PubMed Health⌕ Search

Biomedical subjects

Marc G Jeschke

Publications and source records attributed to Marc G Jeschke.

At least 19 recordsLinked to original sources
PubMed2026

High-Dose Intravenous Vitamin C and Mortality and Organ Dysfunction in Severe Burn Injury: The VICTORY Randomized Clinical Trial.

IMPORTANCE: Severe burn injury triggers systemic inflammation that can lead to multiple organ dysfunctions and death. High-dose intravenous vitamin C has been proposed to mitigate these effects, but strong evidence in patients with burn injury is lacking. OBJECTIVE: To evaluate the efficacy of high-dose intravenous vitamin C in patients with severe burn injury. DESIGN, SETTING, AND PARTICIPANTS: Randomized, double-blind, placebo-controlled phase 3 trial conducted across 24 burn centers in North, Central, and South America; Europe; and Asia. Adults (≥18 years) with deep second- and/or third-degree burns covering 20% or more of total body surface area and requiring skin grafting were enrolled between August 18, 2020, and September 12, 2025. Final follow-up was completed in March 2026. The trial was stopped early after the first prespecified interim analysis for futility/harm. INTERVENTIONS: Patients were randomly assigned (1:1) to receive intravenous vitamin C (50 mg/kg every 6 hours for 96 hours) or matched placebo. MAIN OUTCOMES AND MEASURES: The primary outcome was a composite of 28-day mortality and persistent organ dysfunction (defined as dependence on mechanical ventilation, kidney replacement therapy, or vasopressor/inotrope support at day 28). The main secondary outcome was time to discharge alive from hospital within 90 days. RESULTS: Among 238 patients enrolled (mean age, 48.9 [SD, 19.1] years; 79% male; mean total body surface area, 37.0% [SD, 14.6%]), 120 were assigned to vitamin C and 118 to placebo. The primary composite outcome occurred in 49 patients (40.8%) in the vitamin C group and 35 patients (29.7%) in the placebo group (adjusted risk ratio [RR], 1.28 [95% CI, 0.99-1.65]; P = .06), crossing the prespecified futility/harm threshold and prompting early trial termination. Time to discharge alive from hospital within 90 days was not improved (adjusted subdistribution hazard ratio, 0.85 [95% CI, 0.62-1.16]; P = .31). Twenty-eight-day mortality was higher in the vitamin C group (15.0% vs 7.6%; adjusted RR, 1.96 [95% CI, 1.32-2.90]; P = .001), as was hospital mortality (23.3% vs 16.1%; adjusted RR, 1.44 [95% CI, 1.03-2.00]; P = .03). CONCLUSIONS AND RELEVANCE: Among patients with severe burn injury, high-dose intravenous vitamin C did not reduce 28-day mortality and persistent organ dysfunction and is possibly harmful. TRIAL REGISTRATION: ClinicalTrials.gov Identifier: NCT04138394.

Humans↗
PubMed2007

Blood transfusions are associated with increased risk for development of sepsis in severely burned pediatric patients.

OBJECTIVE: To determine the risk of developing sepsis following transfusion of blood products in severely burned pediatric patients. DESIGN: Retrospective, cohort study. SETTING: Shriners Hospital for Children and University Hospital. PATIENTS: Severely burned pediatric patients with >30% total body surface area (TBSA) burn. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Two hundred seventy-seven pediatric burn patients over a period of 7 yrs (1997-2004) were included in the study, with 25 patients being septic at admission and therefore excluded. Patients were stratified according to TBSA burn and presence or absence of inhalation injury. The amounts of packed red blood cells (RBCs) and fresh frozen plasma (FFP) were recorded during hospital stay before the development of sepsis. Blood product administration was normalized for the number of surgeries and divided into two groups: high (RBCs>20/FFP>5) or low (RBCs<20/FFP<5) amount of blood products. Sepsis was diagnosed based on the criteria set by the Society of Critical Care Medicine in conjunction with positive blood culture or presence of organisms in the organs at autopsy. By stratifying the groups into low and high blood transfusion, we found that patients with >60% TBSA burn with inhalation injury have an 8% risk of developing sepsis in the low RBC group, which increases to 58% in the high RBC group (p<.05). Similar results were found for RBCs per operation, FFP, and FFP per operation (p<.05). There were no differences in age and gender between groups. CONCLUSIONS: Pediatric burn suffering from a 60% TBSA burn with concomitant inhalation injury are more likely to develop sepsis if they are given high amounts of blood products, indicating an immunocompromised state following blood transfusion.

