scholarly journals Myostatin Upregulation in Patients in the Chronic Phase of Severe Burn Injury Leads to Muscle Cell Catabolism

2019 ◽  
Vol 60 (1-2) ◽  
pp. 86-96 ◽  
Author(s):  
Christoph Wallner ◽  
Julika Huber ◽  
Marius Drysch ◽  
Sonja Verena Schmidt ◽  
Johannes Maximilian Wagner ◽  
...  
Keyword(s):  
Muscle Wasting ◽  
Burn Injury ◽  
Muscle Protein ◽  
Chronic Phase ◽  
Severe Burn ◽  
Term Survival ◽  
Long Term Survival ◽  
Severe Burn Injury

Background: Burn injury leads to a hypercatabolic response and ultimately muscle wasting with drastic implications for recovery of bodily functions, patient’s quality of life (QoL), and long-term survival. Several treatment options target the body’s initial stress response, but pharmacological approaches to specifically address muscle protein metabolism have only been poorly investigated. Objective: The aim of this study was to assess the role of myostatin and follistatin in burn injury and its possible implications in muscle wasting syndrome. Methods: We harvested serum from male patients within 48 h and again 9–12 months after severe burn injury (>20% of total body surface area). By means of myoblast cultures, immunohistochemistry, immunoblotting, and scratch assay, the role of myostatin and its implications in post-burn muscle metabolism and myoblast proliferation and differentiation was analyzed. Results: We were able to show increased proliferative and myogenic capacity, decreased myostatin, decreased SMAD 2/3, and elevated follistatin concentrations in human skeletal myoblast cultures with serum conditioned medium of patients in the acute phase of burn injury and conversely a reversed situation in patients in the chronic phase of burn injury. Thus, there is a biphasic response to burn trauma, initiated by an anabolic state and followed by long-term hypercatabolism. Conclusion: We conclude that the myostatin signaling pathway plays an important regulative role in burn-associated muscle wasting and that blockade of myostatin could prove to be a valuable treatment approach improving the rehabilitation process, QoL, and long-term survival after severe burn injury.

Long-Term Survival in a Patient With Abdominal Sarcomatosis From Uterine Leiomyosarcoma: Role of Repeated Laparoscopic Surgery in Treatment and Follow-Up

2016 ◽  
Vol 23 (6) ◽  
pp. 1003-1008 ◽  
Author(s):  
Antonio Macciò ◽  
Paraskevas Kotsonis ◽  
Giacomo Chiappe ◽  
Luca Melis ◽  
Fausto Zamboni ◽  
...  
Keyword(s):  
Laparoscopic Surgery ◽  
Uterine Leiomyosarcoma ◽  
Term Survival ◽  
Long Term Survival

Hyperosmotic NaCl and severe hemorrhagic shock: role of the innervated lung

1981 ◽  
Vol 241 (6) ◽  
pp. H883-H890 ◽  
Author(s):  
O. U. Lopes ◽  
V. Pontieri ◽  
M. Rocha e Silva ◽  
I. T. Velasco
Keyword(s):  
Cardiac Output ◽  
Arterial Pressure ◽  
Metabolic Response ◽  
Term Survival ◽  
Long Term Survival ◽  
Vagal Blockade ◽  
Intravenous Infusions ◽  
Acid Base Equilibrium

Infusions of hyperosmotic NaCl (2,400 mosmol/l; 4 ml/kg) were given to dogs in severe hemorrhagic hypotension by intravenous injection (72 expts) or intra-aortic injection (25 expts). In 46 experiments intravenous infusions were given during bilateral blockage of the cervical vagal trunks (local anesthesia or cooling). Intravenous infusions (without vagal blockade) restore arterial pressure, cardiac output, and acid-base equilibrium to normal and cause mesenteric flow to overshoot prehemorrhage levels by 50%. These effects are stable, and indefinite survival was observed in every case. Intra-aortic infusions of hyperosmotic NaCl produce only a transient recovery of arterial pressure and cardiac output but no long-term survival. Intravenous infusions with vagal blockage produce only a transient recovery of cardiac output, with non long-term survival. Measurement of pulmonary artery blood osmolarity during and after the infusions shows that a different pattern is observed in each of these three groups and strongly indicates that the first passage of hyperosmotic blood through the pulmonary circulation at a time when vagal conduction is unimpaired is essential for the production of the full hemodynamic-metabolic response, which is needed for indefinite survival.

