Objective To study lymphocyte subsets changes in patients with malignant tumors during chemoimmunotherapy and the clinical significance. Metheds Fifty one cases were treated with chemotherapy and twenty six cases with chemoimmunotherapy. Lymphocyte subsets were determined by flow cytometry. Results Chemotherapy significantly decreased CD 3 +, CD 4 + and NK cells ( P 0 05). Chemoimmunotherapy elevated CD 8 + and NK cells ( P

Background Sclera remodeling process in axial elongation is one of the main pathological mechanisms of axial myopia progression.Studies confirmed that transforming growth factor-β1(TGF-β1) participates in the sclera remodeling process,and Smad3 is one of TGF-β1 downstream signal gene transcriptive factors,so to explore its role in sclera remodeling process of myopic eyes is of great significance for pathogenesis and prevention research of myopia.Objective This study was to investigate the expressions of type Ⅰ collagen and Smad3,a TGF-31 downstream target,in sclera of form deprivation myopic (FDM) eyes and explore the impact of TGF-β1-Smad3-type Ⅰ collagen signaling pathway on collagen remodeling in myopic sclera.Methods Seventy-five 1-week-old guinea pigs were randomly divided into normal control group (25 guinea pigs) and FDM group (50 guinea pigs).Monocular FDM was induced by occluding the left eyes of guinea pigs in FDM group with translucent latex balloons for 2,4,6 weeks,respectively,and consecutive occluding for 4 weeks followed by uncovering for 1 week (4/-1 weeks).The refractive power was detected by retinoscopy and axial length was measured with A-type ultrasound.Immunohistochemistry and reverse transcription-PCR were employed to detect the dynamic expressions of type Ⅰ collagen and Smad3 protein ad mRNA in the sclera of guinea pigs with emmetropia and experimental myopia,ard the relationship between collagen Ⅰ and Smad3 levels was analyzed.Results The refraction was hypermetropic in both normal control group and FDM group before occluding of eyes (P＞0.05),and the hypermetropic power was gradually reduced over time in the normal control group.In the FDM group,the refractive power was gradually changed from (+2.09 ± 0.31)D before occluding to (-1.23±0.69),(-4.17±0.59),(-7.07±0.56) and (-4.30±0.58)D,and the axial length was increased from (5.93-±0.39)mm to (6.62±0.36),(7.30±0.34),(7.99--0.32),and (7.21 ±0.36) mm at weeks 2,4,6,and 4/-1 after occluding,respectively,indicating significant differences in refractive power and axial length over time in the FDM group from normal control group and self-control group (all at P＜0.05).The expressions of Smad3 and type Ⅰ collagen protein and mRNA in the sclera of the FDM group was significantly lower than those of the control group and self-control group in various time points (all at P＜0.05).The positive correlation were found in the expression of Smad3 on the myopic sclera with that of type Ⅰ collagen in both protein and mRNA levels (protein:r=0.993,P＜0.05;mRNA:r=0.954,P＜0.05).Conclusions The myopic power and ocular axis increase dependent upon occluding time,and the expressions of Smad3 and type Ⅰ collagen in the sclera are correspondingly weakened in FDM eyes.A consistent expression trend is found between Smad3 and type Ⅰ collage,suggesting Smad3 and type Ⅰ collagen participate in the regulation of sclera remodeling in myopia by TGF-β1-Smad3-Collagen Ⅰ signaling pathway.

Objective To explore the clinical characteristics and medicine treatment of patients with severe ulcerative colitis (UC),the efficacy of rescue treatment in patients with glucocorticoid (GCS) resistant severe UC,and the clinical risk factors in patients with GCS-refractory severe UC.Methods From January 2001 to December 2012,clinical,laboratory,endoscopy,imaging data and medication of treatment of 106 patients with severe UC were retrospectively analyzed.Then the patients were followed up,and the clinical efficacy and under endoscopic presentation of Mayo score were evaluated.Logistic regression analysis was performed to analyze the high risk factor of GCS-refractory severe UC.Results Among 106 patients with severe UC,95 were chronic relapse type accounting for 89.6 ％.The percentage of patients with defecation times over six was 73.6％ (78/106),with severe purulent bloody stool was 51.0％ (54/106),and with moderately or severe abdominal pain was 83.0％ (88/106).The percentage of diffuse colon type was 83.0％ (88/106),endoscopic presentation of Mayo score over two was 87.7％ (93/106).Hemoglobin decreased in 65.1％ (69/106) patients,blood platelet increased in 48.1％ (51/106) patients,C-reaction protein elevated in 88.7％ (94/106) patients,and hypoalbuminemia decreased in 42.5％ (45/106) patients.Account to 89.6％ (95/106) of patients with severe UC received GCS treatment,and the percentage of induced remission was 64.2％ (61/95),effective rate was 16.8％ (16/95),and ineffective rate was 18.9％ (18/95).The percentage of GCS refractory was 35.8％(34/95).There were 23 patients with GCS resistance and 11 patients with GCS dependence.Ten patients with GCS resistant severe UC accepted medicine rescue therapy.Five cases were treated with cyclosporin A,of which two cases induced remission,one case was effective,and two cases were ineffective.Another five cases were treated with infliximab,of which three cases induced remission,and two cases were ineffective.The results of Logistic regression analysis showed that severe anemia (OR=6.750,95％CI:2.656 to 17.152,P＜0.01),elevated blood platelets (OR=4.032,95％CI:1.226 to 13.261,P=0.015) and albumin level less than 25 g/L (OR =3.022,95 ％ CI:1.236 to 7.390,P =0.022) were risk factors of GCS-refractory severe UC.Conclusions GCS resistant or dependent occurred in part of patients with severe UC.Patients with G-CS resistant severe UC receive rescue treatment of cyclosporin A or infliximab.Severe anemia,elevated blood platelets,albumin less than 25 g/L may be clinical predicting factors in patients with GCS-refractory severe UC.

