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Query: UMLS:C0344329 (collapse)
 28,634 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 73-year-old woman had dyspnea associated with gradually increasing pulmonary collapse. Despite intensive investigation, the diagnosis was only reached at autopsy 18 months later, when histologic examination of the lungs showed changes of both fibrosing alveolitis and alveolar cell carcinoma.
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PMID:Another presentation of fibrosing alveolitis and alveolar cell carcinoma. 18 Dec 13

Spirographic investigations were carried out in a lot of 125 children and adolescents with surgical exeresis or collapse, performed between 1965 and 1972 for suppurations, tuberculosis and other thoraco-pulmonary diseases. Spirographic determinations before and 1--2 months after surgery showed that the postoperative sequelae were milder in children than in adults. Recovery of the ventilation function was more complete than that of the pulmonary circulation. The necessity of a correct postoperative care and systematic, prolonged respiratory kinesitherapy is emphasized.
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PMID:[Respiratory consequences of thoracopulmonary surgical operations in children and adolescents]. 18 17

The property of the neuronal membrane to be permeable to metabolic modifiers of two regulatory enzymes has been utilized to manipulate the spike activity of inspiratory (I) and expiratory-inspiratory (EI) neurons of the bulbar respiratory centre. The neurons have been classified according to their response to lung distention or collapse (alpha- or beta-type) and to hyperventilation (tonic firing denoted by "+", cessation of activity by "-"). Using extracellular microelectrodes for single unit recording, the medulla oblongata was superfused with a metabolite-containing CSF. The various neuronal sub-types exhibited a differential activating or inhibitory response to one or several metabolic effectors. For example Ialpha+ units were activated by 5 mM glucose-6-phosphatase (G-6-P) and 3.5 mM 3-phosphoglycerate (3-PGA), which both inhibited Ibeta+ neurons, while 5 mM AMP inhibited Ialpha+ much more strongly than Ibeta+ cells. The spike density of Ialpha- and Ibeta- neurons was increased in the presence of 2.5 mM fructose-6-phosphate and 3.5--5 mM AMP, but became reduced by G-6-P. In contrast, 3 mM fructose-1,6-diphosphate and 5 mM 3-PGA activated the Ialpha- but inhibited the Ibeta- neurons. The EIbeta units were characteristically activated by 10 mM citrate, which inhibited all I-type neurons. Activations of the Ialpha and Ibeta neurons led to an accelerated respiratory rate and a higher tidal volume, while the opposite was true for EIbeta neurons. Intravenous injection of metabolites could not duplicate the striking effects under local applications.
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PMID:Metabolic control of respiratory neuronal activity and the accompanying changes in breathing movements of the rabbit. 1. Mainpulation of inspiratory and expiratory-inspiratory neurons. 18 80

Expiratory-related neurons have been classified according to their phase relation within the respiratory cycle, their response to lung distension and collapse (alpha- and beta-type), and to hyperventilation (tonic firing denoted by "+", cessation of activity by "-"). The dorsal surface of the medulla oblongata was superfused with a metabolite-containing CSF solution and the activity of expiratory (E) and inspiratory-expiratory (IE) neurons was extracellulary recorded. The neuronal sub-types established by their functional behaviour could equally be distinguished by their differential response to one or several metabolites. In contrast to inspiratory (I) neurons, Ealpha- Ebeta-, Ebeta- and IEbeta- neurons are inhibited by 3.5 mM AMP, but are activated by 10 mM citrate (with the exception of Ebeta+ units). Furthermore I cells are activated by ATP, while Ealpha and Ebeta units become inhibited. Vagotomy in some instances affected the response of some IEbeta units. An increase in spike density of IEbeta+ and Ealpha- cells is paralleled by a reduction of both the respiratory rate and the tidal volume, while a lower spike density in IEbeta+, IEbeta- and Ealpha- units is accompanied by increases in respiratory rate and tidal volume. In the case of Ebeta+ and Ebeta- cells lower activity is associated with an increased tidal volume. No metabolite-induced changes could be obtained with cardiovascular or unspecific reticular neurons.
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PMID:Metabolic control of respiratory neuronal activity and the accompanying changey-expiratory neurons. 18 81

