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51.
A case of avascular necrosis of whirlbone in a young man affected by multiple sclerosis and treated with high doses of corticosteroids
is described. The authors discuss the causes of this collateral effect underlining the risks of underevaluating the symptoms. 相似文献
52.
Much of the laboratory and medical equipment in resource-poor settings is out-of-service. The most commonly cited reasons
are (1) a lack of spare parts and (2) a lack of highly trained technicians. However, there is little data to support these
hypotheses, or to generate evidence-based solutions to the problem. We studied 2,849 equipment-repair requests (of which 2,529
were out-of-service medical equipment) from 60 resource-poor hospitals located in 11 nations in Africa, Europe, Asia, and
Central America. Each piece of equipment was analyzed by an engineer or an engineering student and a repair was attempted
using only locally available materials. If the piece was placed back into service, we assumed that the engineer’s problem
analysis was correct. A total of 1,821 pieces of medical equipment were placed back into service, or 72%, without requiring
the use of imported spare parts. Of those pieces repaired, 1,704 were sufficiently documented to determine what knowledge
was required to place the equipment back into service. We found that six domains of knowledge were required to accomplish
99% of the repairs: electrical (18%), mechanical (18%), power supply (14%), plumbing (19%), motors (5%), and installation
or user training (25%). A further analysis of the domains shows that 66% of the out-of-service equipment was placed back into
service using only 107 skills covering basic knowledge in each domain; far less knowledge than that required of a biomedical
engineer or biomedical engineering technician. We conclude that a great majority of laboratory and medical equipment can be
put back into service without importing spare parts and using only basic knowledge. Capacity building in resource-poor settings
should first focus on a limited set of knowledge; a body of knowledge that we call the biomedical technician’s assistant (BTA).
This data set suggests that a supported BTA could place 66% of the out-of-service laboratory and medical equipment in their
hospital back into service. 相似文献
53.
Patients with acquired defects or congenital malformations of the palate exhibit disturbances in speech, including hypernasality, nasal emission, and decreased intelligibility of speech. Maxillofacial prosthetic treatment can reestablish the palatopharyngeal integrity to provide the potential for acceptable speech. This article describes a case series of patients with palatopharyngeal disorders and their treatment approaches. 相似文献
54.
55.
BACKGROUND: Acute administration of mitochondrial adenosine triphosphate-dependent potassium channel openers preconditions the heart, but whether their long-term administration induces a permanent state of protection is unknown. These studies investigate the effect of long-term treatment with the mitochondrial adenosine triphosphate-dependent potassium channel opener nicorandil on the response of the human myocardium to ischemia and preconditioning. METHODS: Right atrial tissue obtained from patients regularly treated with or without nicorandil (mean of 20 mg/d for 18.6 +/- 2.5 months) and undergoing cardiac surgery was sliced and equilibrated for 30 minutes and then subjected to 90 minutes of simulated ischemia, followed by 120 minutes of reoxygenation. In study 1 the following groups were studied to investigate the effect of nicorandil on the susceptibility of the myocardium to ischemia and on the protective effect of ischemic and pharmacologic preconditioning: (1) aerobic control; (2) simulated ischemia and reoxygenation alone; (3) ischemic preconditioning with 5 minutes of simulated ischemia and 5 minutes of reoxygenation; and (4) phenylephrine (0.1 micromol/L) for 5 minutes and 5 minutes' washout before simulated ischemia and reoxygenation. In study 2 the following groups were studied to investigate the effect of nicorandil on the responsiveness of mitochondrial adenosine triphosphate-dependent potassium channels: (1) aerobic control; (2) simulated ischemia and reoxygenation; (3) ischemic preconditioning; (4) diazoxide (100 micromol/L) for 10 minutes before simulated ischemia and reoxygenation, and (5) 5-hydroxydecanoate (1 mmol/L) for 10 minutes before simulated ischemia and reoxygenation. In study 3 the following groups were included to investigate the effect of the long-term administration of nicorandil on the kinase pathway involved in preconditioning: (1) aerobic control; (2) simulated ischemia and reoxygenation alone; (3) ischemic preconditioning; (4) phorbol 12-myristate 13-acetate (1 micromol/L), a protein kinase C activator, for 10 minutes before simulated ischemia and reoxygenation; and (5) anisomycin (1 nmol/L), a p38 mitogen-activated protein kinase activator, for 10 minutes before simulated ischemia and reoxygenation. At the end of each protocol, the leakage of creatine kinase (in units per