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Fredriksson Sundbom, MarcusORCID iD iconorcid.org/0000-0002-3586-4197
Publications (4 of 4) Show all publications
Fredriksson Sundbom, M., Sangfelt, A., Lindgren, E., Nyström, H., Johansson, G., Brändstrom, H. & Haney, M. (2022). Respiratory and circulatory insufficiency during emergent long-distance critical care interhospital transports to tertiary care in a sparsely populated region: a retrospective analysis of late mortality risk. BMJ Open, 12(2), Article ID e051217.
Open this publication in new window or tab >>Respiratory and circulatory insufficiency during emergent long-distance critical care interhospital transports to tertiary care in a sparsely populated region: a retrospective analysis of late mortality risk
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2022 (English)In: BMJ Open, E-ISSN 2044-6055, Vol. 12, no 2, article id e051217Article in journal (Refereed) Published
Abstract [en]

Objectives: To test if impaired oxygenation or major haemodynamic instability at the time of emergency intensive care transport, from a smaller admitting hospital to a tertiary care centre, are predictors of long-term mortality.

Design: Retrospective observational study. Impaired oxygenation was defined as oxyhaemoglobin %–inspired oxygen fraction ratio (S/F ratio)<100. Major haemodynamic instability was defined as a need for treatment with norepinephrine infusion to sustain mean arterial pressure (MAP) at or above 60 mm Hg or having a mean MAP <60. Logistic regression was used to assess mortality risk with impaired oxygenation or major haemodynamic instability.

Setting: Sparsely populated Northern Sweden. A fixed-wing interhospital air ambulance system for critical care serving 900 000 inhabitants.

Participants: Intensive care cases transported in fixed-wing air ambulance from outlying hospitals to a regional tertiary care centre during 2000–2016 for adults (16 years old or older). 2142 cases were included.

Primary and secondary outcome measures: All-cause mortality at 3 months after transport was the primary outcome, and secondary outcomes were all-cause mortality at 1 and 7 days, 1, 6 and 12 months.

Results: S/F ratio <100 was associated with increased mortality risk compared with S/F>300 at all time-points, with adjusted OR 6.3 (2.5 to 15.5, p<0.001) at 3 months. Major haemodynamic instability during intensive care unit (ICU) transport was associated with increased adjusted OR of all-cause mortality at 3 months with OR 2.5 (1.8 to 3.5, p<0.001).

Conclusion: Major impairment of oxygenation and/or major haemodynamic instability at the time of ICU transport to get to urgent tertiary intervention is strongly associated with increased mortality risk at 3 months in this cohort. These findings support the conclusion that these conditions are markers for many fold increase in risk for death notable already at 3 months after transport for patients with these conditions.

Place, publisher, year, edition, pages
BMJ Publishing Group Ltd, 2022
National Category
Anesthesiology and Intensive Care
Identifiers
urn:nbn:se:umu:diva-192545 (URN)10.1136/bmjopen-2021-051217 (DOI)000780118100029 ()35168967 (PubMedID)2-s2.0-85124679769 (Scopus ID)
Funder
Region Västerbotten
Available from: 2022-02-16 Created: 2022-02-16 Last updated: 2023-09-05Bibliographically approved
Fredriksson Sundbom, M., Sandberg, J., Johansson, G., Brändstrom, H., Nyström, H. & Haney, M. (2021). Total Mission Time and Mortality in a Regional Interhospital Critical Care Transport System: A Retrospective Observational Study. Air Medical Journal, 40(6), 404-409
Open this publication in new window or tab >>Total Mission Time and Mortality in a Regional Interhospital Critical Care Transport System: A Retrospective Observational Study
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2021 (English)In: Air Medical Journal, ISSN 1067-991X, E-ISSN 1532-6497, Vol. 40, no 6, p. 404-409Article in journal (Refereed) Published
Abstract [en]

Objective: We assessed the mortality risk related to the time for intensive care unit transport in a geographically large regional health care system.

