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71.
72.
The induction of apoptosis by anticancer drugs and its relationship to stages of the cell cycle was studied in cells derived from a solid tumour; a highly malignant hamster fibrosarcoma (Met B). Asynchronously proliferating cells were treated with a wide variety of agents such as actinomycin-D, 1--D-arabinofuranosyl cytosine, camptothecin, cisplatin, cyclophosphamide, daunorubicin, 5-flurouracil, 6-mercaptopurine, hydroxyurea, ionomycin, methotrexate and vincristine. With the exception of cyclophosphamide and hydroxyurea, a 36 h exposure to these drugs resulted in inhibition of cell growth and apart from cyclophosphamide, hydroxyurea, 6-mercaptopurine and cisplatin the induction of apoptosis. Studies using a decreased concentration of drug and exp osure time (12 h) followed by examination of cells using flow cytometry indicated that most drugs were capable of affecting cell cycle progression without induction of apoptosis. However when cells were synchronised at G0/G1, S and G2/M phases and then exposed to these decreased concentrations of drug apart from 6MP an HU, apoptosis was observed and for the majority of drugs it took place in the same phase in which progression through the cell cycle was blocked by the drug. Cells synchronised in G0/G1 phase were more susceptible to methotrexate, whereas S-phase cells were more susceptible to camptothecin and 5-flurouracil and G2/M phase cells more susceptible to actinomycin D, 1--D-arabinofuranosyl cytosine, daunorubicin and cisplatin. In contrast, vincristine blocked cells in G2/M phase but exerted its apoptotic effect in S-phase cells, ionomycin had no effect on the cell cycle, but G2/M cells appeared to be more susceptible to the effect of this drug. These data indicate that entry into apoptosis by this fibrosarcoma may occur at any point in the cell cycle. They also demonstrate a correlation between the action of some anticancer drugs on the cell cycle and the subsequent induction of apoptosis which may be useful in chemotherapeutic design. 相似文献
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Summary The pivotal event in Wallerian degeneration is the breakdown of the axon. Establishing the pathophysiology of axonal degeneration has implications for the understanding of the pathogenesis of other types of nerve degenerations. A key aspect of the pathophysiology is the spatiotemporal pattern of spread after transection, an issue that has remained controversial. We have studied the progression of axonal degeneration in the dorsal columns of the rat following L4L5L6 dorsal radiculotomy. Axonal degeneration proceeds in a proximo-distal fashion, beginning near the site of transection and spreading up the dorsal columns at a net rate of about 3 mmh–1. In addition, there was early degeneration of the preterminal axons in the gracile nuclei. This pattern suggests that the clearing of axonally transported materials from the distal stump by continued anterograde transport may underlie axonal breakdown after transection. 相似文献
75.
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Food-related illness and death in the United States. 总被引:62,自引:0,他引:62
P S Mead L Slutsker V Dietz L F McCaig J S Bresee C Shapiro P M Griffin R V Tauxe 《Emerging infectious diseases》1999,5(5):607-625
To better quantify the impact of foodborne diseases on health in the United States, we compiled and analyzed information from multiple surveillance systems and other sources. We estimate that foodborne diseases cause approximately 76 million illnesses, 325,000 hospitalizations, and 5,000 deaths in the United States each year. Known pathogens account for an estimated 14 million illnesses, 60, 000 hospitalizations, and 1,800 deaths. Three pathogens, Salmonella, Listeria, and Toxoplasma, are responsible for 1,500 deaths each year, more than 75% of those caused by known pathogens, while unknown agents account for the remaining 62 million illnesses, 265,000 hospitalizations, and 3,200 deaths. Overall, foodborne diseases appear to cause more illnesses but fewer deaths than previously estimated. 相似文献
77.
78.
