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Artikel ; Online: Ensuring Equitable Use of Bariatric Surgery in Adolescents.

Cummins, Claire B / Bowen-Jallow, Kanika A

The Journal of adolescent health : official publication of the Society for Adolescent Medicine

2019 Band 65, Heft 3, Seite(n) 311–312

Mesh-Begriff(e)	Adolescent ; Bariatric Surgery ; Child ; Humans ; Obesity, Morbid
Sprache	Englisch
Erscheinungsdatum	2019-08-23
Erscheinungsland	United States
Dokumenttyp	Editorial ; Research Support, N.I.H., Extramural ; Comment
ZDB-ID	1063374-1
ISSN	1879-1972 ; 1054-139X
ISSN (online)	1879-1972
ISSN	1054-139X
DOI	10.1016/j.jadohealth.2019.04.024
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: Burn-Induced Cardiac Mitochondrial Dysfunction via Interruption of the PDE5A-cGMP-PKG Pathway.

Wen, Jake J / Cummins, Claire B / Radhakrishnan, Ravi S

International journal of molecular sciences

2020 Band 21, Heft 7

Abstract: Burn-induced heart dysfunction is a key factor for patient mortality. However, the molecular mechanisms are not yet fully elucidated. This study sought to understand whether burn-induced heart dysfunction is associated with cardiac mitochondrial ... ...

Abstract	Burn-induced heart dysfunction is a key factor for patient mortality. However, the molecular mechanisms are not yet fully elucidated. This study sought to understand whether burn-induced heart dysfunction is associated with cardiac mitochondrial dysfunction and interruption of the PDE5A-cGMP-PKG pathway. Sixty percent total body surface area (TBSA) scald burned rats (±sildenafil) were used in this study. A transmission electron microscope (TEM), real-time qPCR, O2K-respirometer, and electron transport chain assays were used to characterized molecular function. Cardiac mitochondrial morphological shapes were disfigured with a decline in mitochondrial number, area, and size, resulting in deficiency of cardiac mitochondrial replication. Burn induced a decrease in all mitDNA encoded genes. State 3 oxygen consumption was significantly decreased. Mitochondrial complex I substrate-energized or complex II substrate-energized and both of respiratory control ratio (RCRs) were decreased after burn. All mitochondrial complex activity except complex II were decreased in the burn group, correlating with decreases in mitochondrial ATP and MnSOD activity. Sildenafil, a inhibitor of the PDE5A-cGMP-PKG pathway, preserved the mitochondrial structure, respiratory chain efficiency and energy status in cardiac tissue. Furthermore, sildenafil treatment significantly restored ADP-conjugated respiration in burned groups. In conclusion, cardiac mitochondrial damage contributes to burn-induced heart dysfunction via the PDE5A-cGMP-PKG pathway.
Mesh-Begriff(e)	Animals ; Burns/complications ; Burns/metabolism ; Burns/pathology ; Cyclic GMP/metabolism ; Cyclic GMP-Dependent Protein Kinases/metabolism ; Cyclic Nucleotide Phosphodiesterases, Type 5/metabolism ; Male ; Mitochondria, Heart/metabolism ; Mitochondria, Heart/pathology ; Oxygen Consumption ; Rats ; Rats, Sprague-Dawley ; Signal Transduction
Chemische Substanzen	Cyclic GMP-Dependent Protein Kinases (EC 2.7.11.12) ; Cyclic Nucleotide Phosphodiesterases, Type 5 (EC 3.1.4.35) ; Pde5a protein, rat (EC 3.1.4.35) ; Cyclic GMP (H2D2X058MU)
Sprache	Englisch
Erscheinungsdatum	2020-03-28
Erscheinungsland	Switzerland
Dokumenttyp	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms21072350
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: Cardiac Dysfunction after Burn Injury: Role of the AMPK-SIRT1-PGC1α-NFE2L2-ARE Pathway.

Wen, Jake J / Cummins, Claire B / Szczesny, Bartosz / Radhakrishnan, Ravi S

Journal of the American College of Surgeons

2020 Band 230, Heft 4, Seite(n) 562–571

Abstract: Background: Mitochondrial oxidative stress plays a prominent role in the development of burn-induced cardiac dysfunction. AMP-activated kinase (AMPK), an energy sensor, has a central role in the pathogenesis of heart failure. However, its role in ... ...

