[Analysis and forecast of burden of pancreatic cancer along with attributable risk factors in Asia countries between 1990 and 2019].

Objective: To analyze the disease burden of pancreatic cancer in major Asian countries and forecast the burden of that in China, which helps to provide reference for the prevention and control of pancreatic cancer. Methods: Data on disease burden of pancreatic cancer among global and major Asian countries from on the Global Burden of Disease (GBD) 2019 were collected to describe burden distribution through the absolute numbers or standardized rates of incidence, death and disability adjusted life years (DALY) by year, sex and socio-demographic index. Estimated annual percentage changes (EAPC) was used to assess the trend of standardized rate. The proportion of deaths attributable to risk factors for pancreatic cancer in 2019 was used to compare by age, sex and region. ARIMA model was performed with R language to predict change of age-standardized incidence and death rates of pancreatic cancer from 2020 to 2029. Results: From 1990 to 2019, the standardized incidence rates of pancreatic cancer in China increased from 3.17/100 000 to 5.78/100 000, and the standardized death rate increased from 3.34/100 000 to 5.99/100 000. The increases exceeded other high-income Asia countries. In the past three decades, the standardized incidence, death and DALY rates of pancreatic cancer in global have increased year by year. Among the major countries in Asia, China has the highest growth rate of disease burden (EAPC of standardized incidence rates=2.32%, 95% CI: 2.10%-2.48% and EAPC of standardized death rate=2.25%, 95% CI: 2.03%-2.42%). In addition, incidence and death rates of pancreatic cancer in China are expected to continue on the rise between 2000 and 2029 by ARIMA model. Incidence rate is expected to increase 15.92% and death rate is expected to increase 15.86%. Conclusions: The standardized incidence and death rates of pancreatic cancer in China increase year by year with an increasing trend for the burden of disease. The disease burden of pancreatic cancer is expected to rise due to the increase and aging of the population. Preventive measures should be adopted to decrease the burden of the pancreatic cancer.

[The optimal thresholds of the quantitative fecal immunochemical test for opportunistic screening of colorectal neoplasia].

Objective: To investigate the significance of quantitative fecal immunochemical test (FIT) for opportunistic screening of colorectal neoplasia, and to propose the most optimal thresholds to improve the screening level of early colorectal neoplasia. Methods: The opportunistic screening participants were recruited from the Department of Gastroenterology & GI Endoscopy Center of the Seventh Medical Center of PLA General Hospital, and stool sample was collected before colonoscopy and the quantitative FIT was analyzed by OC-MICRO analysator for each patient. We assessed test performance in detecting colorectal neoplasia (advanced adenoma and CRC)with different thresholds on sensitivity, specificity, positive predictive value (PPV) and negative predictive value (NPV). Results: A total of 1 448 objects were enrolled in this study, including 714 male (49.3%)and 734 female (50.7%).All participants were classified according to the result of colonoscopy and pathology, and 242 cases of colorectal neoplasia were found, containing 157 advanced adnoma and 85 colorectal cancer. The FIT threshold increased from 50 µg/L to 200 µg/L, while the positivity rate dropped from 11.5% to 8.6% and the sensitivity in detecting colorectal neoplasia dropped from 47.9% to 38.8%. However, the specificity increased from 96.8% to 98.2% and the positive predictive value increased from 82.3% to 87.0%.The miss rate of colorectal cancer increased from 11.8% (n=10) to 17.6% (n=15) along with the increase in FIT thresholds, but the miss rate of 100 µg/L and 150 µg/L was the same as 12.9% (n=11). Conclusions: Quantitative FIT,which is simple and fast,with the threshold of 100 µg/L for opportunistic screening, has a high sensitivity and specificity for the diagnosis of colorectal neoplasia,and is an important index in screening and diagnosis of colorectal neoplasia.

LECT2 association with macrophage-mediated killing of Helicobacter pylori by activating NF-κB and nitric oxide production.