C Davies G Grimshaw M Kendall A Szczepura C Griffin V Toescu 《International journal of health care quality assurance incorporating Leadership in health services》1999,12(2-3):87-91
OBJECTIVE AND STUDY DESIGN: To assess quality of a quick and early diagnosis route (QED) by determining effectiveness and cost-effectiveness of five clinics compared with three conventional outpatient clinics. Prospective economic evaluation. Six-month cohort of all referrals (November 1996-April 1997). SUBJECTS: All referrals for suspected cancers of: upper gastro-intestinal tract; urinary tract, prostate and testis; skin. EFFECTIVENESS: Median days saved between GP referral and date of: diagnostic appointment; consultant decision; intervention. RESULTS: GP referral to diagnostic appointment: QED was effective (median days) for all clinics. Diagnostic appointment to consultant decision: QED was effective for testicular and haematuria clinics. Consultant decision to intervention: QED was effective for haematuria, testicular and melanoma clinics. COST-EFFECTIVENESS: Extra (incremental) NHS cost per patient diagnosed. RESULTS: Less than 5 Pounds per day saved between GP referral and diagnostic appointment for: endoscopy; haematuria; prostate; testicular; melanoma. Less than 3 Pounds per day saved between GP referral and consultant decision for: testicular; haematuria. Less than 3 Pounds per day saved between GP referral and intervention for: endoscopy; haematuria; testicular; melanoma. CONCLUSION: A "quick and early" diagnostic route provides a higher quality service through improved effectiveness and cost-effectiveness compared to conventional outpatients. 相似文献
79.
Cerebral spinal fluid involvement by Hodgkin's disease diagnosed by CSF cytology and immunocytochemistry 总被引:3,自引:0,他引:3
Perez-Jaffe LA Salhany KE Green RJ Griffin T Stadtmauer EA Gupta PK 《Diagnostic cytopathology》1999,20(4):219-223
A 39-yr-old man with stage IV Hodgkin's disease (HD) involving bone marrow was being evaluated for autologous bone marrow transplantation when he developed diplopia, prompting a lumbar puncture tap for cerebral spinal fluid (CSF) examination. Cytologic examination of the CSF revealed numerous Reed-Sternberg (RS) cells in a polymorphous inflammatory background of small lymphocytes, monocytes, rare plasma cells, and eosinophils. However, magnetic resonance imaging (MRI) studies of the brain and spinal cord failed to reveal evidence of leptomeningeal disease or intracranial masses. Repeat CSF examination again demonstrated cytologic evidence of HD. Immunocytochemical stains established that the RS cells and mononuclear Hodgkin's cells were positive for CD30 and CD20 but negative for CD15; this phenotype was identical to that of RS cells in the initial diagnostic bone marrow biopsy, confirming CSF involvement by HD. The patient was treated with intrathecal methotrexate, 15 mg, 6 days after his bone marrow transplant. After treatment, all subsequent CSF cytology specimens were negative for tumor. In this case of disseminated HD, cytologic examination allowed for early detection of CNS involvement by lymphoma prior to development of radiographically detectable lesions. 相似文献
80.
Karson CN Mrak RE Schluterman KO Sturner WQ Sheng JG Griffin WS 《Molecular psychiatry》1999,4(1):39-45
An impairment of prefrontal cortical functioning in schizophrenia ('hypofrontality') has been suggested by clinical, neuroimaging, and postmortem brain tissue studies. We used Western immunoblot and Northern hybridization analyses of postmortem brain tissue obtained from 14 schizophrenic patients and 12 control patients of similar ages to measure tissue levels of synaptophysin (a structural synaptic vesicle protein) and of SNAP-25 (a 25-kDa presynaptic protein), and their encoding mRNAs, in Brodmann's area 10 of prefrontal cortex. There were significant decreases in tissue levels of both of these proteins in prefrontal cortex of schizophrenic patients relative to controls. In contrast, tissue levels for the mRNAs encoding these proteins were not decreased in schizophrenic patients. Subsequent labeling of the same Western immunoblots showed no difference in tissue levels of glial fibrillary acidic protein (GFAP) in schizophrenic and control patients. Similarly, subsequent hybridization of the same Northern hybridization membranes showed no difference in tissue levels of GFAP mRNA or of 28S rRNA in schizophrenic and control patients. These alterations in tissue levels of synaptophysin and SNAP-25 are consistent with the idea that the clinically observed 'hypofrontality' of schizophrenia arises from abnormalities of synaptic number or structural integrity in prefrontal cortex. 相似文献