• Early warning model
• Machine learning (ML)
• Sepsis
• XGBoost

• Humans
• Machine Learning
• Sepsis/diagnosis
• Aged
• Male
• Female
• Aged, 80 and over
• Intensive Care Units
• Early Warning Score
• ROC Curve

• 2022BEG02045 science and technology department of Ningxia Hui Autonomous Region

• Golgi apparatus
• gene co-expression network
• immune infiltration
• sepsis
• signature

• National Outstanding Youth Science Fund Project of National Natural Science Foundation of China
• Natural Science Foundation of Inner Mongolia Autonomous Region

• PICU mortality
• children
• lymphocytes
• predictive model
• sepsis

• Clinical management4
• Ferritin5
• Macrophage activation syndrome1
• Pathogenesis3
• Sepsis2

• Humans
• Macrophage Activation Syndrome/immunology
• Macrophage Activation Syndrome/etiology
• Sepsis/immunology
• Sepsis/therapy
• Animals
• Macrophages/immunology

• 81873870（Z-HT) National Natural Science Foundation of China

• acute kidney injury
• immune
• inflammation
• lymphocyte-to-C-reactive protein ratio
• sepsis

• apoptosis
• bioinformatics
• function analysis
• gene signature
• immune landscape
• sepsis

• National Natural Science Foundation of China

• CRP-albumin-lymphocyte index
• immune
• inflammation
• nutrition
• prognosis
• sepsis

• Humans
• Male
• Female
• Sepsis/mortality
• Retrospective Studies
• Critical Illness
• Middle Aged
• Intensive Care Units
• Prognosis
• Aged
• C-Reactive Protein/analysis
• C-Reactive Protein/metabolism
• Lymphocytes
• Predictive Value of Tests
• Biomarkers/blood
• Serum Albumin/analysis
• Serum Albumin/metabolism
• China/epidemiology

• ARDS
• FFL
• MD simulation
• TLR6
• WGCNA

• PI3K/AKT/mTOR
• Xuebijing injection
• apoptosis
• autophagy
• sepsis induced myocardial injury

• Endotoxemia
• LPS
• Neuroinflammation
• Sepsis
• Sickness Response

The present study is aimed at investigating the biochemical and clinical effects of electroacupuncture in patients with sepsis.

Patients with sepsis treated at Guangdong Provincial Hospital of Chinese Medicine from July 2019 to December 2020 were included. Patients were randomly assigned to treatment with routine Western medicine (WM group) or treatment with Western medicine plus electroacupuncture based on Western medicine (EA group). Indices associated with immune function and clinical efficacy were determined before and at 3 and 5 days after treatment. Indicators of immune function included the percentage of T lymphocyte subsets, natural killer (NK) cells, and soluble programmed death protein 1 (sPD-1) levels. Indicators of clinical efficacy included infection-related indicators in whole blood; levels of tumor necrosis factor-α (TNF-α), C-reactive protein (CRP), and interferon-γ (INF-γ); and assessments using acute physiology and chronic health evaluation-II (APACHE-II) and sequential organ failure assessment (SOFA) scores.

Baseline data were not different between WM (N = 30) and EA groups (N = 30). At day 5 following treatment, the level of sPD-1 in the EA group was lower than that in the WM group. Proportions of CD3 + T lymphocytes, CD4 + T lymphocytes, and NK cells, the percentage of lymphocytes, and INF-γ levels in the EA group were significantly higher than those in the WM group. Compared with the WM group, the white blood cell count (WBC), percentage and count of neutrophils, ratio of neutrophils to lymphocytes, and levels of CRP and TNF-α were significantly decreased in the EA group 5 days after treatment. The APACHE-II score of the EA group was significantly lower than that of the WM group 5 days after treatment.

Electroacupuncture may regulate the immune function of patients with sepsis through the PD-1 pathway to achieve an anti-inflammatory state and improve clinical symptoms.

