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71.
Abstract: Scalene muscle injections are used to confirm the diagnosis of neurogenic thoracic outlet syndrome and predict the response of patients to surgery. We performed a retrospective study to determine if relief of pain was related to brachial plexus blockade in these patients. Methods: We reviewed the charts of 12 patients who had anterior and middle scalene muscle injections, for neurogenic thoracic outlet syndrome, between April 2009 and September 2010. The injections were performed under ultrasound guidance wherein 2 to 5 mL of 0.25% bupivacaine was injected into the belly of the anterior and scalene muscles. The following were noted: (1) sites of preprocedure pain; (2) volume injected into each of the anterior and middle scalene muscles; (3) presence of numbness after injection; and (4) presence and duration of pain relief. Results: All 12 patients had relief of their pain. Six of the twelve patients developed numbness, which ranged from blockade of the C4‐5, C6‐7, and C4‐T1 dermatomes. In the patients who developed numbness, there was no relationship between the duration of numbness and the duration of pain relief or the location of numbness and the location of pain relief. Conclusions: The relief from scalene muscle injections in patients with neurogenic thoracic outlet syndrome is not related to blockade of the brachial plexus. ?  相似文献   
72.
Children and young people are seen as fundamental to the design and delivery of clinical research as active and reflective participants. In Europe, involvement of children and young people in clinical research is promoted extensively in order to engage young people in research as partners and to give them a voice to raise their own issues or opinions and for their involvement in planning and decision making in addition to learning research skills. Children and young people can be trained in clinical research through participation in young person advisory groups (YPAGs). Members of YPAGs assist other children and young people to learn about clinical research and share their experience and point of view with researchers, thereby possibly influencing all phases of research including the development and prioritization of research questions, design and methods, recruitment plans, and strategies for results dissemination. In the long term, the expansion of YPAGs in Europe will serve as a driving force for refining pediatric clinical research. It will help in a better definition of research projects according to the patients’ needs. Furthermore, direct engagement of children and young people in research will be favorable to both researchers and young people.  相似文献   
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Canavan disease (CD) is a fatal neurological disorder caused by defects in the gene that encodes for a critical metabolic enzyme. The enzyme aspartoacylase catalyzes the deacetylation of N-acetylaspartate to produce acetate required for fatty acid biosynthesis in the brain. The loss of aspartoacylase activity leads to the demyelination and disrupted brain development that is found in CD patients. Sixteen different clinical mutants of aspartoacylase have been cloned, expressed and purified to examine their properties and the relationship between enzyme properties and disease phenotype. In contrast to numerous cell culture studies that reported virtually complete loss of function, each of these purified mutant enzymes was found to have measureable catalytic activity. However, the activities of these mutants are diminished, by as little as three-fold to greater than 100-fold when compared to the native enzyme. Many of these mutated enzyme forms show decreased thermal stability and an increased propensity for denaturation upon exposure to urea, but only four of the 16 mutants examined showed both diminished thermal and diminished conformational stability. Significantly, each of these lower stability mutants are responsible for the more severe phenotypes of CD, while patients with milder forms of CD have aspartoacylase mutants with generally high catalytic activity and with either good thermal or good conformational stability. These results suggest that the loss of catalytic function and the accumulation of N-acetylaspartate in Canavan disease is at least partially a consequence of the decreased protein stability caused by these mutations.  相似文献   
75.
The treatment of keloid and hypertrophic scar is challenging with no universally accepted mode for permanent ablation. Conventional therapies yield unpredictable results, significant complications and require elaborate hardware.

Objective

The objective was to establish the safety and efficacy of intralesional 5-fluorouracil (5-FU) for the treatment of keloids and hypertrophic scars.

Study design

Randomized controlled trial (RCT).

Place and duration

It was conducted at the Jinnah Burn and Reconstructive Surgery Center/Allama Iqbal Medical College, Lahore, Pakistan from May 2012 to March 2013.

Subjects and methods

We included 120 patients divided in two groups. The group A patients received intralesional triamcinolone acetonide (TAC) and the group B patients received both 5-FU and TAC. 8 injections at a week interval were given and patients were evaluated at the start of treatment and then at 4th and at 8th week during the treatment and then 4 weeks after the end of treatment. Patents were assessed for mean reduction in scar height, efficacy and complications.

Results

Total of 108 patients completed the study. The mean reduction in the scar height in group B (5-FU + TAC) 1.144 + .4717 was markedly better than that of group A (TAC alone) 1.894 + 1.0751 (t = 4.781, p = .000). The efficacy (defined previously as >50% reduction in initial scar height) was superior in group B 44 (77.2%) than that of group A 25 (49.0% (X2 = 9.260, p = .002). Recurrence was seen in 39.2% (20) of patients of the group A while in only 17.5% (10) of the cases of group B (P = 0.012). Mean follow up was of 22 months.

Conclusion

5-FU + TAC is safe, easy to administer and effective treatment for problematic scars and has the lower rate of recurrence on larger follow up.  相似文献   
76.
Diabetic peripheral neuropathy in people with type 2 diabetes is poorly managed because of its insidious onset, delayed diagnosis and more complex aetiology resulting from the contribution of not only hyperglycaemia, but also ageing, hyperlipidaemia, hypertension and obesity. Because there is no US Food and Drug Adminstration-approved disease-modifying therapy for diabetic peripheral neuropathy, the key to ameliorating it in type 2 diabetes has to be through earlier diagnosis and timely multi-factorial risk factor reduction. The management of painful diabetic peripheral neuropathy also requires a detailed appraisal of the choice of therapy, taking into account efficacy, patient wishes, comorbidities, side effect profile and potential for abuse.  相似文献   
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