Acute brain injury is usually complicated by systemic inflammatory response syndrome (SIRS) which is initiated by cytokines and inflammatory mediators and induces a series of adverse physiological changes, culminating in the development of multiple organ failure. SIRS plays a pivotal role on the function of brain and extra cerebral organs, exacerbates the brain edema, and increases the septic rate. The diagnostic criteria and pathological courses of SIRS, and its relationship with acute brain injury and sepsis are briefly reviewed.

The metabolic response to traumatic brain injury includes hypermetabolism, hypercatabolism, hyperglycemia, acute phase response and immunosuppression, which are mediated mainly by hypothalamus pituitary adrenal axis and cytokines. Sufficient nutritional support and appropriate metabolic intervention are believed clinically to play an important role on the mitigation of secondary brain damage, reduction of septic rate and improvement of patient′s outcomes.

In recent years,with the development of molecular biology,people gradually realize the tumor is composed of a series of development of the molecular mechanisms that trigger.The progress of targeted therapy for cancer patients brings new hope.Cetuximab through competitive combination with growth factor receptor blocking selective the growth of tumor cells,and achieved significant results.This is cetuximab in colo rectal cancer research progress of targeted therapy are reviewed in this paper.

To study the etiology and treatment of relapsing polychondritis, especially tracheostenosis, 3 patients with severe relapsing polychondritis complicated with severe tracheostenosis were presented. The clinical features, criteria of diagnosis, etiology, therapy and prognosis were discussed. All the 3 cases were female. They were misdiagnosed as laryngopharyngeal inflammation with severe tracheostenosis, so that their correct diagnosis and treatment were delayed. The report and discussion of such cases are helpful to its early diagnosis and improve ment of their prognosis.

Objective To study the expression and signiifcance of phospholipid transfer protein (PLTP) and macrophage migration inhibitory factor (MIF) in mice with bronchopulmonary dysplasia (BPD). Methods Ninety-six 4-day-old mice were randomly divided into oxygen group and air group. Mice in oxygen group were exposed to a FiO2 of 65%, and mice in air group were exposed to air. On day 7, 14, 21 and 28, blood and lung tissue samples from 12 randomly selected mice in each group were obtained. The serum levels of MIF and PLTP were measured by ELISA assay. The morphological changes of lung tissue were ob-served with HE staining. Results The mice in oxygen group showed thickened lung parenchyma and obvious pulmonary ifbrosis. The radioactive alveolar count was signiifcantly lower in oxygen group than that in air group (P<0.01). PLTP level in air group was increased gradually from day 7 to day 21, and began to decrease on day 28. PLTP level in oxygen group was increased from day 7 to day 14, and decreased on day 21 and day 28. MIF level in air group did not change during the experiment. MIF level in oxygen group was signiifcantly increased from day 7 to day 21, and began to decrease on day 28. Conclusions MIF and PLTP may be good biomarkers for the diagnosis of BPD.

Objective:The aim of the current study was to investigate the expression of nuclear factor-?B(NF-?B) and metalloproteinase-9(MMP-9) in the small intestine and to explore the potential role of NF-?B and MMP-9 in the damage of gut mucosal barrier after traumatic brain injury.Methods:The trauma was produced by a free-falling weight on the exposed dura of right parietal lobe.The rats were randomly divided into control group and traumatic brain injury groups at hours 3,12,24 and 72,and on day 7.NF-?B binding activity in the small intestine was studied by electrophoretic mobility shift assay(EMSA),and the expression of MMP-9 was studied by immunohistochemistry.Results:The results showed that NF-?B binding activity and MMP-9 expression in the small intestine was progressively increased,reached the maximum at 72 h and kept at high level up to 7 d after TBI.Concomitant upregulation of NF-?B~()and MMP-9 was observed.MMP-9 positively immunostained cells were mainly located at villous interstitium,lamina propria,crypt and submucosal layer,including endothelial cells,lymphocytes and neutrophils.Conclusion:It was concluded that cortical contusion trauma could induce a concomitant and persistent upregulation of NF-?B binding activity and MMP-9 expression in the small intestine which might play a central role in the~()damage of gut mucosal barrier.

Objectives: The aim of the current study was to explore the alterations of intestinal mucosa morphology and barrier function, and to determine how rapidly impairment of gut barrier function occurs and how long it persists following traumatic brain injury. Methods: Male Wistar rats were randomly divided into six groups (6 rats each group) including controls without brain injury and traumatic brain injury groups at hours 3, 12, 24, 72 and days 7. The intestinal mucosa structure was detected by histopathological examination and electron microscopy. Gut barrier dysfunction was evaluated by detecting serum endotoxin and intestinal permeability. The level of serum endotoxin and intestinal permeability were measured by using chromogenic limulus amebocyte lysate and lactulose/mannitol (L/M) ratio, respectively. Results: After traumatic brain injury, the histopathological alterations of gut mucosa occurred rapidly as early as 3 hours and progressed to a serious state, including shedding of epithelial cells, fracture of villi, focal ulcer, fusion of adjacent villi, dilation of central chyle duct, mucosal atrophy, and vascular dilation, congestion and edema in the villous interstitium and lamina propria. Apoptosis of epithelial cells, fracture and sparseness of microvilli, loss of tight junction between enterocytes, and damage of mitochondria and endoplasm were found by electron microscope. The villous height, crypt depth and surface area in jejunum decreased progressively with the time of brain injury. The level of serum endotoxin and L/M ratio were significantly higher in traumatic brain injury groups than that in control (P