Sepsis is a clinical syndrome common in critical care settings. In the present study, the therapeutic effect of thymoquinone (TQ) on the expression of sepsis-related microRNAs (miRNAs/miRs), levels of inflammatory markers, organ dysfunction and mortality were investigated in a cecal ligation and puncture (CLP) rat model. A single dose of TQ (1 mg/kg) was administered to animals 24 h after CLP and the mortality rate was assessed up to 7 days following the induction of sepsis. In addition, blood samples were collected at different time points and the expression levels of miRNAs (i.e. miR-16, miR-21, miR-27a and miR-34a) were examined, along with the levels of inflammatory cytokines (i.e. TNF-α, IL-1α, IL-2, IL-6 and IL-10) and sepsis markers (i.e. C-reactive protein, endothelial cell-specific molecule-1, VEGF, procalcitonin and D-dimer). Liver, kidney and lung tissues were also collected for further histological examination. Treatment with TQ significantly downregulated the miRNA expression levels, as well as the levels of inflammatory cytokines and early-stage sepsis biomarkers by 30-70% at 12-36 h (P<0.05). Furthermore, CLP model rats treated with TQ exhibited an ~80% increase in survival rate compared with that in the untreated CLP group. In addition, TQ induced the preservation of organ function and structure. In conclusion, the present study demonstrated a promising therapeutic effect of TQ against the sequelae of sepsis.

The purpose of our study was to explore the prognostic value of complete blood count and myocardial markers combination with Sequential Organ Failure Assessment (SOFA) score in predicting the 28-day mortality among sepsis patients.

A retrospective observational cohort study was performed. Three hundred and nineteen sepsis patients who were hospitalized at the Second Affiliated Hospital of Chongqing Medical University, China, from January 2019 to September 2021 were included. The clinical and laboratory data, the Acute Physiological and Chronic Health Evaluation II (APACHE II) score and SOFA score at the time of the initial sepsis diagnosis were collected, and the predictive values of the single and combination variables for 28-day mortality were compared.

The derivation cohort consisted of 221 patients and included 59 (26.7%) died. The area under the curve (AUC) [95% confidence interval (CI)] of RDW and cTnT were 0.735 (0.663–0.807) and 0.753 (0.678–0.827) for mortality, and the cut-off value were 14.05% and 0.039 ng/mL, respectively. The combination of RDW, cTnT and the SOFA score showed a better performance for the prediction of mortality, and the AUC was significantly higher than that of the SOFA score (0.791 vs 0.726, DeLong test: P=0.032). Multivariate Cox analysis identified that the combination of RDW, cTnT and the SOFA score (HR=6.133, P=0.004) and APACHE II score (HR=1.093, P<0.001) were independent detrimental factors for 28-day mortality. The validation cohort consisted of 98 patients and included 23 (23.5%) died. Similarly, the AUC of the RDW, cTnT and the SOFA score combination is significantly higher than that of the SOFA score (0.821 vs 0.739, DeLong test: P=0.035).

RDW and cTnT showed good performance in predicting 28-day mortality rates among patients with sepsis. Combined RDW and cTnT with the SOFA score can significantly improve the predictive value of SOFA score for the prognosis of sepsis.

• the Chongqing Special Research Project for Novel Coronavirus Pneumonia Prevention and Control
• Emergency Research Project of COVID-19 of Chongqing Health Commission

The way of cell death can be roughly divided into two categories: cell necrosis and PCD(programmed cell death). Pyroptosis is a kind of PCD, its occurrence depends on the gasdermin protein family and it will produce inflammatory response. With constant research in recent years, more and more evidences show that pyroptosis is closely related to the occurrence and development of tumors. The treatment of tumors is a big problem worldwide. We focus on whether we can discover new potential tumor markers and new therapeutic targets from the mechanism. If we can understand the mechanism of pyroptosis and clear the relationship between pyroptosis and the development of tumors, this may provide a new reference for clinical cancer treatment.

• antitumor immunity
• cancer treatment
• gasdermin family
• programmed cell death
• pyroptosis

• sepsis
• PD‑L1
• immunotherapy
• survival analysis
• apoptosis

Sepsis was first described by the ancient Greek physicians over 2000 years ago. The pathophysiology of the disease, however, is still not fully understood and hence the mortality rate is still unacceptably high due to lack of specific therapies. In the last decade, great progress has been made by shifting the focus of research from systemic inflammatory response syndrome (SIRS) to multiple organ dysfunction syndrome (MODS). Sepsis has been re-defined as infection-induced MODS in 2016. How infection leads to MODS is not clear, but what mediates MODS becomes the major topic in understanding the molecular mechanisms and developing specific therapies. Recently, the mechanism of infection-induced extensive immune cell death which releases a large quantity of damage-associated molecular patterns (DAMPs) and their roles in the development of MODS as well as immunosuppression during sepsis have attracted much attention. Growing evidence supports the hypothesis that DAMPs, including high-mobility group box 1 protein (HMGB1), cell-free DNA (cfDNA) and histones as well as neutrophil extracellular traps (NETs), may directly or indirectly contribute significantly to the development of MODS. Here, we provide an overview of the mechanisms and consequences of infection-induced extensive immune cell death during the development of sepsis. We also propose a pivotal pathway from a local infection to eventual sepsis and a potential combined therapeutic strategy for targeting sepsis.

