A brief history of studies on anti-tumor remedies in China

This paper gives a general introduction to the studies on the formulation and invention of anti-tumor remedies from 1950s-1980s. Beginning from 50s, antitumor antibiotics were investigated. New alkylicompoun and antibiotics were found in the 60s, while more new natural compounds were found in the 70s. Researches were proceeded in the 80s based on the former achievements. Through the process of about 30 years, nearly 80 new species were produced, many anti-tumor pharmaceutical corporations established, and a contigent of high level research workers was formed. However, there still exist a rather large gap between the urgent clinical needs for clinical chemotherapeutics and the actual status. Based on some 30 years of experience in China, the following points were summarized, i.e., shifting from merely imitation to invention, developing the spirit of massive cooperation, investigating the thesaurus of TCM, developing China's plant resources, and traditional Chinese preventive idea, so that the stress point for research be laid on the invention of preventive anti-tumor remedies.     

兴山五味子的质量研究

兴山五味子;;襄五脂素;;主要药理作用     

Effect of melatonin on the regulation of proenkephalin and prodynorphin mRNA levels induced by kainic acid in the rat hippocampus

The in vivo short-term effect of melatonin on kainic acid (KA)-induced proenkephalin (proENK) or prodynorphin (proDYN) mRNA, and on AP-1 protein levels in the rat hippocampus, were studied. Melatonin (5 mg/kg) or saline was administered intraperitoneally (i.p.) to rats 30 min prior to and immediately after i.p. injection of KA (10 mg/kg). Rats were sacrificed 1 and 3 h after KA injection. The proENK and proDYN mRNA levels were significantly increased 3 h after KA administration. The elevations of both proENK and proDYN mRNA levels induced by KA were significantly inhibited by the preadministration with melatonin. The increases of proENK and proDYN mRNA levels induced by KA were well-correlated with the increases of c-Fos, Fra-2, FosB, c-Jun, and JunB protein levels, which were significantly increased 3 h after KA administration and effectively inhibited by administration with melatonin. In an electrophoretic mobility shift assay, both AP-1 and ENKCRE-2 DNA binding activities were increased by KA, which were also attenuated by the administration of melatonin. In addition, cross-competition studies revealed that AP-1 or ENKCRE-2 DNA binding activity was effectively reduced by the 50x unlabeled cross-competitor. Therefore, these data suggest that melatonin has an inhibitory role in KA-induced gene expression, such as proENK and proDYN mRNA expression, and this may be due to a reduction of KA-induced AP-1 or ENKCRE-2 DNA binding activity.     

Peak height velocity as a maturity indicator for males with idiopathic scoliosis

We retrospectively studied 43 adolescent boys treated with orthoses for idiopathic scoliosis to assess the usefulness of the timing of peak height velocity for predicting growth remaining and the likelihood of curve progression when compared with Risser sign, closure of the triradiate cartilage, and chronologic age. We compared the peak height velocity data in boys to our previous work for girls with adolescent idiopathic scoliosis. We found the median height velocity plots showed a similar high peak and sharp decline as is found in girls. All 13 patients with a curve magnitude > 30 degrees at the time of peak height velocity had progression of their scoliosis to > 45 degrees despite bracing. Four of 29 patients (14%) with curves < or = 30 degrees at peak height velocity progressed to 45 degrees. These values generate a sensitivity of 76%, specificity of 100% and accuracy of 91% in predicting progression to 45 degrees. Similar values have been found in female patients. The use of peak height velocity to predict the length of time for remaining growth was superior to Risser sign and chronologic age for boys with idiopathic scoliosis. Closure of the triradiate cartilage approximated the timing of peak height velocity in boys.     

