Objective: To evaluate the effects of a new timing strategy of band adjustment on the short-term outcome of obese women operated
with adjustable silicone gastric banding. Subjects: The outcome of 30 women without binge-eating disorder operated with laparoscopic
adjustable silicone gastric banding with a wider intraoperatory band calibration (LAP-BAND) was compared to that of 30 body
mass index-matched women without binge-eating disorder previously operated with adjustable silicone gastric banding (ASGB)
applied by laparotomy with the usual intraoperatory band calibration. The patients were evaluated 3, 6 and 12 months after
surgery. Measurements: (1) weight loss; (2) total daily energy intake; (3) percent as liquid, soft or solid food; (4) vomiting
frequency; (5) rate of postoperative percutaneous band adjustments; (6) rate of band-related complications. Results: Both
the weight loss and the daily energy intake did not differ between patients with LAP-BAND and patients with ASGB. After surgery,
the patients with LAP-BAND ate more solid food and less liquid food than the patients with ASGB. Vomiting frequency was higher
in patients with ASGB than in patients with LAP-BAND. The total number of percutaneous band adjustments was higher in women
with LAP-BAND than in women with ASGB. Band inflation because of weight stabilization was performed in six (20.0%) women with
ASGB and in 19 (63.3%) women with LAP-BAND. Neostoma stenosis occurred in one women with ASGB, but in none of the women with
LAP-BAND. One patient with LAP-BAND presented band slippage. Conclusions: The wider intraoperatory band calibration performed
in patients with LAP-BAND did not reduce the short-term efficacy of adjustable silicone gastric banding. This new timing strategy
of band adjustment required more postoperative percutaneous band inflations, but it improved the eating pattern of the patients
(low vomiting frequency and high intake of solid food). 相似文献
Expression of tau protein in non-neuronal cells can result in a redistribution of the microtubule cytoskeleton into thick bundles of tau-containing microtubules (Lewis et al.: Nature 342:498-505, 1989; Kanai et al.: J Cell Biol 109:1173-1184, 1989). We reconstituted microtubule bundles using purified tubulin and tau in order to study the assembly of these structures. Taxol-stabilized tubulin polymers were incubated with various concentrations of recombinant human tau and examined by electron microscopy. With increasing concentrations of tau 3 (tau isoform containing three microtubule binding domains) or tau 4 (isoform containing four microtubule binding domains) the microtubules changed orientation from a random distribution to loosely and tightly packed parallel arrays and then to thick cables. In contrast, tau 4L, the tau isoform containing four microtubule binding domains plus a 58-amino acid insert near the N-terminus, showed minimal bundling activity. tau 4-induced bundling could be inhibited by the addition of 0.5 M NaCl or 0.4 mM estramustine phosphate, conditions which are known to inhibit tau binding to microtubules. A tau construct that contained only the microtubule binding domains plus 19 amino acids to the C-terminus was fully capable of bundling microtubules. Phosphorylation of tau 3 with cAMP-dependent protein kinase had no effect on its ability to induce microtubule bundling. These results indicate that tau protein is directly capable of bundling microtubules in vitro, and suggests that different tau isoforms differ in their ability to bundle microtubule filaments. 相似文献
The epsilon-sarcoglycan gene (SGCE) on human chromosome 7q21 has been reported to be a major locus for inherited myoclonus-dystonia. Linkage to the SGCE locus has been detected in the majority of families tested, and mutations in the coding region have been found recently in families with autosomal dominant myoclonus-dystonia. To evaluate the relevance of SGCE in myoclonus-dystonia, we sequenced the entire coding region of the epsilon-sarcoglycan gene in 16 patients with either sporadic or familial myoclonus-dystonia. No mutations were found. This study suggests that epsilon-sarcoglycan does not play an important role in sporadic myoclonus-dystonia and supports genetic heterogeneity in familial cases. 相似文献
Isolated or combined labyrinthine, neural, and vascular damage account for failure to preserve hearing during removal of acoustic neuromas. However, the specific mechanisms of auditory impairment remain unclear unless surgical maneuvers can be related to peri- and postoperative hearing on the basis of intraoperative monitoring of auditory function.
