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141.
MAAGs were introduced as a result of the 1989 White Paper 'Working for Patients', with the remit to direct, coordinate and monitor medical audit activities in general practice. They were funded through the new FHSA management budget and each MAAG was responsible to its own FHSA. They were accepted as a completely new institution as a part of the introduction of an innovative management structure in a reformed NHS. When viewed in an historical context, MAAGs can actually be seen as a part of an expanding culture of greater objectivity and critical analysis which has burgeoned in medical practice over the last two decades. Although MAAGs began with an educational role with uniprofessional medical audit, they have embraced multiprofessional clinical audit in primary care in the context of the wider aspects of quality in practice. The last 20 years have seen the development of clinical guidelines, evidence-based medicine and application of business management theory to clinical quality. All these have reflected the increasing demand for explicit standards of care which has also formed the basis of clinical audit and MAAG activity. MAAGs should be seen as an inevitable concomitant of this historical trend to improve the application of scientific rigour in medical practice. With the adoption of clinical effectiveness, incorporating all these themes, as one of the NHS Executive's six medium-term priority areas, MAAGs are uniquely placed to act as agents of change to enhance the quality of primary health care. 相似文献
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EJ Goldstein DM Citron M Hudspeth S Hunt Gerardo CV Merriam 《Canadian Metallurgical Quarterly》1997,41(7):1552-1557
The in vitro activity of Bay 12-8039, a new oral 8-methoxyquinolone, was compared to the activities of 11 other oral antimicrobial agents (ciprofloxacin, levofloxacin, ofloxacin, sparfloxacin, azithromycin, clarithromycin, amoxicillin clavulanate, penicillin, cefuroxime, cefpodoxime, and doxycycline) against 250 aerobic and 140 anaerobic bacteria recently isolated from animal and human bite wound infections. Bay 12-8039 was active against all aerobic isolates, both gram-positive and gram-negative isolates, at < or = 1.0 microg/ml (MICs at which 90% of isolates are inhibited [MIC90s < or = 0.25 microg/ml) and was active against most anaerobes at < or = 0.5 microg/ml; the exceptions were Fusobacterium nucleatum and other Fusobacterium species (MIC90s, > or = 4.0 microg/ml) and one strain of Prevotella loeschii (MICs, 2.0 microg/ml). In comparison, the other quinolones tested had similar in vitro activities against the aerobic strains but were less active against the anaerobes, including peptostreptococci, Porphyromonas species, and Prevotella species. The fusobacteria were relatively resistant to all the antimicrobial agents tested except penicillin G (one penicillinase-producing strain of F. nucleatum was found) and amoxicillin clavulanate. 相似文献
144.
Phenotypic heterogeneity of mutational changes at a conserved nucleotide in 16 S ribosomal RNA 总被引:1,自引:0,他引:1
RNA sites that contain unpaired or mismatched nucleotides can be interaction sites for other macromolecules. C1054, a virtually universally conserved nucleotide in the 16 S (small subunit) ribosomal RNA of Escherichia coli, is part of a highly conserved bulge in helix 34, which has been located at the decoding site of the ribosome. This helix has been implicated in several translational events, including peptide chain termination and decoding accuracy. Here, we observed interesting differences in phenotype associated with the three base substitutions at, and the deletion of, nucleotide C1054. The phenotypes examined include suppression of nonsense codons on different media and at different temperatures, lethality conditioned by temperature and level of expression of the mutant rRNA, ribosome profiles upon centrifugation through sucrose density gradients, association of mutant 30 S subunits with 50 S subunits, and effects on the action of tRNA suppressor mutants. Some of our findings contradict previously reported properties of individual mutants. Particularly notable is our finding that the first reported 16 S rRNA suppressor of UGA mutations was not a C1054 deletion but rather the base substitution C1054A. After constructing deltaC1054 by site-directed mutagenesis, we observed, among other differences, that it does not suppress any of the trpA mutations previously reported to be suppressed by the original UGA suppressor. In general, our results are consistent with the suggestion that the termination codon readthrough effects of mutations at nucleotide 1054 are the result of defects in peptide chain termination rather than of decreases in general translational accuracy. The phenotypic heterogeneity associated with different mutations at this one nucleotide position may be related to the mechanisms of involvement of this nucleotide, the two-nucleotide bulge, and/or helix 34 in particular translational events. In particular, previous indications from other laboratories of conformational changes associated with this region are consistent with differential effects of 1054 mutations on RNA-RNA or RNA-protein interactions. Finally, the association of a variety of phenotypes with different changes at the same nucleotide may eventually shed light on speculations about the coevolution of parts of ribosomal RNA with other translational macromolecules. 相似文献
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146.
