Relevant bibliographies by topics / Lung disorder

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Lung disorder'

Author: Grafiati
Published: 4 June 2025
Last updated: 23 June 2025

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Journal articles on the topic "Lung disorder"

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Rannels, S. R., S. L. Rannels, J. G. Sneyd, and E. G. Loten. "Fetal lung development in rats with a glycogen storage disorder." American Journal of Physiology-Lung Cellular and Molecular Physiology 260, no. 6 (1991): L419—L427. http://dx.doi.org/10.1152/ajplung.1991.260.6.l419.

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A New Zealand strain of rats (NZR/Mh) is unable to mobilize liver glycogen due to a deficiency of phosphorylase b kinase. Affected homozygous rats (gsd/gsd) were used to assess the developmental relationship between lung glycogen loss and surfactant phospholipid and protein biosynthesis. Phosphorylase a and phosphorylase b kinase activities were negligible in gsd/gsd fetal lungs compared with controls from gestational day (D18) until postnatal day 1 (D + 1). At D20, tissue glycogen content was 158 +/- 5 and 181 +/- 6 mumol/g lung for control and gsd/gsd, respectively. Control rats mobilized 84% of their lung glycogen by D + 1, whereas the gsd/gsd strain retained 70–80% of D19–20 levels. This apparent fall in gsd/gsd glycogen per gram lung was due to an increase in cellular protein and size. Thus, in controls, total glycogen per lung decreased 65% from D20 to D + 1, whereas DNA doubled. In contrast, gsd/gsd lung growth resulted in a doubling of total lung glycogen, whereas the glycogen-to-DNA ratio remained constant. A lack of cellular glycogenolysis was confirmed by electron microscopy where gsd/gsd type II cells remained large and glycogen-rich over the entire perinatal interval. The potential for glycogen breakdown by a lysosomal alpha-amyloglucosidase in gsd/gsd lungs was estimated in tissue homogenates, whereas rates of hydrolysis of glycogen or p-nitrophenylglucoside were significant and equal to controls at all ages tested. Incorporation of [14C]choline into phosphatidylcholine (PC) of incubated lung slices increased 1.7-fold in control lungs from D20–D21. Over the same interval, PC synthesis in gsd/gsd lungs was 40% lower and did not change.(ABSTRACT TRUNCATED AT 250 WORDS)
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Bakhtiar, Arief, and Renny Irviana Eka Tantri. "Faal Paru Dinamis." Jurnal Respirasi 3, no. 3 (2019): 89. http://dx.doi.org/10.20473/jr.v3-i.3.2017.89-96.

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Pulmonary function is an examination to measure lung volume function using spirometry. Tests with spirometry to detect abnormalities associated with respiratory distress. Spirometry examination is not only to determine the diagnosis but also to assess the severity of obstruction, restriction, and the effects of treatment. Spirometry examination is a test to measure the volume of a person’s static and dynamic lungs with a spirometer tool. Dynamic lung spirometry consists of Forced vital capacity (FVC), Forced expiratory volume (FEVT), Forced expiratory flow200-1200 / FEF 200-1200, Forced expiratory flow25% -75% / FEF 25% -75%, Peak expiratory flow rate / PEFR, Maximum voluntary ventilation / MVV / MBC, FEV1 / FVC Ratio. Ventilation disorders consist of: restriction and obstruction disorders. Restriction is a disorder of lung development by any cause. In obstruction disorder, it shows a decrease in velocity of expiratory flow and normal vital capacity. FEV values, which are widely used are FEV1 / FVC, abnormal when <80%, FEV1 / FVC ratio <80%. This parameter is very important because the accuracy level for obstruction in the central airway is quite large. In obstructive disorder there is generally a decrease in pulmonary dynamic volume. Significant parameters are FEV 1 / FVC, PEFR, and FEF 25-75. The FEV1 / FVC ratio is important because the accuracy level for obstruction in the central airway is considerable, whereas FEF 25-75 indicates obstruction in the small airway.
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Ilyina, N. A., S. L. Ivanov, I. E. Myagkova, and K. V. Prusakova. "The role of radiological research methods in the diagnosis of rare forms of interstitial lung diseases in newborns." Regional blood circulation and microcirculation 22, no. 1 (2023): 92–102. http://dx.doi.org/10.24884/1682-6655-2023-22-1-92-102.

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Introduction. Interstitial lung diseases in newborns associated with diffuse pulmonary developmental disorders are a difficult to detect, as they are rare, formed at the early stages of embryonic development, clinically manifested in the first hours of life as severe respiratory distress syndrome in newborns. The aim. To demonstrate the role of radiation research methods and the difficulties of differential diagnosis of rare forms of interstitial lung diseases associated with diffuse impaired lung development. Materials and methods. Clinical cases of congenital alveolar dysplasia and alveolar-capillary dysplasia with an abnormal location of the pulmonary veins are described in detail, the radiological data, confirmed by the histological data, are presented. Results. Specific changes in the lungs in ILD of newborns associated with a diffuse disorder of lung development, according to X-ray data in the first day of life, are not determined, however, a progressive negative trend has been noted. The lungs computed tomography allows a detailed diagnosis of structural changes in the lung parenchyma, their severity and prevalence. Issues of differential diagnosis of diffuse disorders of lung development in newborns are discussed; the obtained results correlate with the published data. Conclusions. Histological examination is the “gold standard” in the diagnosis of interstitial lung diseases associated with diffuse lung developmental disorders in newborns, but is most often performed at autopsy. The role of radiological methods in the algorithmic approach of diagnostics is increasing due to the accumulated data, the improvement in the quality of detection and recognition of rare variants of interstitial lung diseases in newborns according to CT of the chest organs.
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Mehta, Pankaj, and Girish Trikha. "Lymphoproliferative Disorder of the Lung." Chest 140, no. 4 (2011): 69A. http://dx.doi.org/10.1378/chest.1113561.

