi.org/10.1152/jappl.1994.76.6.2840.
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On the basis of the knowledge that the pulmonary and bronchial circulations have extensive anastomoses, we hypothesized that gene transfer to the endothelium of both pulmonary and bronchial circulations might be achieved with replication-deficient recombinant adenovirus (Ad) vectors administered to the pulmonary circulation. To evaluate this concept, the right upper lobe branches of the sheep pulmonary artery and vein were temporarily occluded and a replication-deficient recombinant Ad vector containing the Escherichia coli lacZ reporter gene coding for beta-galactosidase (beta-Gal) was infused into the lumen of the occluded pulmonary artery. After 15 min, the pulmonary circulation was restored, and 1 or 4 days later the lungs were evaluated by histochemical analysis for beta-Gal activity. Gene transfer and expression were positive in 13 of 17 evaluated sheep. No beta-Gal activity was detected in any category of cells of uninfected lobes. As hypothesized, beta-Gal activity was detected in endothelial cells of the right upper lobe pulmonary and bronchial circulations. Unexpectedly, gene transfer was also observed in epithelial cells of the alveoli and the airways (bronchi and bronchioles) as well as in the epithelium of submucosal glands. These studies demonstrate that it is possible to use Ad vectors for transfer and expression of genes to lung parenchymal cells served by both the pulmonary and bronchial circulations. Furthermore, whereas administration of such vectors via the airways results in gene transfer only to the epithelium, pulmonary artery administration permits gene transfer to both endothelium and epithelium, thus expanding the target range of Ad gene transfer to the lungs.
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Kim, Jinho, John D. O’Neill, N. Valerio Dorrello, Matthew Bacchetta, and Gordana Vunjak-Novakovic. "Targeted delivery of liquid microvolumes into the lung." Proceedings of the National Academy of Sciences 112, no. 37 (August 31, 2015): 11530–35. http://dx.doi.org/10.1073/pnas.1512613112.
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The ability to deliver drugs to specific sites in the lung could radically improve therapeutic outcomes of a variety of lung diseases, including cystic fibrosis, severe bronchopneumonia, chronic obstructive pulmonary disease, and lung cancer. Using conventional methods for pulmonary drug administration, precise, localized delivery of exact doses of drugs to target regions remains challenging. Here we describe a more controlled delivery of soluble reagents (e.g., drugs, enzymes, and radionuclides) in microvolume liquid plugs to targeted branches of the pulmonary airway tree: upper airways, small airways (bronchioles), or the most distal alveoli. In this approach, a soluble liquid plug of very small volume (<1 mL) is instilled into the upper airways, and with programmed air ventilation of the lungs, the plug is pushed into a specific desired (more distal) airway to achieve deposition of liquid film onto the lung epithelium. The plug volume and ventilation conditions were determined by mathematical modeling of plug transport in a tubular geometry, and targeted liquid film deposition was demonstrated in rat lungs by three different in vivo imaging modalities. The experimental and modeling data suggest that instillation of microvolumes of liquid into a ventilated pulmonary airway could be an effective strategy to deliver exact doses of drugs to targeted pathologic regions of the lung, especially those inaccessible by bronchoscopy, to increase in situ efficacy of the drug and minimize systemic side effects.
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Poynter, Matthew E., Rebecca L. Persinger, Charles G. Irvin, Kelly J. Butnor, Hans van Hirtum, Wendy Blay, Nicholas H. Heintz, et al. "Nitrogen dioxide enhances allergic airway inflammation and hyperresponsiveness in the mouse." American Journal of Physiology-Lung Cellular and Molecular Physiology 290, no. 1 (January 2006): L144—L152. http://dx.doi.org/10.1152/ajplung.00131.2005.
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In addition to being an air pollutant, NO2 is a potent inflammatory oxidant generated endogenously by myeloperoxidase and eosinophil peroxidase. In these studies, we sought to determine the effects of NO2 exposure on mice with ongoing allergic airway disease pathology. Mice were sensitized and challenged with the antigen ovalbumin (OVA) to generate airway inflammation and subsequently exposed to 5 or 25 ppm NO2 for 3 days or 5 days followed by a 20-day recovery period. Whereas 5 ppm NO2 elicited no pathological changes, inhalation of 25 ppm NO2 alone induced acute lung injury, which peaked after 3 days and was characterized by increases in protein, LDH, and neutrophils recovered by BAL, as well as lesions within terminal bronchioles. Importantly, 25 ppm NO2 was also sufficient to cause AHR in mice, a cardinal feature of asthma. The inflammatory changes were ameliorated after 5 days of inhalation and completely resolved after 20 days of recovery after the 5-day inhalation. In contrast, in mice immunized and challenged with OVA, inhalation of 25 ppm NO2 caused a marked augmentation of eosinophilic inflammation and terminal bronchiolar lesions, which extended significantly into the alveoli. Moreover, 20 days postcessation of the 5-day 25 ppm NO2 inhalation regimen, eosinophilic and neutrophilic inflammation, pulmonary lesions, and AHR were still present in mice immunized and challenged with OVA. Collectively, these observations suggest an important role for NO2 in airway pathologies associated with asthma, both in modulation of degree and duration of inflammatory response, as well as in induction of AHR.
