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101.
Antonio Claudio L. Nóbrega M.D. Sc.D. Amália Faria dos Reis M.D. M.Sc. Ruy S. Moraes M.D. Sc.D. Bianca Gouvêa Bastos M.D. Elton L. Ferlin B.Sc.EE Jorge P. Ribeiro M.D. Sc.D. 《Clinical autonomic research》2001,11(1):11-17
The purpose of this study was to determine the effect of the oral administration of pyridostigmine bromide on indices of heart rate variability (HRV) in healthy young volunteers. Seventeen healthy participants (11 men, 6 women; aged 27 +/- 8 y) submitted to a randomized, crossover, double-blind protocol, in which they received 30 mg pyridostigmine bromide (PYR) or placebo orally at 8-hour intervals for 24 hours, on two separate days. Venous blood samples were collected 2 and 24 hours after the first dose for determination of serum cholinesterase activity. Holter tapes were recorded during the 24-hour period and analyzed using a semiautomatic technique to evaluate time- and frequency-domain indices of HRV and to build three-dimensional return maps for later quantification. Symptoms were mild and occurred similarly during administration of PYR and placebo (p = 0.140). Serum cholinesterase activity was reduced by 15% at 2 hours (p = 0.013) and by 14% at 24 hours (p = 0.010) after the first dose of PYR, but not after administration of placebo. Pyridostigmine administration caused a significant increase in the mean 24-hour R-R interval (placebo: 814 +/- 20 msec; PYR: 844 +/- 18 msec; p = 0.003) and in time-domain indices of HRV, such as the standard deviation of all R-R intervals (SDNN; placebo: 151 +/- 9 msec; PYR: 164 +/- 9 msec; p = 0.017), and the percentage of pairs of adjacent R-R intervals differing by more than 50 msec (pNN50; placebo: 12.8 +/- 1.8%; PYR: 13.9 +/- 1.5%; p = 0.029). Pyridostigmine had no significant effect on frequency-domain indices of HRV, but resulted in significant increase in P2, a parasympathetic index derived from the three-dimensional return map (placebo: 93 +/- 13 msec; PYR: 98 +/- 13 ms; p = 0.029). In conclusion, low-dose pyridostigmine reduced mean heart rate and increased HRV during a 24-hour period in healthy young subjects. 相似文献
102.
Tait D; Riccio M; Sittler A; Scherzinger E; Santi S; Ognibene A; Maraldi NM; Lehrach H; Wanker EE 《Human molecular genetics》1998,7(6):991-997
It has been reported that the ataxin-3 protein containing a polyglutamine
sequence in the pathological range (61-84Q) is localized within the nucleus
of neuronal cells, whereas ataxin-3 with a normal repeat length (12-37Q) is
predominantly a cytoplasmic protein. In this study, the subcellular
localization of the full-length ataxin-3 protein with a glutamine sequence
in the normal range (Q3KQ22) was analysed in two mammalian cell lines.
Using two affinity-purified polyclonal antibodies raised against the N- or
C-terminal portion of ataxin-3, the protein was detected predominantly, but
not exclusively, in the nucleus of COS-7 as well as neuroblastoma cells by
immunofluorescence and confocal laser scanning microscopy (CLSM). The
distribution of the protein in these cellular compartments was confirmed by
biochemical subcellular fractionations. Furthermore, CLSM revealed that the
ataxin- 3 protein present in the nucleus of neuroblastoma cells is
associated with the inner nuclear matrix. Our results taken together with
the finding of a nuclear localization signal in ataxin-3 indicate that the
ataxin-3 protein per se translocates to the nucleus and that an expanded
glutamine repeat is not essential for this transport.