Methods: Patient-level data from critical care ambulance missions were analyzed for 2,067 cases, mission time, and relevant patient factors. Mission time was used as a surrogate for the “distance” to tertiary care, and mortality at 7 days and other intervals was assessed.

Results: No increased mortality risk was found at 7 days in an unadjusted regression analysis (odds ratio = 1.00; range, 0.999-1.002; P = .66). In a secondary analysis, an increased mortality risk was observed in longer mission time subgroups and at later mortality assessment intervals (> 375 mission minutes and 90-day mortality; adjusted hazard ratio = 1.56; range, 1.07-2.28; P = .02). Negative changes in oxygenation and hemodynamic status and transport-related adverse events were associated with the longest flight times. Measurable but small changes during flight were noted for mean arterial pressure and oxygenation.

Conclusion: The main finding was that there was no overall difference in mortality risk based on mission time. We conclude that transport distances or accessibility to critical care in the tertiary care center in a geographically large but sparsely populated region is not clearly associated with mortality risk.

Place, publisher, year, edition, pages
Elsevier, 2021
Keywords
Emergency, Emergency Medicine, Intensive Care, Critical Care, Fixed-wing
National Category
Anesthesiology and Intensive Care
Identifiers
urn:nbn:se:umu:diva-189651 (URN)10.1016/j.amj.2021.08.005 (DOI)2-s2.0-85115193240 (Scopus ID)
Funder
Region Västerbotten
Available from: 2021-11-17 Created: 2021-11-17 Last updated: 2022-04-14Bibliographically approved
Thanikkal, E. J., Kumar Gahlot, D., Liu, J., Fredriksson Sundbom, M., Gurung, J. M., Ruuth, K., . . . Francis, M. S. (2019). The Yersinia pseudotuberculosis Cpx envelope stress system contributes to transcriptional activation of rovM. Virulence, 10(1), 37-57
Open this publication in new window or tab >>The Yersinia pseudotuberculosis Cpx envelope stress system contributes to transcriptional activation of rovM
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2019 (English)In: Virulence, ISSN 2150-5594, E-ISSN 2150-5608, Vol. 10, no 1, p. 37-57Article in journal (Refereed) Published
Abstract [en]

The Gram-negative enteropathogen Yersinia pseudotuberculosis possesses a number of regulatory systems that detect cell envelope damage caused by noxious extracytoplasmic stresses. The CpxA sensor kinase and CpxR response regulator two-component regulatory system is one such pathway. Active Cpx signalling upregulates various factors designed to repair and restore cell envelope integrity. Concomitantly, this pathway also down-regulates key determinants of virulence. In Yersinia, cpxA deletion accumulates high levels of phosphorylated CpxR (CpxR~P). Accumulated CpxR~P directly repressed rovA expression and this limited expression of virulence-associated processes. A second transcriptional regulator, RovM, also negatively regulates rovA expression in response to nutrient stress. Hence, this study aimed to determine if CpxR~P can influence rovA expression through control of RovM levels. We determined that the active CpxR~P isoform bound to the promoter of rovM and directly induced its expression, which naturally associated with a concurrent reduction in rovA expression. Site-directed mutagenesis of the CpxR~P binding sequence in the rovM promoter region desensitised rovM expression to CpxR~P. These data suggest that accumulated CpxR~P inversely manipulates the levels of two global transcriptional regulators, RovA and RovM, and this would be expected to have considerable influence on Yersinia pathophysiology and metabolism.