Determination of hip position in the Pavlik harness

Fourteen children treated for developmental dysplasia of the hip with a Pavlik harness were evaluated at the time of harness application with clinical examination, hip ultrasonography, and anteroposterior radiography. Ten orthopedic surgeons with experience levels varying from residents to experienced pediatric orthopedic surgeons evaluated the studies to determine hip position in the harness. Clinical examination agreed with hip ultrasonography for hip position in 100% of hips. Interpretation of radiographs agreed with ultrasonography in only 49% of cases in which the hip was judged to be dislocated and in 82% of cases in which the hip was judged to be reduced. When imaging is used to aid in assessing hip position during treatment with a Pavlik harness, ultrasonography appears to be superior to anteroposterior radiography for assessing hip position.     

中医对延缓衰老的认识

衰老是生命运动的必然规律，但怎样使衰老推迟，让生命延长却可人持之。现社会是一个安定、物质可满足的社会，追求长寿延缓衰老是每个人都在追求的目标，生活中都把它摆在第一位。中医工作者长寿者多，已成不争的事实，何也?因摄生在中医文献中占很大比例，生气通天、法于自然、恬儋虚无、精神内守是中医延缓衰老的准则。人体是通过气血运行来维持生命活动的，精神是气血的外在表现，是养生要解决的一个问题。     

A phase II trial of capecitabine in previously untreated patients with advanced and/or metastatic gastric cancer.

BACKGROUND: Capecitabine (Xeloda) is a novel, oral, selectively tumor-activated fluoropyrimidine with proven activity in the treatment of advanced colorectal cancer. This trial was conducted to evaluate the efficacy, safety and feasibility of capecitabine in previously untreated patients with advanced and/or metastatic gastric cancer, with a view to replacing 5-fluorouracil (5-FU) in such patients. PATIENTS AND METHODS: Forty-four patients received capecitabine 1250 mg/m2 twice daily (2500 mg/m2/day) for 14 days followed by 7 days of rest, for up to six cycles. RESULTS: Capecitabine produced an objective response rate of 34% (all partial responses) and stable disease in 14 patients (30%). The median time to disease progression (TTP) was 3.2 months [95% confidence interval (CI) 2.7-6.4 months] and median overall survival was 9.5 months (95% CI 6.9-13.2 months). Hand-foot syndrome (HFS), nausea, anorexia, diarrhea and vomiting were the most common adverse events. While HFS was the most frequent grade 3/4 toxicity (National Cancer Institute Common Toxicity Criteria), only 9% of patients experienced grade 3 HFS. Severe myelosuppression was not reported during the study. CONCLUSIONS: Capecitabine monotherapy is active and well tolerated as first-line therapy in patients with advanced/metastatic gastric cancer. Larger comparative trials investigating capecitabine-based combination regimens in patients with advanced gastric cancer are warranted.     

Arsenic trioxide induces selective tumour vascular damage via oxidative stress and increases thermosensitivity of tumours.

It has previously been found that the anti-leukaemia agent Arsenic Trioxide (ATO) causes vascular shutdown in solid tumours and markedly sensitizes tumours to hyperthermia. The present study was designed to evaluate the mechanism of action and dose-dependence of ATO-induced thermosensitization in FSaII and SCK murine tumours. The role of oxidative stress was studied by observing ATO-induced vascular shutdown in vivo and ATO-induced endothelial cell adhesion molecule expression in vitro in the presence or absence of an anti-oxidant. It was found that a dose as low as 2 mg/kg ATO impaired vascular function, as estimated by 86Rb uptake, in the tumour. The degree of tumour growth delay induced by 1 h of hyperthermia at 42.5 degrees C, applied 2 h after ATO injection, was proportional to the dose of ATO administered. In addition, it was found that ATO can directly thermosensitize tumour cells in vitro. The development of massive tissue necrosis in the tumour was observed in the days after treatment, especially with the combination of ATO and heating. ATO-induced adhesion molecule expression in vitro was abolished when the anti-oxidant n-acetyl-cysteine (NAC) was introduced prior to exposure, while the addition of NAC in vivo partially blocked ATO-induced vascular shutdown. These results suggest that the expression of adhesion molecules by the vasculature due to oxidative stress contribute to the ATO-induced selective tumour vascular effects observed and that the clinical use of ATO to increase tumour thermosensitivity via direct cellular and vascular effects appears feasible.