Conditions affecting either or both extremities offer unique opportunities and challenges for investigators and clinicians. When the condition is purely unilateral, observations on the unaffected extremity may be used as a within-patient control, and thereby strengthen the ability to identify changes in the affected limb. However, such use presumes that the condition will not subsequently develop in the unaffected extremity. Bilateral presentations or subsequent development of disease in the unaffected extremity is common in conditions such as the carpal tunnel syndrome (CTS). Treatment of one extremity may lead to development or aggravation of CTS in the other extremity. Since both extremities may be necessary to perform certain activities, it can be difficult to clearly identify treatment effects when looking at functional outcomes. In an effort to avoid these complexities, investigators have used one of two approaches in studying CTS: either selecting only those patients with unilateral disease, or analyzing results by extremity, often avoiding any outcome measures that might depend upon both extremities (such as driving). We illustrate some of the shortcomings of this approach, such as loss of patients and data, with preliminary information from our ongoing prospective study of carpal tunnel surgery outcomes. We develop a dynamic model that incorporates etiologic factors and treatment effects to describe changes in CTS over time. This model accounts for extremity-specific and systemic factors, as well as possible interaction of the disease process in both hands. The advantages of this model include a more rational approach to research and care of extremity disorders, and research strategies which address a wider scope of patients and outcomes; however, its application is limited by the need for more extensive data collection. 相似文献
147.
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149.
PJ Cagnoni Y Nieto EJ Shpall SI Bearman AE Barón M Ross S Matthes SE Dunbar RB Jones 《Canadian Metallurgical Quarterly》1998,16(5):1661-1668
PURPOSE: To evaluate the feasibility of high-dose chemotherapy (HDC) with autologous hematopoietic progenitor-cell support (AHPCS) as part of combined modality therapy (CMT) in patients with inflammatory breast cancer (IBC). PATIENTS AND METHODS: From April 1993 to March 1997, 30 patients with IBC were treated at our program. Twenty-three patients received neoadjuvant chemotherapy (NAC) before HDC; 18 patients also received adjuvant chemotherapy following surgery, but before HDC. All patients received HDC with high-dose cyclophosphamide, cisplatin, and carmustine (BCNU) with AHPCS. Every patient underwent surgery either before (27 patients) or after (three patients) HDC. Patients received radiotherapy after HDC in addition to tamoxifen if their tumors were estrogen receptor-positive. RESULTS: Thirteen patients experienced grade 3 or 4 nonhematologic noninfectious toxicities. In 12 patients (40%), this represented drug-induced lung injury, which in all cases responded to a 10-week course of corticosteroids. The only treatment-related death was secondary to hemolytic-uremic syndrome (HUS). Another patient suffered grade 4 CNS toxicity, which was completely reversible. All patients engrafted promptly. Eight patients relapsed, five of whom had a poor pathologic response to NAC. Relapses were local (five patients), local plus systemic (one), or systemic only (two). Median follow-up time from diagnosis and HDC is 23.5 (range, 7 to 49) and 19 (range, 4 to 44) months, respectively. Twenty-one patients (70%; 95% confidence interval [CI], 51% to 86%) remain alive and free of disease 4 to 44 months after HDC. Median disease-free survival (DFS) and overall survival have not yet been reached. CONCLUSION: HDC as part of CMT is feasible in patients with IBC. The toxicity of this treatment program is significant, but tolerable. Despite the short follow-up duration, the promising DFS observed in this group of patients warrants randomized studies that include a HDC-containing arm in patients with IBC. 相似文献
150.
R Wiger JA Holme JK Hongslo G Brunborg K Haug V Rodilla E Dybing EJ S?derlund 《Canadian Metallurgical Quarterly》1998,14(4):267-282
We investigated 1,2-dibromo-3-chloropropane (DBCP)-induced DNA damage, cell cycle alterations and cell death in two cell lines, the human leukemia HL-60 and the pig kidney LLCPK1, both of which are derived from potential target sites for DBCP-induced toxicity. DBCP (30-300 micromol/L) caused a concentration-dependent increase in the levels of DNA single-strand breaks in both cell lines as well as in cultured human renal proximal tubular cells. After extended DBCP exposure in LLCPK1 cells (100 micromol/L, 30 h), the level of DNA breaks returned almost to control values. Incubation for 48 h showed a clear reduction of growth with DBCP concentrations as low as 10 micromol/L. Flow cytometric analysis showed that DBCP (1-10 micromol/L) exposure for 24 h caused an accumulation of LLCPK1 cells in the G2/M-phase. In HL-60 cells the accumulation in G2/M-phase was less marked, and at higher concentrations the cells accumulated in S-phase. Flow cytometric studies of HL-60 and LLCPK1 cells exposed to 100-500 micromol/L DBCP showed increased number of apoptotic cells/bodies with a lower DNA content than that of the G1 cells. Microscopic studies revealed that there were increased numbers of cells with nuclear condensation and fragmentation, indicating that apoptosis was the dominant mode of death in these cell lines, following exposure to DBCP. The characteristic ladder pattern of apoptotic cells was observed when DNA from DBCP-treated HL-60 cells and LLCPK1 cells was electrophoresed in agarose. The finding that DBCP can cause an accumulation of cells in G2/M-phase and induce apoptosis in vitro may be of importance for the development of DBCP-induced toxicity in vivo. 相似文献