Synonyms for peribronchial or Related words with peribronchial

peribronchiolar              perivenular              hypercellularity              periportal              perifollicular              microabscesses              hyalinization              perisinusoidal              subepithelial              hilar              bronchiolar              hypodense              periductal              lymphohistiocytic              eosinophiles              leukocytic              subpleural              pbln              centrilobular              mesangium              subsynovial              perineural              intrapancreatic              histiocytes              midzonal              endomysial              noninflamed              eosinophilia              intrafollicular              inflammtion              perivascular              cryptitis              hyperaemia              leptomeninges              morphometrically              lymphnode              neutrophilia              peribroncheal              polymorphonuclears              desmoplasia              pericentral              basophilia              honeycombing              perimysial              vacuolation              periductular              eosinophillic              cosinophils              aveolar              inflammatorycell             



Examples of "peribronchial"
Peribronchial cuffing is seen in a number of conditions including:
Acute HP is characterized by poorly formed noncaseating interstitial granulomas and mononuclear cell infiltration in a peribronchial distribution with prominent giant cells.
As peribronchial cuffing is a sign rather than a symptom or condition, there is no specific treatment except to treat the underlying cause.
Peribronchial cuffing, also referred to as peribronchial thickening or bronchial wall thickening, is a radiologic sign which occurs when excess fluid or mucus buildup in the small airway passages of the lung causes localized patches of atelectasis (lung collapse). This causes the area around the bronchus to appear more prominent on an X-ray. It has also been described as donut sign, considering the edge is thicker, and the center contains air.
In a study investigating the impact of sarafotoxin-b on respiratory properties, it was found that there was a marked increase in airway resistance. This was likely caused by bronchoconstriction. Bronchoconstriction occurred due to constriction of smooth muscle and airway wall thickening due to peribronchial edema. This peribronchial edema is likely caused by impairment of left ventricular relaxation, elevating microvascular hydrostatic pressure. Proving this theory of edema, during investigation, abundant and frothy fluid was found in tracheal cannulas after sarafotoxin injection.
The mechanism responsible for pneumopericardium is the ‘Macklin effect’ – There is initially an increased pressure gradient between the alveoli and the interstitial space. Increased pressure leads to alveolar rupture, resulting in air getting through to the pericapillary interstitial pulmonary space. This space is continuous with the peribronchial and pulmonary perivascular sheaths. From here, the air tracks to the hilum of the lung and then to the mediastinum. In case of a pericardial tear, this air enters the pericardial cavity and pneumopericardium develops. The condition may remain asymptomatic or may progress to life-threatening conditions like tension pneumopericardium or cardiac tamponade.
X-rays can be used to examine the lung tissue, however it can not be used to positively diagnose geotrichosis. X-rays may show cavitation that is located the walls of the lungs tissues. The lung tissue resemble the early signs of tuberculosis. The results of an x-ray examination of pulmonary geotrichosis presents smooth, dense patchy infiltrations and some cavities. Bronchial geotrichosis shows peribronchial thickening with fine mottling may be present on middle or basilar pulmonary fields. Bronchial geotrichosis usually present itself as non-specific diffuse peribronchical infiltration.
The Intrapulmonary nodes or Lymphatic Vessels of the Lungs originate in two plexuses, a superficial and a deep. The superficial plexus is placed beneath the pulmonary pleura. The deep accompanies the branches of the pulmonary vessels and the ramifications of the bronchi. In the case of the larger bronchi the deep plexus consists of two net-works—one, submucous, beneath the mucous membrane, and another, peribronchial, outside the walls of the bronchi. In the smaller bronchi there is but a single plexus, which extends as far as the bronchioles, but fails to reach the alveoli, in the walls of which there are no traces of lymphatic vessels. The superficial efferents turn around the borders of the lungs and the margins of their fissures, and converge to end in some glands situated at the hilus; the deep efferents are conducted to the hilus along the pulmonary vessels and bronchi, and end in the tracheobronchial lymph nodes. Little or no anastomosis occurs between the superficial and deep lymphatics of the lungs, except in the region of the hilus.
While "SIGLEC8" and mouse "Siglecf " do not appear to derive from the same ancestral gene (they are paralogous, not orthologous), they share a binding preference for 6′-sulfo-sialyl Lewis X and 6′-sulfated sialyl "N"-acetyl-D-lactosamine, similar but distinct patterns of cellular expression, and similar inhibitory functions. For example, Siglec-F is expressed by eosinophils, like Siglec-8, but is also expressed by alveolar macrophages and has not been detected on mouse mast cells or basophils. This functional convergence of Siglec-8 and Siglec-F has permitted in vivo studies to be performed in mouse models of eosinophil-mediated disorders that may provide information about the human system. In a chicken ovalbumin (OVA) model of allergic airway inflammation, the Siglec-F knockout mouse exhibits increased lung eosinophilia, enhanced inflammation, delayed resolution, and exacerbated peribronchial fibrosis. Antibody ligation of Siglec-F has also been shown to inhibit eosinophil-mediated intestinal inflammation and airway remodeling in OVA challenge models. The ST3Gal-III enzyme is necessary for the generation of the natural Siglec-F ligand, which remains unknown but is induced by IL-4 and IL-13 in the airway. Loss of this enzyme leads to enhanced allergic eosinophilic airway inflammation. Despite evidence that Siglec-F binds specifically to 6′-sulfo-sialyl Lewis X and 6′-sulfated sialyl "N"-acetyl-D-lactosamine, in which galactose is sulfated at carbon 6, mice deficient in the two known galactose 6-"O"-sulfotransferases, keratan sulfate galactose 6-"O"-sulfotransferase (KSGal6ST) and chondroitin 6-"O"-sulfotransferase 1 (C6ST-1), express equivalent levels of Siglec-F ligand. These models may shed some light on the regulation of human eosinophil biology by Siglec-8 and the production of natural Siglec-8 ligands in humans. Also like Siglec-8, Siglec-F ligation leads to the apoptosis of eosinophils. However, Siglec-F–induced eosinophil apoptosis is mediated by a mechanism distinct from that employed by Siglec-8, hindering direct comparisons between the mouse and human systems. Siglec-F-induced apoptosis is mediated by caspase activation in mouse eosinophils and does not involve ROS, in contrast to the mechanism reported in Siglec-8–induced apoptosis of human eosinophils. This apoptotic mechanism also does not involve Src family kinases, SHP-1, or NADPH.