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Das, Santanu, Stuart Horowitz, Carolyn G. Robbins, Marwan Eid El-Sabban, Namita Sahgal, and Jonathan M. Davis. "Intracellular uptake of recombinant superoxide dismutase after intratracheal administration." American Journal of Physiology-Lung Cellular and Molecular Physiology 274, no. 5 (May 1, 1998): L673—L677. http://dx.doi.org/10.1152/ajplung.1998.274.5.l673.
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We have previously demonstrated that recombinant human copper-zinc superoxide dismutase (rhCu,ZnSOD) is rapidly incorporated into cells of airways, respiratory bronchioles, and alveoli after intratracheal administration. The present study examines whether this cellular uptake is specific for rhCu,ZnSOD or whether other proteins are similarly incorporated into lung cells. Twenty-two newborn piglets (2–3 days old, 1.2–2.0 kg) were intubated and mechanically ventilated. Eight piglets received fluorescently labeled recombinant human manganese superoxide dismutase (rhMnSOD), six received fluorescently labeled albumin, two received free (unbound) fluorescent label intratracheally, and two piglets served as untreated controls. To determine whether endogenous surfactant was important in the process of intracellular uptake, four additional piglets were made surfactant deficient by repeated bronchoalveolar lavage and then given rhCu,ZnSOD intratracheally. All animals were killed after 30–60 min. Lung sections were examined blindly by laser confocal microscopy. Similar to our previous observations with rhCu,ZnSOD, intracellular uptake of rhMnSOD and albumin was noted throughout the lung. The free label did not localize intracellularly. The uptake of proteins did not appear to be affected by surfactant deficiency. rhMnSOD administration was associated with a greater than twofold increase in lung MnSOD activity. Data suggest that the cellular uptake of antioxidants and other proteins in the lung may reflect a nonspecific host defense system for clearing proteins from the lumen of airways and alveoli.
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Vohra, Poonam, and Harsumeet S. Sidhu. "Evaluation of diffuse lung diseases by high resolution computed tomography of chest." International Journal of Research in Medical Sciences 5, no. 4 (March 28, 2017): 1655. http://dx.doi.org/10.18203/2320-6012.ijrms20171282.
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Background: Diffuse lung diseases describe a heterogeneous group of disorders of the lower respiratory tract characterized by inflammation and derangement of the interstitium and loss of functional alveolar units. The disease is not restricted to the interstitium only, as it involves epithelial, endothelial and mesenchymal cells with the disease process extending into the alveoli, acini and bronchioles. Thus, the entire pulmonary parenchyma is involved. The objective of the study was to evaluate diffuse lung diseases by high resolution computed tomography of chest.Methods: A cross-sectional observational study was done in 30 patients. Adult patients of either sex of age group 18 and above showing reticular opacities on chest X-ray and those patients who were incidentally diagnosed as cases of diffuse lung diseases on HRCT chest were included in present study.Results: Reticular opacities were the most common roentgenographic finding followed by reticulonodular opacities. On HRCT, intra and interlobular septal thickening was the most common finding in Idiopathic interstitial pneumonia (usual interstitial pneumonia).Conclusions: High resolution computed tomography (HRCT) is superior to the plain chest X-ray for early detection and confirmation of suspected diffuse lung diseases. In addition, HRCT allows better assessment of the extent and distribution of disease, and it is especially useful in the investigation of patients with a normal chest radiograph. Coexisting disease is often best recognized on HRCT scanning.
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Korol, Т. М., V. P. Sorokoumov, G. V. Datsenko, V. V. Moshkivskyi, О. О. Tymoshchuk, and S. О. Tymoshchuk. "Morphological peculiarities of pneumonia in the use of antibiotics and antioxidants." Reports of Vinnytsia National Medical University 22, no. 4 (December 28, 2018): 604–9. http://dx.doi.org/10.31393/reports-vnmedical-2018-22(4)-04.