Helicobacter pylori employs unique methods to colonize the stomach, which induces chronic inflammation. It is also able to avoid eradication by macrophages and other immune cells. Leukocyte cell-derived chemotaxin 2 (LECT2), a multi-functional cytokine involved in many pathological conditions, has recently been shown to activate macrophages via the CD209a receptor. Therefore, we aimed to investigate the effects of LECT2 on H. pylori-infected macrophages. Macrophages were treated with recombinant LECT2, and both their ability to kill H. pylori and produce nitric oxide were analyzed. Western blot was performed to determine nuclear translocation and protein phosphorylation of p65, a subunit of nuclear factor (NF)-κB. Transfection experiments were performed to analyze the signaling pathway of LECT2 in macrophages. We found that treatment with LECT2 enhanced H. pylori killing and nitric oxide production in macrophages. In addition, DNA-binding activity and nuclear translocation of p65 were up-regulated by LECT2 treatment. Furthermore, we found that NF-κB activation by LECT2 was mediated by Raf-1 in macrophages, and Raf-1 phosphorylation was specifically altered in response to LECT2. Moreover, LECT2 induced Ser28 phosphorylation in the intracellular domain of CD209a. CD209a Ser28 phosphorylation was required for LECT2-induced Raf-1 and NF-κB activation in RAW264.7 macrophages. Our study showed that the effects of LECT2 on H. pylori killing and nitric oxide production were dependent on CD209a phosphorylation, Raf-1, and NF-κB activation. Together, these results demonstrate for the first time that exposure to LECT2 can modulate specific intracellular mechanisms downstream of CD209a to enhance H. pylori killing and nitric oxide production in macrophages.

Genetic variations of ISL1 associated with human congenital heart disease in Chinese Han people.

Congenital heart disease (CHD) is the most common birth abnormality, but the etiology of CHD is unknown. ISL1 may play a fundamental role in cardiac morphogenesis, and mutations of this gene could cause CHD. To evaluate whether genetic variations of ISL1 are associated with CHD in Chinese Han people, polymerase chain reaction restriction fragment-length polymorphism and SNaPshot were used to examine 9 polymorphisms of ISL1 in 233 patients with CHD as well as 288 healthy controls. We found that one SNP (rs1017) in ISL1 was significantly associated with simple CHD. Genetic variation of ISL1 was confirmed to be associated with the risk of CHD. ISL1 is related to the atrial septal defect group and the ventricular septal defect group, and the genotypes were associated with the occurrence of CHD in the dominant mode of inheritance. We concluded that rs1017 contributed to the risk of CHD in Chinese Han people, and ISL1 may be involved in the formation and development of the heart.

[Fabrication and evaluation of composite hydroxyapatite coating on ordered micro-/nanotextured titanium surface].

Objective: To develope a titanium specimen with good osteogenic activity through fabrication of a composite hydroxyapatite coating on ordered micro-/nanotextured titanium surface. Methods: An ordered micro-/nanotextured structure was prepared on the surface of titanium (the control), and then hydroxyapatite was deposited on the as-prepared ordered micro-/nanotextured structure by alternative loop immersion method. The ordered micro-/nanotextured structures before and after hydroxyapatite deposition were denoted as HA and MN, respectively. Surface morphology was observed using a scanning electron microscope. Bone marrow mesenchymal stem cells (BMMSC) were seeded on the surface of three different materials. Cell morphology was observed with a scanning electron microscope. Cell adhesion and cell proliferation were evaluated using 4', 6-diamidino-2-phenylindole staining and cell counting kit-8 assay, respectively. Extracellular matrix mineralization and the expression levels of osteogenesis-related genes were evaluated by alizarin red staining and real-time quantitative PCR, respectively. Each group has three samples in every experiment. Results: After alternative loop immersing, the MN's original microholes (20 µm in diameter) were retained, and the uniform petal-like hydroxyapatite was deposited on the MN's original titania nanotubes (70 nm in diameter). Compared with the control, BMMSC on MN and HA elongated further and intersected along the micron structure with noticeable pseudopodia and pseudoplates, and the trend was more pronounced especially on HA. The number of early adherent cells on HA was remarkably larger than that on the control and MN at each time point (P<0.05). On day 1, the A value of cell proliferation on HA was significantly higher than that on the control and MN (P<0.05). The A value of cell proliferation on HA was significantly lower than that on the control and MN on day 3 (P<0.05). On day 7, the A value of cell proliferation on HA was significantly lower than that on MN (P<0.05), but there was no statistically significant difference in the A value of cell proliferation between HA and the control on day 7 (P>0.05). The Avalue of extracellular matrix mineralization on HA (0.607±0.011) was significantly higher than that on the control and MN (0.268±0.025 and 0.522±0.022, respectively) (t=-0.25, P<0.001; t=-0.34, P<0.001). The expression levels of bone related genes on HA were significantly higher than those on the control and MN (P<0.05). Conclusions: HA could promote the BMMSC adhesion and osteogenic differentiation, support BMMSC proliferation, and demonstrate good osteogenic activity.