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Mitka, Mike. "Researchers Explore Rare Lung Disorder." JAMA 297, no. 5 (2007): 456. http://dx.doi.org/10.1001/jama.297.5.456.

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Garrett, M. Kathryn. "Combined lung and bone disorder." Seminars in Roentgenology 20, no. 4 (1985): 323–24. http://dx.doi.org/10.1016/0037-198x(85)90039-2.

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Sinha, Tanay, Harshita Mishra, Rosna Thomas, et al. "A case of post renal transplant PTLD of lung." Lung India 40, no. 5 (2023): 465–68. http://dx.doi.org/10.4103/lungindia.lungindia_94_23.

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ABSTRACT Post Transplant Lymphoproliferative Disorder (PTLD) is a heterogeneous group of Lymphoid proliferative disorders that occur in patients post Hematogenous or Solid organ transplants. They are closely associated with Ebstein-Barr Virus and can range from polyclonal lesions to frank lymphomas. PTLD is usually a rare post-transplant complication, with the incidence being higher post Lung or Heart Transplantation and less commonly seen post-renal transplantation. The incidence post renal transplantation is less than 1%, with most of the cases being limited to the Gastro-Intestinal Tract and Lymph nodes, and incidence in the lungs being extremely rare. Here we present a case report of PTLD of the lung in a post-renal transplant recipient.
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Kadir, M. Abdul, Tanvir Noor Baig, and K. Siddique-e. Rabbani. "FOCUSED IMPEDANCE METHOD TO DETECT LOCALIZED LUNG VENTILATION DISORDERS IN COMBINATION WITH CONVENTIONAL SPIROMETRY." Biomedical Engineering: Applications, Basis and Communications 27, no. 03 (2015): 1550029. http://dx.doi.org/10.4015/s1016237215500295.

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Conventional spirometry gives information on the overall ventilation of a person's lung; it cannot detect localized disorders in ventilation as occurring in pulmonary edema, pneumonia, tumor, TB, etc. Here we propose a new technique involving the recently developed focused impedance method (FIM) in combination with conventional spirometry to detect localized lung ventilation disorders. Electrical impedance of lung tissue changes as a function of air content and FIM provides a measurement of localized electrical impedance with sensitivity down to reasonable depths inside the body using a few surface electrodes; here we used a six-electrode version. At least four quadrants of the lungs in the frontal plane can be separately measured using a hand-held probe with spring backed skin surface electrodes. Firstly, spatial sensitivity distribution of the six-electrode FIM was obtained using finite element simulation which verified the focusing effect and its depth sensitivity. Percent change in impedance between maximum inspiration and expiration were measured at four quadrants of the chest of a healthy male subject giving four different values; that at the lower right quadrant was found to be the maximum, as also expected based on anatomy. Changes in impedance at this quadrant of the same subject were found to vary proportionately with exhaled air volumes, measured using a bellows-type spirometer. Similar FIM measurements at lower right lung of seven healthy subjects were found to be almost proportional (R2 = 0.7) to the total exhaled air volumes (vital capacity). This was the basis of the new technique. For a healthy individual, the ratio of the local impedance change to vital capacity (VC) will fall within a certain range for each of the four lung quadrants. A lower value at any quadrant would indicate disorder within that quadrant, while a larger value would indicate disorder in a region outside the particular quadrant. The FIM electrode probe can then be moved to take measurements at the other quadrants to locate the region of disorder. This preliminary study indicates that FIM in combination with conventional spirometry could be used to detect localized ventilation defects.
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Agustiyanto, Catur, and Ariani Permatasari. "Farmer’s Lung Disease." Jurnal Respirasi 7, no. 3 (2021): 152. http://dx.doi.org/10.20473/jr.v7-i.3.2021.152-157.

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Occupational lung disease is a lung disease or disorder that occurs due to the inhalation of dangerous particles, mist, vapors, or gases while a person is working. The materials accumulate in the respiratory tract or lungs. The type of lung disease that occurs depends on the size and type of the inhaled material. Substances that cause occupational lung disease are toxic materials called noksa. Noksa is a substance that can cause damage to the anatomical structure of body organs and cause respiratory tract function disorders. The lung disease that many farmers experience is often called farmer's lung disease (FLD). FLD is part of hypersensitivity pneumonitis (HP). HP, also known as extrinsic allergic alveolitis, is a group of lung diseases caused by the inhalation of various antigenic organic materials. The most common cause is exposure to agricultural biological dust derived from straw, mold spores, or other dust. HP can be a secondary reaction due to repeated and prolonged inhalation of specific antigens in sensitive individuals. Diagnosis of FLD is often inaccurate. Many of these cases are diagnosed as idiopathic interstitial lung disease. A complete anamnesis should be performed, especially regarding the history of exposure to moldy hay, previous work, and domestic animals, to determine the existence of a history of exposure to the antigen and to confirm the diagnosis.
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Zinkin, Valery, Irina Vasilyeva, Vladimir Bespalov, and Aleksandr Osetrov. "HIGH-INTENSITY LOW-FREQUENCY ACOUSTIC VIBRATIONS HAVE THE CRITICAL EFFECT ON THE LUNGS." Akustika 32 (March 1, 2019): 5–9. http://dx.doi.org/10.36336/akustika2019325.

