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1.  Stress-induced intestinal necrosis resulting from severe trauma of an earthquake 
AIM: To investigate the possible reasons and suggest therapeutic plan of stress-induced intestinal necrosis resulting from the severe trauma.
METHODS: Three patients in our study were trapped inside collapsed structures for 22, 21 and 37 h, respectively. The patients underwent 3-4 operations after sustaining their injuries. Mechanical ventilation, intermittent hemodialysis and other treatments were also provided. The patients showed signs of peritoneal irritation on postoperative days 10-38. Small intestinal necrosis was confirmed by emergency laparotomy, and for each patient, part of the small bowel was removed.
RESULTS: Two patients who all performed 3 operations died of respiratory complications on the first and second postoperative days respectively. The third patient who performed 4 operations was discharged and made a full recovery. Three patients had the following common characteristics: (1) Multiple severe trauma events with no direct penetrating gastrointestinal injury; (2) Multiple surgeries with impaired renal function and intermittent hemodialysis treatment; (3) Progressive abdominal pain and tenderness, and peritoneal irritation was present on post-traumatic days 10-38; (4) Abdominal operations confirmed segment ulcer, necrosis of the small intestine, hyperplasia and stiffness of the intestinal wall; and (5) Pathological examinations suggested submucosal hemorrhage, necrosis, fibrosis and hyalinization of the vascular wall. Pathological examinations of all 3 patients suggested intestinal necrosis with fistulas.
CONCLUSION: Intestinal necrosis is strongly asso-ciated with stress from trauma and post-traumatic complications; timely exploratory laparotomy maybe an effective method for preventing and treating stress-induced intestinal necrosis.
doi:10.3748/wjg.v18.i17.2127
PMCID: PMC3342613  PMID: 22563202
Intestinal necrosis; Stress; Trauma; Earthquake; Exploratory laparotomy; Fatty acid binding protein
2.  Two clinically relevant pressures of carbon dioxide pneumoperitoneum cause hepatic injury in a rabbit model 
AIM: To observe the hepatic injury induced by carbon dioxide pneumoperitoneum (CDP) in rabbits, compare the effects of low- and high-pressure pneumoperitoneum, and to determine the degree of hepatic injury induced by these two clinically relevant CDP pressures.
METHODS: Thirty healthy male New Zealand rabbits weighing 3.0 to 3.5 kg were randomly divided into three groups (n = 10 for each group) and subjected to the following to CDP pressures: no gas control, 10 mmHg, or 15 mmHg. Histological changes in liver tissues were observed with hematoxylin and eosin staining and transmission electron microscopy. Liver function was evaluated using an automatic biochemical analyzer. Adenine nucleotide translocator (ANT) activity in liver tissue was detected with the atractyloside-inhibitor stop technique. Bax and Bcl-2 expression levels were detected by western blotting.
RESULTS: Liver functions in the 10 mmHg and 15 mmHg experimental groups were significantly disturbed compared with the control group. After CDP, the levels of alanine transaminase and aspartate transaminase were 77.3 ± 14.5 IU/L and 60.1 ± 11.4 IU/L, respectively, in the 10 mmHg experimental group and 165.1 ± 19.4 IU/L and 103.8 ± 12.3 IU/L, respectively, in the 15 mmHg experimental group, which were all higher than those of the control group (P < 0.05). There was no difference in pre-albumin concentration between the 10 mmHg experimental group and the control group, but the pre-albumin level of the 15 mmHg experimental group was significantly lower than that of the control group (P < 0.05). No significant differences were observed in the levels of total bilirubin or albumin among the three groups. After 30 and 60 min of CDP, pH was reduced (P < 0.05) and PaCO2 was elevated (P < 0.05) in the 10 mmHg group compared with controls, and these changes were more pronounced in the 15 mmHg group. Hematoxylin and eosin staining showed no significant change in liver morphology, except for mild hyperemia in the two experimental groups. Transmission electron microscopy showed mild mitochondrial swelling in hepatocytes of the 10 mmHg group, and this was more pronounced in the 15 mmHg group. No significant difference in ANT levels was found between the control and 10 mmHg groups. However, ANT concentration was significantly lower in the 15 mmHg group compared with the control group. The expression of hepatic Bax was significantly increased in the two experimental groups compared with the controls, but there were no differences in Bcl-2 levels among the three groups. Twelve hours after CDP induction, the expression of hepatic Bax was more significant in the 15 mmHg group than in the 10 mmHg group.