Burns↗
PubMed2007

Serum cytokine differences in severely burned children with and without sepsis.

The aim was to determine whether serum cytokine profiling early after burn can be used to identify patients at high risk of developing and subsequently dying of sepsis. A case series study was designed to determine whether serum cytokine profiling allows identification of patients at highest risk of developing and dying of sepsis at the time of hospital admission. All patients were treated according to the standard of burn care at our facility. Forty-four children (1-19 years old) with more than 40% of total body surface area and admitted within 7 days postburn were studied. None had infections or sepsis at the time of admission. Serum was collected before the first operation, and concentrations of 17 cytokines were measured. Diagnosis of sepsis was made at autopsy with identification of the pathogen. Fifteen patients developed sepsis and died, whereas 29 patients did not develop sepsis and survived. Significant elevations in serum interleukin (IL) 6, IL-8, IL-10, granulocyte-monocyte colony-stimulating factor, interferon gamma (IFN-gamma), tumor necrosis factor (TNF), and IL-12 p70 were found at the time of admission of patients who subsequently developed and died of sepsis when compared with burned patients who did not develop sepsis (P < 0.05). Multiple logistic regression analysis revealed that patients with a combination of elevated IL-6 and IL-12 p70 and lower TNF had an elevated risk of dying of sepsis. Serum IL-6, IL-8, IL-10, granulocyte-monocyte colony-stimulating factor, IFN-gamma, TNF, and IL-12 p70 are expressed differently in patients who die of sepsis versus those who never become septic. In addition, serum IL-6, IL-12 p70, and TNF can be used to identify burned patients who are at high risk of death from sepsis.

Burns↗
PubMed2007

Insulin attenuates the cytokine response in a burn wound infection model.

A massive burn is one of the most serious injuries resulting in major imbalances of the immune system. The aftermath of a burn is frequently complicated by infections and septic events that additionally increase mortality and morbidity. The aim of the present study was to investigate if insulin attenuates the cytokine response of burned mice challenged with Pseudomonas. Male mice (C57/BL/6) received a full thickness burn of 35% of their total body surface area. Mice received 5 IU/kg insulin i.p. or an equal volume of saline for 5 days after burn. Mice were challenged with 5x10 colony forming units Pseudomonas aeruginosa intraperitoneally. Serum was harvested 6 h after the bacterial challenge, and 18 serum cytokines were measured using the Bio-Plex suspension array system (Bio-Rad, Hercules, Calif). All 18 cytokines were elevated after the Pseudomonas challenge. However, mice treated with insulin showed significantly lower proinflammatory cytokine concentrations of interleukin 5, interleukin 6, and keratinocyte-derived chemokine after the Pseudomonas infection when compared with placebo-treated mice (P<0.05). In contrast, serum concentrations of G-CSF were significantly higher in insulin-treated animals when compared with placebo (P<0.05). We conclude, that insulin treatment selectively modulates specific cytokines in a burn wound infection model.

Animals↗
PubMed2006

Gut mucosal homeostasis and cellular mediators after severe thermal trauma and the effect of insulin-like growth factor-I in combination with insulin-like growth factor binding protein-3.

Increased small bowel epithelial cell apoptosis and decreased cell proliferation lead to impairment of gut mucosal integrity and function after thermal injury. Impairment of gut integrity is associated with increased bacterial translocation and incidence of sepsis. The purpose of this study was to determine whether IGF-I/IGF binding protein (IGFBP)-3 can improve small bowel homeostasis after injury and by which cellular mechanisms these changes occur and to identify changes in apoptosis-related genes after burn and the effect of bile acid on small bowel epithelial cell apoptosis after burn. Rats sustained a thermal injury and received saline or the IGF-I/IGFBP-3 complex. Serum and small intestine were taken at 1, 2, 5, and 7 d after injury and serum inflammatory cytokines and mucosal apoptosis, proliferation, villous morphology, and apoptotic and proliferative mediators were measured. Apoptosis-related gene expression and the bile acid pool were determined in separate experiments up to 6 h after burn. Gut epithelial cell apoptosis as well as apoptosis-related genes were increased after the thermal injury, whereas bile acid secretion was significantly decreased (P < 0.05). IGF-I/IGFBP-3 significantly improved villous height and cells per villous by decreasing small bowel epithelial cell apoptosis and increasing proliferation (P < 0.05). Decreased apoptosis was associated with decreased Fas, Fas-ligand, and TNF when compared with saline (P < 0.05). A severe thermal injury caused an up-regulation of apoptosis and apoptosis-related genes and down-regulation of bile acid secretion. IGF-I/IGFBP-3 decreases small bowel epithelial cell apoptosis through down-regulation of the Fas pathway, which improves gut mucosal integrity after a severe thermal injury.

