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.

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.

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: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.

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.

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 aim of the current study was to explore the alterations of TLR4 after traumatic brain injury. Methods: 20 Male ICR rats were randomly divided into four groups(5 rats each group)including control group without brain injury and traumatic brain injury groups(4,24 hours and 7 days).All rats were decapitated at corresponding time point and mid-jejunum samples were taken.The intestinal mucosa structure was detected by histopathological examination.Immunohistochemistry and realtime RNA were used for detection of TLR4 expression in ileum samples.Results: After traumatic brain injury,the histopatholocal alterations of gut mucosa occurred at 4 hours and progressed to a serious state.Compared to control group,TLR4 was significantly up-regulated on the endothelia of microvessels in villous interstitium and lamina propria by 4 h following TBI and maximally expressed at 24 h post-injury.The endothelial TLR4 immunoreactivity in ileum mucosa still remained strong on 7 d post-injury.There was a very low mRNA expression of TLR4 in the gut of control rats and significantly increased at 4 h following TBI(P

Purpose To investigate 1H-MRS in differentiating intracranial lymphoma from tumor-like demyelinating lesions. Materials and Methods Thirty-three cases of intracranial lymphoma confirmed by pathology and 18 cases of tumor-like demyelinating lesions confirmed by pathology or clinic were recruited in this study. Imaging data including single-voxel (TE=144 ms) 1H-MRS was retrospective analyzed. The Cho/Cr and Cho/NAA area ratios were calculated. The lipid and lactate peak was visually categorized into 5 grades based on the ratio of Lip-Lac peak to the height of the Cr peak. 1H-MRS findings of the intracranial lymphoma and the tumor-like demyelinating lesions were compared. The differentiation of the two diseases diagnosed by 1H-MRS and conventional MR were evaluated by use of receiver operating characteristic curves. Results There were significant difference of Cho/Cr, Cho/NAA ratio and Lip-Lac peak level between the intracranial lymphoma and tumor-like demyelinating lesions (P<0.001). It was more likely to be intracranial lymphoma when Cho/Cr ratio was>2.56, Cho/NAA ratio was>1.71, and Lip-Lac peak grade was>3. Cho/Cr, Cho/NAA ratio and Lip-Lac peak grade were found higher in atypical intracranial lymphomas when compared with those of tumor-like demyelinating lesions. The area under the receiver operating characteristic curve of conventional MR was increased from 0.827 to 0.870 when Cho/NAA ratio was added for analysis in the 28 uncertain cases. Conclusion 1H-MRS has great clinical significance for differentiating intracranial lymphoma from tumor-like demyelinating lesions. The values of Cho/Cr ratio>2.56, Cho/NAA ratio>1.71 and Lip-Lac grade >3 suggest intracranial lymphoma rather than TDLs. When the conventional MR imaging features can not do the differentiation, Cho/NAA ratio is a useful complement.

AIM:To observe the changes in heme oxygenase-1(HO-1) expression in the lung after ischmia-reperfusion of hind limbs in rats.METHODS:Hind limbs ischemia was made by clamping infrarenal aorta with a microvascular clip and lung injury was made by following reperfusion. Lung tissue was obtained from the animals subjected to sham operation, 4 h ischemia without reperfusion and 4 h, 8 h, 16 h, 24 h, 48 h reperfusion following 4 h ischemia. The levels of HO-1 mRNA and protein were measured at different times by Northern blot and Western blot. Immunohistochemistry technique was used to determine the cell types responsible for limb ischemic reperfusion induced HO-1 expression. RESULTS:After ischemia-reperfusion of limbs, HO-1 mRNA increased by 4 h, reached a peak at 16 h, and returned toward baseline at 24-48 h. This time course correlated with increased HO-1 protein. Immunohistochemical studies showed HO-1expressed in a variety of cell types, including the airway epithelium, alveolar macrophages and vascular smooth muscular cells. There were no positive signals in sham group and ischemia group both in mRNA levels and protein levels. CONCLUSION:The expression of HO-1 in the lung is not induced by limb ischemia or sham operation, but induced by limb reperfusion after ischemia in rats.