Abstract	Background: Mitochondrial oxidative stress plays a prominent role in the development of burn-induced cardiac dysfunction. AMP-activated kinase (AMPK), an energy sensor, has a central role in the pathogenesis of heart failure. However, its role in cardiac dysfunction after burn injury is unclear. Our hypothesis is that burn injury acts through the AMPK-sirtuin 1-PGC1α-nuclear factor erythroid 2-related factor 2 (NFE2L2)-ARE signaling pathway, leading to cardiac mitochondrial impairment, resulting in cardiac dysfunction. Study design: Male Sprague-Dawley rats underwent sham procedure or 60% total body surface area full-thickness burn. Echocardiograms were performed 24 hours post burn. Heart tissue was harvested at 24 hours post burn for biochemistry/molecular biologic analysis. AC16 cardiomyocytes were treated with either sham or burned rat serum (±AMPK inhibitor/AMPK activator/PGC1α activator) for evaluation of cardiomyocyte mitochondrial function by using seahorse in vitro. Results: Burn injury-induced cardiac dysfunction was measured by echocardiogram. Burn injury suppressed cardiac AMPK, sirtuin 1, and PGC1 expression, leading to acetylation of cardiomyocyte proteins. In addition, burn injury caused NFE2L2 and NFE2L2 regulated antioxidants (heme oxygenase 1, NADH quinone oxidoreductase 1, glutamatecysteine ligase catalytic subunit, manganese superoxide dismutase, and glutathione peroxidase) to decrease, resulting in cardiac oxidative stress. In vitro, AMPK1 activator and PGC1α agonist treatment improved Ac16 cell mitochondrial dysfunction, and AMPK1 inhibitor treatment worsened Ac16 cellular damage. Conclusions: Burn-induced cardiac dysfunction and cardiac mitochondrial damage occur via the AMPK-sirtuin 1-PGC1α-NFE2L2-ARE signaling pathway. AMPK and PGC1α agonists might be promising therapeutic agents to reverse cardiac dysfunction after burn injury.
Mesh-Begriff(e)	AMP-Activated Protein Kinases/physiology ; Animals ; Antioxidant Response Elements/physiology ; Burns/complications ; Heart Diseases/etiology ; Male ; NF-E2-Related Factor 2/physiology ; Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha/physiology ; Rats ; Rats, Sprague-Dawley ; Signal Transduction/physiology ; Sirtuin 1/physiology
Chemische Substanzen	NF-E2-Related Factor 2 ; Nfe2l2 protein, rat ; Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha ; Ppargc1a protein, rat ; AMP-Activated Protein Kinases (EC 2.7.11.31) ; Sirt1 protein, rat (EC 3.5.1.-) ; Sirtuin 1 (EC 3.5.1.-)
Sprache	Englisch
Erscheinungsdatum	2020-02-04
Erscheinungsland	United States
Dokumenttyp	Journal Article
ZDB-ID	1181115-8
ISSN	1879-1190 ; 1072-7515
ISSN (online)	1879-1190
ISSN	1072-7515
DOI	10.1016/j.jamcollsurg.2019.12.029
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel: The Genetic Evidence of Burn-Induced Cardiac Mitochondrial Metabolism Dysfunction.

Wen, Jake J / Cummins, Claire B / Williams, Taylor P / Radhakrishnan, Ravi S

Biomedicines

2020 Band 8, Heft 12

Abstract: Burn-induced cardiac dysfunction is thought to involve mitochondrial dysfunction, although the mechanisms responsible are unclear. In this study, we used our established model of in vivo burn injury to understand the genetic evidence of burn-induced ... ...