Animals↗
PubMed2006

IGF-1 protects intestinal epithelial cells from oxidative stress-induced apoptosis.

BACKGROUND: Reactive oxygen species (ROS) are involved in the pathogenesis of necrotizing enterocolitis (NEC) in premature infants. We have recently found that activation of multiple cellular signaling transduction pathways occurs during ROS-induced intestinal cell apoptosis; the phosphatidylinositol 3-kinase (PI3-K) pathway plays an anti-apoptotic role during this process. Insulin-like growth factor (IGF)-1 activates PI3-K pathway to promote cell survival; however, the effects of IGF-1 treatment during gut injury are not clearly defined. The purpose of this study was to determine whether IGF-1 protects intestinal cells from ROS-induced apoptosis. MATERIALS AND METHODS: Rat intestinal epithelial (RIE)-1 cells were treated with either IGF-1 (100 nm), hydrogen peroxide (H2O2; 500 microm), or combination. Western blotting was performed to assess phosphorylation of Akt, a downstream effector of PI3-K. Cell Death Detection ELISA, DCHF, and JC-1 assays were performed to demonstrate protective effects of IGF-1. Wortmannin, an inhibitor of PI3-K, was used to show PI3-K-dependent mechanism of action for IGF-1. RESULTS: H2O2 treatment resulted in increased intestinal epithelial cell apoptosis with intracellular ROS generation and mitochondrial membrane depolarization; IGF-1 pre-treatment attenuated this response without affecting ROS production. H2O2-induced phosphorylation of Akt was further increased with IGF-1 treatment; wortmannin abolished these effects in RIE-1 cells. CONCLUSIONS: PI3-K pathway is activated during ROS-induced intestinal epithelial cell injury; IGF-1 exerted an anti-apoptotic effect during this response by PI3-K activation. A better understanding of the exact role of IGF-1-mediated activation of PI3-K may allow us to facilitate the development of novel therapy against NEC.

Animals↗
PubMed2006

Immunohistochemical staining of transgenic beta-galactosidase in burned skin is a better indicator of transfection efficiency than histochemical techniques.

The non-mammalian reporter gene LacZ, encoding the protein beta-galactosidase (beta-Gal), has long been used to test the efficiency of gene transfer into cells in culture or tissues in vivo. Biodistribution and dose-response transfection experiments rely upon a sensitive and specific technique for accurate results. We conducted an experiment to compare two techniques of identifying beta-galactosidase expression. The presence of beta-Gal was detected by dual staining transfected murine skin by both immunohistochemical (alkaline phosphatase) as well as histochemical staining (5-bromo-indolyl-beta-o-galactopyranoside [Bluo-Gal]). We demonstrated an almost two-fold increase in beta-galactosidase transfected dermal cell staining using immunohistochemistry as compared with histochemical staining. This translates to nearly 63% cells that were transfected with LacZ but were not identified by Bluo-Gal. The superior sensitivity of immunostaining suggests that anti-beta-Gal antibody represents the preferred analytical tool for light microscopic evaluation of LacZ gene transfer, promoter analysis in transgenic animals. Thus, identification of activity as opposed to presence of the enzyme underestimates gene expression following LacZ gene transfer in skin.

Animals↗
PubMed2006

Cytokine expression profile over time in severely burned pediatric patients.