• damage-associated molecular patterns (DAMPs)
• extensive immune cell death
• extracellular histones
• immunosuppression
• multiple organ dysfunction syndrome (MODS)
• sepsis

• Apoptosis
• Flow cytometry
• Hypothermia
• IL-10
• PD-L1

• bacterial translocation
• gut microbiota
• gut-derived infection
• intestinal barrier
• intestinal epithelium
• mucosal immunity

• Animals
• Bacterial Infections/etiology
• Bacterial Infections/immunology
• Bacterial Infections/microbiology
• Critical Illness
• Dysbiosis/immunology
• Dysbiosis/microbiology
• Gastrointestinal Microbiome/physiology
• Humans
• Immunity, Mucosal/physiology
• Intestinal Mucosa/microbiology
• Permeability
• Sepsis/etiology
• Sepsis/immunology
• Sepsis/microbiology

• Community-acquired severe sepsis
• ICU-acquired infection
• Mortality
• T helper cells

A major challenge in sepsis intervention is unclear risk stratification. We postulated that a panel of biomarkers of lymphocyte apoptosis and immune function, termed the “lymphocyte apoptosis model,” would be an effective tool for predicting 28-day survival for sepsis patients.

A total of 52 consecutive sepsis patients were enrolled. Peripheral blood samples were collected on day 1 of admission for quantification of biomarkers of lymphocyte apoptosis and immune function, including lymphocyte count, lymphocyte apoptotic percentage, expression on monocyte HLA-DR, CD4⁺/CD8⁺ T cell ratio, T helper type 1 to type 2 ratio (Th1/Th2), cytochrome c levels, and various proinflammatory cytokine levels. Sepsis severity was classified using Acute Physiology and Chronic Health Evaluation II (APACHE II) and Sequential Organ Failure Assessment (SOFA) scores. Survival was assessed at 28 days.

Compared with survivors, non-survivors had significantly higher lymphocyte apoptotic percentages and plasma cytochrome c levels and significantly lower lymphocyte counts, Th1/Th2 ratios, and HLA-DR expression on day 1 of admission. Multivariate analysis identified cytochrome c levels (odds ratio [OR]1.829, p = 0.025), lymphocyte apoptotic percentage (OR 1.103, p = 0.028), lymphocyte count (OR 0.150, p = 0.047), and HLA-DR expression (OR 0.923, p = 0.021) as independent predictors of 28-day mortality. A logistic regression equation incorporating the independent risk factors predicted 28-day mortality with greater accuracy than did the APACHE II score or single components biomarkers.

The “lymphocyte apoptosis model” may be useful for risk stratification and predicting prognosis of sepsis patients.

• Biomarker
• Immune function
• Lymphocyte apoptosis
• Predictive model
• Prognosis
• Sepsis

People with critical illness (CI) commonly develop various forms of immune dysfunction, however, there is limited information concerning immune dysfunction in dogs with CI.

The immune response in CI dogs differs from that of healthy dogs.

Immunologic variables were compared between 14 dogs with CI, defined as APPLE_fast score of >20 points, admitted to the University of Missouri Veterinary Health Center Small Animal Clinic Intensive Care Unit and healthy controls (n = 15).

Cohort study evaluating constitutive and lipopolysaccharide (LPS)‐stimulated TNF‐α, IL‐6, and IL‐10 production, phagocytosis of opsonized E. coli and respiratory burst capacity after opsonized E. coli or phorbol 12‐myristate 13‐acetate (PMA) stimulation, peripheral blood lymphocyte phenotype, and monocyte expressions of HLA‐DR and TLR‐4.

Lipopolysaccharide‐stimulated leukocyte TNF‐α (median, Q1, Q3; CI, 49, 49, 120; control, 655, 446, 1174 pg/mL; P = < 0.001), IL‐6 (median, Q1, Q3; CI, 49, 49, 64; control, 100, 49, 166 pg/mL; P = 0.029), and IL‐10 (CI, 49, 49, 56; control, 96, 49, 203 pg/mL; P = 0.014) production and both E. coli (median, Q1, Q3; CI, 60.5, 43, 88.5; control, 86.6, 81, 89.2%; P = 0.047) and PMA (CI, 40, 11.7, 70; control, 93, 83, 97.6%; P = < 0.001)‐stimulated respiratory burst capacity significantly decreased in CI dogs. Percentage of monocytes expressing TLR‐4 greater in the CI dogs (median, Q1, Q3; CI, 46.9, 24.3, 64.2; control, 16.4, 9.4, 26.2%; P = 0.005).