Abstract	Burn-induced cardiac dysfunction is thought to involve mitochondrial dysfunction, although the mechanisms responsible are unclear. In this study, we used our established model of in vivo burn injury to understand the genetic evidence of burn-induced mitochondrial confusion dysfunction by describing cardiac mitochondrial metabolism-related gene expression after burn. Cardiac tissue was collected at 24 hours after burn injury. An O2K respirometer system was utilized to measure the cardiac mitochondrial function. Oxidative phosphorylation complex activities were determined using enzyme activity assays. RT Profiler PCR array was used to identify the differential regulation of genes involved in mitochondrial biogenesis and metabolism. The quantitative qPCR and Western blotting were applied to validate the differentially expressed genes. Burn-induced cardiac mitochondrial dysfunction was supported by the finding of decreased state 3 respiration, decreased mitochondrial electron transport chain activity in complex I, III, IV, and V, and decreased mitochondrial DNA-encoded gene expression as well as decreased levels of the corresponding proteins after burn injury. Eighty-four mitochondrial metabolism-related gene profiles were measured. The mitochondrial gene profile showed that 29 genes related to mitochondrial energy and metabolism was differentially expressed. Of these 29 genes, 16 were more than 2-fold upregulated and 13 were more than 2-fold downregulated. All genes were validated using qPCR and partial genes were correlated with their protein levels. This study provides preliminary evidence that a large percentage of mitochondrial metabolism-related genes in cardiomyocytes were significantly affected by burn injury.
Sprache	Englisch
Erscheinungsdatum	2020-12-03
Erscheinungsland	Switzerland
Dokumenttyp	Journal Article
ZDB-ID	2720867-9
ISSN	2227-9059
ISSN	2227-9059
DOI	10.3390/biomedicines8120566
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: Burn-Induced Cardiac Mitochondrial Dysfunction via Interruption of the PDE5A-cGMP-PKG Pathway

Jake J. Wen / Claire B. Cummins / Ravi S. Radhakrishnan

International Journal of Molecular Sciences, Vol 21, Iss 7, p

2020 Band 2350

Abstract	Burn-induced heart dysfunction is a key factor for patient mortality. However, the molecular mechanisms are not yet fully elucidated. This study sought to understand whether burn-induced heart dysfunction is associated with cardiac mitochondrial dysfunction and interruption of the PDE5A-cGMP-PKG pathway. Sixty percent total body surface area (TBSA) scald burned rats (±sildenafil) were used in this study. A transmission electron microscope (TEM), real-time qPCR, O2K-respirometer, and electron transport chain assays were used to characterized molecular function. Cardiac mitochondrial morphological shapes were disfigured with a decline in mitochondrial number, area, and size, resulting in deficiency of cardiac mitochondrial replication. Burn induced a decrease in all mitDNA encoded genes. State 3 oxygen consumption was significantly decreased. Mitochondrial complex I substrate-energized or complex II substrate-energized and both of respiratory control ratio (RCRs) were decreased after burn. All mitochondrial complex activity except complex II were decreased in the burn group, correlating with decreases in mitochondrial ATP and MnSOD activity. Sildenafil, a inhibitor of the PDE5A-cGMP-PKG pathway, preserved the mitochondrial structure, respiratory chain efficiency and energy status in cardiac tissue. Furthermore, sildenafil treatment significantly restored ADP-conjugated respiration in burned groups. In conclusion, cardiac mitochondrial damage contributes to burn-induced heart dysfunction via the PDE5A-cGMP-PKG pathway.
Schlagwörter	burn injury ; mitochondria ; oxygen consumption ; electron transport chain ; sildenafil ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
Sprache	Englisch
Erscheinungsdatum	2020-03-01T00:00:00Z
Verlag	MDPI AG
Dokumenttyp	Artikel ; Online
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Artikel ; Online: Predicting General Surgery Match Outcomes Using Standardized Ranking Metrics.

Mao, Rui-Min D / Williams, Taylor P / Price, Anthony / Colvill, Kayla M / Cummins, Claire B / Radhakrishnan, Ravi S

The Journal of surgical research

2022 Band 283, Seite(n) 817–823

Abstract: Introduction: Objective measurements for applicant ranking are becoming increasingly important, not only to help address the growing number of general surgery applicants each year but also to minimize bias and ensure consistency. We assessed if our ... ...

