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991.
Guang-Hua Xu Young-Hee Kim Soo-Jin Choo In-Ja Ryoo Jae-Kuk Yoo Jong-Seog Ahn Ick-Dong Yoo 《Archives of pharmacal research》2010,33(3):369-373
Two acetylated megastigmane glycosides, matenosides A (1) and B (2), have been isolated from the MeOH extract of Ilex paraguariensis leaves, and their structures were elucidated on the basis of spectroscopic analysis. Compounds 1 and 2 exhibited human neutrophil elastase (HNE) inhibitory activity with IC50 values of 50.4 μM and 11.1 μM, respectively. 相似文献
992.
B Y Ryoo Y K Kang Y H Im Y J Kim B S Kim T Y Kim S H Jung J H Park H J Baek Y C Kim Y M Shim C M Kim J I Zo 《American journal of clinical oncology》1999,22(3):253-257
Gastric adenocarcinomas involving the esophagogastric junction represent a particular therapeutic problem because they lie in the border area between two body cavities: the thorax and the abdomen. The prognosis of gastric adenocarcinomas involving esophagogastric junction is poor because there is widespread lymphatic metastasis, making curative resection difficult. Even in patients with localized disease who are potentially curable, the 5-year survival rate is approximately 20% with curative resection only, somewhat lower than for those with cancer elsewhere in the stomach. The authors conducted a pilot study to evaluate the safety and possible efficacy of adjuvant chemotherapy with cisplatin, etoposide, and 5-fluorouracil (PEF) after curative resection of gastric adenocarcinoma involving esophagogastric junction. Three cycles of adjuvant PEF chemotherapy with cisplatin (20 mg/m2/day intravenously on days 1-5), etoposide (100 mg/m2/day intravenously on days 1, 3, and 5), and 5-fluorouracil (800 mg/m2/day continuous intravenous infusion on days 1-5) were given every 3 weeks after curative resection of gastric adenocarcinoma involving the esophagogastric junction. Between November 1989 and June 1995, a total of 50 patients with postoperative stage II, IIIA, or IIIB disease entered this trial. In 14 of 50 patients (28%), the disease recurred during the follow-up of 4-83 months (median 26 months). Disease-free survival was 4-83+ months (median 48 months), and the actuarial 5-year disease-free survival rate was 48% (95% CI: 41% to 55%). Overall survival was 4-83+ months (median 62 months), and the actuarial 5-year survival rate was 54% (95% CI: 40% to 68%). The prognostic factor analysis showed that the postoperative N stage and the interval between surgery and chemotherapy affected disease-free survival and overall survival. The toxicities of PEF adjuvant chemotherapy were leukopenia, nausea/vomiting, and alopecia, but they were mostly mild and reversible except in one patient who died because of treatment-related sepsis. Adjuvant chemotherapy with three cycles of PEF regimen was well tolerated and seems to be a promising treatment for gastric adenocarcinoma involving the esophagopstric junction, in comparison with previous treatments. To define the efficacy of adjuvant PEF chemotherapy for gastric adenocarcinoma involving esophagogastric junction, prospective randomized trials are warranted. 相似文献
993.
The hyperactivity of ionotropic glutamate receptors has been implicated in the development of the neuronal cell death seen in many neurodegenerative processes including ischemic stroke, traumatic brain injury, and epilepsy. Thus neuronal protection against glutamate-induced neurotoxicity is considered as an appropriate therapeutic strategy for preventing and treating neurodegenerative diseases. Whilst searching for blockers of glutamate-induced toxicity in mouse cortical cells, we isolated p-terphenyl curtisians A - D from the mushroom Paxillus curtisii. Curtisians protected cortical neurons from glutamate-induced toxicity in a dose-dependent manner. Among the glutamate receptor subtypes, curtisians were found to block NMDA receptor-mediated but not AMPA/kainate-mediated cell death. In addition, we found that curtisians exhibited potent antioxidative activity against iron-mediated oxidative damage which was generated by H2O2 neurotoxocity and lipid peroxidation, but no activity was detected in the superoxide, DPPH and ABTS radical scavenging systems, and in protection of N18-RE-105 cells subjected to glutamate-induced glutathione depletion. This effect was likely due to the iron chelating properties of curtisians. The iron chelation ability of curtisians was then further investigated on DNA single strand breakage (SSB) induced by the addition of iron and H2O2, and curtisians prevented DNA SSB like the iron chelator desferrioxamine. These results suggest that the neuroprotective action of curtisians is dependent on their ability to chelate iron as well as to block the NMDA receptor, and that in this context curtisians may be useful as neuroprotective agents against neurological disorders which result in neuronal cell death. 相似文献
994.
995.