A severe burn leads to hypermetabolism and catabolism resulting in compromised function and structure of essential organs. The massive release of cytokines is implicated in this hypermetabolic response. The aim of the present study was to compare cytokine expression profiles from severely burned children without signs of infections or inhalation injury (n = 19) to the cytokine profiles from normal, noninfected, nonburned children (n = 14). The Bio-Plex suspension array system was used to measure the concentration of 17 cytokines. The expression of proinflammatory and anti-inflammatory cytokines was maximal during the first week after thermal injury. Significant increases were measured for 15 mediators during the first week after thermal injury: interleukin (IL) 1beta, IL-2, IL-4, IL-5, IL-6, IL-7, IL-8, IL-10, IL-12 p70, IL-13, IL-17, interferon gamma, monocyte chemoattractant protein 1, macrophage inflammatory protein 1beta, and granulocyte colony-stimulating factor (P < 0.05). Granulocyte-macrophage colony-stimulating factor was significantly increased during the second week after burn (P < 0.05). Within 5 weeks, the serum concentrations of most cytokines decreased, approaching normal levels. When compared with the cytokine levels measured in normal children, a total of 16 cytokines were significantly altered (P < 0.05). After severe burn, a specific cytokine expression profile is observed in patients without complications such as inhalation injury or sepsis. The cytokine concentrations decrease during 5 weeks after burn but remain elevated over nonburned values. Furthermore, the elevation in most serum cytokine levels during the first week after burn may indicate a potential window of opportunity for therapeutic intervention.

Adolescent↗
PubMed2006

The influence of age and gender on resting energy expenditure in severely burned children.

INTRODUCTION: Recent evidence suggests that female severely burned children have higher endogenous anabolic hormone levels and a shorter ICU stay compared with males. The purpose of this study was to analyze the influence of age and gender on resting energy expenditure (REE) in severely burned children from acute hospitalization through 12 months postburn. METHODS: A total of 100 pediatric patients with > 40% total body surface area (TBSA) burn were enrolled in a prospective study and followed by indirect calorimetry measurements. The REE was expressed as actual REE kcal/d, percent of predicted REE, and REE/ body mass index (BMI). Statistical analysis was performed by Student t test and one-way ANOVA for repeated measures. Significance was accepted at P < 0.05. RESULTS: The measured REE was significantly higher in males versus females at all time points (P < 0.05). The percent of predicted REE was significantly higher in males versus females during the acute hospitalization, at discharge, 6 and 9 months postburn (P < 0.05). The REE/BMI showed a significant difference between males and females at the acute and discharge time period (P < 0.05). In children 3 to 9.9 years of age, the measured REE and the percent of predicted REE were significantly higher in males versus females during the acute study, at discharge and 6 months postburn (P < 0.05). The measured REE at discharge, 9 and 12 months postburn for children >10 years of age was significantly higher in males compared with females (P < 0.05). CONCLUSION: Data show that female children exert a decreased hypermetabolic response compared with male children, which may improve burn outcomes in females.

Adolescent↗
PubMed2006

Beneficial effects of extended growth hormone treatment after hospital discharge in pediatric burn patients.

OBJECTIVE: To study the efficacy of growth hormone given to severely burned children from discharge to 12 months after burn and for 12 months after the drug was discontinued. SUMMARY BACKGROUND DATA: We have previously shown that low-dose recombinant human growth hormone (rhGH), given to children after a severe thermal injury, successfully improved lean muscle mass, bone mineral content, and growth. The aim of the present study was to investigate long-term functional improvements after treatment. METHODS: Forty-four pediatric patients with over 40% total body surface area burns were studied for 24 months after burn. Patients were randomized to receive either rhGH (0.05 mg/kg body weight) or placebo. Height, weight, body composition, serum hormones, resting energy expenditure, cardiac function, muscle strength, and number of reconstructive procedures performed were measured during rhGH treatment and for 12 months after treatment was discontinued. Statistical analysis used Tukey's multiple comparison test. Significance was accepted at P < 0.05. RESULTS: Height, weight, lean body mass, bone mineral content, cardiac function, and muscle strength significantly improved during rhGH treatment compared with placebo (P < 0.05). This treatment significantly increased GH, IGF-I, and IGFBP-3, whereas serum cortisol decreased (P < 0.05). The number of operative reconstructive procedures was significantly lower with rhGH (P < 0.05). Improvements in height, bone mineral content, and IGF-1 concentrations persisted after rhGH treatment (P < 0.05). No side effects with rhGH were observed. CONCLUSIONS: Administration of rhGH for 1 year after burn was safe and improved recovery. These salutary effects continued after rhGH treatment was discontinued.