These findings suggest dogs with CI develop immune system alterations that result in reduced respiratory burst function and cytokine production despite upregulation of TLR‐4.

• Cytokines
• Phagocytosis
• Respiratory burst
• Sepsis

• complications
• diabetes
• infections
• resource utilization
• sepsis
• septic shock

• R01 GM029507 NIGMS NIH HHS
• R01 GM061656 NIGMS NIH HHS
• R37 GM029507 NIGMS NIH HHS
• T32 HL007517 NHLBI NIH HHS

• adaptive immune dysfunction
• immune suppression sepsis
• inflammation
• innate immune dysfunction
• sepsis

• 脓毒症
• ω-3多不饱和脂肪酸
• 淋巴细胞
• 凋亡
• 大鼠
• sepsis
• ω-3 polyunsaturated fatty acid
• lymphocyte
• apoptosis
• rats

• Animals
• Apoptosis/drug effects
• Dose-Response Relationship, Drug
• Fatty Acids, Omega-3/pharmacology
• Female
• Lymphocytes/drug effects
• Lymphocytes/pathology
• Rats
• Rats, Sprague-Dawley
• Sepsis/drug therapy
• Sepsis/pathology
• Spleen/pathology
• Thymus Gland/pathology

• NF-κB pathways
• NLRP3
• Picroside II
• apoptosis
• inflammation
• sepsis

Sepsis, a systemic inflammatory response to infection, is often accompanied by abnormalities of blood coagulation. Prior work with a mouse model of sepsis induced by cecal ligation and puncture (CLP) suggested that the protease factor XIa contributed to disseminated intravascular coagulation (DIC) and to the cytokine response during sepsis. We investigated the importance of factor XI to cytokine and coagulation responses during the first 24 hours after CLP. Compared to wild type littermates, factor XI-deficient (FXI^-/-) mice had a survival advantage after CLP, with smaller increases in plasma levels of TNF-α and IL-10 and delayed IL-1β and IL-6 responses. Plasma levels of serum amyloid P, an acute phase protein, were increased in wild type mice 24 hours post-CLP, but not in FXI^-/- mice, supporting the impression of a reduced inflammatory response in the absence of factor XI. Surprisingly, there was little evidence of DIC in mice of either genotype. Plasma levels of the contact factors factor XII and prekallikrein were reduced in WT mice after CLP, consistent with induction of contact activation. However, factor XII and PK levels were not reduced in FXI^-/- animals, indicating factor XI deficiency blunted contact activation. Intravenous infusion of polyphosphate into WT mice also induced changes in factor XII, but had much less effect in FXI deficient mice. In vitro analysis revealed that factor XIa activates factor XII, and that this reaction is enhanced by polyanions such polyphosphate and nucleic acids. These data suggest that factor XI deficiency confers a survival advantage in the CLP sepsis model by altering the cytokine response to infection and blunting activation of the contact (kallikrein-kinin) system. The findings support the hypothesis that factor XI functions as a bidirectional interface between contact activation and thrombin generation, allowing the two processes to influence each other.

• Animals
• Coinfection/enzymology
• Coinfection/metabolism
• Cytokines/metabolism
• Enzyme Activation
• Factor XI Deficiency/metabolism
• Mice
• Peptide Hydrolases/metabolism
• Sepsis/enzymology
• Sepsis/metabolism

• HL58837 NHLBI NIH HHS
• GM116184 NIGMS NIH HHS
• HL81326 NHLBI NIH HHS
• R01 HL058837 NHLBI NIH HHS
• R01 HL101972 NHLBI NIH HHS
• R01 GM116184 NIGMS NIH HHS
• R01 HL081326 NHLBI NIH HHS

