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Article ; Online: The impact of catecholamines on skeletal muscle following massive burns: Friend or foe?

Blears, Elizabeth / Ross, Evan / Ogunbileje, John O / Porter, Craig / Murton, Andrew J

Burns : journal of the International Society for Burn Injuries

2021 Volume 47, Issue 4, Page(s) 756–764

Abstract: Profound skeletal muscle wasting in the setting of total body hypermetabolism is a defining characteristic of massive burns, compromising the patient's recovery and necessitating a protracted period of rehabilitation. In recent years, the prolonged use ... ...

Abstract	Profound skeletal muscle wasting in the setting of total body hypermetabolism is a defining characteristic of massive burns, compromising the patient's recovery and necessitating a protracted period of rehabilitation. In recent years, the prolonged use of the non-selective beta-blocker, propranolol, has gained prominence as an effective tool to assist with suppressing epinephrine-dependent burn-induced hypermetabolism and by extension, blunting muscle catabolism. However, synthetic β-adrenergic agonists, such as clenbuterol, are widely associated with the promotion of muscle growth in both animals and humans. Moreover, experimental adrenodemedullation is known to result in muscle catabolism. Therefore, the blunting of muscle β-adrenergic signaling via the use of propranolol would be expected to negatively impair muscle protein homeostasis. This review explores these paradoxical observations and identifies the manner by which propranolol is thought to exert its anti-catabolic effects in burn patients. Moreover, we identify potential avenues by which the use of beta-blocker therapy in the treatment of massive burns could potentially be further refined to promote the recovery of muscle mass in these critically ill patients while continuing to ameliorate total body hypermetabolism.
MeSH term(s)	Adrenergic beta-Antagonists/adverse effects ; Adrenergic beta-Antagonists/pharmacology ; Burns/complications ; Burns/drug therapy ; Catecholamines/adverse effects ; Catecholamines/pharmacology ; Humans ; Muscle, Skeletal/drug effects
Chemical Substances	Adrenergic beta-Antagonists ; Catecholamines
Language	English
Publishing date	2021-02-02
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	197308-3
ISSN	1879-1409 ; 0305-4179
ISSN (online)	1879-1409
ISSN	0305-4179
DOI	10.1016/j.burns.2021.01.009
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Article ; Online: Methods matter - Tailoring SARS-CoV-2 antibody targets to vaccination status.

Rapp, Alexandra R / Ogunbileje, John O / Djouodo-Nemzou, Diane / Okorodudu, Anthony O

Clinica chimica acta; international journal of clinical chemistry

2021 Volume 519, Page(s) 140–141

Abstract: Individuals who have been vaccinated for COVID19 should have IgG antibody in response to the specific antigen that is the target in the vaccine development. There are several options for targeted COVID19 antigen, but most manufacturers have focused on ... ...

Abstract	Individuals who have been vaccinated for COVID19 should have IgG antibody in response to the specific antigen that is the target in the vaccine development. There are several options for targeted COVID19 antigen, but most manufacturers have focused on the spike protein. Using our understanding of the targeted antigen for vaccine development, we can develop testing algorithmic scheme for anti-spike and anti-nucleocapsid antibody assays to aid delineation of infection versus vaccination in our patient population. Clear communication from laboratories specifying the specific SARS-CoV-2 antibodies (i.e., anti-spike, anti-nucleocapsid, or both) in their antibody tests at both the ordering and reporting levels will play crucial role in the development of this approach and is essential to avoid potential provider/patient confusion in the interpretation of serologic testing.
MeSH term(s)	Antibodies, Viral ; COVID-19 ; Humans ; SARS-CoV-2 ; Spike Glycoprotein, Coronavirus ; Vaccination
Chemical Substances	Antibodies, Viral ; Spike Glycoprotein, Coronavirus
Language	English
Publishing date	2021-04-17
Publishing country	Netherlands
Document type	Letter
ZDB-ID	80228-1
ISSN	1873-3492 ; 0009-8981
ISSN (online)	1873-3492
ISSN	0009-8981
DOI	10.1016/j.cca.2021.04.009
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Article ; Online: Brown adipose tissue recruitment in a rodent model of severe burns.