gram wet weight) and the reduction of 3-[4,5 dimethylthiazol-2-yl]-2,5 diphenyltetrazolium bromide into insoluble formazan dye (in millimoles per gram wet weight) were measured. RESULTS: In study 1 the leakage of creatine kinase and the reduction of 3-[4,5 dimethylthiazol-2-yl]-2,5 diphenyltetrazolium bromide induced by simulated ischemia and reoxygenation were similar in the groups with or without nicorandil (creatine kinase, 3.4 +/- 0.1 and 3.5 +/- 0.2, respectively; 3-[4,5 dimethylthiazol-2-yl]-2,5 diphenyltetrazolium bromide, 74.6 +/- 3.9 and 67.9 +/- 7.3, respectively; P >.2 in each instance). Ischemic preconditioning and pharmacologic preconditioning protected the myocardium from patients without nicorandil (creatine kinase, 2.3 +/- 0.1 and 2.4 +/- 0.1, respectively; 3-[4,5 dimethylthiazol-2-yl]-2,5 diphenyltetrazolium bromide, 131.4 +/- 4.9 and 128.4 +/- 5.6, respectively; P < 0.001 vs simulated ischemia and reoxygenation alone in each instance) but not the myocardium from patients receiving nicorandil (creatine kinase, 3.3 +/- 0.1 and 3.3 +/- 0.2, respectively; 3-[4,5 dimethylthiazol-2-yl]-2,5 diphenyltetrazolium bromide, 89.7 +/- 6.5 and 86.4 +/- 5.2, respectively; P >.2 vs simulated ischemia and reoxygenation alone in each instance). In study 2 the administration of diazoxide had identical protection to that of ischemic preconditioning in the myocardium of patients not receiving nicorandil (creatine kinase, 2.1 +/- 0.2 and 2.3 +/- 0.1, respectively; 3-[4,5 dimethylthiazol-2-yl]-2,5 diphenyltetrazolium bromide, 141.4 +/- 7.4 and 131.4 +/- 4.9, respectively; P < 0.001 vs simulated ischemia and reoxygenation alone in each instance) but failed to precondition the myocardium from patients treated with nicorandil (creatine kinase, 3.3 +/- 0.2 and 3.4 +/- 0.1, respectively; 3-[4,5 dimethylthiazol-2-yl]-2,5 diphenyltetrazolium bromide, 90.1 +/- 7.2 and 86.4 +/- 5.2, respectively; P > 0.2 vs simulated ischemia and reoxygenation alone in each instance). In study 3 phorbol 12-myristate 13-acetate or anisomycin given for 10 minutes before simulated ischemia and reoxygenation afforded similar protection to that of ischemic preconditioning in the myocardium from patients with (creatine kinase, 1.5 +/- 0.3 and 1.4 +/- 0.1, respectively; 3-[4,5 dimethylthiazol-2-yl]-2,5 diphenyltetrazolium bromide, 147.0 +/- 4.9 and 160.0 +/- 16.1, respectively; P < 0.001 vs simulated ischemia and reoxygenation alone in each instance) and without nicorandil (creatine kinase, 1.7 +/- 0.4 and 1.4 +/- 0.2, respectively; 3-[4,5 dimethylthiazol-2-yl]-2,5 diphenyltetrazolium bromide, 160.3 +/- 13.6 and 158.3 +/- 11.8, respectively; P <.001 vs simulated ischemia and reoxygenation alone in each instance). CONCLUSION: The myocardium of patients chronically treated with nicorandil cannot be preconditioned either by ischemia or pharmacologically, and this is because of unresponsive mitochondrial adenosine triphosphate-dependent potassium channels. However, protection can be obtained by protein kinase C and p38 mitogen-activated protein kinase activation, which are downstream of mitochondrial adenosine triphosphate-dependent potassium channels in the signaling transduction pathway of preconditioning. 相似文献
56.
Ang ER Zimmerman JC Malkin E 《The Journal of the American Board of Family Practice / American Board of Family Practice》2002,15(3):229-233
BACKGROUND: Pseudotumor cerebri, or idiopathic intracranial hypertension, is a condition most commonly affecting women of childbearing age who are obese or who have experienced recent weight gain. Frequently the patient complains of headache accompanied by dizziness, nausea, or visual defects, and it is characterized by elevated intracranial pressure in the absence of a space-occupying lesion or infection METHODS: A patient had been prescribed minocycline and subsequently developed symptoms 6 weeks after an increase in the original dosage. She was initially examined by an ophthalmologist, then was sent to the Emergency Department, and finally admitted under the family practice service. Articles were searched through MEDLINE, MD Consult, and Google. Key words included "pseudotumor cerebri," benign intracranial hypertension," idiopathic intracranial hypertension," and "minocycline." RESULTS AND CONCLUSION: Although the pathogenesis of pseudotumor cerebri is not completely understood, an association has been observed with minocycline use. This report describes a 16-year-old girl who developed idiopathic intracranial hypertension while taking minocycline for acne. Symptoms of blurred vision and severe headache unrelated to position or activity; an absence of fever, bilateral disk edema, and focalizing neurologic signs; negative neuroradiographic findings; increased cerebrospinal fluid pressure with a normal cell count; and exclusion of systemic or structural cause of increased intracranial pressure satisfy the criteria for the diagnosis of idiopathic intracranial hypertension. Minocycline is often used by family physicians for the treatment of acne, and this complication requires vigilance to protect against potential vision loss. 相似文献
57.