Phase shifts between inspiratory-related and expiratory-related discharge patterns can be reversibly induced in respiratory neurons following volume changes of the lung, hypocapnic apnea as a result of hyperventilation, or superfusion with certain metabolic modifiers. Phase-spanning expiratory-inspiratory or inspiratory-expiratory discharges are frequently induced in those neurons which are activated either by pulmonary stretch receptors or collapse afferents. The same is true for regulatory effectors which activate key steps of the neuronal metabolism such as ADP, 3-phosphoglycerate, L-glutamine, fructose-6-phosphate and fructose-1,6-diphosphate. In contrast, inhibitory vagal inputs or superfusion with citrate, an inhibitory metabolic modifier, revert preexisting expiratory-inspiratory discharges into a phase-coupled inspiratory pattern. It is postulated that the respiratory neuronal networks represents a time-optimal control system which strives to adjust to a new equilibrium value in a minimum of time, following a given mechanical or chemical perturbation. Following the hypothesis advanced by Cohen (1974) that the phase-spanning units modulate the activity of the in-phase neurons, it is suggested that the additional recruitment of expiratory-inspiratory and inspiratory-expiratory units provides a measure of the quality of time-optimal control and hence a performance index of the system.
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PMID:Metabolic control of respiratory neuronal activity and the accompanying changes in breathing movements of the rabbit. III. Phase shifts in respiratory neurons induced by inflation and collapse of the lung, hyperventilation, or metabolic modifiers. 18 82

A mouse hepatitis virus, strain JHM, grown on DBT cell culture was inoculated intranasally into ICR-SLC weanling mice, and histopathological lesions were studied in relation to viral growth. In the spleen virus titer reached a peak of 10(3) PFU/0.2G 48 H after inoculation, and later it decreased gradually. No virus was detected from the liver throughout the experiment, while some early inflammatory reactions appeared in the spleen and liver without any further development. At 48 h postinoculation there existed degeneration and necrosis in the nasal mucosa and submocosa. In the brain and spinal cord active viral growth was seen at 48 h postinfection or later. In the olfactory bulb mitral cells were also affected with accumulation of glial cells and some meningitis. At 72 to 96 h postinoculation, degeneration of neurons and glial cells were remarkable in the tructus olfactorius, cortex of lobus piriformis, septa pellucidum and commissura anterior accompanying meningitis. At 120 h postinfection, pyramidal cells in the hippocumpus were also degenerated and necrotized, and nodular proliferation and collapse of glial cells, small foci of demyelination and perivascular cuffing were seen in the interbrain. At 144 h postinoculation or later, the lesions developed through the whole brain including the pons and medulla oblongata as well as spinal cord. Brain virus titers showed 10(5) PFU/0.2g at 120 h and 10(4) PFU/0.2g at 144 h postinfection. In mice surviving at 168 hr after inoculation severe demyelinating lesions were observed despite of a decreased virus titer. These findings suggest that intranasally inoculated virus might invade the olfactory bulb through the tractus olfactorius and then produce necrotizing lesions, extending later towards the posterior parts of the central nervous system.
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PMID:Nasoencephalopathy of mice infected intrananasally with a mouse hepatitis virus, JHM strain. 19 27

Obstructive pulmonary collapse was produced by ligation of lobar bronchus in 41 healthy dogs. The atelectatic lung was examined electronmicroscopically by means of vapour fixation, ruthenium red procedure and tricomplex flocculation. The equilibration stability index of Pattle was determined and compared to the electromicroscopic findings. The experimentally produced obstructive pulmonary collapse was a mechanical phenomenon which secondarily caused qualitative changes in the production of the alveolar lining layer.
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PMID:The alveolar lining film in experimental pulmonary collapse. 19 8