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The paper summarizes the findings of experimental studies on animals and literature data to show the characteristics of the lungs exposure to low-frequency acoustic vibrations. Experimental studies were performed on laboratory animals of different species (mice, rats, rabbits, dogs) exposed to low-frequency acoustic vibrations on the test bench set for several months. To assess lung injury, broncho-alveolar lavage, surfactant, biologically active substances in the tissues of the lung, extracellular low-molecular blood DNA were investigated, computerized tomography and postmortem methods were used. It has been established that that prolonged action of high-intensity low-frequency acoustic waves leads to structural damage to the lung parenchyma, lung airiness disorder, bronchi patency and metabolic functions of the lungs. The revealed disorders can serve as a structural basis for the development of such lung diseases as chronic non-specific lung disease of the obstructive bronchitis and/or focal emphysema type. Morphological and functional parameters of the lungs can be considered as criteria for the harmful effect of low-frequency acoustic vibrations on the human body and animals. The obtained experimental data allow us to formulate the concept of the mechanisms of the harmful effect of this physical factor on the lungs. The respiratory system is a critical organ in relation to low-frequency acoustic vibrations. It is necessary to correct the ideas of professional ‘noise’ pathology with regard to the damage to the hearing organ only in the form of neurosensory hearing loss. As it can be seen from the presented findings, the nature of disorders in the body is determined by the noise parameters (intensity, duration and spectral composition).
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Dissertations / Theses on the topic "Lung disorder"

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Bhogal, Ranjev. "The characterisation of binding sites for islet amyloid polypeptide and calcitonin gene-related peptide in mammalian lung." Thesis, Imperial College London, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.261471.

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Pouliot, Robert A. "DEVELOPMENT AND CHARACTERIZATION OF LUNG DERIVED EXTRACELLULAR MATRIX HYDROGELS." VCU Scholars Compass, 2016. http://scholarscompass.vcu.edu/etd/4465.

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Chronic obstructive pulmonary disease (COPD) including emphysema is a devastating condition, increasing in prevalence in the US and worldwide. There remains no cure for COPD, rather only symptomatic treatments. Due to unique challenges of the lung, translation of therapies for acute lung injury to target chronic lung diseases like COPD has not been successful. We have been investigating lung derived extracellular matrix (ECM) hydrogels as a novel approach for delivery of cellular therapies to the pulmonary system. During the course of this work we have developed and characterized a lug derived ECM hydrogel that exhibits “injectability,” allowing cells or dugs to be delivered in a liquid and encapsulated at body temperature. The hydrogel self assembles in <5 minutes and achieves mechanical stiffness similar to other soft tissue ECM hydrogels. The hydrogel can support 3D cell growth and encapsulated cell viability. Encapsulated hMSCs can also still be activated by simulated inflammatory environments. Naïve mouse macrophages exposed to the fully formed gel were not significantly induced to express markers for pro or anti-inflammatory polarized phenotypes, but increased expression for several secreted inflammatory mediators was observed. We also investigated a novel approach for preparing and solubilizing the isolated ECM proteins, using digestion time as a variable for controlling hydrogel density (interconnectivity), mechanical stiffness, component protein size distribution, and cell behavior on fully formed gels. The potential future impact for the presented research includes optimization for future animal studies, expansion to additional applications, and the development of new derivative materials.
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Improgo, Ma Reina D. "Regulation and Function of Neuronal Nicotinic Acetylcholine Receptors in Lung Cancer: A Dissertation." eScholarship@UMMS, 2011. https://escholarship.umassmed.edu/gsbs_diss/550.

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Lung cancer is the leading cause of cancer-related mortality worldwide. The main risk factor associated with lung cancer is cigarette smoking. Research through the years suggests that nicotine in cigarettes promotes lung cancer by activating signaling pathways that lead to cell proliferation, cell survival, angiogenesis, and metastasis. Nicotine’s cellular actions are mediated by its cognate receptors, nicotinic acetylcholine receptors (nAChRs). Here, I describe the expression levels of all known human nAChR subunit genes in both normal and lung cancer cells. Of note, the genes encoding the α5, α3, and β4 subunits (CHRNA5/A3/B4) are over-expressed in small cell lung carcinoma (SCLC), the most aggressive form of lung cancer. This over-expression is regulated by ASCL1, a transcription factor important in normal lung development and lung carcinogenesis. The CHRNA5/A3/B4 locus has recently been the focus of a series of genetic studies showing that polymorphisms in this region confer risk for both nicotine dependence and lung cancer. I show that CHRNA5/A3/B4 depletion results in decreased SCLC cell viability. Furthermore, while nicotine promotes SCLC cell viability and tumor growth, blockade of α3β4 nAChRs inhibits SCLC cell viability. These results suggest that increased expression and function of nAChRs, specifically the α3β4α5 subtype, potentiate the effects of nicotine in SCLC. This dual hit from the carcinogens in tobacco and the cancer-promoting effects of nicotine, may provide a possible mechanism for the increased aggressiveness of SCLC. In addition, nAChRs can be activated by the endogenous ligand, acetylcholine, which acts as an autocrine/paracrine growth factor in SCLC. Increased function of α3β4α5 nAChRs in SCLC could also potentiate acetylcholine’s mitogenic effects. This mechanism, combined with other known autocrine/paracrine growth loops in SCLC, may help explain the ineffectiveness of available therapies against SCLC. In an effort to add to the current arsenal against SCLC, I screened a 1280-compund library using a bioluminescence-based viability assay I developed for high-throughput applications. Primary screening, followed by secondary and tertiary verification, indicate that pharmacologically active compounds targeting neuroendocrine markers inhibit SCLC cell viability.
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Malaney, Prerna. "Significance of PTEN Phosphorylation and its Nuclear Function in Lung Cancer." Scholar Commons, 2016. http://scholarcommons.usf.edu/etd/6539.