Abstract	Introduction: Objective measurements for applicant ranking are becoming increasingly important, not only to help address the growing number of general surgery applicants each year but also to minimize bias and ensure consistency. We assessed if our general surgery applicant scoring system was an effective tool for accurately predicting the results of the resident match. Methods: A retrospective review of applicant rank lists from 2017 to 2020 was conducted. Applicants were ranked based on the sum of preinterview and interview scores. The preinterview score is an objective metric related to the applicant's academic portfolio. The interview score is a standardized score based on interview performance. We reviewed match results from ranked candidates and categorized them as academic categorical (AC), community categorical (CC), preliminary surgical (PS), nonsurgical specialty (NS), or unmatched (UM) positions. Results: A total of 378 applicants were interviewed. Forty-nine percent matched into AC, 22% into CC, 11% into PS, and 5% into NS positions, while 13% of the interviewees were UM. Applicants who matched into AC positions had significantly higher preinterview and interview scores than applicants in other categories. Applicants who matched into CC positions had significantly higher interview scores than those categorized as UM, but their preinterview scores did not differ significantly from the UM group. Applicants who did not match into a categorical position (PS, NS, or UM) did not have significantly different preinterview or interview scores from one another. Conclusions: Our standardized scoring system was effective in stratifying which applicants would match into categorical general surgery residency programs.
Mesh-Begriff(e)	Internship and Residency ; Retrospective Studies ; General Surgery/education
Sprache	Englisch
Erscheinungsdatum	2022-12-05
Erscheinungsland	United States
Dokumenttyp	Review ; Journal Article
ZDB-ID	80170-7
ISSN	1095-8673 ; 0022-4804
ISSN (online)	1095-8673
ISSN	0022-4804
DOI	10.1016/j.jss.2022.11.038
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel: Heart Rate Variability Can Detect Blunt Traumatic Brain Injury Within the First Hour.

Zhu, Min / Blears, Elizabeth E / Cummins, Claire B / Wolf, Jordan / Nunez Lopez, Omar A / Bohanon, Fredrick J / Kramer, George C / Radhakrishnan, Ravi S

Cureus

2022 Band 14, Heft 7, Seite(n) e26783

Abstract: Introduction: In patients with multi-organ system trauma, the diagnosis of coinciding traumatic brain injury can be difficult due to injuries from the hemorrhagic shock that confound clinical and radiographic signs of traumatic brain injury. In this ... ...

Abstract	Introduction: In patients with multi-organ system trauma, the diagnosis of coinciding traumatic brain injury can be difficult due to injuries from the hemorrhagic shock that confound clinical and radiographic signs of traumatic brain injury. In this study, a novel technique using heart rate variability was developed in a porcine model to detect traumatic brain injury early in the setting of hemorrhagic shock without the need for radiographic imaging or clinical exam. Methods: A porcine model of hemorrhagic shock was used with an arm of swine receiving hemorrhagic shock alone and hemorrhagic shock with traumatic brain injury. High-resolution heart rate frequencies were collected at different time intervals using waveforms based on voltage delivered from the heart rate monitor. Waveforms were analyzed to assess statistically significant differences between heart rate variability parameters in those with hemorrhagic shock and traumatic brain injury versus those with only hemorrhagic shock. Stochastic analysis was used to assess the validity of results and create a model by machine learning to better assess the presence of traumatic brain injury. Results: Significant differences were found in several heart rate variability parameters between the two groups. Additionally, significant differences in heart rate variability parameters were found in swine within 1 hour of inducing hemorrhage in those with traumatic brain injury versus those without. These results were confirmed with stochastic analysis and machine learning was used to generate a model which determined the presence of traumatic brain injury in the setting of hemorrhage shock with 91.6% accuracy. Conclusions: Heart rate variability represents a promising diagnostic tool to aid in the diagnosis of traumatic brain injury within 1 hour of injury.
Sprache	Englisch
Erscheinungsdatum	2022-07-12
Erscheinungsland	United States
Dokumenttyp	Journal Article
ZDB-ID	2747273-5
ISSN	2168-8184
ISSN	2168-8184
DOI	10.7759/cureus.26783
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: Nuclear Factor Erythroid 2-Related Factor 2 Activation and Burn-Induced Cardiac Dysfunction.

