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101.
Trabecular bone architecture in female renal allograft recipients-- assessed by computed tomography 总被引:1,自引:0,他引:1
Grotz WH; Mundinger FA; Muller CB; Rasenack J; Schulte-Monting J; Langer MF; Schollmeyer PJ 《Nephrology, dialysis, transplantation》1997,12(3):564-569
BACKGROUND: Osteopenia with decreased bone mineral density (BMD) is a
frequent finding in renal allograft recipients. Data concerning the bone
architecture in these patients do not exist, however. METHODS: We compared
the bone architecture of 33 randomly assigned women (age 49 +/- 12 years),
who had received renal allografts 5.6 +/- 5.3 years before the
investigation, with 74 women (age 50 +/- 14 years) who were admitted for
osteodensitometry. All patients underwent single-energy computed tomography
(SEQCT) and a midvertebral high-resolution tomography with
computer-assisted analysis of the trabecular vertebral body architecture.
RESULTS: Progressive alteration of bone architecture was associated with
increasing vertebral height loss of the vertebral body. Height reduction of
a vertebral body of more than 15% was associated with a significantly lower
BMD (-2.3 +/- 0.8 versus -1.1 +/- 1.1 standard deviations below normal
BMD), a lower trabecular bone area (13 +/- 8% versus 42 +/- 22%) and a
lower trabecular diameter (1.4 +/- 0.5 mm versus 2.2 +/- 0.8 mm) compared
to recipients without height reduction. In comparison to a matched group of
patients with similarly reduced BMD (1.1 +/- 1.2 versus 1.2 +/- 1.1 SD
below normal BMD), renal allograft recipients showed a lower number of
trabecular plates (5.6 +/- 3.1 versus 7.0 +/- 3.7) and a smaller
intertrabecular surface (54 +/- 116 mm versus 75 +/- 138 mm). CONCLUSIONS:
Alterations of bone architecture in renal allograft recipients were
associated with progressive vertebral height loss. Despite similar bone
mineral density, differences of bone architecture could be observed between
renal allograft recipients and patients with osteoporosis.
相似文献
102.
GE Lancioni MF O'Reilly J. Sigafoos NN Singh D. Oliva G. Basili 《Disability and rehabilitation》2004,26(21):1291-1294
Purpose: To assess whether a young man with multiple disabilities and minimal motor behaviour would learn to control environmental stimulation using chin movements and a mechanical microswitch. Method: The study was carried out according to an ABAB design in which A represented baseline and B intervention phases. The chin movements controlled the stimulation only during the intervention phases. A 2-month post-intervention check was conducted. Results: The man increased the frequency of his chin movements, thus increasing the level of environmental stimulation, during the intervention phases. This performance was maintained at the post-intervention check. Conclusion: The use of chin movements is a practical strategy for enabling individuals with minimal motor movements to control environmental stimulation. Future research should examine whether similar types of movements may enable some individuals to control voice-output communication devices. 相似文献
103.
Quality systems and total process control in blood banking 总被引:3,自引:0,他引:3
Blood banking has dramatically changed in the past few years. Is the old business hierarchy and medical model for management still workable? How do we want to organize our work today for success in the future? Implementation of quality systems may seem overwhelmingly complex at this time to many blood banking establishments. However, by methodically adhering to the requirements of organization development described in this review, blood centers can achieve goals of quality improvement and TPC. The FDA and the pharmaceuticals and medical device industries have set the direction and provided guidance to blood establishments. The AABB, American Society for Quality Control, the American Society for Training and Development, and numerous other professional organizations can contribute information and materials. The FDA's document on quality assurance and the CFR are the basic texts guiding the approach presented in this paper. The organization's structure and processes may need to be reengineered to meet the requirements of a culture based on quality and process control. 相似文献
104.