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Phosphorylation mediated inactivation of PTEN leads to multiple malignancies with increased severity. However, the consequence of such inactivation on downstream functions of PTEN are poorly understood. Therefore, the objective of my thesis is to ascertain the molecular mechanisms by which PTEN phosphorylation drives lung cancer. PTEN phosphorylation at the C-terminal serine/threonine cluster abrogates its tumor suppressor function. Despite the critical role of the PTEN C-tail in regulating its function, the crystal structure of the C-tail remains unknown. Using bioinformatics and structural analysis, I determined that the PTEN C-tail is an intrinsically disordered region and is a hot spot for post-translational modifications (particularly phosphorylation) and protein-protein interactions. Evolutionary analysis of PTEN and its interacting proteins revealed that the PTEN C-tail has only recently evolved to acquire the ability to engage in a myriad of protein-protein interactions, resulting in its versatile functions. Replacement of the PTEN C-tail serine/threonine residues with alanines generated an artificial mutant, PTEN-4A, which remained “phospho-deficient” and therefore constitutively active. Interestingly, PTEN-4A suppressed cell proliferation and migration to a greater extent than PTEN-WT. PTEN-4A preferentially localized to the nucleus where it suppressed E2F-mediated transcription of cell cycle genes. PTEN physically interacted with the E2F1 protein and at E2F1-binding sites on chromatin, a likely mechanism for its transcriptional function. Further, deletion analysis on various PTEN domains revealed that the C2 domain of PTEN is indispensable for suppression of E2F-related genes. Systematic transcriptional promoter-reporter assays identified disease-associated C2 domain mutations that lose their ability to suppress E2F-mediated transcription, supporting the concept that these mutations are oncogenic in patients. Consistent with my findings, I observed increased level of PTEN phosphorylation and reduced nuclear PTEN levels in lung cancer patient samples. Further, to determine whether the enhanced growth-suppressive properties of PTEN-4A may be due to differential protein-protein interactions, I performed a comparative proteomic profiling of PTEN-WT and PTEN-4A interactomes using the SILAC methodology. Galectin-1 was identified as a candidate protein that binds preferentially to PTEN-WT and inhibits its tumor suppressive function. Taken together, the various tumor suppressive mechanisms of PTEN-4A may be harnessed therapeutically as adjunctive cancer therapy. Use of small molecule inhibitors that hinder PTEN C-tail phosphorylation is a plausible approach to activate PTEN function to reduce tumor burden.
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Lee, Sherman. "The effect of acute cigarette smoke exposure on regional pulmonary blood flow, volume, red cell transit and polymorphonuclear leukocyte retention in the rabbit lung." Thesis, University of British Columbia, 1985. http://hdl.handle.net/2429/24840.

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Regional pulmonary blood flow and volume was measured in ten rabbits anesthetized with pentobarbital (30 mg/kg). Tracheostomy was performed and catheters were placed into the jugular vein and carotid artery. The cardiac ⁹⁹mtc output was measured using the indicator-dilution technique using Tc labelled RBC followed by an injection of radiolabelled macroaggregates (MAA) to mark regional blood flow. Measurements were made both before and after either exposure to cigarette smoke (3 cigarettes for ten minutes at 4 puffs/minute) or sham exposure to air. The animals were sacrificed and the lungs were removed with the vessels tied. The lungs were then inflated and rapidly frozen over liquid nitrogen. The lungs were sampled into slices by vertical height, each slice was further sampled and then gamma counted for the injected isotopes. Regional pulmonary blood flow was calculated by setting the total lung MAA counts for each MAA equal to the cardiac output so that the sample flow was calculated as the fraction of sample counts to total counts times the cardiac output. The blood volume was marked by the labelled RBC and RBC transit was calculated as blood volume (ml) divided by blood flow (ml/sec). In a second series of experiments (N=10) , ⁵¹Cr PMN were injected as a bolus along with ⁹⁹mtc RBC in an indicator-dilution run. Following the injection of the cells, the blood flow was marked with MAAs and then the same sham or smoke treatments were given as in the previous experiments. At the end of ten minutes, the animals were sacrificed and the lungs were processed the same as before. Regional PMN retention was calculated as the [formula omitted]. The data show that smoke exposure increased pulmonary blood volume (p<.01), pulmonary transit time (p<C.05) and the ratio of lung blood volume to central blood volume (p <C-05) without changing central blood volume or cardiac output. Smoke exposure also caused a redistribution of blood flow from upper to lower lung regions (p <C-05). This lengthened the regional RBC transit times in all regions but particularly in the upper zones. These changes in RBC transit had no effect on PMN retention. We conclude that acute smoke exposure lengthens the RBC transit through the pulmonary circulation by increasing blood volume and redistributing blood flow. This change in red cell behavior was not associated with a consistent change in PMN retention in the lungs.<br>Medicine, Faculty of<br>Pathology and Laboratory Medicine, Department of<br>Graduate
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Langhammer, Arnulf. "Respiratory symptoms, lung function, and bone mineral density in a comprehensive population study : The Nord-Trøndelag Health Study 1995-97, The Bronchial Obstruction in Nord-Trøndelag Study." Doctoral thesis, Norwegian University of Science and Technology, Faculty of Medicine, 2003. http://urn.kb.se/resolve?urn=urn:nbn:no:ntnu:diva-126.