Objective: To investigate the changes of sTNFR in rats with MODS and its clinical implication. Methods: Rat delayed two phase models of MODS were replicated, then serum sTNFR were measured respectively pre and post MODS by ELISA method. Results: Serum sTNFRⅠ pre and post MODS was (112.15?24.95) pg/ml and (438.06? 67.06) pg/ml ( P

Objective: To explore the expression changes of transmembrane tumor necrosis factor receptor in rats with multiple organ dysfunction syndrome(MODS). Methods: Thirty two healthy male SD rats were randomly divided into 2 groups. Sixteen rats (MODS group) were subjected to two hit to establish MODS model, the other 16 rats (control group) were without any intervention. RT PCR and immunohistochemistry methods were applied to detect the expression of mTNFR 1 at the levels of mRNA and protein. Results: mTNFR 1 was expressed in normal liver, lung and kidney whereas the most abundant expression was found in liver. Compared with normal liver tissue, the expression of mTNFR 1 in MODS group was significantly higher ( P 0.05). Serum concentration of ALT had correlation with mTNFR 1 gene expression level in liver,but no correlation existed between serum concentration of BUN and mTNFR 1 gene expression level in kidney. Conclusion: The expression of mTNFR 1 increases after the occurence of MODS, which indicates that the impact of TNF can be modulated at the level of receptor.

Objective To observe the protective effects of soluble Nogo-66 receptor (NgR1 )antagonist (sNgR1-Fc) on cortical axons after cortical infarction in rats,and to study the phenomenon and molecular mechanism of its protective effects on and regeneration of axons.Methods The cortical infarction was induced by photochemistry,termed photothrombotic cortical injury (PCI).Fifteen Sprague Dawley rats were randomly divided into three groups:Sham-operated group,PBS (phosphate buffered solution) group,and s-NgR1-Fc group.In PBS group,PBS was injected into the lateral ventricle of rats; and in sNgR1-Fc group,sNgR1-Fc was injected instead of PBS. The ipsilateral cortex with lesion was harvested for histomorphometry and transmission electron microscope observation 7 days after PCI. Proteins including GTP-RhoA,p-JNK,p-c-JUN and p-ATF-2 were detected by Western blot,as well as Total-J and Total-RhoA.Results The cortical infarction in rats was successfully induced by photochemistry.Compared with sham-operated group,the pathological changes in PBS groups were more serious,including extensive edema or disappearance of axoplasm of fiber without medulla sheath involved and extensive thickening or layer derangement in axoplasm of fiber with medulla sheath involved.These changes were improved significantly after sNgR1-Fc treatment.The levels of GTP-RhoA,p-JNK1,p-JNK2,p-c-JUN and p-ATF-2 in the PBS group were significantly higher than those in the sham-operation group ( P ＜ 0.05 ),whereas the levels of Total-RhoA,Total-JNKl and Total-JNK2 were not different significantly between these two groups (P ＞0.05 ).The sNgR1-Fc treatment up-regulated the levels of these proteins ( P ＜ 0.05 ).Conclusions There is pathological change in axon induced by cerebral hypoxia-ischemia for a long period after cortical infarction.The mechanisms may be associated with RhoA/ROCK/JNK/c-Jun signal way,which is activated by ischemia injury and related to the inhibition of regeneration in axon.Our study shows that NgR1-Fc may inhibit this pathway significantly,and then promote the regeneration of axon partially.