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The study of pneumonia and its treatment have been going on for decades, but complex therapy is still not effective enough, which makes it relevant in our time. The purpose of the work is to reveal the morphogenesis of pneumonia in conditions of application of antioxidants. In this work a comparative description of the results of lung necropolis and analyzes of patients' protocols in the treatment of antibiotics with antioxidants and without their using was made, morphological features were compared with different types of pneumonia. Data were obtained from the Vinnytsia Oblast Department of Pathology and Anatomy (OSPAB). 16 patients were divided into 4 groups of 4 people in each (A - died of lobar pneumonia, B - died of gangrenous pneumonia, B - died of segmental pneumonia, G - died of focal pneumonia). Patients are divided into 2 subgroups, depending on the method of treatment (I subgroup - therapy with antibiotics and antioxidants, II subgroup - antibiotics without the use of antioxidants). This allowed us to detect the direct role of antioxidants in the treatment of various types of pneumonia. When we compared morphological differences, depending on the type of treatment, a number of criteria were taken into account, namely: the degree of filling of the alveoli with air, the number of erythrocytes, leukocytes and neutrophils in the field of view. As a result, we have found indisputable evidence that antioxidants are an important element in the treatment of pneumonia. Based on the research, it was found that antioxidant therapy positively affects the course of pneumonia. The histological picture of cranial, gangrenous and segmental pneumonia is characterized by a decrease in segmental neutrophils in the alveoli, and with focal pneumonia in bronchioles. With clover and gangrenous pneumonia, an increase in air in the alveoli and moderate hypertrophy in the vasculature was observed. Morphological changes in pulmonary tissue with the use of antioxidants were to reduce the number of neutrophils and erythrocytes in the exsudate, the presence of small amounts of air in the alveoli, whereas in the other therapy, the alveoli were irritable. Flexibility of interalveolar membranes in the application of antioxidant therapy was more moderate than without its application.
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Fujita, Katsuhide, Sawae Obara, Junko Maru, and Shigehisa Endoh. "Pulmonary inflammation following intratracheal instillation of cellulose nanofibrils in rats: comparison with multi-walled carbon nanotubes." Cellulose 28, no. 11 (May 28, 2021): 7143–64. http://dx.doi.org/10.1007/s10570-021-03943-2.
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Abstract Safety assessment of cellulose nanofibrils (CNFs) is required to accelerate the utilization of these materials in industrial applications. The present study aimed to characterize the effects on rat pulmonary inflammation over a period of 90 days following intratracheal instillation of three types of CNFs or multi-walled carbon nanotubes (MWCNTs) at doses of 0.5, 1.0, or 2.0 mg/kg. The pulmonary inflammatory responses induced by phosphorylated CNFs (CNF1), 2,2,6,6-tetramethylpiperidine-1-oxyl radical (TEMPO)-oxidized CNFs (CNF2), CNFs produced via mechanical defibrillation (CNF3), and MWCNTs were investigated using bronchoalveolar lavage fluid analysis, histopathological findings, and comprehensive gene expression profiling of rat lungs. CNF1 and CNF2 with approximately equal diameter (7.0–8.0 nm) and length (0.8–1.0 µm) distributions induced inflammation after dosing, which was attenuated 90 days post-instillation. CNF3 of relatively greater thickness (21.2 nm) and longer length (1.7 μm) deposited around the terminal bronchioles were observed after instillation. Acute inflammatory responses in the alveoli induced by CNF3 were mild compared with those induced by other materials and attenuated 90 days post-instillation. MWCNTs induced severe pulmonary inflammatory responses that continued during the test period. The inflammation failed to resolve within 90 days post-instillation. A hierarchical cluster analysis revealed comparable gene expression profiles for CNF1, CNF2, and CNF3, whereas profiles of MWCNTs were different from those of other test substances. This study suggests that pulmonary inflammation is associated with the diameter and length distributions of CNFs and that the pulmonary inflammation caused by CNFs is mild compared with that caused by MWCNTs. Graphic abstract
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Flores, Eduardo F., Rudi Weiblen, Margareti Medeiros, Sônia A. Botton, Luiz F. Irigoyen, David Driemeier, Luis F. Schuch, and Mauro Moraes. "A retrospective search for bovine respiratory syncytial virus (BRSV) antigens in histological specimens by immunofluorescence and immunohistochemistry." Pesquisa Veterinária Brasileira 20, no. 4 (December 2000): 139–43. http://dx.doi.org/10.1590/s0100-736x2000000400002.