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<p>The prevalence of respiratory symptoms and diseases like asthma and chronic obstructive pulmonary disease (COPD), seem to have increased the last decades. The reason for the increase in asthma related symptoms and allergy is uncertain. Some, but not all, of this increase might be ascribed to lowered threshold for use of the diagnosis by medical doctors, change in diagnostic criteria, and increased awareness of symptoms in the population. Studies have indicated that increased prevalence might be explained by a reduction during the last decades in exposure to environmental factors in infancy, These factors are supposed to stimulate the change from Th-2 to TH-1 helper cells (hygiene hypothesis), but even low level of allergen exposure seems to contribute to increase in risk for allergy. The increase in COPD in developed countries is closely related to the smoking pattern during the last two to four decades, and the increased therefore, is mainly seen in women. Further, studies have indicated that women are more vulnerable for the deleterious effects of tobacco smoking than men are; if this is true the current smoking pattern with increased female smoking, is worrying. </p><br>Paper 1 reprinted with kind permission of Journal of Epidemiology and Community Health. Papers 2 and 3 reprinted with kind permission of European Respiratory Society Journals Ltd. Paper 4 reprinted with kind permission of John Wiley and Sons Limited.
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Ekta, Rani. "Ayurvedic ways to treat lung disorders." Thesis, Буковинський державний медичний університет, 2012. http://dspace.bsmu.edu.ua:8080/xmlui/handle/123456789/1422.

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Heeley, Emma Louise. "Lung surfactant and secretory phospholipase A←2 in inflammatory lung disorders." Thesis, University of Southampton, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.323970.

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Kotecha, Sailesh. "The role of cytokines in chronic lung disease of prematurity." Thesis, Imperial College London, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.244032.

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Gonzalez, Brian David. "Prevalence, Predictors, and Correlates of Patient Concealment of a Lung Cancer Diagnosis." Scholar Commons, 2013. http://scholarcommons.usf.edu/etd/4679.

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Most cases of lung cancer have a commonly-understood behavioral etiology. Thus, individuals with lung cancer are often blamed for their illness by others and may therefore seek to avoid this blame by concealing their diagnosis from others. This study sought to determine the prevalence of diagnosis concealment, examine potential predictors of concealment, and test parts of a cognitive-affective-behavioral model of the effects of concealing a concealable stigma among individuals receiving treatment for lung cancer. With regard to predictors of concealment, it was hypothesized that concealment would be positively associated with male gender, introversion, and trait social anxiety and would be negatively associated with social support and the use of seeking guidance and support as a coping strategy. Hypothesized correlates of concealment included poorer self-esteem as well as greater anxiety, cancer-specific distress, and social avoidance. A sample of 117 participants receiving chemotherapy or radiation for stage I-IV non-small cell lung cancer and limited to extensive stage small cell lung cancer was recruited during routine outpatient visits. A medical chart review was conducted to assess clinical factors and participants completed a standard demographic questionnaire as well as measures of coping strategies, introversion, trait social anxiety, social avoidance, social support, anxiety, depression, cancer-specific distress, self-esteem, perceived stigma, public self-consciousness, and private self-consciousness. Results indicated that 31% of participants concealed their diagnosis from others since their diagnosis and 26% concealed their diagnosis in the month preceding their participation in the study. Hypotheses regarding predictors and correlates of concealment were not supported. However, exploratory analyses identified use of alcohol, recency of a recurrence of lung cancer, use of positive reappraisal as a coping strategy, and social support as predictors of concealment as well as internalized shame as a correlate of concealment. These findings serve to extend existing literature on concealing a concealable stigma and support parts of an existing model on the effects of concealment. Future research should aim to test the impacts of concealment in the context of certain social situations to examine longitudinal relationships between predictors and consequences of concealment.
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Books on the topic "Lung disorder"

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Kaushik, Nag, ed. Lung surfactant function and disorder. Taylor & Francis, 2005.

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Fishman, Alfred P. Fishman's pulmonary diseases and disorders. 4th ed. McGraw-Hill Medical, 2008.

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P, Fishman Alfred, ed. Update--Pulmonary diseases and disorders. McGraw-Hill, 1992.

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Sperber, Miriam, ed. Diffuse Lung Disorders. Springer London, 1999. http://dx.doi.org/10.1007/978-1-4471-3440-4.

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P, Fishman Alfred, and Fishman Alfred P, eds. Pulmonary diseases and disorders. 2nd ed. McGraw-Hill, 1988.

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P, Fishman Alfred, and Kotloff Robert Mark, eds. Pulmonary diseases and disorders: Companion handbook. 2nd ed. McGraw-Hill, 1994.

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1952-, Müller B., Wichert P. von, and International Symposium on Lung Surfactant (4th : 1992 : Marburg, Germany), eds. Lung surfactant: Basic research in the pathogenesis of lung disorders. Karger, 1994.

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Pokorski, Mieczyslaw, ed. Lung Cancer and Autoimmune Disorders. Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-09752-7.

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A, Kelly C., ed. Lung disease in rheumatology disorders. Baillière Tindall, 1993.

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P, Fishman Alfred, ed. Fishman's manual of pulmonary diseases and disorders. 3rd ed. McGraw-Hill, 2002.

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Book chapters on the topic "Lung disorder"

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Lakshman Narayana, V., R. S. M. Lakshmi Patibandla, V. Pavani, and P. Radhika. "Optimized Nature-Inspired Computing Algorithms for Lung Disorder Detection." In Nature-Inspired Intelligent Computing Techniques in Bioinformatics. Springer Nature Singapore, 2022. http://dx.doi.org/10.1007/978-981-19-6379-7_6.