Activation and/or recruitment of the host plasmin, a fibrinolytic enzyme also active on extracellular matrix components, is a common invasive strategy of bacterial pathogens. Yersinia pestis, the bubonic plague agent, expresses the multifunctional surface protease Pla, which activates plasmin and inactivates fibrinolysis inhibitors. Pla is encoded by the pPla plasmid. Following intradermal inoculation, Y. pestis has the capacity to multiply in and cause destruction of the lymph node (LN) draining the entry site. The closely related, pPla-negative, Y. pseudotuberculosis species lacks this capacity. We hypothesized that tissue damage and bacterial multiplication occurring in the LN during bubonic plague were linked and both driven by pPla. Using a set of pPla-positive and pPla-negative Y. pestis and Y. pseudotuberculosis strains in a mouse model of intradermal injection, we found that pPla is not required for bacterial translocation to the LN. We also observed that a pPla-cured Y. pestis caused the same extensive histological lesions as the wild type strain. Furthermore, the Y. pseudotuberculosis histological pattern, characterized by infectious foci limited by inflammatory cell infiltrates with normal tissue density and follicular organization, was unchanged after introduction of pPla. However, the presence of pPla enabled Y. pseudotuberculosis to increase its bacterial load up to that of Y. pestis. Similarly, lack of pPla strongly reduced Y. pestis titers in LNs of infected mice. This pPla-mediated enhancing effect on bacterial load was directly dependent on the proteolytic activity of Pla. Immunohistochemistry of Pla-negative Y. pestis-infected LNs revealed extensive bacterial lysis, unlike the numerous, apparently intact, microorganisms seen in wild type Y. pestis-infected preparations. Therefore, our study demonstrates that tissue destruction and bacterial survival/multiplication are dissociated in the bubo and that the primary action of Pla is to protect bacteria from destruction rather than to alter the tissue environment to favor Y. pestis propagation in the host.

The hallmark of bubonic plague, a disease that ravaged Medieval Europe and is still prevalent in several countries, is the bubo, a highly inflammatory and painful lymph node, which is characterized by high concentrations of bacteria within a severely damaged organ. Yersinia pestis, the causative agent, expresses a surface protease, Pla, critical to the development of bubonic plague. This multitarget protease has the potential to activate the fibrinolytic pathway and to promote destruction of extracellular protein networks within tissues. Hence, it was expected that Pla was responsible for the tissue destructions of the bubo, and consequently, for bacterial propagation and virulence. However, we found, using various engineered Yersinia strains in a mouse model of bubonic plague, that Pla proteolytic activity was dispensable for lymph node alteration, but was required to achieve high bacterial loads in the organ. Further analysis showed that Pla is essential for preventing the bacteria from being destroyed in the host. Therefore, the role of Pla as a virulence factor is to protect Y. pestis survival and integrity in the host, rather than to assist its spread through tissue destruction.

• Animals
• Bacterial Proteins/metabolism
• Disease Models, Animal
• Immunohistochemistry
• Mice
• Mutagenesis, Site-Directed
• Plague/enzymology
• Plague/microbiology
• Plague/pathology
• Plasminogen Activators/metabolism
• Virulence/physiology
• Virulence Factors/metabolism
• Yersinia pestis/enzymology
• Yersinia pestis/pathogenicity
• Yersinia pseudotuberculosis/enzymology
• Yersinia pseudotuberculosis/pathogenicity
• Yersinia pseudotuberculosis Infections/enzymology
• Yersinia pseudotuberculosis Infections/microbiology
• Yersinia pseudotuberculosis Infections/pathology

• Adrenergic alpha-1 Receptor Antagonists/pharmacology
• Animals
• Apoptosis/drug effects
• Cells, Cultured
• Cytokines/metabolism
• HSP90 Heat-Shock Proteins/chemistry
• HSP90 Heat-Shock Proteins/drug effects
• Infarction, Middle Cerebral Artery/drug therapy
• Infarction, Middle Cerebral Artery/pathology
• Mice
• Models, Molecular
• Phosphoglycerate Kinase/chemistry
• Phosphoglycerate Kinase/drug effects
• Prazosin/analogs & derivatives
• Prazosin/pharmacology
• Protein Conformation
• Rats
• Sepsis/drug therapy
• Stress, Physiological/drug effects
• Stroke/drug therapy

• P01 HL048675 NHLBI NIH HHS
• P01 HL103526 NHLBI NIH HHS
• HL48675 NHLBI NIH HHS

• Apoptosis/immunology
• Dendritic Cells/immunology
• Humans
• Inflammation/immunology
• Macrophages/immunology
• Multiple Organ Failure/immunology
• Neutrophils/immunology
• Sepsis/immunology
• Sepsis/mortality
• T-Lymphocytes/immunology

