Animals ; Male ; NF-kappa B ; metabolism ; Otitis Media with Effusion ; immunology ; metabolism ; physiopathology ; Rats ; Rats, Sprague-Dawley ; Th1 Cells ; cytology ; Th2 Cells ; cytology

Adolescent ; Adult ; Ear, Middle ; diagnostic imaging ; Female ; Humans ; Imaging, Three-Dimensional ; Male ; Mastoid ; diagnostic imaging ; Middle Aged ; Tomography, X-Ray Computed ; Young Adult

Synaptic plasticity of barrel cortex is one of the most widely studied topics in neuroscience in recent years. The primary somatosensory cortex of the rodent has a good topology character,which provides an ideal experimental model for plasticity study. This system displays very strong experience-dependent plasticity both during development and in adulthood. The changes of sensory cortex's neural circuit can induce experience-dependent plasticity. In the synaptic level,thalamocortical synapse is considered to be the main location of plasticity. In the circuit level,both synapses from layer 4 to layer 2/3 and those within layer 2/3 are also the necessary parts of achieving synaptic plasticity in primary somatosensory cortex. The GABAergic inhibitory circuit may be involved in this plasticity of S1, but the exact mechanism remains unknown.
Animals ; Neural Pathways ; physiology ; Neuronal Plasticity ; Somatosensory Cortex ; physiology ; Synapses ; physiology ; Thalamus ; physiology ; Vibrissae ; physiology

OBJECTIVETo study the biological effects of 585 nm pulsed dye laser (FLPDL) in the treatment of congestive scar.

METHODSBy histological study, collagen VG staining and microvascular staining, we investigated the changes of collagen fibers and the density of microvessels in the congestive scars after FLPDL treatment.

RESULTSHistological and immunohistochemistry examinations showed that FLPDL achieved normal vascularity in the scar after over 3 times of treatment.

CONCLUSIONSPDL treatment can change fundamentally the physiology of wound healing if applied in the early phases.

Adolescent ; Adult ; Cicatrix ; therapy ; Female ; Humans ; Lasers, Dye ; Low-Level Light Therapy ; methods ; Male ; Middle Aged ; Reconstructive Surgical Procedures ; methods ; Treatment Outcome ; Wound Healing ; Young Adult

BACKGROUNDHepatocyte growth factor (HGF) treats ischemic disease by promoting arteriogenesis, however, its mechanism of action is not known. The notch signaling pathway plays an important role in neovascularization. The relationship between the proliferation and migration ability of artery endothelial cells and the Dll4-Notch-Hey2 signaling pathway in the process of arteriogenesis was investigated as a mechanism of action of HGF.

METHODSBased on the prophase study cells and supernatant were harvested at the indicated time after human femoral artery endothelial cells (HFAECs) were infected with adenovirus-HGF (Ad-HGF) at 200 pfu/cell. Cells were analyzed for HGF expression and Notch1, Dll4 and Hey2 expression by ELISA and reverse transcription-PCR (RT-PCR). The changes in the proliferation and migration ability of HFAECs were observed by MTT and Transwell migration experiments. Ad-GFP-infected HFAECs were used as control.

RESULTSCompared with the control group the Ad-HGF group's HGF expression was not increased with time, and the induction by HGF of Notch1, Dll4 and Hey2 gene transcription was not enhanced with an increase of HGF. The proliferation ability of Ad-HGF-transduced HFAECs was enhanced and their migration ability was also enhanced in the presence of HGF.

CONCLUSIONSThrough activating the Dll4-Notch-Hey2 signaling pathway, HGF indirectly promotes the proliferation and migration ability of cells, so that offspring artery branches are formed.

Basic Helix-Loop-Helix Transcription Factors ; genetics ; metabolism ; Cell Line ; Enzyme-Linked Immunosorbent Assay ; Hepatocyte Growth Factor ; genetics ; metabolism ; Humans ; Intercellular Signaling Peptides and Proteins ; genetics ; metabolism ; Receptors, Notch ; genetics ; metabolism ; Repressor Proteins ; genetics ; metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; Signal Transduction ; genetics ; physiology

OBJECTIVETo study the effects of Lipopolysaccharide (LPS) on the maturation and secretion of human peripheral dendritic cells (DCs).