Burns↗
PubMed2006

Body composition changes with time in pediatric burn patients.

BACKGROUND: Major trauma and burns are associated with whole body catabolism which can persist for 1 or more years after injury. This study investigates body composition in massively burned children for up to 2 years. METHODS: Twenty-five pediatric patients with greater than 40% total body surface area burns were studied. At discharge, 6, 12, 18, and 24 months after burn height, weight, body composition, resting energy expenditure (REE), serum growth hormone, insulin-like growth factor-I (IGF-I), IGF binding protein-3 (IGFBP-3), insulin, cortisol, parathyroid hormone, and thyroid hormones were measured. Tukey's test was used for analysis. Significance was accepted at p < 0.05. RESULTS: Lean body mass, fat mass, bone mineral content, height, and weight increased significantly during the second year after burn. Percent predicted REE decreased significantly, whereas IGFBP-3 and parathyroid hormone levels increased significantly over time. Insulin and T3 uptake were significantly higher at discharge. CONCLUSIONS: Body composition of severely burned children significantly improved in the second year compared with the first year after injury. This demonstrates a need for long-term rehabilitation in these burn patients.

Absorptiometry, Photon↗
PubMed2005

Tissue engineered fetal skin constructs for pediatric burns.

The management of patients with partial thickness (second degree) burns is problematic due to the different treatments needed for varying depths of injury. A report recently published in The Lancet describes a novel treatment for deep second degree burns using a fetal skin construct (FSC). The authors included eight pediatric patients with small second degree burns. They showed that FSCs reduced the need for autografting of deep second degree burns, with little hypertrophy of new skin and no skin contraction. This technology is new and exciting, but in our opinion several issues must be addressed before FSCs can enter the clinical arena. All of the patients were included in the treatment group, and therefore no comparison with conventional skin substitutes was possible. There is no mention of the use of laser Doppler in any initial assessment of patients. The debridement carried out before application of the FSC is not elaborated upon, and the surface areas involved in the study were very small in most cases, which limits the relevance to patients with larger burns. The use of FSCs gives us an additional option in a range of possible treatments for this notoriously difficult-to-treat patient group.

Biological Dressings↗
PubMed2005

The effect of growth hormone on gut mucosal homeostasis and cellular mediators after severe trauma.

BACKGROUND: Gut mucosal integrity and function is impaired after severe trauma with associated increases in small bowel epithelial cell apoptosis and decreases in cell proliferation. Growth hormone improves gastrointestinal function during chemotherapy and has anabolic effects on protein synthesis. The purpose of this study was to determine whether growth hormone can improve small bowel homeostasis after injury and by which cellular mechanisms these changes occur. MATERIALS AND METHODS: Rats were pair-fed, given a thermal trauma, and received saline (n = 28) or GH (2.5 mg/kg every 24 h, n = 28). Small intestine and serum were taken at 1, 2, 5, and 7 days after injury. Measures were mucosal apoptosis, proliferation, villous morphology, apoptotic, and proliferative mediators, such as Caspases-3, -8, Fas and Fas-Ligand, Bcl-2, and Bcl-x. In addition serum cytokines were determined. RESULTS: Gut epithelial cell apoptosis and proliferation were increased in both groups after the thermal injury (P < 0.05). GH had neither an effect on small bowel epithelial cell apoptosis or proliferation, nor dependent cellular mediators after thermal injury. However, GH significantly improved villous morphology (height and cell number) when compared with controls (P < 0.05). RhGH was found to significantly increase serum TNF-alpha compared to controls (P < 0.05). CONCLUSION: Growth hormone improves small bowel homeostasis after severe trauma independent from small bowel epithelial cell apoptosis or proliferation, probably by increasing the life span.

Animals↗
PubMed2005

Treatment of second degree facial burns with allografts--preliminary results.