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Bovine respiratory syncytial virus (BRSV) has been only sporadically identified as a causative agent of respiratory disease in Brazil. This contrasts with frequent reports of clinical and histopathological findings suggestive of BRSV-associated disease. In order to examine a possible involvement of BRSV in cases of calf pneumonia, a retrospective search was performed for BRSV antigens in histological specimens submitted to veterinary diagnostic services from the states of Rio Grande do Sul and Minas Gerais. Ten out of 41 cases examined (24.4%) were positive for BRSV antigens by immunohistochemistry (IPX). Eight of these cases (19.5%) were also positive by indirect immunofluorescence (IFA), and 31 cases (75.6%) were negative in both assays. In the lungs, BRSV antigens were predominantly observed in epithelial cells of bronchioles and less frequently found in alveoli. In one case, antigens were detected only in the epithelium of the alveolar septae. The presence of antigen-positive cells was largely restricted to epithelial cells of these airways. In two cases, positive staining was also observed in cells and cellular debris in the exudate within the pulmonary airways. The clinical cases positive for BRSV antigens were observed mainly in young animals (2 to 12 month-old) from dairy herds. The main microscopic changes included bronchointerstitial pneumonia characterized by thickening of alveolar septae adjacent to airways by mononuclear cell infiltrates, and the presence of alveolar syncytial giant cells. In summary, the results demonstrate the suitability of the immunodetection of viral antigens in routinely fixed tissue specimens as a diagnostic tool for BRSV infection. Moreover, the findings provide further evidence of the importance of BRSV as a respiratory pathogen of young cattle in southeastern and southern Brazil.
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Cutlip, Randall C., Howard D. Lehmkuhl, Kim A. Brogden, and Nan-Jung Hsu. "Lesions in Lambs Experimentally Infected with Ovine Adenovirus Serotype 6 and Pasteurella Haemolytica." Journal of Veterinary Diagnostic Investigation 8, no. 3 (July 1996): 296–303. http://dx.doi.org/10.1177/104063879600800304.
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Twenty-five colostrum-deprived lambs reared in isolation were inoculated with a US variant of ovine adenovirus serotype 6 (OAV-6) strain RTS-151, Pasteurella haemolytica, or a combination of the 2 agents. Although severe pulmonary lesions were caused by each agent, the lesions were more severe and lasted longer with the combined infection. Lesions induced by OAV-6 alone developed 6–9 days after inoculation and lasted for 15 days, the length of the experiment. The lesions were characterized by suppurative inflammation at the junction of the terminal bronchioles and alveoli. Air spaces were filled with neutrophils and sloughed epithelial cells, which often contained large intranuclear inclusions. Lesions induced by P. haemolytica alone developed within 1 day and persisted for no more than 10 days and were characterized by severe pulmonary edema with variable amounts of fibrin. Lesions induced by the combined infection had aspects of each infection alone and resulted in severe disease in 4 of 8 lambs that were permitted to live more than 1 day after inoculation with bacteria. Early pulmonary lesions included edema, limited fibrin deposition, and slight purulent bronchiolitis and alveolitis. Later lesions included necrosis and more fibrin. For lambs inoculated with both pathogens, resolution was incomplete 15 days after inoculation of virus (10 days after inoculation of P. haemolytica). The results presented here corroborate previous findings indicating that the RTS-151 variant of OAV-6 is common in lambs and acts in concert with P. haemolytica to cause severe and often fatal pneumonia.
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Adhikari, Sanjib, Ramesh Sharma Regmi, Siddanta Pandey, Parash Paudel, Nischal Neupane, Shyam Chalise, Ashok Dubey, Sarad Chandra Kafle, and Komal Raj Rijal. "Bacterial Etiology of Bronchoalveolar Lavage Fluid in Tertiary Care Patients and Antibiogram of the Isolates." Journal of Institute of Science and Technology 26, no. 1 (June 17, 2021): 99–106. http://dx.doi.org/10.3126/jist.v26i1.37833.