Wen, Jake J / Mobli, Keyan / Rontoyanni, Victoria G / Cummins, Claire B / Radhakrishnan, Geetha L / Murton, Andrew / Radhakrishnan, Ravi S

Journal of the American College of Surgeons

2022 Band 234, Heft 4, Seite(n) 660–671

Abstract: Background: Our previous studies have found that burn injury induces cardiac dysfunction through interruption of the antioxidant-response element (ARE) pathway in cardiac mitochondria. Nuclear factor erythroid 2-related factor 2 (Nrf2) is a key ... ...

Abstract	Background: Our previous studies have found that burn injury induces cardiac dysfunction through interruption of the antioxidant-response element (ARE) pathway in cardiac mitochondria. Nuclear factor erythroid 2-related factor 2 (Nrf2) is a key regulator that activates many antioxidant enzymes. Oltipraz (Olti) is a Nrf2 activator and a well-known inducer of NQO1 along with other enzymes that comprise the Nrf2-associated antioxidants. We propose that Nrf2 activation will induce the ARE pathway, leading to abrogation of burn-induced cardiac dysfunction. Study design: In this study, we investigated the effect of Nrf2-deficiency in mice on burn-induced cardiac dysfunction. Wild-type (WT) and Nrf2-deficient mice received 30% total body surface area burn injury and were treated with or without Olti and then harvested at 3 hours and 24 hours post burn (3 hpb and 24 hpb). Results: As expected, Nrf2-deficient mice exhibited exacerbated cardiac dysfunction after burn injury, as measured by Vevo 2100 echocardiography. Electron microscopy showed that Nrf2 depletion worsened burn injury-induced cardiac mitochondrial damage. In addition, Nrf2 depletion increased cardiac mitochondrial dysfunction and myocardial fibrosis after burn injury. Treatment with Olti ameliorated the heart dysfunction in burned Nrf2-/+ mice, improved cardiac mitochondrial structure and oxidative phosphorylation, as well as decreased cardiac fibrosis. These results suggest that Nrf2 and its downstream targets modulate cardiac function after burn injury. Conclusions: In summary, Nrf2 depletion worsens cardiac dysfunction after burn injury. Nrf2 activation, with a drug such as Olti, offers a promising therapeutic strategy for abrogating burn-induced cardiac dysfunction.
Mesh-Begriff(e)	Animals ; Antioxidant Response Elements ; Antioxidants ; Burns/metabolism ; Heart Diseases/etiology ; Mice ; NF-E2-Related Factor 2 ; Signal Transduction
Chemische Substanzen	Antioxidants ; NF-E2-Related Factor 2 ; Nfe2l2 protein, mouse
Sprache	Englisch
Erscheinungsdatum	2022-03-11
Erscheinungsland	United States
Dokumenttyp	Journal Article
ZDB-ID	1181115-8
ISSN	1879-1190 ; 1072-7515
ISSN (online)	1879-1190
ISSN	1072-7515
DOI	10.1097/XCS.0000000000000119
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: Education of pediatric surgery residents over time: Examining 15 years of case logs.

Cummins, Claire B / Bowen-Jallow, Kanika A / Tran, Sifrance / Radhakrishnan, Ravi S

Journal of pediatric surgery

2020 Band 56, Heft 1, Seite(n) 85–98

Abstract: Background/purpose: Surgical indications and techniques have changed over the last 15 years. The number of Pediatric Surgery training programs has also increased. We sought to examine the effect of these changes on resident education by examining case ... ...