Bhattarai, Nisha / Rontoyanni, Victoria G / Ross, Evan / Ogunbileje, John O / Murton, Andrew J / Porter, Craig

Burns : journal of the International Society for Burn Injuries

2020 Volume 46, Issue 7, Page(s) 1653–1659

Abstract: Background: Severe burns results in a prolonged hypermetabolic response. Brown adipose tissue (BAT), abundant in uncoupling protein 1 (UCP1), plays a key role in non-shivering thermogenesis. We set out to determine if BAT is recruited in response to ... ...

Abstract	Background: Severe burns results in a prolonged hypermetabolic response. Brown adipose tissue (BAT), abundant in uncoupling protein 1 (UCP1), plays a key role in non-shivering thermogenesis. We set out to determine if BAT is recruited in response to severe burns. Methods: Male balb-c mice underwent scald burns on approximately 20-25% of their total body surface. BAT was harvested from the interscapular fat pad of sham and burned mice at 3h, 24h, 4 days, and 10 days after injury. High-resolution respirometry was used to determine mitochondrial respiratory function in BAT. BAT protein concentration, and mitochondrial enzyme activity were also determined. Results: Respiration increased in BAT of burned mice, peaking at 24h after injury (after injury, P<0.001). While UCP1 independent respiration was not significantly altered by burn, UCP1 dependent respiration increased >2-fold at 24h after injury when compared to the 3h and sham group (P<0.01). Normalized to citrate synthase activity, total uncoupled (P<0.05) and UCP1 dependent (P<0.01) respiration remained elevated at 24h after injury. Conclusions: We show a time-dependent recruitment of rodent BAT in response to severe burns. Given recent reports that humans, including patients with severe burns, have functional BAT, these data support a role for BAT in the hypermetabolic response to severe burns.
MeSH term(s)	Adipose Tissue, Brown/metabolism ; Animals ; Burns/metabolism ; Male ; Mice ; Mice, Inbred BALB C ; Thermogenesis ; Uncoupling Protein 1/metabolism
Chemical Substances	Uncoupling Protein 1
Language	English
Publishing date	2020-05-19
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	197308-3
ISSN	1879-1409 ; 0305-4179
ISSN (online)	1879-1409
ISSN	0305-4179
DOI	10.1016/j.burns.2020.04.034
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Article ; Online: The Role of Mitochondrial Stress in Muscle Wasting Following Severe Burn Trauma.

Ogunbileje, John O / Herndon, David N / Murton, Andrew J / Porter, Craig

Journal of burn care & research : official publication of the American Burn Association

2017 Volume 39, Issue 1, Page(s) 100–108

Abstract: Increased resting metabolic rate and skeletal muscle wasting are hallmarks of the pathophysiological stress response to severe burn trauma. However, whether these two responses occur independently in burn patients or are in fact related remains unclear. ... ...

Abstract	Increased resting metabolic rate and skeletal muscle wasting are hallmarks of the pathophysiological stress response to severe burn trauma. However, whether these two responses occur independently in burn patients or are in fact related remains unclear. In light of recent evidence demonstrating that increased proteolysis in skeletal muscle of burned patients is accompanied by mitochondrial hypermetabolism, oxidative stress, and protein damage; in this article, we discuss the evidence for a role for the mitochondrion in skeletal muscle wasting following severe burn trauma. In particular, we focus on the role of mitochondrial superoxide production in oxidative stress and subsequent proteolysis, and discuss the role of the mitochondrion as a signaling organelle resulting in protein catabolism in other cellular compartments following severe burn trauma.
MeSH term(s)	Basal Metabolism/physiology ; Burns/complications ; Burns/metabolism ; Humans ; Mitochondria/physiology ; Muscle, Skeletal ; Muscular Atrophy/etiology ; Oxidative Stress/physiology ; Superoxides
Chemical Substances	Superoxides (11062-77-4)
Language	English
Publishing date	2017-04-27
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2224246-6
ISSN	1559-0488 ; 1559-047X
ISSN (online)	1559-0488
ISSN	1559-047X
DOI	10.1097/BCR.0000000000000553
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Article ; Online: Identification and Quantification of Human Brown Adipose Tissue.