CONCLUSION: A CDP pressure of 15 mmHg caused more substantial hepatic injury, such as increased levels of acidosis, mitochondrial damage, and apoptosis; therefore, 10 mmHg CDP is preferable for laparoscopic operations.
doi:10.3748/wjg.v17.i31.3652
PMCID: PMC3180024  PMID: 21987614
Carbon dioxide pneumoperitoneum; Hepatic injury; Rabbit; Mitochondria; Apoptosis
3.  Management of patients with sphincter of Oddi dysfunction based on a new classification 
AIM: To propose a new classification system for sphincter of Oddi dysfunction (SOD) based on clinical data of patients.
METHODS: The clinical data of 305 SOD patients documented over the past decade at our center were analyzed retrospectively, and typical cases were reported.
RESULTS: The new classification with two more types (double-duct, biliary-pancreatic reflux) were set up on the basis of the Milwaukee criteria. There were 229 cases of biliary-type SOD, including 192 (83.8%) cases cured endoscopically, and 29 (12.7%) cured by open abdominal surgery, and the remaining 8 (3.5%) cases observed with unstable outcomes. Eight (50%) patients with pancreatic-type SOD were cured by endoscopic treatment, and the remaining 8 patients were cured after open abdominal surgery. There were 19 cases of double-duct-type SOD, which consisted of 7 (36.8%) patients who were cured endoscopically and 12 (63.2%) who were cured surgically. A total of 41 cases were diagnosed as biliary-pancreatic–reflux-type SOD. Twenty (48.8%) of them were treated endoscopically, 16 (39.0%) were treated by open abdominal surgery, and 5 (12.2%) were under observation.
CONCLUSION: The newly proposed SOD classification system introduced in this study better explains the clinical symptoms of SOD from the anatomical perspective and can guide clinical treatment of this disease.
doi:10.3748/wjg.v17.i3.385
PMCID: PMC3022301  PMID: 21253400
Sphincter of Oddi dysfunction; Classification; Diagnosis; Treatment
4.  Effects of Neurolytic Celiac Plexus Block on Liver Regeneration in Rats with Partial Hepatectomy 
PLoS ONE  2013;8(9):e73101.
Liver regeneration is the basic physiological process after partial hepatectomy (PH), and is important for the functional rehabilitation of the liver after acute hepatic injury. This study was designed to explore the effects of neurolytic celiac plexus block (NCPB) on liver regeneration after PH. We established a model of PH in rats, assessing hepatic blood flow, liver function, and serum CRP, TNF-α, IL-1β and IL-6 concentrations of the residuary liver after PH. Additionally, histopathological studies, immunohistochemistry, and western blotting were also performed. Our results indicated that NCPB treatment after PH improved liver regeneration and survival rates, increased hepatic blood flow, reduced hepatocyte damage, decreased the secretion and release of inflammatory cytokines, increased the expression of B cell lymphoma/leukemia-2 (Bcl-2), and decreased the expression of Bcl-2 associated X protein (Bax). Additionally, Western blotting revealed that the expression of NF-κB p65 and c-Jun were decreased in liver after NCPB. In conclusion, the results of our present study indicate that NCPB treatment has a favorable effect on liver regeneration after PH. We suggest that NCPB can be utilized as an effective therapeutic method to help the functional rehabilitation of the liver after acute hepatic injury or liver cancer surgery.
doi:10.1371/journal.pone.0073101
PMCID: PMC3764180  PMID: 24039865

Results 1-4 (4)