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Aydin Acar, Cigdem. "Cystic Fibrosis: Clinical Characteristics, Molecular Mechanisms and Treatment." In Molecular Approaches in Medicine. Nobel Tip Kitabevleri, 2024. http://dx.doi.org/10.69860/nobel.9786053359524.7.

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Cystic Fibrosis (CF) is a genetic disorder that primarily affects the respiratory and digestive systems. This chapter provides a comprehensive overview of CF, including its pathophysiology, clinical manifestations, diagnosis and treatment. CF is caused by mutations in the CFTR gene, which encodes the cystic fibrosis transmembrane conductance regulator protein. This protein is crucial for the regulation of chloride and sodium ions across epithelial membranes. Mutations lead to the production of thick, sticky mucus that clogs the airways and various channels throughout the body. This chapter describes the main symptoms of CF, including chronic cough, progressive lung damage due to recurrent lung infections, and gastrointestinal problems such as pancreatic enzyme deficiency, malabsorption, and meconium ileus in newborns. CF can also affect the liver, sweat glands, and reproductive system. Diagnostic criteria for CF are discussed and the importance of newborn screening, sweat chloride testing, and genetic testing is emphasized. This chapter also reviews current treatment options aimed at managing symptoms and improving quality of life. The role of CFTR modulators, a new class of drugs targeting the underlying genetic disorder, is also highlighted and concludes with a discussion of new therapies and ongoing research aimed at finding a cure for CF.
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Kallianos, Kimberly. "Pulmonary Vascular Disease." In IDKD Springer Series. Springer Nature Switzerland, 2025. https://doi.org/10.1007/978-3-031-83872-9_7.

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Abstract Familiarity with the CT features of pulmonary vascular disease, including pulmonary embolism and pulmonary hypertension, is essential to ensure diagnostic accuracy. Acute and chronic pulmonary emboli have characteristic imaging findings; however, the diagnosis of pulmonary embolism can be challenging due to the high prevalence of image artifacts. Foreign materials may also embolize within the pulmonary arterial system. While relatively uncommon, pulmonary hypertension is disorder where accurate interpretation of CT imaging features is of critical importance. The World Health Organization (WHO) has defined a classification scheme with five groups of pulmonary hypertension patients. Characteristic lung parenchymal findings, in addition to pulmonary arterial abnormalities, are useful in distinguishing the etiology of pulmonary hypertension and in determining the most appropriate management.
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Bromberg, Philip A., and M. Patricia Rivera. "Hematological Disorders." In Diffuse Lung Disorders. Springer London, 1999. http://dx.doi.org/10.1007/978-1-4471-3440-4_13.

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Sperber, Miriam, and D. Novak. "Environmental Lung Disorders." In Diffuse Lung Disorders. Springer London, 1999. http://dx.doi.org/10.1007/978-1-4471-3440-4_9.

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Poletti, Venerino, Gian Luca Casoni, Sara Piciucchi, et al. "Lymphoproliferative Lung Disorders." In Orphan Lung Diseases. Springer London, 2014. http://dx.doi.org/10.1007/978-1-4471-2401-6_31.

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Poletti, Venerino, Sara Piciucchi, Sara Tomassetti, et al. "Lymphoproliferative Lung Disorders." In Orphan Lung Diseases. Springer International Publishing, 2023. http://dx.doi.org/10.1007/978-3-031-12950-6_39.

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Pearly, A. Agnes, and B. Karthik. "A Hybrid Deep Learning Framework for Lung Disorder Detection Using Multi-Scale Feature Extraction and Ensemble Classification." In Communications in Computer and Information Science. Springer Nature Switzerland, 2025. https://doi.org/10.1007/978-3-031-86293-9_10.

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Trigaux, J. P., A. Simonds, and S. W. Clarke. "Cystic Lung Disorders." In Radiologic Diagnosis of Chest Disease. Springer US, 1990. http://dx.doi.org/10.1007/978-1-4684-0347-3_21.

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Poletti, Venerino, Pier Luigi Zinzani, Sara Tomassetti, and Marco Chilosi. "Lymphoproliferative Lung Disorders." In Diffuse Parenchymal Lung Disease. KARGER, 2007. http://dx.doi.org/10.1159/000102700.

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Conference papers on the topic "Lung disorder"

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Eluri, Rama Krishna, Pentyala Tanuja, M. Venkat Rao, Vutla Lavanya, and M. Mokshagna. "Optimizing the Powerhouse: Fine-Tuning CNNs for Superior Lung Disorder Detection." In 2024 First International Conference on Innovations in Communications, Electrical and Computer Engineering (ICICEC). IEEE, 2024. https://doi.org/10.1109/icicec62498.2024.10808691.

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Gurram, Anjaneyulu, and Parthasarathy Ramadass. "Magnetic Resonance Image based Lung Disorder Detection Models in Deep Learning-A Comprehensive Survey." In 2024 5th International Conference on Smart Electronics and Communication (ICOSEC). IEEE, 2024. http://dx.doi.org/10.1109/icosec61587.2024.10722364.

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Pearly, A. Agnes, and B. Karthik. "HybridNet-X: A Hybrid Deep Learning Network with Fuzzy-Enhanced Firefly Algorithm for Lung Disorder Diagnosis Using X-Ray Images." In 2024 International Conference on Innovative Computing, Intelligent Communication and Smart Electrical Systems (ICSES). IEEE, 2024. https://doi.org/10.1109/icses63760.2024.10910459.