Full textAbstract:
Bronchoalveolar Lavage (BAL) is a medical technique by which cells and fluids from bronchioles and lung alveoli are withdrawn for diagnosis of disease or evaluation of treatment. Patients with various pulmonary infections follow the procedure of BAL for the disease diagnosis as it has high sensitivity and reliability in diagnosis. To examine the bacterial etiology of BAL fluids among tertiary care patients with pulmonary infections, a cross-sectional study was conducted over a period of three months from August to November 2018. A total of 149 BAL fluid samples were examined and the bacterial agents were isolated and identified by conventional microbiological methods. Out of the 149 samples, 142 samples were culture positive. Among 6 different isolates (4 Gram-negative and 2 Gram-positive), Pseudomonas aeruginosa (45 %) was predominant followed by Klebsiella pneumoniae (25.3 %). A higher infection rate was seen among males (62.4 %) and in the age group 60-70 years (30.0 %). In addition, 25.4 % (36/149) samples were positive in Acid Fast staining. Bacterial recovery from the BAL fluid was significantly associated with the gender and age of the patients (p<0.05). Gentamycin was the least resisted (1.5 %) by Gram-negative isolates followed by Polymyxin-B (3 %). For Gram-positive isolates, Ofloxacin was the most effective drug resisted by none of the isolates followed by Gentamycin. Among the 157 isolates, 125 (79.6 %) were MDR and 35.0 % of Enterobacteriaceae were ESBL producers. Detection of bacterial agents from BAL fluid can be a basis for successful antimicrobial therapy for patients with pulmonary infections.
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Elia, Davide, Olga Torre, Roberto Cassandro, Antonella Caminati, and Sergio Harari. "Ultra-rare cystic disease." European Respiratory Review 29, no. 157 (September 2, 2020): 190163. http://dx.doi.org/10.1183/16000617.0163-2019.
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Diffuse cystic lung diseases include a group of heterogeneous disorders characterised by the presence of cysts within the lung parenchyma, sometimes showing a characteristic computed tomography scan pattern that allows diagnosis. The pathogenetic mechanisms underlying cyst formation in the lung are still not clear and a number of hypotheses have been postulated according to the different aetiologies: ball-valve effect, ischaemic dilatation of small airways and alveoli related to infiltration and obstruction of small vessels and capillaries that supply the terminal bronchioles and connective tissue degradation by matrix metalloproteases. A wide number of lung cyst diseases have been classified into six diagnostic groups according to the aetiology: neoplastic, congenital/genetic, lymphoproliferative, infective, associated with interstitial lung diseases, and other causes. This article focuses on lymphangioleiomyomatosis, pulmonary Langerhans cell histiocytosis and Erdheim–Chester disease, Birt–Hogg–Dubé, follicular bronchiolitis and lymphocytic interstitial pneumonia, light-chain deposition disease and amyloidosis, congenital lung disease associated with aberrant lung development and growth, and cystic lung disease associated with neoplastic lesion. These cystic diseases are epidemiologically considered as ultra-rare conditions as they affect fewer than one individual per 50 000 or fewer than 20 individuals per million. Despite the rarity of this group of disorders, the increasing use of high-resolution computed tomography has improved the diagnostic yield, even in asymptomatic patients allowing prompt and correct therapy and management without the need for a biopsy.
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Khoor, A., M. T. Stahlman, M. E. Gray, and J. A. Whitsett. "Temporal-spatial distribution of SP-B and SP-C proteins and mRNAs in developing respiratory epithelium of human lung." Journal of Histochemistry & Cytochemistry 42, no. 9 (September 1994): 1187–99. http://dx.doi.org/10.1177/42.9.8064126.
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We determined the temporal and spatial distribution of surfactant protein B (pro-SP-B) and C (pro-SP-C) mRNAs and proteins by immunohistochemistry and in situ hybridization in fetal, neonatal, and adult human lung. Pro-SP-B and SP-B mRNA were detected in bronchi and bronchioles by 15 weeks' gestation. After 25 weeks, pro-SP-B, active SP-B peptide, and SP-B mRNA were co-localized in bronchiolo-alveolar portal cells and in Type II epithelial cells. In adult lung, pro-SP-B and SP-B mRNA were detected primarily in non-ciliated bronchiolar epithelial cells and in Type II cells in the alveolus. Pro-SP-C and SP-C mRNA were detected in cells lining terminal airways from 15 weeks' gestation and thereafter. After 25 weeks, SP-C mRNA and precursor protein were detected in epithelial cells of the bronchiolo-alveolar portals and in Type II cells, where expression increased with advancing gestational age. Distinct cellular patterns of staining for pro-SP-B compared with SP-B active peptide support the concept that its proteolytic processing or cellular routing may be influenced by cell type and/or cell differentiation. SP-B and SP-C are expressed primarily in distal conducting and terminal airway epithelium of human fetal lung well in advance of surfactant lipid synthesis or physiologic requirements to produce pulmonary surfactant at the time of birth.