Facial burns are very common and have significant clinical impact. However, the treatment regimen for superficial to deep facial burns is not well defined. The purpose of this study was to investigate the effects of cadaver skin grafting in deep partial thickness facial burns in comparison to standard care. In a prospective open study design severely injured patients with superficial and deep partial thickness burns were randomized into the group receiving open treatment with silversulfadiazine (standard n=5) or into the group receiving early superficial debridement followed by coverage with glycerolized cadaver skin (n=5). The outcome measures were time and quality of wound healing, and incidence of hypertrophic scarring at 3 and 6 months post burn. There were no significant differences in demographics between groups. In the group treated with the allogenic material time to reepithelialization was 10.5 days, while it was 12.4 days in the silversulfadiazine group (p<0.05). Scar quality was found to be significantly improved in the allogenic treatment group. Three and 6 months postburn there were no patients with significant hypertrophic scarring in the allogenic group while there were two patients who developed hypertrophic scars in the silversulfadiazine group (p<0.05). In this study, we demonstrated that glyzerolized cadaver allograft skin represents a superior biological dressing for shallow and deep partial thickness facial burns. This is in concordance with other reports on scalds. It would be worthwhile to perform more clinical studies with a larger number of patients to further evaluate the effect and function of allogenic skin for facial burns.

Adult↗
PubMed2005

Insulin prevents liver damage and preserves liver function in lipopolysaccharide-induced endotoxemic rats.

BACKGROUND/AIMS: Liver integrity and function are crucial for survival of patients suffering from trauma, operations or infections. Insulin decreased mortality and prevented the incidence of multi organ failure and infection in critically ill patients. The aim of the present study was to determine whether insulin exerts positive effects on hepatic homeostasis and function during endotoxemia. METHODS: Endotoxemic rats received either saline or insulin. Hepatic morphology and function was determined by measuring the effect of insulin on liver proteins, enzymes, hepatocyte apoptosis and proliferation including caspases-3 and -9 and Bcl-2. Intrahepatic ATP, glucose and lactate concentration were determined by bioluminescence. To determine possible molecular changes the effect of insulin on hepatic cytokine mRNA and gene profile analysis were assessed. RESULTS: Insulin significantly improved hepatic protein synthesis by increasing albumin and decreasing c-reactive protein, P<0.05. Insulin attenuated hepatic damage by decreasing AST and ALT, P<0.05. Improved liver morphology was due to decreased hepatocyte apoptosis along with decreased caspase-3 concentration and increased hepatocyte proliferation along with Bcl-2 concentration, P<0.05. Insulin decreased hepatic IL-1beta, IL-6 and MIF mRNA and improved hepatic glucose metabolism and glycolysis, P<0.05. GeneChip analysis revealed an anti-inflammatory effect of insulin. CONCLUSIONS: Insulin improves hepatic integrity, hepatic glucose metabolism and hepatic function by increasing cell survival and attenuating the hepatic inflammatory response in endotoxemic rats.

Acute-Phase Proteins↗
PubMed2005

The effect of hepatocyte growth factor on gut mucosal apoptosis and proliferation, and cellular mediators after severe trauma.

BACKGROUND: A severe burn injury is associated with an impairment of gut mucosal integrity and function, which is due to increases in small-bowel epithelial cell apoptosis and decreases in cell proliferation. Hepatocyte growth factor (HGF) was shown to improve regeneration in the liver, mesentery, and skin. The purpose of this study was to determine whether HGF can improve small-bowel homeostasis after injury and the cellular mechanisms by which these changes occur. METHODS: Rats were pair-fed, underwent thermal trauma, and received saline (0.9% NaCl; n = 28) or HGF (200 microg/kg iv every 12 hours, n = 28). Small intestine and serum were taken at 1, 2, 5, and 7 days after injury. Measures were mucosal apoptosis, proliferation, villous morphology, and apoptotic and proliferative mediators, such as caspase-3 and caspase-7, Fas and Fas-ligand, Bcl-2, and Bax. In addition, serum cytokines were determined. RESULTS: Gut epithelial cell apoptosis was increased in the saline and HGF groups after the thermal injury. Despite an increase in serum tumor necrosis factor-alpha and interleukin-1beta, HGF did not affect small-bowel cell apoptosis, but it improved proliferation at days 1 and 2 after injury, which was associated with increased villous height and cell per villous, compared with saline controls, P < .05. Increased mucosal cell proliferation was associated with increased Bcl-2 in the HGF group, P < .05. HGF had no effect on apoptotic mediators, such as Fas, Fas-L, or caspase-3 and caspase-7. CONCLUSIONS: HGF improves small-bowel morphology after a severe burn by increasing mucosal Bcl-2 and, concomitantly, small-bowel epithelial cell proliferation.

Animals↗