• Calcium-sensing receptor
• Cytokine
• Lymphocytes
• Sepsis
• Transient receptor potential channel

• Calcium-sensing receptor
• Cytokine
• Lymphocyte
• Sepsis
• Signaling transduction pathway

• Complication
• Gastrectomy
• Gastric cancer
• International Study Group on Pancreatic Fistula classification
• Pancreatic fistula

• Age Factors
• Aged
• Chi-Square Distribution
• Critical Care
• Female
• Gastrectomy/adverse effects
• Humans
• Japan
• Logistic Models
• Lymphocyte Count
• Male
• Middle Aged
• Multivariate Analysis
• Odds Ratio
• Pancreatic Fistula/diagnosis
• Pancreatic Fistula/etiology
• Pancreatic Fistula/therapy
• Predictive Value of Tests
• Retrospective Studies
• Risk Factors
• Severity of Illness Index
• Stomach Neoplasms/surgery
• Treatment Outcome

Lymphocyte apoptosis is one reason for immunoparalysis seen in sepsis, although the triggers are unknown. We hypothesized that molecules in plasma, which are up-regulated during sepsis, may be responsible for this. In this study, peripheral lymphocyte apoptosis caused by extracellular histones was confirmed both in mouse and human primary lymphocytes, in which histones induced lymphocyte apoptosis dose-dependently and time-dependently. To identify which intracellular signal pathways were activated, phosphorylation of various mitogen-activated protein kinases (MAPKs) were evaluated during this process, and p38 inhibitor (SB203580) was used to confirm the role of p38 in lymphocyte apoptosis induced by histones. To investigate the mitochondrial injury during these processes, we analyzed Bcl2 degradation and Rhodamine 123 to assess mitochondrial-membrane stability, via cyclosporin A as an inhibitor for mitochondrial permeability transition (MPT). Then, caspase 3 activation was also checked by western-blotting. We found that p38 phosphorylation, mitochondrial injury and caspase 3 activation occurred dose-dependently in histones-mediated lymphocyte apoptosis. We also observed that p38 inhibitor SB203580 decreased lymphocyte apoptotic ratio by 49% (P<0.05), and inhibition of MPT protected lymphocytes from apoptosis. Furthermore, to investigate whether histones are responsible for lymphocyte apoptosis, various concentrations of histone H4 neutralization antibodies were co-cultured with human primary lymphocytes and plasma from cecal ligation and puncture (CLP) mice or sham mice. The results showed that H4 neutralization antibody dose-dependently blocked lymphocyte apoptosis caused by septic plasma in vitro. These data demonstrate for the first time that extracellular histones, especially H4, play a vital role in lymphocyte apoptosis during sepsis which is dependent on p38 phosphorylation and mitochondrial permeability transition. Neutralizing H4 can inhibit lymphocyte apoptosis, indicating that it could be a potential target in clinical interventions for sepsis associated immunoparalysis.

• Adult
• Animals
• Apoptosis
• Enzyme Inhibitors/pharmacology
• Histones/metabolism
• Humans
• Imidazoles/pharmacology
• Lymphocytes/metabolism
• Lymphocytes/pathology
• Male
• Mice
• Mitochondria/metabolism
• Mitochondria/pathology
• Mitochondrial Membrane Transport Proteins/metabolism
• Mitochondrial Permeability Transition Pore
• Phosphorylation/drug effects
• Pyridines/pharmacology
• p38 Mitogen-Activated Protein Kinases/antagonists & inhibitors
• p38 Mitogen-Activated Protein Kinases/metabolism

• Chemokine
• Cytokines
• Dexamethasone
• Histology
• Lung mechanics
• Oxidative stress

• Adolescent
• Adult
• Aged
• Antioxidants/metabolism
• Antioxidants/pharmacology
• Apoptosis/drug effects
• Ascorbic Acid/blood
• Ascorbic Acid/pharmacology
• Child
• Dietary Supplements
• Double-Blind Method
• Female
• Humans
• In Situ Nick-End Labeling
• Lymphocyte Count
• Lymphocytes/drug effects
• Lymphocytes/radiation effects
• Male
• Micronutrients/metabolism
• Micronutrients/pharmacology
• Middle Aged
• Oxidative Stress/drug effects
• Selenium/blood
• Selenium/pharmacology
• Ultraviolet Rays
• Vitamin A/blood
• Vitamin A/pharmacology
• Young Adult
• beta Carotene/blood
• beta Carotene/pharmacology