Place, publisher, year, edition, pages
Taylor & Francis Group, 2019
Keywords
Environmental stress responsiveness, gene expression control, metabolic networks, microbial behaviour, growth and survival, fitness
National Category
Microbiology Microbiology in the medical area
Research subject
Microbiology; Molecular Biology; Infectious Diseases
Identifiers
urn:nbn:se:umu:diva-154425 (URN)10.1080/21505594.2018.1556151 (DOI)000453473300001 ()30518290 (PubMedID)2-s2.0-85058727745 (Scopus ID)
Funder
Swedish Research Council, 2009-3660Swedish Research Council, 2014-6652
Available from: 2018-12-17 Created: 2018-12-17 Last updated: 2023-03-24Bibliographically approved
Gouveia-Figueira, S., Karlsson, J., Deplano, A., Hashemian, S., Svensson, M., Fredriksson Sundbom, M., . . . Fowler, C. J. (2015). Characterisation of (R)-2-(2-Fluorobiphenyl-4-yl)-N-(3-Methylpyridin-2-yl)Propanamide as a Dual Fatty Acid Amide Hydrolase: Cyclooxygenase Inhibitor. PLOS ONE, 10(9), Article ID e0139212.
Open this publication in new window or tab >>Characterisation of (R)-2-(2-Fluorobiphenyl-4-yl)-N-(3-Methylpyridin-2-yl)Propanamide as a Dual Fatty Acid Amide Hydrolase: Cyclooxygenase Inhibitor
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2015 (English)In: PLOS ONE, E-ISSN 1932-6203, Vol. 10, no 9, article id e0139212Article in journal (Refereed) Published
Abstract [en]

Background Increased endocannabinoid tonus by dual-action fatty acid amide hydrolase (FAAH) and substrate selective cyclooxygenase (COX-2) inhibitors is a promising approach for pain-relief. One such compound with this profile is 2-(2-fluorobiphenyl-4-yl)-N-(3-methylpyridin-2-yl)propanamide (Flu-AM1). These activities are shown by Flu-AM1 racemate, but it is not known whether its two single enantiomers behave differently, as is the case towards COX-2 for the parent flurbiprofen enantiomers. Further, the effects of the compound upon COX-2-derived lipids in intact cells are not known. Methodology/Principal Findings COX inhibition was determined using an oxygraphic method with arachidonic acid and 2-arachidonoylglycerol (2-AG) as substrates. FAAH was assayed in mouse brain homogenates using anandamide (AEA) as substrate. Lipidomic analysis was conducted in unstimulated and lipopolysaccharide + interferon gamma-stimulated RAW 264.7 macrophage cells. Both enantiomers inhibited COX-2 in a substrate-selective and time-dependent manner, with IC50 values in the absence of a preincubation phase of: (R)-Flu-AM1, COX-1 (arachidonic acid) 6 mu M; COX-2 (arachidonic acid) 20 mu M; COX-2 (2-AG) 1 mu M; (S)-Flu-AM1, COX-1 (arachidonic acid) 3 mu M; COX-2 (arachidonic acid) 10 mu M; COX-2 (2-AG) 0.7 mu M. The compounds showed no enantiomeric selectivity in their FAAH inhibitory properties. (R)-Flu-AM1 (10 mu M) greatly inhibited the production of prostaglandin D2 and E2 in both unstimulated and lipopolysaccharide + interferon.-stimulated RAW 264.7 macrophage cells. Levels of 2-AG were not affected either by (R)-Flu-AM1 or by 10 mu M flurbiprofen, either alone or in combination with the FAAH inhibitor URB597 (1 mu M). Conclusions/Significance Both enantiomers of Flu-AM1 are more potent inhibitors of 2-AG compared to arachidonic acid oxygenation by COX-2. Inhibition of COX in lipopolysaccharide + interferon.-stimulated RAW 264.7 cells is insufficient to affect 2-AG levels despite the large induction of COX-2 produced by this treatment.

National Category
Pharmacology and Toxicology
Identifiers
urn:nbn:se:umu:diva-110569 (URN)10.1371/journal.pone.0139212 (DOI)000361800700192 ()26406890 (PubMedID)2-s2.0-84947261212 (Scopus ID)
Available from: 2015-11-06 Created: 2015-10-23 Last updated: 2023-03-23Bibliographically approved
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ORCID iD: ORCID iD iconorcid.org/0000-0002-3586-4197

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