Symptomatic diffuse esophageal spasm as a major ictal manifestation of post-traumatic epilepsy: a case report.

Post-traumatic epilepsy (PTE) can create diagnostic confusion when typical epileptic seizures are not manifest. Abdominal symptoms as a manifestation of PTE are rare in this setting. We present a 43-year-old female with paroxysmal chest and abdominal pain, nausea, salivation, and intermittent dysphagia. Esophageal testing demonstrated diffuse esophageal spasm, but smooth muscle relaxants provided no relief. Finally, after history revealed that a motor vehicle accident temporally preceded symptom onset, video electroencephalography confirmed PTE. Therapy with anti-epileptic drug completely resolved symptoms, and the esophageal motor pattern normalized. We speculate that abnormal epileptiform discharges from the seizure focus altered cerebral input to intrinsic esophageal innervation, resulting in inhibitory dysfunction and a picture resembling diffuse esophageal spasm. This is the first report of symptomatic esophageal spasm as a major ictal manifestation of PTE.

Differential Expression ESTs Associated with Fluorosis in Rats Liver.

The fluoride has volcanic activity and abundantly exists in environment combining with other elements as fluoride compounds. Recent researches indicated that the molecular mechanisms of intracellular fluoride toxicity were very complex. However, the molecular mechanisms underlying the effects on gene expression of chronic fluoride-induced damage is unknown, especially the detailed regulatory process of mitochondria. In the present study, we screened the differential expression ESTs associated with fluorosis by DDRT-PCR in rat liver. We gained 8 genes, 3 new ESTs, and 1 unknown function sequence and firstly demonstrated that microsomal glutathione S-transferase 1 (MGST1), ATP synthase H(+) transporting mitochondrial F(0) complex subunit C1, selenoprotein S, mitochondrial IF1 protein, and mitochondrial succinyl-CoA synthetase alpha subunit were participated in mitochondria metabolism, functional and structural damage process caused by chronic fluorosis. This information will be very helpful for understanding the molecular mechanisms of fluorosis.

Storage Rot of Dragon Fruit Caused by Gilbertella persicaria.

In October 2011, a new disease of dragon fruit (Hylocereus costaricensis) was discovered in a fruit market in Yuanjiang, Yunnan Province, China. Small, light brown, water-soaked spots appeared initially and then coalesced, extending to the entire fruit in 6 days. Hyaline hyphae and light brown sporangia were observed over the entire surface of the infected fruit. On potato sucrose agar (PSA) the fungus produced a white, appressed colony that covered a 9-cm diameter petri dish in less than 5 days at 25°C. The sporangiophores were hyaline, light brown to grayish, 44.71 to 143.14 (average = 85.10) µm long, and arose directly from the non-septate substrate hyphae. The sporangia were spherical, single, and terminal and yellow-brown to brown when young turning to dark brown or black at maturity. Both the sporangiophores and sporangia were covered with calcium oxalate crystals. When mounted in a drop of water, the sporangium immediately broke longitudinally into two halves, releasing the spores and exposing a large pyriform columella at the tip of the sporangiophore. The spores were mostly globose to ellipsoid, aseptate, and 5.15 (3.71 to 7.86) × 6.30 (4.08 to 9.19) µm (n = 300). Two to three slender, hyaline appendages were attached to the ends of the spores. The cardinal growth temperatures of the pathogen were 10, 30, and 40°C and it grew faster in the dark than under 12-h alternating light-dark cycles. The fungus was identified as Gilbertella persicaria (1). To confirm the identification, the internal transcribed spacer region of the nuclear rDNA of one isolate was amplified using the fungal primers ITS1 and ITS4. The nucleotide sequence (Accession No. JQ951601) showed 98% homology with G. persicaria in GenBank (HM999958). Pathogenicity tests were carried out on two species of dragon fruit, H. costaricensis and H. undatus, by placing a 6-mm diameter young mycelial PSA agar disc on the surface of an asymptomatic fruit, either unwounded or wounded with a sterile needle. As the control, a plain PSA disc was used. Each inoculated fruit was placed in a moist chamber and incubated at 25°C. Three fruits were used per treatment and the experiment was repeated twice. The fruits rotted in 2 to 3 days, and the disease was especially serious on wounded fruits and on H. costaricensis. The fungus was reisolated from infected fruits. The controls did not show any disease symptoms. Inoculation studies were also made on other fruits but rot was produced only on peach, pear, and wounded tomato. To our knowledge, this is the first record of dragon fruit rot caused by G. persicaria. The fungus had been reported in China but caused no diseases (2). In India, it caused fruit rot of pear, tomato, and peach (3). To minimize the disease, dragon fruit should be stored at low temperature and in uncovered containers. References: (1) G. L. Benny. Mycologia 83:150, 1991. (2) J. Y. Cheng and H. Y. Mei. Acta Phytotax. Sin. 10:105, 1965. (3) M. D. Mehrotra. Mycopath. Mycol. Appl. 29:151, 1966.