Chondronikola, Maria / Porter, Craig / Ogunbileje, John O / Sidossis, Labros S

Methods in molecular biology (Clifton, N.J.)

2017 Volume 1566, Page(s) 159–176

Abstract: Brown adipose tissue (BAT) has attracted significant interest as a potential target tissue against obesity and its associated metabolic perturbations. The purpose of this chapter is to provide an overview of some of the methodological approaches that can ...

Abstract	Brown adipose tissue (BAT) has attracted significant interest as a potential target tissue against obesity and its associated metabolic perturbations. The purpose of this chapter is to provide an overview of some of the methodological approaches that can be used to identify and quantify BAT in people. Specifically, we will provide a step-by-step description of the following procedures: quantification of BAT in vivo using positron emission tomography-computed tomography (PET/CT) with 2-deoxy-2-[
Language	English
Publishing date	2017
Publishing country	United States
Document type	Journal Article
ISSN	1940-6029
ISSN (online)	1940-6029
DOI	10.1007/978-1-4939-6820-6_16
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Article ; Online: Skeletal Muscle Bioenergetics in Critical Limb Ischemia and Diabetes.

Rontoyanni, Victoria G / Blears, Elizabeth / Nunez Lopez, Omar / Ogunbileje, John / Moro, Tatiana / Bhattarai, Nisha / Randolph, Amanda C / Fry, Christopher S / Fankhauser, Grant T / Cheema, Zulfiqar F / Murton, Andrew J / Volpi, Elena / Rasmussen, Blake B / Porter, Craig

The Journal of surgical research

2023 Volume 288, Page(s) 108–117

Abstract: Introduction: Mitochondrial dysfunction is implicated in the metabolic myopathy accompanying peripheral artery disease (PAD) and critical limb ischemia (CLI). Type-2 diabetes mellitus (T2DM) is a major risk factor for PAD development and progression to ... ...

Abstract	Introduction: Mitochondrial dysfunction is implicated in the metabolic myopathy accompanying peripheral artery disease (PAD) and critical limb ischemia (CLI). Type-2 diabetes mellitus (T2DM) is a major risk factor for PAD development and progression to CLI and may also independently be related to mitochondrial dysfunction. We set out to determine the effect of T2DM in the relationship between CLI and muscle mitochondrial respiratory capacity and coupling control. Methods: We studied CLI patients undergoing revascularization procedures or amputation, and non-CLI patients with or without T2DM of similar age. Mitochondrial respiratory capacity and function were determined in lower limb permeabilized myofibers by high-resolution respirometry. Results: Fourteen CLI patients (65 ± 10y) were stratified into CLI patients with (n = 8) or without (n = 6) T2DM and were compared to non-CLI patients with (n = 18; 69 ± 5y) or without (n = 19; 71 ± 6y) T2DM. Presence of CLI but not T2DM had a marked impact on all mitochondrial respiratory states in skeletal muscle, adjusted for the effects of sex. Leak respiration (State 2, P < 0.025 and State 4 Conclusions: Skeletal muscle mitochondrial respiratory capacity was blunted by ∼35% in patients with CLI. T2DM was not associated with muscle oxidative capacity and did not moderate the relationship between muscle mitochondrial respiratory capacity and CLI.
MeSH term(s)	Adult ; Humans ; Chronic Limb-Threatening Ischemia ; Muscle, Skeletal ; Peripheral Arterial Disease/complications ; Risk Factors ; Energy Metabolism ; Ischemia/complications ; Ischemia/metabolism ; Treatment Outcome ; Limb Salvage ; Diabetes Mellitus
Language	English
Publishing date	2023-03-22
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	80170-7
ISSN	1095-8673 ; 0022-4804
ISSN (online)	1095-8673
ISSN	0022-4804
DOI	10.1016/j.jss.2023.02.015
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Article ; Online: Comparative effects of cocaine and cocaethylene on alveolar epithelial type II cells.