Objective To investigate the clinic effect of Linezolid for community acquired methicillin resistant staphylococcus aureus (MRS A) pneumonia. Methods The clinic data of the patient- were collected from the First Affiliated Hospital of Sun Yat-Sen University, in addition, the body temperature and white blood cell counts were obtained as the index of treatment. Results It was proved that Linezolid was effective in treating community acquired MRSA pneumonia and showed well tolerance with few adverse events. Conclusion Linezolid demonstrated good clinical and antibacterial activity but very few adverse reactions in elderly patients with community acquired MRSA pneumonia.

Objective To explore the mechanism of Zibu Piyin Recipe (ZBPYR) on spleen yin deficiency diabetes-associated cognitive disorder (DACD). Methods The rats were randomly divided into control group, diabetes mellitus (DM) group, spleen yin deficiency group, spleen yin deficiency DM group and spleen yin deficiency DM+ZBPYR group (treatment group). Type 2 DM models were established by high-fat food feeding and low dose STZ intraperitoneal injection for 4 weeks. Then the classical compound method was used to construct spleen yin deficiency rat models by improper diet, over exertion and yin fluids exhaustion. The treatment group was given ZBPYR by gavage for 15 days, and the other groups were given the same amount of normal saline. Then cerebral cortex, hippocampus, stomach and liver were obtained and the changes of protein expression of PDHE1α in them were observed by Western Blot. Results The protein expression of PDHE1αin cortex of DM group and spleen yin deficiency DM group were lower than control group (P<0.05). PDHE1α expression of treatment group in cortex and stomach increased more significantly than spleen yin deficiency DM group (P<0.05). The expression of PDHE1α protein showed no significant difference among all groups in hippocampus and liver. Conclusion ZBPYR improved spleen yin deficiency DACD by regulating PDHE1αin cortex and stomach.

Objective To investigate the variation of biomarker of coagulation, anti-coagulation, fibrinolysis in elderly critical patients and find out whether they are related to the disease severity. Methods Sixty-seven patients were no less than 60 years old. Eligible criteria: coincidence with the diagnostic criteria of systemic inflammatory response syndrome (SIRS) and APACHE Ⅱ score was no less than 10 scores. Blood sample was drawn from the venous for the test of biomarker (APTT, PT, TT, D-D, Fib, AT-Ⅲ , PC, PAI-1). According to the existent status,all the patients were divided into two groups:survival group (43 cases) and death group(24 cases) ,meanwhile,according to the diagnostic criteria of MODSE,all the patients were divided into MODSE group (30 cases) and non-MODSE group (37 cases). Results There were significant differences in APACHE Ⅱ score between MODSE group and non-MODSE group, survival group and death group [(25.83 ± 1.19) scores vs(18.1±20.73) scores and(18.81±0.72) scores vs(26.50 ± 1.42) scores](P <0.01). The PT and D-D in MODSE group anti death group were higher than those in non-MODSE group and survival group, the differences were significant (P <0.05),while the activity of AT-Ⅲand PC in MODSE group and death group were lower than those in non-MODSE group and survival group, the differences were significant (P <0.05). The PT,D-D and PAI-1 were positively correlated to APACHE Ⅱ score (related coefficients were 0.328, 0.308, 0.335,P <0.05). The AT-Ⅲ and PC were negatively correlated to APACHE Ⅱ score (related coefficients were -0.469, -0.559,P <0.01). Conclusions The abnormality of eoagnlation-fibfinolysis system exists in elderly critical patients. The extended PT, elevated D-D and PAI-1 ,descended PC and AT-Ⅲ are the hints of disease severity and poor prognosis.

OBJECTIVETo study the effect of berberine on the release of nitric oxide (NO) by rat intestinal mucous microvascular endothelial cells (RIMECs) cultured in vitro for exploring the pharmacological mechanism of berberine in treating intestinal disease.

METHODSCultured RIMECs in vitro were identified adopting immunofluorescent stain with factor VIII-related antigen. NO level in the supernatant of normal cell culture or cell culture treated with different concentrations of berberine was detected with colorimetry at the 3rd, 6th, 9th and 12th h and compared.

RESULTSCompared with that in the normal control group, NO level increased more obviously in the berberine treated groups, and the best effect was shown in the 5 microg/mL berberine treated group.

CONCLUSIONOne of the important pharmacological mechanisms of berberine might be through promoting the endogenous NO release to induce endothelium-dependent dilatation of microvascular in intestinal mucosa, thus to improve the local microcirculation of intestine.

Animals ; Berberine ; pharmacology ; Cells, Cultured ; Colorimetry ; Endothelial Cells ; cytology ; drug effects ; metabolism ; Intestinal Mucosa ; blood supply ; cytology ; Nitric Oxide ; biosynthesis ; Rats ; Time Factors