Objective:To summarize the clinical characteristics of single-center children with low and intermediate-risk neuroblastoma (NB), report the long-term follow-up results of the growth and survival quality, and provide a basis for further clinical research.Methods:Clinical characteristics, including the sex, age, stage, risk of disease, and metastatic site of 370 newly treated children with low and intermediate-risk NB admitted to Hematology Oncology Center, Beijing Children′s Hospital from March 2007 to June 2019 were retrospectively analyzed.Kaplan-Meier method was used for survival analysis.WHO Anthro Plus was used for calculating Z score.Results:A total of 370 eligible children with low and intermediate-risk NB were included, with the mean age at onset of 16.8 months (1-191 months). Among them, 148 cases (40%) were younger than 12 months old.Mediastinal region was the most common primary site of NB (47.8%, 177 cases), followed by retroperitoneum/adrenal gland (41.4%, 153 cases). The median follow-up time of 370 patients was 31 months (0.3-157.0 months), the 5-years event free survival (EFS) and 5-year overall survival (OS) were 86.2% and 96.9%, respectively.Thirty-seven cases had growth and deve-lopment problems, of which 22 cases had stunted growth, 6 cases had low body mass, 9 cases had wasting, and 7.3%(27/370 cases) had scoliosis.5.5% of them had heart damage and 5.0%(18/357 cases) had kidney damage, involving 12 cases related to the primary tumor and 6 cases were surgically related.30.2%(95/315 cases) of them had hair changed after chemotherapy, and curly hair was the most common change.Compared with before treatment, 14.9% of the children had a personality change, with an impatient being the most common.Conclusions:The 5-year overall survival rate of the single-center large sample of low and intermediate-risk NB was high, mediastinal was the most common primary site of tumor, and the long-term quality of life is good, but there were still treatment-related side effects, and further clinical monitoring and long-term follow-up were needed.

It is critical to regulate the senescence-associated secretory phenotype (SASP) due to its effect on promoting malignant phenotypes and limiting the efficiency of cancer therapy. In this study, we demonstrated that marchantin M (Mar-M, a naturally occurring bisbibenzyl) suppressed pro-inflammatory SASP components which were elevated in chemotherapy-resistant cells. Mar-M treatment attenuated the pro-tumorigenic effects of SASP and enhanced survival in drug-resistant mouse models. No toxicity was detected on normal fibroblast cells or in animals following this treatment. Inactivation of transcription factor EB (TFEB) and nuclear factor-B (NF-B) by Mar-M significantly accounted for its suppression on the components of SASP. Furthermore, inhibition of SASP by Mar-M contributed to a synergistic effect during co-treatment with doxorubicin to lower toxicity and enhance antitumor efficacy. Thus, chemotherapy-driven pro-inflammatory activity, seen to contribute to drug-resistance, is an important target for Mar-M. By decreasing SASP, Mar-M may be a potential approach to overcome tumor malignancy.

Alzheimer's disease (AD) is a kind of neurodegenerative diseases, the most common cause of dementia. Although AD has been studied more than, 100 years and the Aβ and tau theory are most widely accepted among the theories achieved, yet it is not really clear what the mechanism related to AD works up to now. However, it is certain that AD is a kind of diseases resulting from multi-causes. Except for causes correlated with heredity, aging and life habits, environmental role is worth taking into consideration as well. Some metals, such as copper, aluminum, zinc and iron et al, can also have close relationship with AD. Now, we make an overview on the correlative researches in the field.

OBJECTIVETo study the liposoluble ingredients of Quchiling (LQ), which enter the blood and the brain,and to confirm the active ingredients of LQ in vivo.

METHODSerum pharmacochemistry and gas chromatography mass spectroscopy were used to analyze ingredients of LQ entering the blood and the brain.

RESULTThere were eleven ingredients of LQ to enter the blood and six ingredients of LQ to enter the brain.

CONCLUSIONIt is confirmed that eleven ingredients of LQ entered the blood, which are beta-asarone, schisandrol A, schisandrol B, deoxyschisandrin, schisandrin B, schisantherrin A, schisantherrin B, schisantherrin C, delta-cadinene, delta-cadinol and calamendiol in the blood, and that six ingredients are beta-asarone, schisandrol A, schisandrol B, deoxyschisandrin, schisandrin B and calamendiol in the brain.

Animals ; Anisoles ; chemistry ; metabolism ; Brain ; metabolism ; Cyclooctanes ; chemistry ; metabolism ; Dioxoles ; chemistry ; metabolism ; Drugs, Chinese Herbal ; chemistry ; metabolism ; pharmacokinetics ; Female ; Gas Chromatography-Mass Spectrometry ; Lignans ; chemistry ; metabolism ; Male ; Polycyclic Compounds ; chemistry ; metabolism ; Rats ; Rats, Sprague-Dawley

Aim The pharmacodynamics and mechanism of Kadsura heteroclita on the Alzheimers disease (AD) model mice were studied. Methods The Kunming mice were treated with D-galactose and AlCl 3(90 d)to make the AD animal model. The therapy groups were treated with HS 2 (po, 40 d) respectively since d51. The Morris water-maze test, the expressions of PS1, BACE, as well as the pathological observation of the hippocampus and cerebral cortex were carried out to evaluate the effect of HS 2 on the AD model mice. Resluts By oral administration with HS 2, the capacity of learning and memory of the AD model mice was improved. HS 2 can downregulate the expression of PS1, BACE and decrease the amount of senile plaque in their brains. Conclusion HS 2 can meliorate AD model mice's learning and memory deficiency as well as decrease the mRNA content of PS1, BACE and senile plaque in their brains.