Bazuaye-Ekwuyasi, Eseosa A / Ogunbileje, John O / Kaphalia, Bhupendra S / Eltorky, Mahmoud A / Okorodudu, Anthony O

Toxicology mechanisms and methods

2015 Volume 25, Issue 8, Page(s) 604–613

Abstract: Abuse of cocaine (COC) and alcohol have been among the leading causes of non-prescription drug-related deaths in the USA and are known to cause acute and chronic lung diseases. The co-abuse of COC and alcohol results in the production of an active ... ...

Abstract	Abuse of cocaine (COC) and alcohol have been among the leading causes of non-prescription drug-related deaths in the USA and are known to cause acute and chronic lung diseases. The co-abuse of COC and alcohol results in the production of an active metabolite, cocaethylene (CE). The effects of COC and its metabolites on the respiratory system have been scarcely studied. This study was aimed at comparing the toxic effects of eqimolar concentration (1 mM) of COC and CE on alveolar epithelial type II cells. This was performed by measuring cell growth, viability, clonogenic activity, cell cycle and reactive oxygen species (ROS) generation. The treatment of CE and COC resulted in a significant inhibition of cell proliferation with the formation of an average of three colonies which measured about 1.74×10(-15) m each and 25 colonies each of about 5.73×10(-15) m, respectively, while untreated cells yielded 31 colonies of 8.75×10(-15) m (p<0.05). The treatments of CE and COC resulted in the reduction of the growth fraction of alveolar epithelial type II cells without significant decrease in viability. In addition, there was an approximately twofold increase in ROS generation as compared to the controls (p<0.05). Therefore, CE-induced inhibition of cellular proliferation may contribute to the pathogenesis of diffuse alveolar damage in co-abusers of COC and alcohol.
MeSH term(s)	Alveolar Epithelial Cells/drug effects ; Alveolar Epithelial Cells/metabolism ; Cell Cycle/drug effects ; Cell Line, Tumor ; Cell Proliferation/drug effects ; Cell Survival/drug effects ; Cocaine/analogs & derivatives ; Cocaine/toxicity ; Colony-Forming Units Assay ; Dopamine Uptake Inhibitors/toxicity ; Humans ; Oxidative Stress/drug effects ; Reactive Oxygen Species/metabolism ; Street Drugs/toxicity
Chemical Substances	Dopamine Uptake Inhibitors ; Reactive Oxygen Species ; Street Drugs ; cocaethylene (FJO3071W5Y) ; Cocaine (I5Y540LHVR)
Language	English
Publishing date	2015
Publishing country	England
Document type	Comparative Study ; Journal Article
ZDB-ID	2081252-8
ISSN	1537-6524 ; 1537-6516 ; 1051-7235
ISSN (online)	1537-6524
ISSN	1537-6516 ; 1051-7235
DOI	10.3109/15376516.2015.1045658
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Article ; Online: Differential acute and chronic effects of burn trauma on murine skeletal muscle bioenergetics.

Porter, Craig / Herndon, David N / Bhattarai, Nisha / Ogunbileje, John O / Szczesny, Bartosz / Szabo, Csaba / Toliver-Kinsky, Tracy / Sidossis, Labros S

Burns : journal of the International Society for Burn Injuries

2016 Volume 42, Issue 1, Page(s) 112–122

Abstract: Altered skeletal muscle mitochondrial function contributes to the pathophysiological stress response to burns. However, the acute and chronic impact of burn trauma on skeletal muscle bioenergetics remains poorly understood. Here, we determined the ... ...

