Adult ; Diagnosis, Differential ; Female ; Granulomatous Disease, Chronic ; metabolism ; pathology ; Hodgkin Disease ; metabolism ; pathology ; Humans ; Ki-1 Antigen ; metabolism ; Lewis X Antigen ; metabolism ; Lymphoma, Large B-Cell, Diffuse ; metabolism ; pathology ; Lymphoma, Large-Cell, Anaplastic ; metabolism ; pathology ; Young Adult

Burkitt Lymphoma ; diagnosis ; pathology ; Female ; Hodgkin Disease ; diagnosis ; pathology ; Humans ; Lymphoma ; classification ; diagnosis ; pathology ; Lymphoma, Extranodal NK-T-Cell ; diagnosis ; pathology ; Lymphoma, Follicular ; diagnosis ; pathology ; Lymphoma, Large B-Cell, Diffuse ; diagnosis ; pathology ; Male ; Precursor Cell Lymphoblastic Leukemia-Lymphoma ; diagnosis ; pathology

Adult ; Antigens, CD20 ; metabolism ; CD3 Complex ; metabolism ; Diagnosis, Differential ; Facial Dermatoses ; metabolism ; pathology ; surgery ; Follow-Up Studies ; Humans ; Lymphoma, B-Cell, Marginal Zone ; metabolism ; pathology ; Lymphoma, Large-Cell, Anaplastic ; metabolism ; pathology ; Male ; Pseudolymphoma ; metabolism ; pathology ; surgery ; Skin Neoplasms ; metabolism ; pathology

Actins ; metabolism ; Adult ; Diagnosis, Differential ; Granzymes ; metabolism ; Histiocytic Sarcoma ; metabolism ; pathology ; Humans ; Ki-1 Antigen ; metabolism ; Lymph Nodes ; metabolism ; pathology ; Lymphoma, Large-Cell, Anaplastic ; metabolism ; pathology ; Male ; Neoplasms, Muscle Tissue ; metabolism ; pathology ; Protein-Tyrosine Kinases ; metabolism ; Receptor Protein-Tyrosine Kinases

0.05).Conclusions Both CBZ and OXC are effecive in treating typical frontal lobe seizures.

BACKGROUNDDepression related cognitive deficits are frequently considered as simple epiphenomena of the disorder. However, whether or not the depression might directly bring about cognitive deficits is still under investigation. This study was to investigate the distinct pattern of cognitive deficits in patients with depression by comparing the cognitive function before and after anti-depressive drug therapy.

METHODSSixty cases of patients, first-time diagnosed with depression, were assessed by 17-item Hamilton Rating Scale for Depression (HAMD17scale). The memory ability was tested by quantitatively clinical memory scale, while the attention ability by modified Ruff 2&7 Selective Attention Test. Forty-two healthy volunteers were recruited as controls. The depressive patients were treated with Venlafaxine (75 - 300 mg/d), Fluoxetine (20 - 40 mg/d), Paroxetine (20 - 40 mg/d), and Sertraline (50 - 150 mg/d). After 12 weeks treatment, patients were tested again by HAMD17scale, quantitatively clinical memory scale, and modified Ruff 2&7 selective attention test to assess the effect of anti-depressive drugs on cognitive deficits.

RESULTSThe memory quotient (MQ) was significantly lowered in depressive patients. The selection speed was also significantly decreased and the number of missing and error hits increased in the depression group as compared to control. However, there was no significant difference in clinical memory scale and Ruff 2&7 selective attention test between mild-to-moderate and severe depression group. Importantly, after anti-depressive drug therapy, the HAMD17 scale scores in depressive patients were significantly decreased, but the MQ, directional memory (DM), free recall (FR), associative learning (AL), and face recognition were comparable with those before the treatment. Furthermore, the selection speed and the number of missing and error hits were also not significantly different after anti-depressive drugs treatment.

CONCLUSIONSDepressive patients suffer from short-term memory deficits, and attention extent, stability and rearrangement deficiency. Even though anti-depressive drugs sufficiently relieve the cardinal presentation of depression, they could not successfully alleviate the accompanying cognitive deficits. This might indicate a distinct pattern of cognitive deficits in patients with depression.

Adolescent ; Adult ; Antidepressive Agents ; therapeutic use ; Cognition Disorders ; etiology ; physiopathology ; Depression ; complications ; drug therapy ; physiopathology ; Female ; Humans ; Male ; Memory ; drug effects ; physiology ; Middle Aged ; Neuropsychological Tests ; Young Adult

Objective To study the chemical constituents from the bark of Juglans mandshurica. Methods The compounds were isolated and purified by column chromatography on silica gel,HPLC,and recrystallization.Their structures were elucidated by the physicochemical and spectroscopic evidences. Results Fifteen compounds were identified as:4,8-dihydroxynaphthalenyl-O-?D-(6′-acetoxyl)gluco- pyranoside(Ⅰ),dihydrokaempferol(Ⅱ),juglone(Ⅲ),daucosterol(Ⅳ),kaempferol(Ⅴ),4,8-dihy- droxynaphthalenyl-1-O-?-D-[6′-O-(3″,5″-dimethoxy-4″-hydroxybenzoyl)] glucopyranoside(Ⅵ), kaempferol-3-O-?-L-rhamnoside(Ⅶ),3,3′-dimethoxylellagic acid(Ⅷ),naringenin(Ⅸ),quercetin (Ⅹ),reginolone(Ⅺ),quercetin-3-O-?-L-rhamnoside(Ⅻ),naringenin-7-O-?-D-glucoside(ⅩⅢ),4,8- dihydroxynaphthalenyl-1-O-?-glucoside(ⅩⅣ),4,5,8-trihydroxy-?-tetralone-5-O-?-D-[6′-O-(4″-hy- droxy-3″,5″-dimethoxy-benzoyl)] glucoside(ⅩⅤ).Conclusion CompoundⅠ(juglamanol)is a new compound.CompoundsⅡ,Ⅶ—Ⅸ,Ⅻ,andⅩⅢare isolated from plants of Carya Nutt.for the first time.