OBJECTIVE:The bioequivalence and pharmacokinetics of two kinds of domestic meloxicam tablets were studied in 20 healthy male volunteers METHODS:A dose of 15mg of domestic or imported meloxicam(test and reference preparation)was given according to arandomized 2-way cross-over design,blood samples were withdrawn up to 96 hours post administration,and plasma concentration of meloxicam was determined by high performance liquid chromatography(HPLC)method RESULTS:The peak plasma levels(Cmax)of meloxicam test drug and reference drug were (2 736 2?312 0)and(2 665 6?333 8)?g/L,respectively,the peak time(Tmax)were(4 25?1 16)h and(4 00?1 30)h,respectively,T1/2ke were(21 67?3 81)h and(21 05?3 30)h,respectively,and AUC0～t were(96 454 6?25 526 6)and(95 692 5?24 532 6)?g/(h?L),respectively There were no significant differences in AUC0～t,Tmax,Cmax and T1/2ke between two kinds of tablet CONCLUSION:The relative bioavailability data obtained in the study furnished definite proof of bioequivalence of both domestic meloxicam tablets and imported meloxicam tablets The relative bioavailablility of the test drug was(101 3?11 9)%

Objective To investigate the effect of parent artery occlusion with liquid embolic agents (Onyx)for the treatment of distal intracranial aneurysms. Methods The clinical data of 27 patients with 29 ruptured distal intracranial aneurysms were analyzed retrospectively.Seventeen aneurysms located in the posterior inferior cerebellar artery,3 in the anterior inferior cerebellar artery,2 in the superior cerebellar artery,2 in the posterior cerebral artery,1 in the anterior cerebral artery,and 4 in the middle cerebral artery.Twenty-eight aneurysms were treated with Onyx to occlude proximal parent arteries and aneurysms, and 1 distal middle cerebral artery aneurysm was occluded spontaneously. Results All the aneurysms treated were occluded completely.One patient died of intraoperative hemorrhage.The remaining patients were followed up for 8 to 67 months.The final Glasgow outcome scale (GOS)scores were 5 in 23 patients and 4 in 3 patients. 17 patients were followed up with digital subtraction angiography (DSA)and 5 were followed up with computed tomography angiography (CTA)after procedure.There was no recurrence of the aneurysm. Four patients were followed up clinically.No new neurological disturbance or rebleeding was found in all the survived patients. Conclusion Medium-long term follow-up results have shown that the clinical efficacy of proximal parent artery occlusion with Onyx for the treatment of distal intracranial aneurysms is satisfactory,and the recurrence rate is low.

Objective To investigate the expression of pSTAT5 in 7 pancreatic carcinoma cell lines,and the change of expression of pSTAT5 in pancreatic carcinoma cells SW1990 after growth hormone (GH) treatment, and explore its molecular mechanism. Methods Human pancreatic carcinoma cell lines (SW1990, Cap-1, Colo, Mia, AsPc, P3, PANC1) were cultured in vitro, and Western blotting was used to detect the expression of pSTAT5 in these cell lines. SW1990 in exponential growth phase was collected and nude Balb/c mice were inoculated with SW1990 cells. When tumors became palpable after inoculation, mice (normal saline group). 1 h, 2 h and 24 h after the last dose of GH treatment, the mice were sacrificed.Western blotting was used to detect the expression of pSTAT5 in SW1990 and inoculation tumor cells after GH injection. Results Positive expression of pSTAT5 was observed in all human pancreatic carcinoma cell lines (SW1990, Cap-1, Colo, Mia, Aspc, P3, PANC1). 5 minutes after GH (50 ng/ml) stimulation, the expression of pSTAT5 in SW1990 was 0.57 ±0.05, which was significantly increased; and it reached 0.64 ±0.04 at 10 minutes, then decreased to 0.39 ±0.03 at 15 minutes, however, it remained higher than that in the control group at 1 h (0.33 ± 0.02 vs 0.25 ± 0.06), and its expression at 2 h was 0.26 ± 0.03 and returned to the normal level. The expression of pSTAT5 in xenograft was not significantly changed. Conclusions GH could rapidly up-regulate the expression of pSTAT5 in SW1990 but the effect lasted for a relatively short period. GH had no significant effect on the expression of pSTAT5 in xenograft.