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Shchebentovska, O. M., and M. V. Holubtsova. "Pathogistological changes in the lungs of Felis silvestris catus when infected with Aelurostrongylus abstrusus." Scientific Messenger of LNU of Veterinary Medicine and Biotechnologies 22, no. 97 (May 7, 2020): 169–74. http://dx.doi.org/10.32718/nvlvet9727.
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Aelurostrongylus abstrusus is a parasite that belongs to Nematoda type, Metastrongyloidea superfamily, Angiostrongylidae family, Aelurostrongylus genus and is known as feline helminth, whose intermediate hosts are slugs and snails and reservoir hosts are mice and birds. In cats, Aelurostrongylus abstrusus parasitizes in bronchioles and alveoli, causing specific inflammatory changes in the lower respiratory tract and enables the development of such clinical signs as cough, shortness of breath as well as mucous-purulent discharge from the nasal cavity, when complicated by bacterial infections. Females of parasite lay eggs, which the larvae of L1 hatch from. Subsequently, these larvae cough with bronchial mucus and are swallowed by an animal. They pass through the digestive channel without changes and together with the faeces are released into the environment. The first stage larvae actively penetrate into the body of the slugs, fade twice and are becoming invasive. Duration of larvae development from the stage L1 to L3 depends on the biological cycle of intermediate hosts – slugs and snails. Cats are becoming infected by eating slugs or snails with invasive larvae of the third stage (L3), which are transmitted from the digestive channel of the definitive host (cat) with blood flow to the lungs. Usually, the pathogen has low pathogenicity and invasions are primarily detected after animal’s death, during pathoanatomical dissection. Acute clinical signs of the disease have not been described much up to date. The article presents the results of pathomorphological examination of the cat's lungs infected by Aelurostrongylus abstrusus. The severity of pathomorphological changes of the cat’s pulmonary tissue depends on the intensity of the invasion. When dissected, the lungs appear unevenly coloured, dark red with light and slightly denser areas, where focal parasitic nodules are clearly distinct, surrounded by pink halo and different in size but mostly round, dense consistency. Main morphological characteristic of Aelurostrongylus abstrusus infection is the presence of numerous eggs and L1 larvae in the alveoli but also in the bronchi. Helminth eggs accumulated in the alveolar lumps, surrounded by a thin shell; a severe cellular reaction from lymphocytes, macrophages and histiocytes occurred around this shell. An inflammatory reaction resulted in the thickening of the interstitial tissue with a strong vascular response, characterized by fraying and edema of the vessel walls. The results of pathomorphological researches have shown that the main changes were localized in the lungs and bronchial tubes with diffuse damage of the pulmonary tissue parenchyma and development of croupous pneumonia.
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Condorelli, Peter, Hye-Won Shin, Anna S. Aledia, Philip E. Silkoff, and Steven C. George. "A simple technique to characterize proximal and peripheral nitric oxide exchange using constant flow exhalations and an axial diffusion model." Journal of Applied Physiology 102, no. 1 (January 2007): 417–25. http://dx.doi.org/10.1152/japplphysiol.00533.2006.
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The most common technique employed to describe pulmonary gas exchange of nitric oxide (NO) combines multiple constant flow exhalations with a two-compartment model (2CM) that neglects 1) the trumpet shape (increasing surface area per unit volume) of the airway tree and 2) gas phase axial diffusion of NO. However, recent evidence suggests that these features of the lungs are important determinants of NO exchange. The goal of this study is to present an algorithm that characterizes NO exchange using multiple constant flow exhalations and a model that considers the trumpet shape of the airway tree and axial diffusion (model TMAD). Solution of the diffusion equation for the TMAD for exhalation flows >100 ml/s can be reduced to the same linear relationship between the NO elimination rate and the flow; however, the interpretation of the slope and the intercept depend on the model. We tested the TMAD in healthy subjects ( n = 8) using commonly used and easily performed exhalation flows (100, 150, 200, and 250 ml/s). Compared with the 2CM, estimates (mean ± SD) from the TMAD for the maximum airway flux are statistically higher ( J′awNO = 770 ± 470 compared with 440 ± 270 pl/s), whereas estimates for the steady-state alveolar concentration are statistically lower (CANO = 0.66 ± 0.98 compared with 1.2 ± 0.80 parts/billion). Furthermore, CANO from the TMAD is not different from zero. We conclude that proximal (airways) NO production is larger than previously predicted with the 2CM and that peripheral (respiratory bronchioles and alveoli) NO is near zero in healthy subjects.
