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Prativa Pandey, Benu Lohani, Holly Murphy
Pandey, Prativa, Benu Lohani, and Holly Murphy. Pulmonary embolism masquerading as high altitude pulmonary edema at high altitude. High Alt Med Biol. 16:000-000, 2016.-Pulmonary embolism (PE) at high altitude is a rare entity that can masquerade as or occur in conjunction with high altitude pulmonary edema (HAPE) and can complicate the diagnosis and management. When HAPE cases do not improve rapidly with descent, other diagnoses, including PE, ought to be considered. From 2013 to 2015, we identified eight cases of PE among 303 patients with initial diagnosis of HAPE...
October 21, 2016: High Altitude Medicine & Biology
Tianbo Jin, Yongchao Ren, Xikai Zhu, Xun Li, Yongri Ouyang, Xue He, Zhiying Zhang, Yuan Zhang, Longli Kang, Dongya Yuan
Previous studies demonstrated that Angiotensin II Receptor 1 (AGTR1) may play an important role in the development of high-altitude pulmonary edema. We envisaged a role for AGTR1 gene variants in the pathogenesis of HAPE and investigated their potential associations with HAPE in a Han Chinese population. We genotyped seven AGTR1 polymorphisms in 267 patients with diagnosed HAPE and 304 controls and evaluated their association with risk of HAPE. Statistically significant associations were found for the single nucleotide polymorphisms (SNPs) rs275651 (p = 0...
October 6, 2016: Oncotarget
Roberta Rosas Petrocinio, Elga Dias Gomes
BACKGROUND: High altitude retinopathy (HAR) includes a number of diseases related to high altitude such as acute mountain sickness (AMS), high altitude pulmonary edema (HAPE) and high altitude cerebral edema (HACE). High altitude retinopathy is mainly characterized by retinal hemorrhages, usually sparing the macular region, a condition specifically known as high altitude retinal hemorrhages (HARH). The pathogenesis of HARH is unclear. Many studies show that lack of oxygen causes an inadequate autoregulation of retinal circulation, causing vascular incompetence...
2016: Aerospace Medicine and Human Performance
Logan Mills, Chris Harper, Sophie Rozwadowski, Chris Imray
Mills, Logan, Chris Harper, Sophie Rozwadowski, and Chris Imray. High altitude pulmonary edema without appropriate action progresses to right ventricular strain: A case study. High Alt Med Biol. 16:000-000, 2016.-A 24-year-old male developed high altitude pulmonary edema (HAPE) after three ascents to 4061 m over 3 days, sleeping each night at 2735 m. He complained of exertional dyspnea, dry cough, chest pain, fever, nausea, vertigo, and a severe frontal headache. Inappropriate continuation of ascent despite symptoms led to functional impairment and forced a return to the valley, but dyspnea persisted in addition to new orthopnea...
August 30, 2016: High Altitude Medicine & Biology
Yongjun He, Xiyang Zhang, Xun Li, Jieli Du, Xue He, Zhiying Zhang, Yuan Zhang, Longli Kang, Tianbo Jin, Dongya Yuan
BACKGROUND: High altitude pulmonary edema (HAPE) is a type of pneumonedema that mostly occurs under conditions such as high altitude, rapid ascent and hypoxia, amongst others. The ACYP2 polymorphism is suggested to be associated with mean telomere length, and telomere length is significantly longer at a moderate attitude than at sea-level or at simulated high attitude. The present study aimed to determine whethher there is any association between ACYP2 polymorphism and the risk of HAPE...
September 2016: Journal of Gene Medicine
Priyanka Pandey, Zahara Ali, Ghulam Mohammad, M A Qadar Pasha
Biomarkers are essential to unravel the locked pathophysiology of any disease. This study investigated the role of biomarkers and their interactions with each other and with the clinical parameters to study the physiology of high-altitude pulmonary edema (HAPE) in HAPE-patients (HAPE-p) against adapted highlanders (HLs) and healthy sojourners, HAPE-controls (HAPE-c). For this, seven circulatory biomarkers, namely, epinephrine, norepinephrine, tyrosine hydroxylase, transforming growth factor beta 1, tumor necrosis factor alpha (TNFα), platelet-derived growth factor beta beta, and C-reactive protein (CRP), were measured in blood plasma of the three study groups...
2016: Therapeutics and Clinical Risk Management
Marta A King, Carrie A Phillipi, Paula M Buchanan, Linda O Lewin
OBJECTIVE: The written history and physical exam (H&P) is an underutilized source of medical trainee assessment. The authors describe development and validity evidence for Pediatric History and Physical Exam Evaluation (P-HAPEE) rubric: a novel tool for evaluating written H&Ps. METHODS: Through an iterative process, the authors drafted, revised, and implemented the 10-item rubric at three academic institutions in 2014. Eighteen attending physicians and 5 senior residents each scored 10 3(rd) year medical student H&Ps...