Handheld cellular telephones and risk of acoustic neuroma 总被引:8,自引:0,他引:8
Muscat JE Malkin MG Shore RE Thompson S Neugut AI Stellman SD Bruce J 《Neurology》2002,58(8):1304-1306
The hypothesis that intracranial energy deposition from handheld cellular telephones causes acoustic neuroma was tested in an epidemiologic study of 90 patients and 86 control subjects. The relative risk was 0.9 (p = 0.07) and did not vary significantly by the frequency, duration, and lifetime hours of use. In patients who used cellular telephones, the tumor occurred more often on the contralateral than ipsilateral side of the head. Further efforts should focus on potentially longer induction periods. 相似文献
58.
59.
Liberatore M Fiore V D'Agostini A Prosperi D Iurilli AP Santini C Baiocchi P Galiè M Di Nucci GD Sinatra R 《European journal of nuclear medicine》2000,27(6):660-667
Sternal wound infections (SWIs) can be subdivided into two types, superficial or deep, that require different treatments. The clinical diagnosis of superficial SWI is normally easy to perform, whereas the involvement of deep tissues is frequently difficult to detect. Therefore, there is a need for an imaging study that permits the assessment of SWIs and is able to distinguish between superficial and deep SWI. The present work was a prospective study aiming to evaluate the role of technetium-99m hexamethylpropylene amine oxime (99mTc-HMPAO) labelled leucocyte scan in SWI management. Twenty-eight patients with suspected SWIs were included in the study. On the basis of clinical examination they were subdivided into three groups: patients with signs of superficial SWI (group 1), patients with signs of superficial SWI and suspected deep infection (group 2) and patients with suspected deep SWI without superficial involvement (group 3). Ten patients previously submitted to median sternotomy, but without suspected SWI, were also included in the study as a control group (group 4). All patients with suspected SWI had bacteriological examinations of wound secretion, if present. In addition 99mTc-HMPAO labelled leucocyte scan was performed in all patients. The patients of groups 1, 2 and 3 were treated on the basis of the clinical signs and microbiological findings, independently of the scintigraphic results. The patients of group 4 did not receive treatment. The final assessment of infection was based on histological and microbiological findings or on long-term clinical follow-up. Sensitivity, specificity, accuracy and positive and negative predictive values for scintigraphic and non-scintigraphic results were calculated. In the diagnosis of superficial and deep SWI, clinical and microbiological examination (combined) yielded, respectively, a sensitivity of 68.7% and 100%, a specificity of 77.3% and 80.8%, an accuracy of 73.7% and 86.8%, a positive predictive value of 68.7% and 70.6% and a negative predictive value of 77.3% and 100%. The scintigraphic results obtained in superficial SWI yielded a sensitivity of 56.2%, a specificity of 90.9%, an accuracy of 76.3%, a positive predictive value of 81.8% and a negative predictive value of 74.1%, while, by contrast, in deep SWI all of these values were 100%. Therefore, one can conclude that 99mTc-HMPAO labelled leucocyte scan permits accurate diagnosis of deep SWI, solving the main clinical problem in this field. In the present study the categorisation of patients without taking into account 99mTc-HMPAO labelled leucocyte planar scan findings caused a non-negligible number of cases of superficial SWI to be treated as though they were deep SWI. This "overestimation" led to unnecessary surgery, increased and prolonged use of antibiotics with more (higher) toxicity and additional expense. 相似文献
60.
Renal function in pediatric patients with β-thalassemia major 总被引:1,自引:0,他引:1
Aldudak B Karabay Bayazit A Noyan A Ozel A Anarat A Sasmaz I Kilinç Y Gali E Anarat R Dikmen N 《Pediatric nephrology (Berlin, Germany)》2000,15(1-2):109-112
In patients with β-thalassemia major, the most important cause of mortality and morbidity is organ failure due to deposits
of iron.. In this study, the nature of the kidney injury and possible pathogenetic factors were investigated. Seventy children
with β-thalassemia major and 14 age and sex-matched healthy children were involved in the study. Blood and timed urine samples
were obtained for hematological and biochemical tests. The mean values of blood urea nitrogen (BUN), serum creatinine, creatinine
clearance, serum sodium, urine osmolality, fractional excretion of sodium, potassium, and uric acid were not statistically
different between the groups. Serum levels of potassium, phosphorus, and uric acid and the urine volume, high urinary protein
to creatinine (UP/Cr), urinary N-acetyl-β-d-glucosaminidase to creatinine (UNAG/Cr), and urinary malondialdehyde to creatinine, (UMDA/Cr) and the tubular phosphate reabsorption (TRP) values were statistically different between two groups (P<0.05). Increased serum levels of potassium, phosphorus, and uric acid in the patient group were attributed to the rapid erythrocyte
turnover. The presence of high UP/Cr, UNAG/Cr and UMDA/Cr ratios shows that in these patients with proximal renal tubular damage may be secondary to oxidative lipid peroxidation mediated
by the iron overload.
Received: 30 September 1999 / Revised: 19 May 2000 / Accepted: 22 May 2000 相似文献