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Caprioli, Rafaela A., Caroline P. de Andrade, Fernando F. Argenta, Luiza P. Ehlers, João Fábio Soares, Saulo P. Pavarini, David Driemeier, and Luciana Sonne. "Angiostrongylosis in Cerdocyon thous (crab-eating fox) and Lycalopex gymnocercus (Pampas fox) in Southern Brazil." Parasitology 146, no. 5 (November 5, 2018): 617–24. http://dx.doi.org/10.1017/s0031182018001865.
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AbstractThe objective of this study was to identify species of Angiostrongylus spp. infecting wild carnivores in Southern Brazil, as well as to describe gross and histopathological findings associated with the infection. Necropsy was conducted in 16 wild carnivores parasitized by Angiostrongylus spp. Analysed lungs revealed multifocal dark-red areas of consolidation; in one case, multifocal firm white nodules spread in all pulmonary lobes were observed. In one animal, a focally extensive area of malacia associated with haemorrhage was noted in the encephalon. Histologically, multifocal granulomatous pneumonia or bronchopneumonia, associated with eggs and larvae in blood vessels, lung interstitium, alveoli, and sometimes in bronchi and bronchioles was observed. Adult nematodes were seen within blood vessels. The lesion observed in the brain was characterized as a focally extensive area of malacia associated with gitter cells, haemorrhage, thrombosis and a free intralesional larva. Through molecular techniques, seven positive samples of Angiostrongylus cantonensis were obtained, including the brain sample, and a positive sample of Angiostrongylus vasorum-like, all in Cerdocyon thous. The positive sample for A. vasorum showed 97% similarity with sequences deposited in GenBank, suggesting a new species or subspecies of Angiostrongylus sp. Infection of Lycalopex gymnocercus by Angiostrongylus spp. was confirmed by histological evaluation.
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Barré, Sébastien F., David Haberthür, Tiziana P. Cremona, Marco Stampanoni, and Johannes C. Schittny. "The total number of acini remains constant throughout postnatal rat lung development." American Journal of Physiology-Lung Cellular and Molecular Physiology 311, no. 6 (December 1, 2016): L1082—L1089. http://dx.doi.org/10.1152/ajplung.00325.2016.
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The pulmonary airways are subdivided into conducting and gas-exchanging airways. The small tree of gas-exchanging airways which is fed by the most distal conducting airway represents an acinus. Very little is known about the development of the number of acini. The goal of this study was to estimate their number throughout rat postnatal development. Right middle rat lung lobes were obtained at postnatal day 4–60, stained with heavy metals, paraffin embedded, and scanned by synchrotron radiation-based X-ray tomographic microscopy or imaged with micro computed tomography after critical point drying. The acini were counted by detection of the transitional bronchioles [bronchioalveolar duct junction (BADJ)] by using morphological criteria (thickness of the walls of airways and appearance of alveoli) during examination of the resulting three-dimensional (3D) image stacks. Between postnatal days 4–60, the number of acini per lung remained constant (5,840 ± 547 acini), but their volume increased significantly. We concluded that the acini are formed before the end of the saccular stage (before postnatal day 4) and that the developmental increase of the lung volume is achieved by an increase of the acinar volume and not by an increase of their number. Furthermore, our results propose that the bronchioalveolar stem cells, which are residing in the BADJ, are as constant in their location as the BADJ itself.
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Sahgal, N., J. M. Davis, C. Robbins, S. Horowitz, E. G. Langenback, R. H. Perry, D. Colflesh, J. Tierney, and S. R. Simon. "Localization and activity of recombinant human CuZn superoxide dismutase after intratracheal administration." American Journal of Physiology-Lung Cellular and Molecular Physiology 271, no. 2 (August 1, 1996): L230—L235. http://dx.doi.org/10.1152/ajplung.1996.271.2.l230.