Abstract	Background/purpose: Surgical indications and techniques have changed over the last 15 years. The number of Pediatric Surgery training programs has also increased. We sought to examine the effect of these changes on resident education by examining case log data. Methods: Accreditation Council for Graduate Medical Education (ACGME) case logs for graduating Pediatric Surgery residents were examined from 2004 to 2018. Using the summary statistics provided, linear regression analysis was conducted on each case log code and category. Results: In 2004, there were 24 Pediatric Surgery training programs and 24 Pediatric Surgery residents graduating with an average of 979.8 total cases logged. In 2018, there were 36 programs with 38 residents graduating with an average of 1260.2 total cases logged. Total case volume of graduating residents significantly increased over the last 15 years (p < 0.001). Significant increases were demonstrated in skin/soft tissue/musculoskeletal (p < 0.01), abdominal (p < 0.001), hernia repair (p < 0.001), genitourinary (p < 0.01), and endoscopy (p < 0.001). No significant changes were seen in the head and neck, thoracic, cardiovascular, liver/biliary, and non-operative trauma categories. No categories significantly decreased over the time period. No significant changes were seen in the number of multiple index congenital cases, including tracheoesophageal fistula/esophageal atresia repair, omphalocele, gastroschisis, choledochal cyst excision, perineal procedure for imperforate anus, and major hepatic resections for tumors. Pertinent increases in specific procedures include diaphragmatic hernia repair (p < 0.01), ECMO cannulation/decannulation(p < 0.05), thyroidectomy (p < 0.001), parathyroidectomy (p < 0.001), biliary atresia (p < 0.001), and circumcision (p < 0.001) as well as most laparoscopic abdominal procedures. Specific procedure codes with significant decreases include tracheostomy (p < 0.05), minimally invasive decortication/pleurectomy/blebectomy (p < 0.001), laparoscopic splenectomy (p < 0.001), as well as most open abdominal procedures. Conclusion: Despite increasing numbers of Pediatric Surgery residents and training programs, the number of cases performed by each graduating resident has increased. This increase is primarily fueled by increase in abdominal, skin/soft tissue/musculoskeletal, hernia repair, genitourinary, and endoscopic cases. Level of evidence: Level II.
Mesh-Begriff(e)	Accreditation ; Child ; Clinical Competence ; Education, Medical, Graduate ; General Surgery/education ; Humans ; Internship and Residency ; Male ; Retrospective Studies ; United States ; Workload
Sprache	Englisch
Erscheinungsdatum	2020-10-06
Erscheinungsland	United States
Dokumenttyp	Journal Article
ZDB-ID	80165-3
ISSN	1531-5037 ; 0022-3468
ISSN (online)	1531-5037
ISSN	0022-3468
DOI	10.1016/j.jpedsurg.2020.09.038
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: The Genetic Evidence of Burn-Induced Cardiac Mitochondrial Metabolism Dysfunction

Jake J. Wen / Claire B. Cummins / Taylor P. Williams / Ravi S. Radhakrishnan

Biomedicines, Vol 8, Iss 566, p

2020 Band 566

Abstract	Burn-induced cardiac dysfunction is thought to involve mitochondrial dysfunction, although the mechanisms responsible are unclear. In this study, we used our established model of in vivo burn injury to understand the genetic evidence of burn-induced mitochondrial confusion dysfunction by describing cardiac mitochondrial metabolism-related gene expression after burn. Cardiac tissue was collected at 24 hours after burn injury. An O2K respirometer system was utilized to measure the cardiac mitochondrial function. Oxidative phosphorylation complex activities were determined using enzyme activity assays. RT Profiler PCR array was used to identify the differential regulation of genes involved in mitochondrial biogenesis and metabolism. The quantitative qPCR and Western blotting were applied to validate the differentially expressed genes. Burn-induced cardiac mitochondrial dysfunction was supported by the finding of decreased state 3 respiration, decreased mitochondrial electron transport chain activity in complex I, III, IV, and V, and decreased mitochondrial DNA-encoded gene expression as well as decreased levels of the corresponding proteins after burn injury. Eighty-four mitochondrial metabolism-related gene profiles were measured. The mitochondrial gene profile showed that 29 genes related to mitochondrial energy and metabolism was differentially expressed. Of these 29 genes, 16 were more than 2-fold upregulated and 13 were more than 2-fold downregulated. All genes were validated using qPCR and partial genes were correlated with their protein levels. This study provides preliminary evidence that a large percentage of mitochondrial metabolism-related genes in cardiomyocytes were significantly affected by burn injury.
Schlagwörter	burn injury ; cardiac dysfunction ; gene profiling ; mitochondrial metabolism ; oxygen consumption ; Biology (General) ; QH301-705.5
Sprache	Englisch
Erscheinungsdatum	2020-12-01T00:00:00Z
Verlag	MDPI AG
Dokumenttyp	Artikel ; Online
Datenquelle	BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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