相似文献
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BACKGROUND: Anticholinergics and beta2-agonists have generally been considered equivalent choices for bronchodilation in chronic obstructive pulmonary disease (COPD). OBJECTIVE: To assess the safety and efficacy of anticholinergics and beta2-agonists in COPD. DESIGN: We comprehensively searched electronic databases from 1966 to December 2005, clinical trial websites, and references from selected reviews. We included randomized controlled trials of at least 3 months duration that evaluated anticholinergic or beta2-agonist use compared with placebo or each other in patients with COPD. MEASUREMENTS: We evaluated the relative risk (RR) of exacerbations requiring withdrawal from the trial, severe exacerbations requiring hospitalization, and deaths attributed to a lower respiratory event. RESULTS: Pooled results from 22 trials with 15,276 participants found that anticholinergic use significantly reduced severe exacerbations (RR 0.67, confidence interval [CI] 0.53 to 0.86) and respiratory deaths (RR 0.27, CI 0.09 to 0.81) compared with placebo. Beta2-agonist use did not affect severe exacerbations (RR 1.08, CI 0.61 to 1.95) but resulted in a significantly increased rate of respiratory deaths (RR 2.47, CI 1.12 to 5.45) compared with placebo. There was a 2-fold increased risk for severe exacerbations associated with beta2-agonists compared with anticholinergics (RR 1.95, CI 1.39 to 2.93). The addition of beta2-agonist to anticholinergic use did not improve any clinical outcomes. CONCLUSION: Inhaled anticholinergics significantly reduced severe exacerbations and respiratory deaths in patients with COPD, while beta2-agonists were associated with an increased risk for respiratory deaths. This suggests that anticholinergics should be the bronchodilator of choice in patients with COPD, and beta2-agonists may be associated with worsening of disease control. 相似文献
108.
Alan S. Pearlman MD FACC J.Geoffrey Stevenson MD Donald W. Baker EE 《The American journal of cardiology》1980,46(7):1256-1262
On the basis of principles that are similar to (but differ slightly from) those that underlie M mode and two dimensional techniques, pulsed Doppler echocardiography permits evaluation of intracardiac blood flow noninvasively. This technique is helpful in the diagnosis and management of patients with valvular and congenital heart disease, and in some circumstances provides information not available from M mode or two dimensional imaging. Despite several notable limitations, pulsed Doppler echocardiography is a useful diagnostic technique whose clinical application is likely to increase as future technologic improvements occur. 相似文献
109.
Nine patients with progressive hairy cell leukemia were treated with subcutaneous injections of recombinant alpha 2 interferon (2 to 10 X 10(6) U/m2) three times weekly. Eight patients completed at least eight weeks of treatment and were evaluable; one patient with refractory thrombocytopenia died of an intracerebral hemorrhage after two doses of interferon. Seven of eight patients responded, with responses occurring as early as two weeks. Four patients also had resolution of their monocytopenia. No complete responses were seen with up to 30 weeks of treatment. Bone marrow biopsies demonstrated improvement in all eight patients. No unforeseen toxicity occurred, but most patients had transient myelosuppression during the first few weeks of treatment. Recombinant alpha 2 interferon is effective in the treatment of hairy cell leukemia, with acceptable toxicity. 相似文献
110.
Dijkstra S Geisert EE JR Gispen WH Bär PR Joosten EA 《The Journal of comparative neurology》2000,428(2):266-277
We examined the expression of CD81 (also known as TAPA, or target of the antiproliferative antibody) after traumatic spinal cord injury in the rat. CD81, a member of the tetraspanin family of proteins, is thought to be involved in reactive gliosis. This is based on the antiproliferative and antiadhesive effects of antibodies against CD81 on cultured astrocytes, as well as its up-regulation after penetrating brain injury. CD81 expression following dorsal hemisection of the spinal cord was determined immunohistochemically at time points ranging from 1 day to 2 months postlesion (p.l.). In the unlesioned cord a low background level of CD81 was observed, with the exception of the ependyma of the central canal and the pia mater, which were strongly CD81-positive. One day p.l., CD81 was diffusely up-regulated in the spinal cord parenchyma surrounding the lesion site. From 3 days onward, intensely CD81-positive round cells entered the lesion site, completely filling it by 7 days p.l. Staining with the microglial markers OX-42 and Iba1 revealed that these cells were reactive microglia/macrophages. At this time, no significant CD81 expression by GFAP-positive reactive astrocytes was noted. From the second week onward, CD81 was gradually down-regulated; i.e., its spatial distribution became more restricted. The CD81-positive microglia/macrophages disappeared from the lesion site, leaving behind large cavities. After 2 months, astrocytes that formed the wall of these cavities were strongly CD81-positive. In addition, CD81 was present on reactive astrocytes in the dorsal funiculus distal from the lesion in degenerated white matter tracts. In conclusion, the spatiotemporal expression pattern of CD81 by reactive microglia and astrocytes indicates that CD81 is involved in the glial response to spinal cord injury. 相似文献