August 10, 2016: Academic Pediatrics
Zhenlei Su, Lili Zhu, Jing Wu, Runzhen Zhao, Hong-Long Ji
Nasal potential difference (NPD), a well-established in vivo clinical test for cystic fibrosis, reflects transepithelial cation and anion transport in the respiratory epithelium. To analyze whether NPD can be applied to diagnose hypoxic lung injury, we searched PubMed, EMBASE, Scopus, Web of Science, Ovid MEDLINE, and Google Scholar, and analyzed data retrieved from eleven unbiased studies for high altitude pulmonary edema (HAPE) and respiratory distress syndrome (RDS) using the software RevMan and R. There was a significant reduction in overall basal (WMD -5...
2016: Scientific Reports
Fabio Gsaller, Peter Hortschansky, Takanori Furukawa, Paul D Carr, Bharat Rash, Javier Capilla, Christoph Müller, Franz Bracher, Paul Bowyer, Hubertus Haas, Axel A Brakhage, Michael J Bromley
Azole drugs selectively target fungal sterol biosynthesis and are critical to our antifungal therapeutic arsenal. However, resistance to this class of drugs, particularly in the major human mould pathogen Aspergillus fumigatus, is emerging and reaching levels that have prompted some to suggest that there is a realistic probability that they will be lost for clinical use. The dominating class of pan-azole resistant isolates is characterized by the presence of a tandem repeat of at least 34 bases (TR34) within the promoter of cyp51A, the gene encoding the azole drug target sterol C14-demethylase...
July 2016: PLoS Pathogens
Matthias Peter Hilty, Stefanie Zügel, Michele Schoeb, Katja Auinger, Christoph Dehnert, Marco Maggiorini
Introduction. Acute exposure to high altitude induces inflammation. However, the relationship between inflammation and high altitude related illness such as high altitude pulmonary edema (HAPE) and acute mountain sickness (AMS) is poorly understood. We tested if soluble urokinase-type plasminogen activator receptor (suPAR) plasma concentration, a prognostic factor for cardiovascular disease and marker for low grade activation of leukocytes, will predict susceptibility to HAPE and AMS. Methods. 41 healthy mountaineers were examined at sea level (SL, 446 m) and 24 h after rapid ascent to 4559 m (HA)...
2016: Mediators of Inflammation
Lee J Martin, Margaret Wong
It is unknown whether DNA damage accumulation is an upstream instigator or secondary effect of the cell death process in different populations of adult postmitotic neurons in the central nervous system. In two different mouse models of injury-induced neurodegeneration characterized by relatively synchronous accumulation of mitochondria, oxidative stress, and DNA damage prior to neuronal apoptosis, we enforced the expression of human 8-oxoguanine DNA glycosylase (hOGG1) and human apurinic-pyrimidinic endonuclease/Ref1 (hAPE) using recombinant adenoviruses (Ad)...
June 27, 2016: Mechanisms of Ageing and Development
Poonam Soree, Rajinder K Gupta, Krishan Singh, Koundinya Desiraju, Anurag Agrawal, Praveen Vats, Abhishek Bharadwaj, T P Baburaj, Pooja Chaudhary, Vijay K Singh, Saroj Verma, Amir Chand Bajaj, Shashi Bala Singh
High altitude pulmonary edema (HAPE) susceptibility is associated with EGLN1 polymorphisms, we hypothesized that HAPE-susceptible (HAPE-S, had HAPE episode in past) subjects may exhibit abnormal HIF1α levels in normoxic conditions. We measured HIF1α levels in HAPE-S and HAPE resistant (HAPE-R, no HAPE episode) individuals with similar pulmonary functions. Hemodynamic responses were also measured before and after normobaric hypoxia (Fi02 = 0.12 for 30 min duration at sea level) in both groups. . HIF1α was higher in HAPE-S (320...
2016: Scientific Reports
Zahara Ali, Mohammad Waseem, Rahul Kumar, Priyanka Pandey, Ghulam Mohammad, M A Qadar Pasha
CONTEXT: Few potential candidate genes coding for type I and II receptors of transforming growth factor beta signaling pathway and the serotonin transporter have been associated with pulmonary hypertension (PH). The latter being a phenotype for high altitude pulmonary edema (HAPE), these genes are hypothesized to be crucial markers to investigate under the hypobaric hypoxic environment of high altitude. AIMS: We hence aimed to investigate bone-morphogenetic protein-2 (BMP2), bone morphogenetic protein receptor type-II (BMPR-2), activin receptor-like kinase-1 (ALK-1), serotonin transporter (5-HTT) and serotonin (5-HT) for their contribution, individually/epistatically, to clinical endpoints by altering downstream signaling molecules...
