Objective] To explore professor Yu Jingmao's clinical experience in coordinating and treating pediatric disease with herbal paste. [Method] By fol owing the teacher clinic, the author summarizes professor Yu Jingmao's academic experience of treatment of children with chronic il ness with herbal paste, and for proven cases. [Result] Professor Yu Jingmao uses herbal paste for modulating pediatric intractable disease with curative effect. In his opinion, herbal paste treatment of pediatric diseases must be combined with disease and syndrome differentiation, and considered in accordance with seasonal conditions and the patient's individuality. Professor Yu considers that herbal paste formulations are suitable for children, and pays attention to regulating and nourishing to strengthen the body focused on harmony, reinforcing with elimination based on balance, protecting and tonifying the spleen and stomach based on enjoying oral application. [Conclusion] According to children's physiological and pathological characteristics, professor Yu Jingmao has rich experiences in using herbal paste for personalized syndrome differentiation treatment of pediatric diseases to strengthen body resistance and eliminate evil, regulate Yin and Yang, which is worth generalizing and applying.

Humans ; Hypoxia-Ischemia, Brain ; diagnosis ; therapy ; Infant, Newborn ; Infant, Premature

Asphyxia Neonatorum ; therapy ; Humans ; Infant, Newborn ; Infant, Newborn, Diseases ; Neonatology ; methods ; Resuscitation ; methods

Asphyxia Neonatorum ; complications ; Humans ; Hypothermia, Induced ; methods ; trends ; Hypoxia-Ischemia, Brain ; diagnosis ; therapy ; Infant, Newborn ; Neurologic Examination

Drugs, Chinese Herbal ; therapeutic use ; Humans ; Medicine, Chinese Traditional ; methods ; Neoplasms ; diagnosis ; drug therapy ; prevention & control ; Phytotherapy ; Treatment Outcome

The possible mechanism of tumor promotion inhibiting activity of garlicextract was studied. The garlic extract could inhibit the cell proliferation of human amnionFL cell in vitro, exerting no influence on the S phase DNA synthesis while exhibitingobvious inhibitory effect on the mitosis of the cells. At suitable concentration, garlic ex-tract could also inhibit the changes of protein kinase C activity induced by tumor promoterTPA, while at higher concentration garlic extract itself could induce changes of proteinkinase C activity mimic to TPA stimulation.

A large number of animal experiments have confirmed that ischemic preconditioning can produce a powerful organ protective effect,but the progress and results of the conversion of animal experiments to clinical trials are unsatisfactory.It has great significance for studying of molecular mechanisms of ischemic preconditioning mediated neuroprotection,searching for safe and effective preconditioning induced ways which can be converted to clinical practice,improving the tolerance of nerve tissue ischemia and hypoxia in stroke and surgical patients and achieving a safe and effective neuroprotection.This article reviews the molecular mechanisms of ischemic preconditioning mediated neuroprotection from the aspects of pretreatment of activated receptor,mitochondria,transcription factor,and protein kinase.

Objective: To investigate the effect of sinomenine on expression of toll like receptor(TLR) 2 and TLR4 of dendritic cells in patients with rheumatoid arthritis in vitro.Methods: The peripheral blood mononuclear cells were isolated from 10 rheumatoid arthritis patients and differentiated into dendritic cells by stimulating with cytokines.Dendritic cells were exposed to high(5mM),middle(2mM),low(1mM) concentration sinomenine and control medium.TLR2 and TLR4 mRNA were detected by real time PCR.Western blot was used to measure the expression of TLR2 and TLR4.Results: In contrast to control,signifi cant lower expression of TLR2,TLR4 mRNA and protein were found in dendritic cells treated with sinomenine,especially in high and middle concentration.Conclusion: The therapeutical effect of sinomenine on rheumatoid arthritis is probably by inhibiting dendritic cells expressing TLR,which can transduce the in? ammatory signal.

Objective: Benzoquinone ansamycin antibiotic, geldanamycin (GA), is a new anticancer agent that could inhibit Hsp90 by occupying its NH2-terminal ATP-binding site. This study was to investigate the antitumor efficacy of GA on Her2/neu tyrosine kinase overexpressing human breast cancer cell line SKBr3. Methods: The degradation of Her2/neu tyrosine kinase was analyzed by Western blotting, the proliferation index was determined by MTT assay, cell cycle distribution was detected by flow cytometry, Cyclin D1 mRNA transcription was measured by RT-PCR and real-time PCR, and cell motility was evaluated by the cell culture insert model. Results: GA induced a dose- and a time-dependent degradation of the Her2/ neu tyrosine kinase protein and concurrently, the inhibition of cancer cell proliferation. The antitumor effects mediated by GA included: GA treatment decreased the survival rates of cancer cells, and led to a dose-dependent G1 arrest. Furthermore, this antitumor effect was proved to be related to declined transcription of Cyclin D1. Concurrently, the motility of cancer cells was reduced by GA. Conclusion: GA treatment could induce the degradation of Her2/neu tyrosine kinase efficiently, inhibit cancer cell proliferation and reduce motility in Her2/neu tyrosine kinase overexpressed human breast cancer cell line SKBr3.

Objective: Benzoquinone ansamycin antibiotic, geldanamycin (GA), is a new anticancer agent that could inhibit Hsp90 by occupying its NH2-terminal ATP-binding site. This study was to investigate the antitumor efficacy of GA on Her2/neu tyrosine kinase overexpressing human breast cancer cell line SKBr3. Methods: The degradation of Her2/neu tyrosine kinase was analyzed by Western blotting, the proliferation index was determined by MTT assay, cell cycle distribution was detected by flow cytometry, Cyclin D1 mRNA transcription was measured by RT-PCR and real-time PCR, and cell motility was evaluated by the cell culture insert model. Results: GA induced a dose- and a time-dependent degradation of the Her2/ neu tyrosine kinase protein and concurrently, the inhibition of cancer cell proliferation. The antitumor effects mediated by GA included: GA treatment decreased the survival rates of cancer cells, and led to a dose-dependent G1 arrest. Furthermore, this antitumor effect was proved to be related to declined transcription of Cyclin D1. Concurrently, the motility of cancer cells was reduced by GA. Conclusion: GA treatment could induce the degradation of Her2/neu tyrosine kinase efficiently, inhibit cancer cell proliferation and reduce motility in Her2/neu tyrosine kinase overexpressed human breast cancer cell line SKBr3.