NF-?B, a group of important transcription factors, are introduced and discussed here on several aspects: their component and molecular structure; their activity control by I?B and IKK, the mechanism of their activation; their important roles in transcriptional regulation for large numbers of genes; and their importance in immunity, inflammation, cell survival, proliferation and apoptosis. The analysis of the relation between NF-?B and disease occurrence, the analysis of the relation between NF-?B and disease therapy, and the application prospect of the new strategy regarding the novel drug design and correlative diseases therapy on the basis of NF-?B as the target, are also included.

Bone Neoplasms ; diagnosis ; pathology ; Breast Neoplasms ; diagnosis ; pathology ; Delayed Diagnosis ; Diagnostic Errors ; Female ; Frozen Sections ; Humans ; Intraoperative Period ; Retrospective Studies ; Thyroid Neoplasms ; diagnosis ; pathology

Adolescent ; Adult ; Ammonia ; adverse effects ; Burns, Chemical ; etiology ; therapy ; Burns, Inhalation ; etiology ; therapy ; Female ; Humans ; Male ; Middle Aged ; Retrospective Studies ; Young Adult

Column chromatography on silica gel was used to study the chemical constituents of traditional Chinese medicine Siegesbeckia pubescens. The chemical structures of the separated compounds were elucidated by spectroscopic data analyses. As a result, eighteen compounds were obtained and identified as 3, 4'-dimethoxy quercetin(1), 3, 3', 4'-trimethoxy quercetin(2), 3, 3'-dimethoxy quercetin(3), 7, 3', 4'-trimethoxy luteolin(4), ursolic acid(5), 2β,19α-dihydroxyursolic acid(6), 2β-hydroxyursolic acid (7), stigmasterol-7-one(8), 5α, 8α-epidioxy-24(R)-methyl-cholesta-6, 22-diene-3β-ol(9), β-sitosterol(10), 2, 6-di(3-hydroxy-4-methoxyphenyl)-3, 7-dioxacyclo [3. 3. 0] octane (11), aurantiamide acetate (12), 3-(m-hydroxyl-p-methoxy)-N-(2'-p-hydroxyl-phenethyl)-2E-acrylamide(13), p-hydroxy benzaldehyde (14), m-hydroxy-p-methoxy benzaldehyde (15), 3, 4, 5-trimethoxybenzoic acid(16), monoethyl malonate(17), and p-hydroxylcinnamic acid(18). Among them, compounds 1-9, 11-18 were isolated from this plant for the first time.
Asteraceae ; chemistry ; Drugs, Chinese Herbal ; chemistry ; isolation & purification ; Luteolin ; chemistry ; isolation & purification ; Medicine, Chinese Traditional ; Plants, Medicinal ; Quercetin ; chemistry ; isolation & purification ; Sitosterols ; chemistry ; isolation & purification ; Triterpenes ; chemistry ; isolation & purification

Objective To investigate the inactivating effect of heat and ultraviolet(UV) light on HCV JFH-1 strain using the cell culture system. Methods The HCV JFH-1 virus stock, with an initial titer of 2.5 × 104 FFU/ml, was exposed in 56℃ water bath or to UV light for varying durations of time for explo-ring their inactivating effects on the virus. The kinetics of virus titer reduction was determined by an indirect immuno-fluorescence assay (IFA). If the cells infected with the exposed virus stock were IFA negative after three blind passages, the virus stock was considered to be inactivated completely. Results After incubation of the HCV JFH-1 virus stock (2.5 × 104 FFU/ml)in 56℃ water bath for 10 min, 20 min and 30 min, the virus titers were reduced to 1.6 × 103 FFU/ml, 3.1 × 102 FFU/ml and 3.3 × 10 FFU/ml, respectively. The exposure of the virus stock to UV light (wavelength 253.7 nm, intensity ≥60 μW/cm2, 30 cm below the UV lamp) for 15 s, 30 s and 45 s resulted in virus fiter reduction to 1.0 × 103 FFU/ml, 1.1 × 102 FFU/ml and 2.7 × 10 FFU/ml, respectively. After 40 min incubation of the virus stock at 56℃, or 1 min exposure to UV light (wavelength 253.7 nm, intensity ≥60 μW/cm2) the virus infectious titer was reduced below the detection limit of IFA, and the IFA was still negative even after three blind passages, indicating that the virus was inactivated completely. Conclusion HCV is sensitive to heat and UV light treatment. For HCV JFH-1 virus stock containing 2.5 × 104 FFU/ml virus, heat treatment at 56℃ for 40 min, or UV light expo-sure at an intensity of ≥60 μW/cm2 for 1 min, resulting in complete virus inactivation.

To investigate the effect of C/EBP βon the neuroinflammation.Recently,neuroinflamma-tion research mainly focused on C/EBP β,more and more researches indicated that C/EBP βmay play an important role in neurodegenerative diseases.We searched the published papers in PubMed,CNKI,and Wan Fang date bases in June 2015.The key words were used asCCAAT enhancer binding protein beta,Neu-ron,Neuroinflammationand so on.According to the inclusion and exclusion criteria, we summaried and analyzed the literatures.Eventually,42 articles were adapted,most of which were foused on the functions and mechanisms of C/EBP βin neuroinflammation.C/EBP βparticipate in multiple signaling pathways of neu-roinflammation,and the regulation mechanism is complicated.Abrogation of C/EBPβexpression or its down-regulation by gene regulation may may serve as a therapeutic target to attenuate deleterious effects in neural tissue and ultimately prevent the development of neurodegenerative disorders.