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MEHTA, PANKAJ, and GIRISH TRIKHA. "Lymphoproliferative Disorder Of The Lung." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a4551.

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Ijpma, G., A. M. Al-Jumaily, and David White. "Lung Simulator for Breathers Assessment and Occlusion Identification." In ASME 2004 International Mechanical Engineering Congress and Exposition. ASMEDC, 2004. http://dx.doi.org/10.1115/imece2004-59102.

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Many respiratory devices are used to help patients to overcome breathing difficulties. As a first step, these equipments are normally tested and calibrated using a lung simulator. Many of the available positive pressure lung simulators achieve the purpose of simulation; however, they neither resemble actual lung vacuum conditions nor can be used for assessing breathing disorders. In this research a special purpose negative pressure simulator is proposed, developed, instrumented and tested. In addition to the lung elasticity, resistance, and compliance, the simulator replicates the vacuum conditions in the lung cavity. It also can be used for occlusion and ailments identification and other disorder diagnostics.
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Hajmurad, M., D. Matthews, and N. Barron. "Post Transplant Lymphoproliferative Disorder Masquerading as a Lung Mass After Lung Transplantation." In American Thoracic Society 2022 International Conference, May 13-18, 2022 - San Francisco, CA. American Thoracic Society, 2022. http://dx.doi.org/10.1164/ajrccm-conference.2022.205.1_meetingabstracts.a3358.

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Mirzan, H., B. Colaco, and V. Arunthari. "Incidental Finding of a Very Rare Congenital Lung Disorder." In American Thoracic Society 2023 International Conference, May 19-24, 2023 - Washington, DC. American Thoracic Society, 2023. http://dx.doi.org/10.1164/ajrccm-conference.2023.207.1_meetingabstracts.a3679.

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Shigdel, R., E. H. Thorarinsdottir, N. O. Jögi, et al. "Lung function and sleep disorder in general population: RHINESA study." In ERS International Congress 2022 abstracts. European Respiratory Society, 2022. http://dx.doi.org/10.1183/13993003.congress-2022.3924.

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Shahzadi, M., T. Nazir, S. Singh, and J. Sharma. "Lung Nodule Dilemma: Differentiating Between Connective Tissue Disorder and Lung Malignancy: A Comprehensive Case Report." In American Thoracic Society 2024 International Conference, May 17-22, 2024 - San Diego, CA. American Thoracic Society, 2024. http://dx.doi.org/10.1164/ajrccm-conference.2024.209.1_meetingabstracts.a5328.

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Kross, EK, DS Davydow, and CL Hough. "Posttraumatic Stress Disorder and Depression among Survivors of Acute Lung Injury." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a4662.

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Reports on the topic "Lung disorder"

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Ly, Lena, Jennifer Philip, Peter Hudson, and Natasha Smallwood. Singing for people with advance chronic respiratory diseases: a qualitative meta-synthesis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, 2022. http://dx.doi.org/10.37766/inplasy2022.8.0017.

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Review question / Objective: This study undertook a meta-synthesis of qualitative data with the aim of collating, synthesizing, and evaluating the current evidence regarding the experiences of singing for people with advanced chronic respiratory disease. Condition being studied: Advanced respiratory illnesses are disorders that impact the airways and other structures of the lung. People with lung cancer, chronic obstructive pulmonary disease (COPD) and interstitial lung disease (ILD) frequently experience progressive, frightening breathlessness, cough and fatigue, which affect their quality of life. Furthermore, people with advanced chronic respiratory disease (CRD) and their carers experience a high prevalence of loneliness and uncertainty, especially if breathlessness is felt to herald death and thus, require both psychological and practical supportive care to cope with their symptoms.
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Zhuo, Guifeng, Hengwang Yu, Ran Liao, et al. Auricular point pressing therapy for obstructive sleep apnea hypoventilation syndrome: A protocol for systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, 2022. http://dx.doi.org/10.37766/inplasy2022.5.0015.

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Review question / Objective: Patients with obstructive sleep apnea hypoventilation syndrome (OSAHS) suffer from repeated hypoxemia, hypercapnia, and sleep structure disorders at night, leading to daytime lethargy and complications of heart, brain, lung, and blood vessel damage, which seriously affect their quality of life and life span. Clinical studies have shown that auricular point pressing therapy has an excellent therapeutic effect on OSAHS, and has the potential to be a complementary and alternative therapy for patients with OSAHS. Currently, systematic reviews and meta-analyses evaluating the efficacy and safety of electroacupuncture for the treatment of OSAHS are lacking. This study aimed to address this deficiency. Information sources: RCTs of auricular point pressing therapy in the treatment of OSAHS were searched in the Web of Science, PubMed, Cochrane Library, Embase, Allied and Complementary Medicine Database (AMED), China Science and Technology Journal Database (VIP), China National Knowledge Infrastructure (CNKI), and Wan-Fang Database. The retrieval time is from database construction to the present.
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99mTc SPECT-CT, Consensus QIBA Profile. Chair Yuni Dewaraja and Robert Miyaoka. Radiological Society of North America (RSNA)/Quantitative Imaging Biomarkers Alliance (QIBA), 2019. https://doi.org/10.1148/qiba/20191021.