Aim This study was designed to investigate the inhibition of matrine on U251 glioma cell line and its mechanism. Methods MTT was used to measure the levels of the proliferation of U251 cultured with matrine in different concentrations.The effects of matrine on cell cycle of U251 were observed by FCM. The expression of proto oncogenes c myc was measured by RT PCR. Results The proliferation of U251 was obviously inhibited by matrine in a dose dependent manner. The inhibitory rate was (53 7?6 0)%,when cultured with matrine at 0 10 g?L -1 . The outcome of FCM showed that the proportion of G 0/G 1 phase cells were decreased. The proportion of S phase cells were reduced obviously,when cultured with matrine at 0 10 g?L -1 in 3 days.The outcome of RT PCR showed that the expression of proto onco gene C myc was notably decreased, when the dose of matrine was increased. Conclusion Matrine can inhibit the proliferation of U251 and inhibit the expression of proto onco gene C myc.

OBJECTIVE:The effects of zinc fructose diphosphate(ZnFDP)in different concentrations on the growth of cultured newborn mouse cerebral cortex neurons were observed METHODS:The newborn mice cerebral cortex neurons were cultured and different dosages of ZnFDP were added with final concentrations of 2 5?g/ml,12 5?g/ml and 125?g/ml The convert phase microscope was used to observe the growth of dendrites and cell bodies of neurons The survival neuron count and LDH assay were carried out to investigate the effect of ZnFDP on the growth and development of neurons in different culture periods RESULTS:After 48h,the number and the length of neural dendrites in 12 5?g/ml ZnFDP group were increased but the maximum diameter of cell bodies of neurons showed no change There were no significant differences in all parameters observed between 2 5?g/ml group and control group,while 125?g/ml ZnFDP obviously inhibited the differentiation of neurons The survival neurons on 12 5?g/ml ZnFDP group outnumbered those in the control group after 3d,7d and 10d culture,and the LDH activity in 12 5?g/ml ZnFDP group was lower than that in control group after 7d and 10d culture CONCLUSION:This study suggests that a suitable dose of ZnFDP can promote the growth and development of cerebral cortex neurons

AIM: This study was designed to investigate the inhibition of tanshinone ⅡA on C6 glioma cell line and its mechanism. METHODS: MTT was used to measure the levels of the proliferation of C6 cultured with tanshinone ⅡA at different concentrations. The effects of tanshinone ⅡA on cell cycle of C6 were observed by FCM. The change of DNA was observed by Sepharose electrophoresis. The expression of proto-oncogenes c-myc was measured by RT-PCR. RESULTS: The proliferation of C6 was obviously inhibited by tanshinone ⅡA in a dose-dependent manner. The outcome of FCM showed that the apoptotic cell rate was 7.7%, when cultured with tanshinone ⅡA at 1.0 mg/L for 3 days. The apoptotic cell rate was 21.6%, when cultured with tanshinone ⅡA at 2.0 mg/L in 3 days. CONCLUSION: Tanshinone ⅡA inhibits the proliferation of C6 cells, induces apoptosis and inhibits the expression of proto-oncogene c-myc.

AIM: This study was designed to investigate the effect of ginsenoside Rg1 on the amyloid ?-protein precursor (APP) and neprilysin (NEP)expression induced by lipopolysaccharide (LPS) in C6 cell line in order to discover effectual Alzheimer's disease (AD)-treated drugs. METHODS: MTT colorimetric analysis was used to measure the survival rate of C6 cultured with ginsenoside Rg1 at different concentrations (2 5, 5, 10 and 20 ?mol?L -1) and LPS (100 mg?L -1). The expression of APP and NEP mRNA was measured by RT-PCR. RESULTS: LPS decreased the survival rate of C6, furthermore, the increase in APP expression and the decrease in NEP expression were observed. On the other hand, the above alteration induced by LPS was reversed by ginsenoside Rg1. CONCLUSION: This study demonstrates that LPS can cause cell damage, the increase in APP expression and the decrease in NEP expression. Ginsenoside Rg1 can exert a neuroprotective action, protect C6 cells against LPS-induced injury via inhibiting APP expression and increasing NEP expression.

AIM: To investigate the inhibitory effect of TanshinoneⅡA on U251 glioma cell line and its mechanism. METHODS: MTT was used to measure the levels of the proliferation in U251 cultured with TanshinoneⅡA at different concentrations. The effects of TanshinoneⅡA on cell cycle of U251 were observed by FCM. The expression of proto-oncogene c-myc was measured by RT-PCR. RESULTS: The proliferation of U251 was obviously inhibited by TanshinoneⅡA in a dose dependent manner. The inhibitory rate came to the peak at (54 2?0 9)%, when cultured with TanshinoneⅡA at 0 10 g/L. The outcome of FCM showed that the proportion of G 0/G 1 phase cells was increased and the proportion of S phase cells was reduced obviously, when cultured with TanshinoneⅡA at 0 10 g/L for 3 days. The RT-PCR experiment showed that the expression of proto-oncogene c-myc was notably decreased, when the dose of TanshinoneⅡA was increased. CONCLUSION: TanshinoneⅡA inhibited the proliferation of U251 and the expression of proto-oncogene c-myc.