Objective To identify the effect of blood pool 18F-FDG activity on liver SUV and to investigate the optimal normalization method.Methods PET/CT and common serological examination items from 1 018 subjects were retrospectively collected.Mean SUV of liver and blood were recorded as SUVmean(L) and SUVmean (B),respectively.The difference and quotient of SUVmean(L) and SUV mean (B) were calculated as SUVmean (L-B) and SUVmean (L/B),respectively.CV of SUVmean (L),SUVmean (L-B) and SUVmean(L/B) were calculated to assess their inter-individual variations.Pearson correlation analysis was used to evaluate the relationship of SUVmean(L),SUVmean(L-B),SUVmean(L/B) with SUVmean(B).Multiple linear stepwise regression was performed to identify their vulnerability to common serological examination items.Results CV of SUVmean(L/B) (15.1％) was less than that of SUmean(L) (23.2％) and SUVmean(L-B) (40.6％).Correlation between SUVmean(L) and SUVmean(B) (r =0.820,P＜0.001) was more significant than that between SUVmean(L-B) and SUVmean(B) (r =0.205,P＜0.001) as well as between SUVmean (L/B) and SUVmean (B) (r=-0.376,P＜0.001).Blood glucose and BMI correlated with SUVmean(L) and SUVmean(L/B),but not with SUV (B).Age and HDL correlated with SUVmean(L) and SUVmean(B),but not with SUV (L/B).Fatty liver was significantly associated with SUV mean (L/B) (β =-0.047,P ＜0.001),but not with SUVmean(L) and SUVmean (B).Conclusions 18 F-FDG activity of blood pool affects liver SUV.SUV mean (L/B) is a simple and reliable normalization method since its inter-individual variation and vulnerability to common serological examination items are relatively lower than liver SUV.

1.0～(?)1.5 cm(14.81%)(P=0.10).There was no lymph node metastasis in tumors less than 1.0 cm in diameter. The 5-year survival rates for cases with or without lymph node involvement were 92.31% and 60.0%,respectively,the difference was significant(P=0.000).The 5-year survival rates of 12 patients showing ground-glass opacity(GGO)on chest CT was 91.67% without any lymph node involvement.Conclusions:There is mediastinal and hilar lymph node involvement even with tumor diameter less than 2 cm.The results of the present study suggested that routine lymph node dissection is necessary even for cases with tumor diameter less than 2 cm.However,if the tumor is within 1.0 cm in diameter with obvious GGO showing on chest CT,these are good candidates for partial resection without mediastinal lymph node dissection.

The phytase was extracted from solid state leavening of Trichoderma Viride LH374.The crude product was purified by(NH_4)_2SO_4 precipitation,gel filtration and ion exchange chromatography.The purified phyatse was 13.3 times of the raw products,and the extraction ration was 27.1%.The study on the enzymology of phyatse showed that the optimal temperature and pH were 55℃ and 6.0,respectively.The Km value of the phytase was 0.15mmol/L.

To investigate whether glutamate and voltage-gated calcium channels-independent calcium influx exists during acute anoxic neuronal damage and its possible relationship to neuronal protective function of NGF. In in vitro model of acute anoxia, hippocampal cultures from newborn rats were exposed to 3 mmol/L KCN. Changes of intracellular Ca(2+) concentration ([Ca(2+)](i)) were monitored by con-focal imaging and cell viability was assayed by PI and cFDA staining. The results showed that after treatment with primary hippocampal cultures with 3 mmol/L KCN for 15 min, [Ca(2+)](i) was significantly increased 6.27-fold compared to pre-anoxia level and 73.3% of the cells died. When combination of 20 mumol/L MK-801 (glutamate receptor antagonist), 40 mumol/L CNQX (AMPA receptor antagonist) and 5 mumol/L nimodipine (voltage-gated calcium channel antagonist) (hereafter denoted as MCN) were administrated to hippocampal cultures, levels of [Ca(2+)](i) and cell death rate induced by KCN were partially reduced by 35.9% and 47.5% respectively. However, Gd(3+) (10 mumol/L) almost completely blocked KCN-mediated [Ca(2+)](i) elevation by 81.9% and reduced neuronal death by 88.8% in the presence of MCN. It is noteworthy that NGF, used in combination with MCN, inhibited KCN-induced [Ca(2+)](i) increase by 77.4% and reduced cell death by 87.1%. Only PLC inhibitor U73122 (10 mumol/L) abolished NGF effects. It is concluded that Gd(3+)-sensitive calcium influx, which is NMDA (glutamate receptor) and voltage-gated calcium channels-independent, is responsible for acute anoxic neuronal death. NGF can inhibit Gd(3+)-sensitive calcium influx and reduce anoxic neuronal death through activating PLC pathway.