Among the different auditory monitoring techniques, recording of cochlear nerve action potentials (CNAPs) from the intracranial portion of the nerve has proven particularly useful for identifying the mechanisms of iatrogenic auditory injury.
The present investigation analyzes intra- and postoperative auditory impairment in relation to surgical steps in a group of 38 subjects with acoustic neuroma (size ranging from 5 to 24 mm) undergoing removal via a retrosigmoid approach.
Coagulation close to the cochlear nerve, drilling of the internal auditory canal, and removal of the intrameatal portion of the acoustic neuroma have prove to be the most critical surgical steps in hearing preservation.
Changes were correlated with intra- and extrameatal tumor size, the relationship between the internal auditory canal and vestibule, and internal auditory canal enlargement, anatomic involvement of the cochlear nerve, preoperative auditory level, and ABR and ENG test findings.
Changes in CNAP morphology and latency are detailed, and mechanisms of injury are analyzed and discussed as a function of these variables.
Previously, we reported that transgenic mice overexpressing endothelin-1 in astrocytes showed more severe neurological deficits and increased infarct after transient focal ischemia. In those studies, we also observed increased level of aldose reductase (AR), the first and rate-limiting enzyme of the polyol pathway, which has been implicated in osmotic and oxidative stress. To further understand the involvement of the polyol pathway, the mice with deletion of enzymes in the polyol pathway, AR, and sorbitol dehydrogenase (SD), which is the second enzyme in this pathway, were challenged with similar cerebral ischemic injury. Deletion of AR-protected animals from severe neurological deficits and large infarct, whereas similar protection was not observed in mice with SD deficiency. Most interestingly, AR(-/-) brains showed lowered expression of transferrin and transferrin receptor with less iron deposition and nitrotyrosine accumulation. The protection against oxidative stress in AR(-/-) brain was also associated with less poly(adenosine diphosphate-ribose) polymerase (PARP) and caspase-3 activation. Pharmacological inhibition of AR by Fidarestat also protected animals against cerebral ischemic injury. These findings are the first to show that AR contributes to iron- and transferrin-related oxidative stress associated with cerebral ischemic injury, suggesting that inhibition of AR but not SD may have therapeutic potential against cerebral ischemic injury. 相似文献
Geste antagonistes, or sensory tricks, are well described in focal dystonia affecting the neck, hand, and face. Improvement in dystonic movements is typically maintained while the trick is performed, but disappears when the geste ends. We investigated the phenomenological features of geste antagoniste maneuvers in 19 patients with idiopathic lower cranial dystonia who were prospectively evaluated over a period of 6 years. Of the 19, 10 were men, mean age of onset was 49.8 years, and the most commonly involved lower cranial area was the jaw (10 patients). In most patients, dystonia was task-specific. Taking advantage of the improvement with a sensory geste, we manufactured oral appliances that mimicked the geste in 8 patients, and 3 continue to use it. 相似文献
Summary 4-amino-1-hydroxybutylidene-1,1-bis-phosphonate (AHButBP) was given intravenously (2.5–25 mg/day for 4 days) to 14 patients
with Paget's disease of bone, five of whom had been treated with dichloromethylidene bisphosphonate (Cl2MBP) 32 months earlier. In the nine patients who had not been treated previously with bisphosphonates, the short course of
AHButBP induced a suppression of serum alkaline phosphatase and urinary hydroxyproline values down to 30% of initial values.
The biochemical suppression of the disease was sustained for 2–18 months and the time to relapse did correlate to the logarithm
of the dose (P<0.001). In the five patients previously treated for Paget's disease, an apparent resistence to treatment with AHButBP was
observed. However, in these patients both serum alkaline phosphatase and urinary hydroxyproline fell to or even below the
nadir values which had previously been achieved with Cl2MBP, irrespective of the degree of relapse. Thus the degree of suppression of Paget's disease of bone, achievable after treatment
with bisphosphonates, seems to be constant for each patient, such that normal levels of serum alkaline phosphatase and urinary
hydroxyproline cannot usually be attained in patients with extremely active disease. 相似文献