Anjum Misbahuddin Mark R Placzek Jan-Willem Taanman Steve Gschmeissner Giampietro Schiavo J Mark Cooper Thomas T Warner 《Movement disorders》2005,20(4):432-440
A single GAG deletion in the DYT1 gene causes primary early-onset, generalized torsion dystonia. The DYT1 protein product, torsinA, belongs to the AAA+ family of proteins. When overexpressed, wild-type torsinA localizes mainly to the endoplasmic reticulum, whereas the mutant forms inclusions of unclear biogenetic origin. In this study, overexpressed wild-type torsinA in human neuroblastoma (SH-SY5Y) cell lines was distributed throughout the cell body and colocalized with a marker for the endoplasmic reticulum, confirming it is an endoplasmic reticulum protein. However, mutant torsinA showed perinuclear staining and formed distinct globular inclusions, which did not colocalize with endoplasmic reticulum markers. Immunoelectron microscopy of the mutant torsinA inclusions revealed membrane whorls staining for torsinA, as well as labeling of lamellae, isolated bilayers, and perinuclear membranes. This finding shows that mutant torsinA redistributes to specific membranous structures, which may represent different stages of maturation of the intracellular inclusions. The mutant torsinA-containing bodies were immunoreactive for vesicular monoamine transporter 2 (VMAT2). VMAT2 expression is important for the exocytosis of bioactive monoamines in neurons. Abnormal processing, transport, or entrapment of VMAT2 within the mutant torsinA membranous inclusions, therefore, may affect cellular dopamine release, providing a potential pathogenic mechanism for the DYT1-dependent dystonia. 相似文献
105.
106.
The heterogeneity of type IIA von Willebrand's disease: studies with protease inhibitors 总被引:6,自引:0,他引:6
Batlle J; Lopez Fernandez MF; Campos M; Justica B; Berges C; Navarro JL; Diaz Cremades JM; Kasper CK; Dent JA; Ruggeri ZM 《Blood》1986,68(6):1207-1212
The absence of large von Willebrand factor (vWF) multimers from plasma is a characteristic of Type IIA von Willebrand's disease (vWD) and is thought to contribute to the clinical expression of this disorder. Recently, three IIA patients have been reported in whom intermediate and large multimers could be restored if blood were collected in 5 mm EDTA, 6 mmol/L N-ethylmaleimide, and 1 mmol/L leupeptin. This suggested that absence of large multimers resulted from in vitro proteolysis. We have now collected blood from ten Type IIA vWD patients in these inhibitors but were not able to detect large multimers in the plasma of any of them. In addition, intermediate-sized multimers were reduced or completely absent in all. The inclusion of inhibitors in the citrate anticoagulant, as compared to citrate alone, was found to increase the relative proportion of intermediate multimers in some patients but had no effect in others, and in none did it restore large multimers to plasma. The results with platelet vWF were more varied. Four patients showed an absence or decrease of large multimers, whereas in seven patients large multimers were present. When compared with citrate anticoagulant alone, the inclusion of inhibitors in the anticoagulant had little or no effect on the platelet multimeric pattern. 1-Deamino-8- D-Arginine Vasopressin (DDAVP) was administered to six patients from five families. Two patients from one family showed complete correction and a third patient showed almost complete correction of her bleeding time. Two patients showed minimal correction and one showed no detectable correction. An increase in multimer size after DDAVP tended to be associated with correction of the bleeding time. However, in no case did the largest multimers appear in plasma even in patients with complete bleeding time correction. The presence or absence of inhibitors in the anticoagulant had little or no effect on the multimeric pattern after DDAVP. These results indicate that Type IIA vWD is a heterogeneous disorder in which absence of largest and intermediate multimers is an in vivo phenomenon. 相似文献
107.