August 22, 2016: Gene
L J Wu
The object in this study was a Han Chinese population in Lhasa, with 3658 m in altitude from Chengdu, which has 505 m in altitude by air. Within 24 to 48 h before the subjects arrived in the plateau, they completed a basic situation questionnaire, under the guidance of medical staff. Within 24 to 48 h after they reached the plateau, the subjects completed an acute plateau disease questionnaire. The diagnostic standard of HAPE and the diagnosis of acute plateau disease were adopted by the Lake Louise diagnostic standards in 1991 and the Chinese Medical Association promulgated the domestic diagnostic criteria on the Third National Plateau Medical Academic Seminar...
2016: Genetics and Molecular Research: GMR
Kevin R Barker, Andrea L Conroy, Michael Hawkes, Holly Murphy, Prativa Pandey, Kevin C Kain
BACKGROUND: The mechanisms underlying acute mountain sickness (AMS) and high-altitude pulmonary edema (HAPE) are not fully understood. We hypothesized that regulators of endothelial function, circulatory homeostasis, hypoxia and cell stress contribute to the pathobiology of AMS and HAPE. METHODS: We conducted a prospective case-control study of climbers developing altitude illness who were evacuated to the CIWEC clinic in Kathmandu, compared to healthy acclimatized climbers...
March 2016: Journal of Travel Medicine
Masatsugu Iwase, Yoshihiro Itou, Kayoko Takada, Kenji Shiino, Yasuchika Kato, Yukio Ozaki
AIMS: Exposure to high altitudes especially with rapid ascent may induce hypoxic pulmonary vasoconstriction (HPV) and pulmonary hypertension (PH) possibly leading to life-threatening high-altitude pulmonary edema (HAPE). The aim of the study was to evaluate the incidence of PH on a 1-day rapid ascent up Mount Fuji (3775 m) in recreational climbers and also to determine the effectiveness of sildenafil for this rapid ascent-induced PH as measured by echocardiography. METHODS AND RESULTS: Twenty-five subjects who climbed Mount Fuji showed significantly increased pulmonary artery systolic pressure (PASP) from 22...
June 2016: Echocardiography
Rajinder K Gupta, G Himashree, Krishan Singh, Poonam Soree, Koundinya Desiraju, Anurag Agrawal, Dishari Ghosh, Deepak Dass, Prassana K Reddy, Usha Panjwani, Shashi Bala Singh
Exaggerated pulmonary pressor response to hypoxia is a pathgonomic feature observed in high altitude pulmonary edema (HAPE) susceptible mountaineers. It was investigated whether measurement of basal pulmonary artery pressure (Ppa) and brain natriuretic peptide (BNP) could improve identification of HAPE susceptible subjects in a non-mountaineer population. We studied BNP levels, baseline hemodynamics and the response to hypoxia (FIo2 = 0.12 for 30 min duration at sea level) in 11 HAPE resistant (no past history of HAPE, Control) and 11 HAPE susceptible (past history of HAPE, HAPE-S) subjects...
2016: Scientific Reports
Wolfgang M Kuebler
No abstract text is available yet for this article.
March 8, 2016: Circulation
Morteza Khodaee, Heather L Grothe, Jonathan H Seyfert, Karin VanBaak
CONTEXT: Athletes at different skill levels perform strenuous physical activity at high altitude for a variety of reasons. Multiple team and endurance events are held at high altitude and may place athletes at increased risk for developing acute high altitude illness (AHAI). Training at high altitude has been a routine part of preparation for some of the high level athletes for a long time. There is a general belief that altitude training improves athletic performance for competitive and recreational athletes...
March 2016: Sports Health
K P Mishra, Navita Sharma, Poonam Soree, R K Gupta, Lilly Ganju, S B Singh
High altitude hypoxia is known to induce an inflammatory response in immune cells. Hypoxia induced inflammatory chemokines may contribute to the development of high altitude pulmonary edema (HAPE) by causing damage to the lung endothelial cells and thereby capillary leakage. In the present study, we were interested to know whether chronic inflammation may contribute to HAPE susceptibility. We examined the serum levels of macrophage inflammatory protein-1α (MIP-1α), monocyte chemoattractant protein-1 (MCP-1) and interleukin-8 in group (1) HAPE Susceptible subjects (n = 20) who had past history of HAPE and group (2) Control (n = 18) consist of subjects who had stayed at high altitude for 2 years without any history of HAPE...
March 2016: Indian Journal of Clinical Biochemistry: IJCB
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