METHODSDCs from healthy human peripheral monocytes (PBMCs) were induced in vitro with rhGM-CSF, rhIL-4, Flt3-L and TNFalpha. The subjects were divided into 3 groups: the long-term group stimulated with LPS 1 microg/ml at day 1, 4, 7, 9 post culture; the short-term group stimulated with LPS 1 microg/ml at day 7 and 8 post culture, and the DCs without LPS stimulation was control group. After 10 days of culture, the morphologic features of DCs were observed by light and electron microscopes, the phenotypic patterns were characterized by flow cytometry, the proliferation of T cell were evaluated with mixed leukocytes reaction (MLR) and the levels of IL-12 and IFNgamma produced by DCs were analyzed with ELISA.

RESULTSCompared with the short-term group, the expressions of HLA-DR (65.81%+/-10.96%), CD86 (48.81%+/-18.13%), CD80 (13.56%+/-5.48%), CD83 (11.52%+/-5.09%), the secretions of IFNgamma(15.60+/-5.83 pg/ml) and IL-12 (51.77+/-11.02 pg/ml) by the DCs in long-term group were decreased obviously (P is less than 0.05) and the proliferation of homogenic lymphocyte cells (1.548+/-0.365) stimulated by DCs was also impaired (P < 0.05).

CONCLUSIONLong-term LPS stimulation can suppress the maturation and secretion of DCs, which might be the reason of poor immunity in the patients with intestinal endotoxemia.

Cells, Cultured ; Dendritic Cells ; cytology ; drug effects ; metabolism ; Humans ; Interleukin-12 ; biosynthesis ; Lipopolysaccharides ; pharmacology ; Monocytes ; cytology ; metabolism

OBJECTIVETo study the potential role of mast cells and the related molecular mechanism in chronic hepatitis (CH) using a rat model system.

METHODSThirty Wistar rats (15 males, 15 females; weight range: 230-290 g) were randomly divided into the normal contrast (NC) group and experimental CH group. The CH group received subcutaneous injection of CCl4 and a diet high in cholesterol and alcohol content and low in protein and choline content. Throughout the 4-week modeling period, aseptic blood samples were taken to test plasma tryptase (TS) and hyaluronic acid (HA) levels. The rats were euthanized to assess the changes in liver mast cells by histology and morphology analyses and the changes in liver expression of c-kit and stem cell factor (SCF) proteins by immunohistochemistry and mRNAs by RT-PCR.

RESULTSCompared to the NC group, the CH group had higher plasma and liver concentration of HA (78.09 +/- 38.55 vs. 145.14 +/- 52.54 ng/ml, 51.58 +/- 20.45 vs. 106.59 +/- 43.15 ng/100 mg; t = 2.457 and 2.825 respectively, both P less than 0.05) and TS (0.416 +/- 0.143 vs 0.753 +/- 0.210 mg/ml; t = 4.165, P less than 0.05). The CH group also showed fatty degeneration and fibrosis with many degranulating and degranulated mast cells filled with purple granula located around the liver blood vessels and in fiber-intervals. The CH livers also showed a significantly higher number of mast cells (2.167 +/- 0.924 vs. NC: 10.92 +/- 1.575; t = 7.633, P less than 0.05) and stronger intensity of c-kit staining (2.783 +/- 0.577 vs. 12.86 +/- 3.126; t = 9.511, P less than 0.05) and SCF staining (3.383 +/- 1.583 vs. 15.58 +/- 6.431; t = 9.625, P less than 0.05). The expressions of c-kit and SCF were positively correlated with HA level (r = 0.478 and 0.556 respectively, both P less than 0.05). The c-kit and SCF mRNA expression levels were also significantly higher in the CH liver tissues.

CONCLUSIONMast cell degranulation and histamine release is significantly increased under conditions of chronic hepatitis, and the related mechanism may involve up-regulation of the membrane receptor c-kit and its ligand SCF.