First Report of Ralstonia solanacearum Causing Bacterial Wilt of Yacon in China.

Yacon (Smallanthus sonchifolius) is an important cash crop in Yunnan Province, China. In 2003, yacon was introduced to Yunnan province as a novelty root crop and as an experimental source of natural sugars; now more than 15 provinces cultivate the crop. Yunnan is one of the major yacon producing areas of China, with up to 10,000 ha yielding up to 50,000 t of yacon, which is nearly half of the production in China. In April and May 2010, bacterial wilt of yacon was observed in the fields of Lion Mountain of Wuding County, Yunnan Province, China. In 2011, the disease occurred in approximately 1 ha of yacon, resulting in 10% crop loss in that area. The initial symptoms observed were irregular, black, necrotic lesions on leaf margins. After 4 to 7 days, leaves became totally necrotic, plants wilted, and black stripes were observed on plant stems. Within 2 to 3 weeks, more than 70% of leaves within the crop were wilted. Subsequently, the plants died and stems became brittle. When dead plants were pulled from the soil, tubers were found to have turned black. When diseased stems and/or petioles were cut with a sterile sharp knife or razor blade, bacterial ooze appeared on the cut ends. High populations of morphologically uniform bacteria were isolated from the diseased plants by conventional methods. When cultured on TZC (2,3,5-Triphenylte tetrazolium chloride) agar medium (3), colonies were large, elevated, fluidal, and entirely white with a pale red center. The isolated bacterium was gram-negative, grew aerobically, and did not form endospores. The cells were 0.5 to 0.7 × 1.5 to 2.0 µm and nonencapsulated. Ralstonia solanacearum was identified and confirmed as the pathogen on the basis of morphological and physiological characteristics, pathogenicity test, and 16S rDNA sequence analysis (1,4). The nucleotide sequence is available in GenBank (Accession No. HQ176322.1). The pathogenic strain belonged to race 1 and biovar 3 according to the pathogenicity and carbohydrate utilization tests (2). Koch's postulates were tested in the greenhouse, with 10 plants inoculated per species. Plants were inoculated with 15 µl of cell suspension containing 106 to 107 CFU ml-1 deposited into the third axilla with a capillary tube. The bacteria could infect tomato, pepper, tobacco, potato, common sage (Salvia dugesii Fernald), and patchouli, and caused typical symptoms of wilt and black lesions, but could not infect leaves of swamp mahogany (Eucalyptus robusta Smith), stramonium (Dature stramonium Datura L.), ginger, or maize. To our knowledge, this is the first report of yacon as a host of R. solanacearum. Since the pathogen has a wide host range, monitoring of the vegetation in and around yacon fields should be implemented as a mandatory management measure to prevent disease spread. References: (1) C. A. Boucher et al. J. Bacteriol. 169:5626, 1987. (2) A. C. Hayward. J. Appl. Bacteriol. 27:265, 1964. (3) A. Kelman. Phytopathology 44:693, 1954. (4) W. G. Weisburg et al. J. Bacteriol. 173:697, 1991.

Long non-coding RNA PVT1 regulates glioma proliferation, invasion, and aerobic glycolysis via miR-140-5p.