Abstract	Altered skeletal muscle mitochondrial function contributes to the pathophysiological stress response to burns. However, the acute and chronic impact of burn trauma on skeletal muscle bioenergetics remains poorly understood. Here, we determined the temporal relationship between burn trauma and mitochondrial function in murine skeletal muscle local to and distal from burn wounds. Male BALB/c mice (8-10 weeks old) were burned by submersion of the dorsum in water (∼ 95 °C) to create a full thickness burn on ∼ 30% of the body. Skeletal muscle was harvested spinotrapezius underneath burn wounds (local) and the quadriceps (distal) of sham and burn treated mice at 3h, 24h, 4d and 10d post-injury. Mitochondrial respiration was determined in permeabilized myofiber bundles by high-resolution respirometry. Caspase 9 and caspase 3 protein concentration were determined by western blot. In muscle local to burn wounds, respiration coupled to ATP production was significantly diminished at 3h and 24h post-injury (P<0.001), as was mitochondrial coupling control (P<0.001). There was a 5- (P<0.05) and 8-fold (P<0.001) increase in respiration in response to cytochrome at 3h and 24h post burn, respectively, indicating damage to the outer mitochondrial membranes. Moreover, we also observed greater active caspase 9 and caspase 3 in muscle local to burn wounds, indicating the induction of apoptosis. Distal muscle mitochondrial function was unaltered by burn trauma until 10d post burn, where both respiratory capacity (P<0.05) and coupling control (P<0.05) were significantly lower than sham. These data highlight a differential response in muscle mitochondrial function to burn trauma, where the timing, degree and mode of dysfunction are dependent on whether the muscle is local or distal to the burn wound.
MeSH term(s)	Acute Disease ; Animals ; Apoptosis ; Back Muscles/metabolism ; Back Muscles/pathology ; Blotting, Western ; Burns/metabolism ; Cell Respiration ; Chronic Disease ; Energy Metabolism ; Male ; Mice ; Mice, Inbred BALB C ; Mitochondria/metabolism ; Muscle Fibers, Skeletal/metabolism ; Muscle Fibers, Skeletal/pathology ; Muscle, Skeletal/metabolism ; Muscle, Skeletal/pathology ; Quadriceps Muscle/metabolism ; Quadriceps Muscle/pathology
Language	English
Publishing date	2016-02
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	197308-3
ISSN	1879-1409 ; 0305-4179
ISSN (online)	1879-1409
ISSN	0305-4179
DOI	10.1016/j.burns.2015.10.026
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Article ; Online: Sepsis Increases Muscle Proteolysis in Severely Burned Adults, but Does not Impact Whole-Body Lipid or Carbohydrate Kinetics.

Murton, Andrew / Bohanon, Fredrick J / Ogunbileje, John O / Capek, Karel D / Tran, Ellen A / Chao, Tony / Sidossis, Labros S / Porter, Craig / Herndon, David N

Shock (Augusta, Ga.)

2018 Volume 52, Issue 3, Page(s) 353–361

Abstract: Sepsis is a common and often fatal consequence of severe burn injury, but its exact effects on whole body and muscle metabolism in the burn patient is unclear. To address this, 13 septic and 11 nonseptic patients (age: 36.9 ± 13.0 years) with burns ... ...

Abstract	Sepsis is a common and often fatal consequence of severe burn injury, but its exact effects on whole body and muscle metabolism in the burn patient is unclear. To address this, 13 septic and 11 nonseptic patients (age: 36.9 ± 13.0 years) with burns encompassing >30% of their total body surface area underwent muscle protein kinetic studies under postabsorptive conditions using bolus injections of ring-C6 and N phenylalanine isotopes. In parallel, whole-body lipid and carbohydrate kinetics were assessed using constant infusions of [U-C6]palmitate, [6,6-H2]glucose, and [H5]glycerol, and during a 2-h hyperinsulinemic euglycemic clamp. Muscle mRNA levels of genes implicated in the development of muscle cachexia were assessed by qPCR. Fractional breakdown rates of mixed-muscle proteins were found to be 2.4-fold greater in septic versus nonseptic patients (P < 0.05). No discernable differences in fractional synthetic rate of mixed-muscle proteins or rate of appearance of plasma free fatty acids, glycerol, or glucose could be observed between patient groups, although the latter was significantly associated with burn size (P < 0.05). Hyperinsulinemia stimulated whole-body glucose uptake and suppressed endogenous glucose production and whole-body lipolytic rate to equivalent degrees in both groups. Muscle mRNA levels of genes spanning autophagy, lysosomal, and ubiquitin proteasome-mediated proteolysis were not enhanced in septic versus nonseptic patients. Our results demonstrate that accelerated muscle proteolysis appears to be the principal metabolic consequence of sepsis in severe burn patients and could be a contributing factor to the accelerated loss of muscle mass in these individuals. The exact mechanistic basis for these changes remains unclear.
MeSH term(s)	Adult ; Aged ; Burns/complications ; Burns/metabolism ; Burns/pathology ; Cachexia/etiology ; Cachexia/metabolism ; Cachexia/pathology ; Humans ; Male ; Middle Aged ; Muscle Proteins/metabolism ; Muscle, Skeletal/metabolism ; Muscle, Skeletal/pathology ; Muscular Diseases/etiology ; Muscular Diseases/metabolism ; Muscular Diseases/pathology ; Proteolysis ; Sepsis/etiology ; Sepsis/metabolism ; Sepsis/pathology ; Trauma Severity Indices
Chemical Substances	Muscle Proteins
Language	English
Publishing date	2018-09-18
Publishing country	United States
Document type	Clinical Trial, Phase II ; Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1185432-7
ISSN	1540-0514 ; 1073-2322
ISSN (online)	1540-0514
ISSN	1073-2322
DOI	10.1097/SHK.0000000000001263
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Article ; Online: Severe Burn Injury Induces Thermogenically Functional Mitochondria in Murine White Adipose Tissue.