Activation of acid-sensing ion channels (ASICs) plays an important role in neuroinflammation.Macrophage recruitment to the sites of inflammation is an essential step in host defense.ASIC 1 and ASIC3 have been reported to mediate the endocytosis and maturation of bone marrow derived macrophages.However,the expression and inflammation-related functions of ASICs in RAW 264.7 cells,another common macrophage,are still elusive.In the present study,we first demonstrated the presence of ASIC 1,ASIC2a and ASIC3 in RAW 264.7 macrophage cell line by using reverse transcriptase polymerase chain reaction (RT-PCR),Western blotting and immunofluorescence experiments.The non-specific ASICs inhibitor amiloride and specific homomeric ASIC 1 a blocker PcTx 1 reduced the production of iNOS and COX-2 by LPS-induced activating RAW 264.7 cells.Furthermore,not only amiloride but also PcTx 1 inhibited the migration and LPS-induced apoptosis of RAW 264.7 cells.Taken together,our findings suggest that ASICs promote the inflammatory response and apoptosis of RAW 264.7 cells,and ASICs may serve as a potential novel target for immunological disease therapy.

To establish neonatal rat cardiac fibroblast inflammatory secretion model by using LPS 100 microg x L(-1) combined with ATP 5 mmol x L(-1), in order to study the inhibitory effect of quercetin on the secretion of inflammatory factors TNF-alpha, IL-1beta and IL-6 of cardiac fibroblasts, further investigate the effect of quercetin on the protein expression of p-NF-kappaB p65 (S276) and p-Akt (S473) by western blot, and discuss the inhibitory effect of quercetin on the inflammatory secretion of cardiac fibroblasts. According to the findings, quercetin with the concentrations between 51.74 micromol x L(-1) and 827.81 micromol x L(-1) had no significant effect on the activity of cardiac fibroblasts. Quercetin with the concentrations of 82.78, 41.39, 20.70 micromol x L(-1) could notably inhibit the increase of TNF-alpha and IL-1beta induced by LPS 100 microg x L(-1) for 3 h and then ATP 5 mmol x L(-1) for 36 h (P < 0.01 or P < 0.05). Quercetin with the concentrations of 82.78, 41.39 micromol x L(-1) could notably inhibit the increase of IL-6 induced LPS 100 microg x L(-1) for 3 h and then ATP 5 mmol x L(-1) for 36 h (P < 0.05), without any notable effect of quercetin with the concentration of 20.70 micromol x L(-1). Quercetin with the concentrations of 82.78, 41.39, 20. 70 micromol x L(-1) could notably inhibit the NF-kappaB p65 (S276) activation induced by LPS 100 microg x L(-1) for 3 h and then ATP 5 mmol x L(-1) for 15 min, with the most significant effect in 20.70 micromol x L(-1). Quercetin with the concentrations of 82.78, 41.39, 20.70 micromol x L(-1) could notably inhibit the increase of p-Akt(473) expression induced by LPS 100 microg x L(-1) for 3 h and then ATP 5 mmol x L(-1) for 240 min (P < 0.05). Therefore, this study believes that quercetin could attenuate the secretion of inflammatory factors TNF-alpha, IL-1beta and IL-6 of cardiac fibroblasts by inhibiting the activation of NF-kappaB p65 (S276) and Akt (473).
Animals ; Cells, Cultured ; Drugs, Chinese Herbal ; administration & dosage ; Endomyocardial Fibrosis ; drug therapy ; genetics ; immunology ; Female ; Fibroblasts ; drug effects ; immunology ; Heart ; drug effects ; Humans ; Interleukin-6 ; genetics ; immunology ; Male ; Proto-Oncogene Proteins c-akt ; genetics ; immunology ; Quercetin ; administration & dosage ; Rats ; Rats, Sprague-Dawley ; Tumor Necrosis Factor-alpha ; genetics ; immunology

Objective To construct recombinant adenovirus Ad/MDC-VP1 and investigate its im-muno-boosting effect of the mice primed with the experimental DNA vaccine against Coxsackievirus infection. Methods The recombinant adenovirus Ad/MDC-VP1 was constructed and packaged. The Western blot analysis was used to verify the target protein. BALB/c mice were divided into four groups: Ad/MDC-VP1 group, pcDNA3/MDC-VP1 group, pcDNA3/MDC-VP1 prime-Ad/MDC-VP1 boost group and PBS group. The mice in each group were immunized intramuscularly. The titers of serum IgG and neutralizing antibody were tested by ELISA and trace neutralization assay, respectively. The lymphocytes proliferation activity and specific CTL cytotoxic activity were tested by CCK-8 assay. The mice in each group were challenged with le-thal dose of Coxsackievirus, and the assay of the serum virus titers and the observation of protection efficacy against Coxsackievirus infection were carried out. Results The recombinant adenovirus Ad/MDC-VP1 was successfully constructed and the target protein was expressed. It was observed that the titers of CVB3 VP1 specific antibody, lymphocyte stimulation index, CTL cytotoxicity activities and protection rate of the pcDNA3/MDC-VP1 prime-Ad/MDC-VP1 boost group were much higher than those of the rest groups( P < 0.05), and the titer of serum virus was lower after CVB3 challenged ( P < 0.05 ). Conclusion Both the cellular and humoral immune responses in mice could been significantly enhanced by the pcDNA3/MDC-VP1 prime-Ad/MDC-VP1 boost strategy.