Transient electron paramagnetic resonance (EPR) methods are used to examine the spin populations of the light-induced radicals produced in spinach chloroplasts, photosystem I particles, and Chlorella pyrenoidosa. We observe both emission and enhanced absorption within the hyperfine structure of the EPR spectrum of P700+, the photooxidized reaction-center chlorophyll radical (Signal I). By using flow gradients or magnetic fields to orient the chloroplasts in the Zeeman field, we are able to influence both the magnitude and sign of the spin polarization. Identification of the polarized radical and P700+ is consistent with the effects of inhibitors, excitation light intensity and wavelength, redox potential, and fractionation of the membranes. The EPR signal of the polarized P700+ radical displays a 30% narrower line width than P700+ after spin relaxation. This suggests a magnetic interaction between P700+ and its reduced (paramagnetic) acceptor, which leads to a collapse of the P700+ hyperfine structure. Narrowing of the spectrum is evident only in the spectrum of polarized P700+, because prompt electron transfer rapidly separates the radical pair. Evidence of cross-relaxation between the adjacent radicals suggests the existence of an exchange interaction. The results indicate that polarization is produced by a radical pair mechanism between P700+ and the reduced primary acceptor of photosystem I. The orientation dependence of the spin polarization of P700+ is due to the g-tensor anisotropy of the acceptor radical to which it is exchange-coupled. The EPR spectrum of P700+ is virtually isotropic once the adjacent acceptor radical has passed the photoionized electron to a later, more remote acceptor molecule. This interpretation implies that the acceptor radical has g-tensor anisotropy significantly greater than the width of the hyperfine field on P700+ and that the acceptor is oriented with its smallest g-tensor axis along the normal to the thylakoid membranes. Both the ferredoxin-like iron-sulfur centers and the X- species observed directly by EPR at low temperatures have g-tensor anisotropy large enough to produce the observed spin polarization; however, studies on oriented chloroplasts show that the bound ferredoxin centers do not have this orientation of their g tensors. In contrast, X- is aligned with its smallest g-tensor axis predominantly normal to the plane of the thylakoid membranes. This is the same orientation predicted for the acceptor radical based on analysis of the spin polarization of P700+, and indicates that the species responsible for the anisotropy of the polarized P700+ spectrum is probably X-. The dark EPR Signal II is shown to possess anisotropic hyperfine structure (and possibly g-tensor anisotropy), which serves as a good indicator of the extent of membrane alignment.
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PMID:Electron spin polarization in photosynthesis and the mechanism of electron transfer in photosystem I. Experimental observations. 20 69

Hepatic fibrosis may result from collapse after hepatocellular necrosis or from new formation of connective tissue. Fibroplasia, particularly within the lobular parenchyma, is a dynamic process. Newer cellular and biochemical investigations clarified its various steps. The process begins with stimulation of cells to connective tissue formation and can be divided into (1) intracellular synthesis, (2) extracellular maturation, and (3) collagen breakdown. The turnover of the connective tissue in the liver is conspicuously increased in chronic hepatitis of any type, as indicated by an elevation of several cellular and metabolic parameters. They are particularly raised in chronic hepatitis and in alcoholic liver injury. Further development of these parameters in the future should facilitate the analysis of the dynamics of fibroplasia. The strongest stimuli for hepatic fibroplasia are hepatocellular necrosis and inflammation, but ethyl alcohol and steatosis are also stimulating, though to a lesser degree. This explains the particular elevation of the fibroplastic parameters in alcoholic hepatitis. It points, however, also to the possibility that cirrhosis might develop without significant hepatocellular necrosis and inflammation. Perihepatocellular, periductular, and septal fibrosis are the functionally most important localizations leading to additional hepatic injury. The initiation of these types of fibrosis by liver injury points to a vicious circle. Specific anti-fibroplastic therapy is still in infancy.
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PMID:[Hepatic fibrosis--mechanism, dynamics and clinical consequences (author's transl)]. 20 39

GTN were evaluated histologically in reference to biologic behavior and response to chemotherapy. GTN requiring more intensive, multiple drug chemotherapy usually exhibited increased mitotic activity, nuclear atypias, compact growth of cytotrophoblast, and little maturation, as compared to lesions that responded more favorably. Fibrinoid at the interface of tumor and host tissues was associated with a favorable response to drug therapy. Patients requiring more intensive chemotherapy were more likely to present with distant metastases and high levels of hCG prior to treatment and to reach remission only after many courses of treatment. The clinical and morphologic features of fatal cases suggest that these represented the extreme of a biologic continuum, with collapse of defense mechanisms despite chemotherapy. The early recognition by the pathologist of those lesions that may be resistant to chemotherapy is important to the clinician in selection of an optimal treatment protocol.
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PMID:Gestational trophoblastic neoplasms: morphologic correlates of therapeutic response. 20 34


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