Animals ; Cell Degranulation ; Disease Models, Animal ; Female ; Hepatitis, Chronic ; metabolism ; pathology ; Hepatocytes ; metabolism ; Liver ; metabolism ; Liver Cirrhosis ; metabolism ; pathology ; Male ; Mast Cells ; metabolism ; physiology ; Proto-Oncogene Proteins c-kit ; metabolism ; RNA, Messenger ; genetics ; Rats ; Rats, Wistar ; Stem Cell Factor ; metabolism

OBJECTIVETo investigate the effects of antihistamine treatment on immune function in rats with experimental hepatitis.

METHODSThirty Wistar rats were randomly allocated into three groups:experimental hepatitis group (EH group), antihistamine treatment group (AH group) and normal control group (NC group). Rats in the EH group received the subcutaneous injection of 40% carbon tetrachloride oil solution and were fed on diet with low-protein, low-choline, high-fat and high-alcohol,while rats in the AH group received antihistamine treatment(ketotifen + vitamin C) additionally.They were sacrificed after 4 weeks, and the levels of serum alanine aminotransferase(ALT), total bilirubin (TBil), histamine(HA), IFNgamma, IL-12, IL-4 and IL-10 were determined. The levels of IL-12 mRNA and IFN-gamma mRNA in liver tissue were determined via real-time reverse transcriptional polymerase chain reaction(RT-PCR).

RESULTS(1) Compared to the NC group, in the EH group, the levels of ALT, TBil, and circulating and intrahepatic HA were significantly increased(P less than 0.05); intrahepatic HA were significantly decreased(P less than 0.05) after antihistamine treatment. (2) Compared to the NC group, in the EH group, the levels of IL-4, IL-10 were significantly increased((0.504+/-0.202)ng/ml and (29.025+/-1.478) pg/ml vs (0.811+/-0.244)ng/ml and (33.72+/-4.293)pg/ml respectively, P less than 0.05), and the levels of IL-12 were decreased ((6.515+/-2.893)pg/ml vs (3.519+/-1.113)pg/ml, P less than 0.05); and after antihistamine treatment the levels of IL-4 and IL-10 were significantly decreased (were (0.423+/-0.168)ng/ml and (30.412+/-3.275)pg/ml, P less than 0.05), the levels of IL-12 were significantly increased (P less than 0.05), but the level of IFNgamma had no significance (P more than 0.05). The levels of intrahepatic IL-12 mRNA and IFNgamma mRNA had similar results.

CONCLUSIONAntihistamine treatment may improve liver function and correct Th1/Th2 unbalance.

Animals ; Ascorbic Acid ; pharmacology ; Disease Models, Animal ; Hepatitis ; immunology ; metabolism ; therapy ; Histamine Antagonists ; pharmacology ; Interferon-gamma ; metabolism ; Interleukin-10 ; metabolism ; Interleukin-12 ; metabolism ; Interleukin-4 ; metabolism ; Ketotifen ; pharmacology ; Liver ; drug effects ; metabolism ; Male ; Rats ; Rats, Wistar ; Th1-Th2 Balance ; Tumor Necrosis Factor-alpha ; metabolism

Adolescent ; Adult ; Aged ; Female ; Humans ; Insulin-Like Growth Factor Binding Proteins ; metabolism ; Liver ; metabolism ; Liver Cirrhosis ; metabolism ; pathology ; Male ; Middle Aged ; Young Adult

Objective： This study was designed to explore the relationship between clinicobiological acting and expression of p21 protein and estrogen receptor(ER) in colorectal cancer. Methods： The intensity of expression of p21 protein and ER for 206 patients with colorectal cancers were determined by labeled-streptokinase avidin-biotin(LSAB) assay. Results： The expression of p21 protein is negatively correlated with that of ER in colorectal cancer(r=-0.6613, P<0.01). The intensity of expression of p21 protein and ER in colorectal cancers were not related with the patients age, sexuality, tumor position, pathological type, histological type, Dukes stage etc.(r< 0.4,P>0.05). Both the expressions were related to the prognosis of colorectal cancer(P<0.01). Higher the intensity of expression of p21 protein worse the patients prognosis, and higher the intensity of expression of ER better the patient s prognosis. Conclusions： The abnormal expression of p21 protein is related to the dysbolism of estrogen in colorectal cancer. The detection of p21 protein and ER are helpful for diagnosis and prognostic evaluation for colorectal cancer.