The article "Long non-coding RNA PVT1 regulates glioma proliferation, invasion, and aerobic glycolysis via miR-140-5p, by Y. Shao, H.-T. Chen, Q.-R. Ma, Y.-W. Zhang, Y.-Q. He, J. Liu published in Eur Rev Med Pharmacol Sci 2020; 24(1): 274-283-DOI: 10.26355/eurrev_202001_19922-PMID: 31957841" has been withdrawn from the authors. The Publisher apologizes for any inconvenience this may cause. https://www.europeanreview.org/article/19922.

Long non-coding RNA PVT1 regulates glioma proliferation, invasion, and aerobic glycolysis via miR-140-5p.

OBJECTIVE: To investigate the regulation of long non-coding RNA plasmacytoma variant translocation 1 (LncRNA PVT1) on proliferation, invasion, and aerobic glycolysis in glioma cells via miR-140-5p. PATIENTS AND METHODS: Sixty patients with glioma treated in our hospital were recruited. The expression of PVT1 in tissues and cells was determined by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR), and the effects on the prognosis were observed. Glioma cell lines U87 and T98MG were either stably or transiently transfected with over-expression or inhibition vectors. Cell counting kit-8 (CCK-8), transwell, glucose, and lactate detection were employed to measure cell proliferation, invasion, and aerobic glycolysis after transfection. The correlation between PVT1 and miR-140-5p was determined by Dual-Luciferase reporter assay. RNA pull-down and RNA immunoprecipitation (RIP) test were adopted to indicate the correlation between PVT1 and miR-140-5p. RESULTS: PVT1 was highly expressed and had superior diagnostic value in gliomas, and the high expression of PVT1 resulted in poor prognosis of patients. Over-expressing PVT1 increased cell proliferation, invasion, and aerobic glycolysis, while inhibiting PVT1 yielded opposite outcome. Dual-Luciferase reporter assay confirmed that PVT1 could target miR-140-5p. Functional analysis showed that over-expression of miR-140-5p inhibited proliferation, invasion, and aerobic glycolysis in glioma cells. Rescue experiment found that the inhibitory effect of miR-140-5p could be eliminated by up-regulating PVT1 expression. CONCLUSIONS: PVT1 promotes proliferation, invasion, and aerobic glycolysis in glioma cells by regulating miR-140-5p.

CYP1A2 is the major isoform responsible for paeonol O-demethylation in human liver microsomes.

1. Paeonol, the primary active component of a traditional Chinese medicine Moutan Cortex, has a wide range of pharmacological activities. In the present study, the metabolism of paeonol by cytochrome P450s (CYPs) was investigated in human liver microsomes. 2. One O-demethylated metabolite was detected in reaction catalysed by human liver microsomes, and was identified as resacetophenone by comparing the tandem mass spectra and the chromatographic retention time with that of the standard compound. 3. The study with a chemical selective inhibitor, cDNA-expressed human CYPs, a correlation assay, and a kinetics study demonstrated that CYP1A2 was the major isoform responsible for the paeonol O-demethylation in human liver microsomes.

Hydroxylation of tanshinone IIa in human liver microsomes is specifically catalysed by cytochrome P4502A6.

Tanshinone IIa, the primary active component of a traditional Chinese medicine Salvia miltiorrhiza (Danshen), has a wide range of pharmacological activities. In the present study, the metabolism of tanshinone IIa (5 microM) by cytochrome P450s (CYPs) was investigated in human liver microsomes. One mono-hydroxylated metabolite was detected in a reaction catalysed by human liver microsomes, and was identified as tanshinone IIb by comparing the tandem mass spectra and the chromatographic retention time with that of the standard compound. The study with a chemical selective inhibitor, cDNA-expressed human cytochrome P450s, correlation assay, and kinetics study demonstrated that CYP2A6 was the specific isozyme responsible for the hydroxyl metabolism of tanshinone IIa (5 microM) in human liver microsomes.

Mutation of GJB2 in a Chinese patient with keratitis-ichthyosis-deafness syndrome and brain malformation.

OBJECTIVE: Keratitis-ichthyosis-deafness syndrome (KID) is a rare congenital disorder. Mutations in the GJB2 gene have recently been identified as the causative mutations of KID. AIM: To define the GJB2 mutation in a Chinese patient with KID and brain malformation. METHODS: Genomic DNA was extracted from peripheral blood and used to amplify the GJB2 gene. Direct sequencing and endonuclease digestion were used for mutation analysis. RESULTS: We identified a heterozygous missense mutation (D50N) in the GJB2 gene in this patient. CONCLUSIONS: These results indicate that KID syndrome in this patient was caused by a dominant mutation of GJB2.