Anthony JH Hall 《Clinical & experimental optometry》2000,83(3):190-194
Purpose : To review the common causes of secondary glaucoma. Methods : Review of current literature. Results : Secondary open and closed angle glaucomas are an important cause of ocular morbidity and vision loss in our community. Secondary glaucoma occurs with acquired ocular diseases (pigment dispersion, pseudoexfoliation, intraocular infection, intraocular inflammation and retinal vascular disease), blunt anterior segment injury, intraocular surgery (especially corneal grafting and congenital cataract surgery) and topical corticosteroid use. The medical treatment of secondary glaucoma is different from that of primary open angle glaucoma and must be tailored for the individual patient. Surgical treatment of secondary glaucoma carries a higher risk of complications and a lower rate of success than does surgical treatment of primary open angle glaucoma. Conclusions : Secondary glaucoma occurs with a variety of intraocular conditions and after a variety of intraocular insults. Awareness of patients at high risk should enable early detection and referral for appropriate management. 相似文献
996.
997.
Pletsa V; Valavanis C; van Delft JH; Steenwinkel MJ; Kyrtopoulos SA 《Carcinogenesis》1997,18(11):2191-2196
The DNA damaging and mutagenic activities of procarbazine, a methylating
drug employed in cancer chemotherapy and suspected of causing
therapy-related leukaemia, were investigated in the liver and bone marrow
of lambda lacZ transgenic mice (MutaMouse). The drug was administered using
two different protocols, a 'high-dose' one involving 5 daily doses of 200
mg/kg, expected to cause depletion of the repair enzyme O6-alkylguanine-DNA
alkyltransferase (AGT) and thus favour the selective accumulation of the
premutagenic lesion O6-methylguanine (O6- meG) relative to other adducts,
and a 'low-dose' one involving 10 daily doses of 20 mg/kg procarbazine.
Substantial accumulation of O6-meG was observed in both tissues examined 6
h after the end of the 'high-dose' treatment, with the liver accumulating
somewhat higher levels than the bone marrow (28.0 +/- 1.8 fmol/microg DNA
and 18.5 +/- 1.1 fmol/microg DNA respectively). However, significant
increases in mutant frequency 10 days after the end of treatment were
observed only in the bone marrow, reaching a 16-fold increase over
background following the 5 x 200 mg/kg treatment. Sequence analysis of the
mutations induced after this treatment revealed a mixed spectrum, in which
G:C-->A:T transitions (characteristic of O6-meG miscoding) were only a
secondary feature: Among 20 mutants analysed, only six such mutations were
found, including three at CpG sites, which might have arisen from
deamination of 5-methylcytosine. The other mutations observed included 1
A:T-->G:C transition, five transversions (one G:C-->T:A, one double
G:C-->C:G, two A:T-->T:A, one A:T-->C:G), five deletions and three
insertions. The mechanistic and clinical significance of these findings is
discussed.
相似文献
998.
Yen CC; Tung SL; Hsieh RK; Chiou TJ; Liu JH; Wang WS; Chen PM 《Japanese journal of clinical oncology》1997,27(5):316-320
For previously treated advanced breast cancer, there is no standard
second-line therapy. Combination chemotherapy with mitoxantrone, high-dose
5-fluorouracil (5-FU) and leucovorin (MFL regimen) had been reported as an
effective and well tolerated regimen. From October 1993 to November 1995,
we treated 13 patients with previously chemotherapy-treated metastatic
breast cancer by mitoxantrone, 12 mg/m2, on day 1 and continuous infusion
of 5-FU, 3000 mg/m2, together with leucovorin, 300 mg/m2, for 48 h from day
1 to 2. Each course of chemotherapy was given every 4 weeks. Most of these
patients had more than two metastatic sites, with lung metastasis
predominant. Seven patients had been treated with anthracycline. Seven
patients had previously received radiotherapy and seven had received
hormone therapy. Median number of courses of MFL regimen given was six and
the median cumulative dose of mitoxantrone was 68.35 mg/m2. One patient had
complete response, seven had stable disease, none had partial response and
five had progressive disease. The overall objective response rate was 7.6%.
The median follow-up period was 14 months. Median survival was 16 months.
Median progression-free survival was 5 months. A complete responder had
relapse-free survival up to 17 months. Major toxicities were cardiotoxicity
and leukopenia. Eight patients were dead in the last follow-up; two of them
died of treatment-related toxicity. The MFL regimen achieves little
palliative benefit and induces severe toxicity at a fairly high rate.
Administration of this regimen to breast cancer patients who have been
treated by chemotherapy and those with impaired heart function requires
careful attention.
相似文献
999.
1000.
The wide array of questions and opportunities for surgical health services research offers important prospects for inquiry
into surgical disparities. In this essay we discuss research that directly or indirectly addresses disparities in surgery,
highlighting the strengths and the future directions such research efforts intimate as potential foci of collective attention.
We then consider possible research approaches—including community-based participatory models—for confronting disparity and
the potential role of research in quality improvement to help achieve the ultimate aim, an optimal level of health care for
all. 相似文献