Porter, Craig / Herndon, David N / Bhattarai, Nisha / Ogunbileje, John O / Szczesny, Bartosz / Szabo, Csaba / Toliver-Kinsky, Tracy / Sidossis, Labros S

Shock (Augusta, Ga.)

2015 Volume 44, Issue 3, Page(s) 258–264

Abstract: Chronic cold exposure induces functionally thermogenic mitochondria in the inguinal white adipose tissue (iWAT) of mice. Whether this response occurs in pathophysiological states remains unclear. The purpose of this study was to determine the impact of ... ...

Abstract	Chronic cold exposure induces functionally thermogenic mitochondria in the inguinal white adipose tissue (iWAT) of mice. Whether this response occurs in pathophysiological states remains unclear. The purpose of this study was to determine the impact of severe burn trauma on iWAT mitochondrial function in mice. Male BALB/c mice (10-12 weeks) received full-thickness scald burns to ∼30% of the body surface area. Inguinal white adipose tissue was harvested from mice at 1, 4, 10, 20, and 40 days postinjury. Total and uncoupling protein 1 (UCP1)-dependent mitochondrial thermogenesis were determined in iWAT. Citrate synthase activity was determined as a proxy of mitochondrial abundance. Immunohistochemistry was performed to assess iWAT morphology and UCP1 expression. Uncoupling protein 1-dependent respiration was significantly greater at 4 and 10 days after burn compared with sham, peaking at 20 days after burn (P < 0.001). Citrate synthase activity was threefold greater at 4, 10, 20, and 40 days after burn versus sham (P < 0.05). Per mitochondrion, UCP1 function increased after burn trauma (P < 0.05). After burn trauma, iWAT exhibited numerous multilocular lipid droplets that stained positive for UCP1. The current findings demonstrate the induction of thermogenically competent mitochondria within rodent iWAT in a model of severe burn trauma. These data identify a specific pathology that induces the browning of white adipose tissue in vivo and may offer a mechanistic explanation for the chronic hypermetabolism observed in burn victims.
MeSH term(s)	Adipose Tissue, White/metabolism ; Adipose Tissue, White/pathology ; Adipose Tissue, White/physiopathology ; Animals ; Burns/complications ; Burns/metabolism ; Burns/pathology ; Burns/physiopathology ; Citrate (si)-Synthase/metabolism ; Ion Channels/metabolism ; Male ; Mice, Inbred BALB C ; Mitochondria/metabolism ; Mitochondria/physiology ; Mitochondrial Diseases/etiology ; Mitochondrial Diseases/metabolism ; Mitochondrial Proteins/metabolism ; Thermogenesis/physiology ; Uncoupling Protein 1
Chemical Substances	Ion Channels ; Mitochondrial Proteins ; Ucp1 protein, mouse ; Uncoupling Protein 1 ; Citrate (si)-Synthase (EC 2.3.3.1)
Language	English
Publishing date	2015-09
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1185432-7
ISSN	1540-0514 ; 1073-2322
ISSN (online)	1540-0514
ISSN	1073-2322
DOI	10.1097/SHK.0000000000000410
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