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Hyperoxia and mechanical ventilation cause acute lung injury which may be mitigated by prophylactic intratracheal (IT) administration of recombinant human CuZn superoxide dismutase (rhSOD). However, little is known about the localization, activity, and metabolism of rhSOD after IT administration by instillation or nebulization. Twenty-six newborn piglets were intubated, mechanically ventilated, and given either saline or fluorescently labeled rhSOD (5 mg/kg IT) by instillation or nebulization. Animals were killed 1, 6, or 12 h later. Intact rhSOD (% total fluorescence still associated with macromolecules) and total SOD activity in lung tissue were then determined. Results indicate that, after 1 and 6 h of administration, the majority of rhSOD present in the lung was still associated with the fluorescent label. By 12 h, most of the rhSOD was no longer fluorescently labeled. At 1 h, lung SOD activity increased by 100% compared with untreated control values, with activity remaining elevated at 6 and 12 h. Laser confocal microscopy of lung tissue showed that at 1 h, labeled rhSOD was found throughout the lung, inside a variety of cell types of airways, respiratory bronchioles, and alveoli. Deposition was more homogeneous after nebulization. Negative controls had minimal background fluorescence. These data indicate that after IT administration, rhSOD is rapidly incorporated into cells in the lung and significantly increases lung SOD activity. These observations have important implications for the clinical use of rhSOD in human trials.
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Davim, André, Tereza Dantas, and Márcia Pereira. "Analysis of the Anti-Inflammatory Potential of Pure and Microemulsified Bullfrog Oil in Acute Lung Injury." Journal of Morphological Sciences 35, no. 02 (June 2018): 102–5. http://dx.doi.org/10.1055/s-0038-1669933.
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AbstractInfectious diseases account for more than a third of all hospital admissions, and are highly prevalent in intensive care units. Currently, sepsis is one of the diseases with the highest morbidity and mortality rates worldwide, with death rates reaching up to 60% among intensive care patients, according to statistics from low-income countries. The prominence of multi-resistant microorganisms is rising, while the possibilities of development of new target drugs are being exhausted. Thus, the objective of the present study was to evaluate the anti-inflammatory potential of bullfrog oil in its pure state and in a microemulsion system in an experimental model of sepsis. Mice were separated into three groups and treated with bullfrog oil in its pure state, in a microemulsion, and with saline solution, and subsequently submitted to induction of sepsis. Bronchoalveolar lavages were performed for cell counts, as well as analyses of lung tissue samples. When the washings were analyzed, no statistically significant difference was observed in cell migration between the experimental groups, but a difference was observed between these groups and the saline solution group. When the lung tissue samples were analyzed, intense tissue wear was observed in the bullfrog oil groups, with the presence of cellular infiltrate and rupture of respiratory bronchioles and alveoli. However, in the microemulsion group, no major tissue wear was observed, and the pulmonary parenchyma was more preserved. Thus, we concluded that bullfrog oil in pure form and in a microemulsion system are good modulators of the inflammatory response, with the microemulsion system being more efficient in protecting lung tissue.
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Sow, Fatoumata B., Jack M. Gallup, Alicia Olivier, Subramaniam Krishnan, Andriani C. Patera, JoAnn Suzich, and Mark R. Ackermann. "Respiratory syncytial virus is associated with an inflammatory response in lungs and architectural remodeling of lung-draining lymph nodes of newborn lambs." American Journal of Physiology-Lung Cellular and Molecular Physiology 300, no. 1 (January 2011): L12—L24. http://dx.doi.org/10.1152/ajplung.00169.2010.
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Respiratory syncytial virus (RSV) is the leading cause of lower respiratory tract infection in children worldwide. The understanding of neonatal RSV pathogenesis depends on using an animal model that reproduces neonatal RSV disease. Previous studies from us and others demonstrated that the neonatal lamb model resembles human neonatal RSV infection. Here, we provide an extensive and detailed characterization of the histopathology, viral load, cellular infiltration, and cytokine production in lungs and tracheobronchial lymph nodes of lambs inoculated with human RSV strain A2 over the course of infection. In the lung, RSV titers were low at day 3 postinfection, increased significantly by day 6, and decreased to baseline levels at day 14. Infection in the lung was associated with an accumulation of macrophages, CD4+ and CD8+ T cells, and a transcriptional response of genes involved in inflammation, chemotaxis, and interferon response, characterized by increased IFNγ, IL-8, MCP-1, and PD-L1, and decreased IFNβ, IL-10, and TGF-β. Laser capture microdissection studies determined that lung macrophage-enriched populations were the source of MCP-1 but not IL-8. Immunoreactivity to caspase 3 occurred within bronchioles and alveoli of day 6-infected lambs. In lung-draining lymph nodes, RSV induced lymphoid hyperplasia, suggesting an ability of RSV to enhance lymphocytic proliferation and differentiation pathways. This study suggests that, in lambs with moderate clinical disease, RSV enhances the activation of caspase cell death and Th1-skewed inflammatory pathways, and complements previous observations that emphasize the role of inflammation in the pathogenesis of RSV disease.