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The quantification of 99mTc labeled biomarkers can add unique value in many different settings, ranging from clinical trials of investigation new drugs to the treatment of individual patients with marketed therapeutics. For example, goals of precision medicine include using companion radiopharmaceutical diagnostics as just-in-time, predictive biomarkers for selecting patients to receive targeted treatments, customizing doses of internally administered radiotherapeutics, and assessing responses to treatment. This Profile describes quantitative outcome measures that represent proxies of target concentration or target mass in topographically specific volumes of interest (VOIs). These outcome measures are usually expressed as the percent injected dose (i.e., radioactivity) per mL of tissue (%ID/mL), a standard uptake value ratio (SUVr), or a target-to-background ratio (TBR). In this profile, targeting is not limited to any single mechanism of action. Targeting can be based on interaction with a cell surface protein, an intracellular complex after diffusion, protein-mediated transport, endocytosis, or mechanical trapping in a capillary bed, as in the case of transarterial administration of embolic microspheres. Regardless, the profile focuses on quantification in well-defined volumes of interest. Technetium-99m based dopamine transporter imaging agents, such as TRODAT, are nearly direct links with some aspects of the predecessor profile on 123I-ioflupane for neurodegenerative disorders. (See www.qibawiki.rsna.org ) Cancer is often a base case of convenience for new material in this profile, but the intent is to create methods that can be useful in other therapeutic areas where the diseases are characterized by spatially-limited anatomical volumes, such as lung segments, or multifocal aggregations of targets, such as white blood cell surface receptors on pulmonary nodules in patients with sarcoidosis. Neoplastic masses that can be measured with x-ray computed tomography (CT) or magnetic resonance imaging (MRI) are the starting point. However, the intent is to create a profile that can be extrapolated to diseases in other therapeutic areas that are also associated with focal, or multi-focal pathology, such as pulmonary granulomatous diseases of autoimmune or infectious etiology, non-oncological diseases of organs such as polycystic kidney disease, and the like. The criteria for measurability are based on the current resolution of most SPECT-CT systems in clinical practice, and are independent of criteria for measurability in other contexts. For this SPECT profile, conformance requires that a “small” VOI must be greater than 30 mL to be measurable. It is understood that much smaller VOIs can sometimes exhibit high conspicuity on SPECT, but these use cases are beyond the scope of this profile and will not be tested for conformance in this version. It is left to individual stakeholders to show the extent to which they can achieve conformance when measuring VOIs less than 30 mL. The detection of smaller changes during clinical trials of large groups can be achieved by referring to the QIBA companion guidance on powering trials. The Claims (Section 2) asserts that compliance with the specifications described in this Profile will produce cross sectional estimates of the concentration of radioactivity [kBq/mL] in a volume of interest (VOI) or a target-to-background ratio (TBR) within a defined confidence interval (CI), and distinguish true biological change from system variance (i.e., measurement error) in individual patients or clinical trials of many patients who will be studied longitudinally with 99mTc SPECT agents. Both claims are founded on observations that target density varies between patients with the same disease as well as within patients with multi-focal disease. The Activities (Section 3) describes the requirements that are placed on the Actors who need to achieve the Claim. Section 3 specifies what the actors must do in order to estimate the amount of radioactivity in a volume of interest, expressed in kBq/mL (ideal) or as a TBR (acceptable) within a 95% CI surrounding the true value. Measurands such as %ID/mL are targets for nonclinical studies in animal models that use terminal sacrifice to establish ground truth for imaging studies. TBRs can be precarious, as the assumptions that depend on the physiology of the background regions matching the volume of interest can be hard to accept sometimes. It is up to each individual stakeholder to qualify the background regions used in their own use case. This profile qualifies only a few in some very limited contexts as examples. The Assessment Procedures (Section 4) for evaluating specific requirements are defined as needed. The requirements are focused on achieving sufficient accuracy and avoiding unnecessary variability of the measurements. The clinical performance target is to achieve a 95% confidence interval for concentration in units of kBq/mL (kilobequerels per milliliter) or %ID/mL (percent injected dose per milliliter) or TBR with both a reproducibility and a repeatability of +/- 8% within a single individual under zero-biological-change conditions. This document is intended to help clinicians basing decisions on these biomarkers, imaging staffs generating measurements of these biomarkers, vendors who are developing related products, purchasers of such products, and investigators designing trials. Note that this document only states requirements to achieve the claims, not “requirements on standard of care” nor compliance with any particular protocol for treating participants in clinical trial settings. Conformance to this Profile is secondary to properly caring for patients or adhering to the requirements of a protocol. QIBA Profiles addressing other imaging biomarkers using CT, MRI, PET and Ultrasound can be found at www.qibawiki.rsna.org.
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CAMHS around the Campfire journal club – Technology-delivered CBT for pediatric anxiety disorders (recording). ACAMH, 2022. http://dx.doi.org/10.13056/acamh.20251.

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For this session we are welcomed Dr. Matti Cervin, Lund University, and Dr Tobias Lundgren, Associate Professor, Karolinska Institutet, to discuss their JCPP paper 'Technology-delivered cognitive-behavioral therapy for pediatric anxiety disorders: a meta-analysis of remission, posttreatment anxiety, and functioning'.
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Critical appraisal - Technology-delivered cognitive-behavioral therapy for pediatric anxiety disorders: a meta-analysis of remission, post treatment anxiety, and functioning'. ACAMH, 2022. http://dx.doi.org/10.13056/acamh.20258.

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This critical appraisal was undertaken by Information Scientist Douglas Badenoch and form part of the wider session for our informal journal club CAMHS around the Campfire. This appraisal, and the session, looked at the JCPP paper by Dr. Matti Cervin, Lund University, 'Technology-delivered cognitive-behavioral therapy for pediatric anxiety disorders: a meta-analysis of remission, posttreatment anxiety, and functioning'.
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