scholarly journals Long-term survival estimates for imatinib versus interferon-? plus low-dose cytarabine for patients with newly diagnosed chronic-phase chronic myeloid leukemia

Cancer ◽  
2004 ◽  
Vol 101 (11) ◽  
pp. 2584-2592 ◽  
Author(s):  
Kevin J. Anstrom ◽  
Shelby D. Reed ◽  
Andrew S. Allen ◽  
G. Alastair Glendenning ◽  
Kevin A. Schulman
Keyword(s):  
Chronic Myeloid Leukemia ◽  
Myeloid Leukemia ◽  
Low Dose ◽  
Chronic Phase ◽  
Newly Diagnosed ◽  
Term Survival ◽  
Long Term Survival ◽  
Low Dose Cytarabine

The Role of Perioperative Transfusion on Long-term Survival of Veterans Undergoing Surgery

2015 ◽  
Vol 261 (1) ◽  
pp. 104-110 ◽  
Author(s):  
Jun Lee ◽  
Vlad Radulescue ◽  
Jahan Porhomayon ◽  
Leili Pourafkari ◽  
Pradeep Arora ◽  
...  
Keyword(s):  
Term Survival ◽  
Long Term Survival

Long-Term Survival and Late Relapse in 5-Year Survivors of Allogeneic Hematopoietic-Cell Transplantation (HCT) for Chronic Myeloid Leukemia (CML) in First Chronic Phase.

Blood ◽  
2009 ◽  
Vol 114 (22) ◽  
pp. 3321-3321
Author(s):  
John M. Goldman ◽  
Navneet S. Majhail ◽  
John P. Klein ◽  
Zhiwei Wang ◽  
Kathleen A. Sobocinski ◽  
...  
Keyword(s):  
General Population ◽  
Conflicts Of Interest ◽  
Chronic Gvhd ◽  
Chronic Phase ◽  
Term Survival ◽  
Long Term Survival ◽  
Late Mortality ◽  
Allogeneic Hct ◽  
Risk Of Relapse

Abstract Abstract 3321 Poster Board III-209 Prior to the advent of tyrosine kinase inhibitors, allogeneic HCT was standard therapy for CML. However, very long-term outcomes of allogeneic HCT for CML are not well described. To evaluate the probability and risk factors for late mortality and relapse in this patient population, we conducted a retrospective cohort study that included 2444 patients who received a myeloablative allogeneic HCT for CML in first chronic phase between 1978 and 1998 and had survived in continuous complete remission for at least 5 years. Relapse was considered the earliest reported date of the following: hematologic recurrence, cytogenetic recurrence or initiation of therapy for recurrence. The median followup of our cohort was 11 years (range, 5-25) from HCT; 377 patients had followup >15 years. Donor sources were HLA-matched siblings (MSD) in 1692, unrelated donors (URD) in 639 and other related donors in 113 patients. The median age at HCT was 35 years and patients primarily received bone marrow grafts (96%) and conditioning using either total-body irradiation (TBI, 61%) or BuCy (38%) regimens. Acute and chronic graft-versus-host disease (GVHD) occurred in 43% and 62% of patients, respectively. The probabilities of overall survival at 15 years were 88% (95% CI, 86-90%) for MSD and 87% (83-90%) for URD recipients. Corresponding cumulative incidences of relapse at 15 years were 8% (7-10%) and 2% (1-4%), respectively. The latest reported relapse occurred 18 years post-HCT. In multivariable analyses addressing the importance of patient, disease and transplant related factors for long-term survival, older age at HCT, use of female donor for a male recipient, use of TBI based conditioning, acute GVHD and chronic GVHD all independently increased the risk of late mortality. Chronic GVHD reduced the risk of relapse, but increased the risk of non-relapse mortality. Recipients of MSD and URD had similar risks of long-term mortality, relapse and non-relapse mortality. Compared to an age, gender and race adjusted general population, 5 year survivors of HCT for CML were 2.9 times (95% CI, 1.9-3.9) more likely to die at 6 years and 2.5 times (1.3-3.7) more likely to die at 10 years after HCT. However, by 15 years after HCT, their relatively mortality (2.3 [0-4.9]) was not significantly different than the general population. In summary, recipients of allogeneic HCT for CML in first chronic phase who remain in remission for at least 5 years after HCT have very favorable subsequent long-term survival with mortality rates eventually approaching those of the general population. There is a small but continuing risk of relapse even in these long-term survivors. Chronic GVHD protects against relapse but increases the risks of non-relapse mortality. Disclosures No relevant conflicts of interest to declare.

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