Histone deacetylase inhibitor trichostatin A modulates cell cycles in A2780 human ovarian cancer cell lines.

PURPOSE OF INVESTIGATION: To analyze the effect and mechanism of TSA on cell cycles in human ovarian cancer cells. METHODS: cells were cultured in RPMI 1640 supplemented. Flow cytometry analysis and RT-PCR were used to examine the distribution of cell cycles and the level of P21(WAF/CIPI) mRNA. RESULTS: TSA induced increase of the G2/M phase accompanied by decrease of the S phase and enhanced level of P21(WAF/CIPI) mRNA in a concentration and time-dependent manner in A2780 cells. CONCLUSION: Trichostatin A affects the activity of cyclin-dependent kinase through increased expression of P21(WAF/CIPI) mRNA. TSA causes A2780 cell blockage in the G2/M phase and inhibits cell proliferation of A2780 cells. The minimum level of active TSA is 100 nM and the minimum time is 12 hours. The effect relies on time and concentration.

[Alteration of oxidative stress and expression of antioxidases in diaphragm of severely burned rats].

Objective: To explore the occurrence of oxidative stress and antioxidases expression in diaphragm of severely burned rats, so that the mechanism of respiratory muscle atrophy and dysfunction post-burn injury will be further clarified. Methods: Eighty male Wistar rats (aged 7 to 8 weeks) were divided into sham injury group and burn injury group according to the random number table, with 40 rats in each group. Rats in burn injury group were inflicted with 50% total body surface area full-thickness scald (hereinafter referred to as burn) on the back and abdomen by immersing into 80 ℃ water for 15 s and 8 s respectively. Immediately after injury, 40 mL/kg normal saline was injected through abdomen for resuscitation, and the wounds were treated with iodine. Except for immersing into 37 ℃ warm water and no resuscitation, the other treatments of rats in sham injury group were the same as those of burn injury group. Whole diaphragms of 8 rats per time point per group were collected after anesthesia at post injury hour (PIH) 2 and on post injury day (PID) 1, 3, 7, and 14, and muscle mass was determined. The protein carbonyl content was determined by microplate reader. The protein expressions of catalase, superoxide dismutase 2 (SOD2), and glutathione peroxidase 1 were determined by Western blotting. Data were processed with analysis of variance of factorial design, t test, and Bonferroni correction. Results: (1) There were no statistically significant differences in the diaphragm mass of rats between the 2 groups at PIH 2 and on PID 1 (t=0.453, 0.755, P>0.05). The diaphragm mass of rats in burn injury group started to decrease from PID 3, which was significantly lower than that of sham injury group (t=3.321, P<0.01). The diaphragm mass of rats in burn injury group started to increase from PID 7 to PID 14, which was significantly lower than that of sham injury group (t=4.622, 4.380, P<0.01). (2) Protein carbonyl content in diaphragm of rats in burn injury group at PIH 2, and on PID 1, 3, 7, and 14 [(2.7±0.3), (2.5±0.5), (2.4±0.4), (2.5±0.4), (3.2±0.6) pg/mL] was significantly higher than that of sham injury group respectively [(1.2±0.4), (1.6±0.3), (1.5±0.7), (1.7±0.3), (1.8±0.4) pg/mL, t=5.994, 3.263, 3.666, 3.158, 5.763, P<0.05 or P<0.01]. (3) Protein expressions of catalase in diaphragm of rats in burn injury group on PID 1 and 3 were close to those of sham injury group (t=0.339, 0.324, P>0.05). There were no statistically significant differences in protein expressions of SOD2 in diaphragm of rats between the 2 groups at PIH 2 and on PID 1, 3, 7, and 14 (t=1.446, 1.385, 0.757, 1.561, 0.531, P>0.05). There were no statistically significant differences in protein expressions of glutathione peroxidase 1 in diaphragm of rats in the 2 groups at PIH 2 and on PID 1, 3, and 7 (t=0.200, 0.729, 0.385, 1.559, P>0.05). Conclusions: Continuous oxidative stress and relatively insufficient expression of antioxidases in diaphragm induced by burn injury could be a contributor to diaphragm atrophy.