Comparison between published clinical success of direct resin composite restorations in vital posterior teeth in 1995–2005 and 2006–2016 periods 下载免费PDF全文
Composites are increasing in popularity as restorative materials. This growing role indicates the necessity of studies on their clinical outcome. In this study, clinical studies published on the performance of posterior composite restorations were included except those of less than a 24‐month assessment period. Results of non‐vital, anterior or primary teeth and cervical single‐surface restorations were also excluded. Records about composite type, number of final recall restorations, failure/survival rate, assessment period and failure reasons were analysed for each decade. Overall survival/failure rates for studies in 1995–2005 were 89.41%/10.59% and for 2006–2016 were 86.87%/13.13%, respectively. In 1995–2005, the reasons for failure were secondary caries (29.47%) and composite fracture (28.84%) with low tooth fracture (3.45%) compared with reasons of failure in 2006–2016, which were secondary caries (25.68%), composite fracture (39.07%), and tooth fracture (23.76%). An increase in incidence of composite fracture, tooth fracture and need for endodontic treatment as failure reasons was noted in the latter decade in addition to a decrease in secondary caries, postoperative sensitivity, unsatisfactory marginal adaptation and wear. The overall rates of failure showed little difference, but the causes showed a notable change. This is believed to be a reflection of increased use of composites for larger restorations and possibly changes of material characteristics. 相似文献
108.
Neonatal neutrophils (PMN) show a well-documented defect in chemotaxis that is associated with several abnormalities of PMN structure and function, including deficient surface expression of CR3 (CD11b), a critical adhesion molecule, on chemoattractant-activated PMN. After activation of PMN with additional stimuli including calcium ionophores, we also found deficient surface CR3 (but normal CR1) expression on neonatal PMN suggesting that abnormal signaling mechanisms are not likely to explain the deficient CR3 expression on activated neonatal PMN. Therefore, we hypothesized that deficient surface expression of CR3 on stimulated neonatal neutrophils is caused by a deficiency in total cell content of CR3. We tested this hypothesis using three different methods to compare the total quantity of CR3 in neonatal versus adult PMN. Western blotting of serial twofold dilutions of PMN lysates from five adult and neonatal pairs, using a monoclonal antibody (MoAb) against CR3 (21PM19C), consistently showed diminished CR3 content in neonatal PMN. A sandwich enzyme-linked immunosorbent assay, in which the CR3 heterodimers in PMN lysates were captured by MoAb to the beta-chain, CD18 (R15.7), then detected with a biotinylated MoAb to the alpha-chain, CD11b (anti-Mac-1), showed that neonatal PMN lysates contain about 66% of adult PMN levels of CR3 (P < 0.03; n = 6). PMN fixed with paraformaldehyde and permeabilized with saponin were studied by immunofluorescence flow cytometry to determine total (surface plus intracellular) CR3 content using phycoerythrin-conjugated MoAb to CR3 (anti-Leu15). Mean total cell CR3 content (in relative fluorescence units) was 58 +/- 14 for adult PMN and 27 +/- 6 for neonatal PMN (n = 5; P = 0.013). In each method, total cell content of CR1 was equivalent for neonatal versus adult PMN. We conclude that neonatal PMN are markedly deficient in total cell CR3 content compared with adult PMN. This result provides a primary explanation for deficient CR3 surface expression on activated neonatal PMN that, in turn, may be important in the chemotactic defect of these cells. 相似文献
109.
BackgroundBetween 1951 and 1995 there was a steady increase in age-standardised deaths from all aortic aneurysms in men, from 2 to 56 per 100,000 population in England &; Wales, supporting an increase in incidence. More recently, evidence from Sweden and elsewhere suggests that now the incidence of abdominal aortic aneurysm (AAA) may be declining.MethodsNational statistics for hospital admissions and deaths from AAA, after population age-standardisation, were used to investigate current trends in England &; Wales and Scotland.ResultsBetween 1997 and 2009 there has been a reduction in age-adjusted mortality from AAA from 40.4 to 25.7 per 100,000 population for England &; Wales and from 30.1 to 20.8 per 100,000 population in Scotland. The decrease in mortality was more marked for men than women. Mortality decreased more than 2-fold in those <75 years versus 25% only in those >75 years. During this same time period the elective hospital admissions for AAA repair have only increased in the population >75 years.ConclusionsThese data suggest that the age at which clinically-relevant aneurysms present has increased by 5–10 years and that incidence of clinically-relevant AAA in men in England &; Wales and Scotland is declining rapidly. The reasons for this are unclear. 相似文献
110.