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Biomedical subjects

B Weller

Publications and source records attributed to B Weller.

At least 19 recordsLinked to original sources

Two-year evaluation of restorations of a packable composite placed in UK general dental practices.

OBJECTIVE: The aim of this study was to assess the clinical performance at two years of 100 Solitaire 2 restorations placed in five United Kingdom dental practices by members of a practice-based research group. METHOD AND MATERIALS: Restorations were assessed after two years by a trained evaluator and the dental practitioner who had placed the material, for anatomic form, marginal adaptation, surface roughness, gingival condition and the presence or absence of secondary caries. In addition, the patients completed a questionnaire requesting details of the comfort and performance of the Solitaire 2 restoration(s). RESULTS: A total of 88 (58 Class II and 30 Class I) restorations of Solitaire 2 placed in 49 patients (mean age 43 years) were assessed. Twelve restorations could not be evaluated because of patient unavailability for the dates of the examinations. Two Class II restorations (2%) had failed by the time of the two-year evaluation and the remaining 86 restorations were found to be intact with no secondary caries. A high percentage of optimal scores were recorded for anatomic form and surface roughness. The colour match of two restorations (2%) was recorded as an obvious mismatch, but otherwise no unacceptable scores were recorded. CONCLUSIONS: After two years of clinical service a high proportion (96%) of the Solitaire 2 restorations that were available for re-examination, placed in general dental practice settings, were found to be performing satisfactorily.

Adhesives↗

Neck irradiation: a risk factor for occlusive carotid artery disease.

OBJECTIVES: to determine whether irradiation is an independent risk factor for carotid atherosclerosis, and propose guidelines for patient follow-up. DESIGN: a retrospective case control study. MATERIALS AND METHODS: two groups of patients with severe carotid artery stenosis (>70%) were compared: 30 post-neck irradiation patients, and a control group of 100 patients with no history of neck irradiation. Disease location and severity were assessed by duplex. The relationship between atherosclerotic risk factors, time since irradiation and carotid artery disease was examined. RESULTS: the average age of study group patients was 67 years (43-86) compared to 69 years (46-89) in the control group. The average interval from irradiation to diagnosis was 14 years (3-53) (median 12.5 years). The study group suffered less from diabetes, ischaemic heart disease, and peripheral vascular disease ( p<0.02). There were no significant differences among risk factors with respect to age, gender, smoking, hypertension, and hypercholesterolemia. Post-neck irradiation patients had a significantly higher prevalence of bilateral disease (p=0.02), and a higher rate of common carotid artery lesions (p<0.002). CONCLUSIONS: neck irradiation should be considered a risk factor for occlusive carotid artery disease. Preoperative angiographic study should be considered, due to frequent involvement of the common carotid artery.

Adult↗

Carotid endarterectomy in awake patients with contralateral carotid artery occlusion.

OBJECTIVES: Patients with severe stenosis of an internal carotid artery with contralateral occlusion (ICO) are at an increased risk for stroke, and therefore surgical treatment is usually recommended. Carotid endarterectomy (CEA) under regional anesthesia enables constant monitoring of neurologic status and selective shunting in cases of clinically evident cerebral ischemia. In this study, we assess the selective use of shunts based solely on changes in neurological status in awake patients with ICO undergoing CEA as well as their complication rates. METHODS: During 1996-1998, we studied intraoperative findings and results of CEA under regional anesthesia with clinical monitoring of neurological status in two groups: (1) patients with stenosis (> 70% by NASCET) and contralateral occlusion (n = 50) and (2) patients with stenosis and no contralateral occlusion (n = 94). RESULTS: Shunt insertion was required in 42% of group 1, and 6% in group 2. All of the patients in group 1 requiring shunts had stump pressures < 50 torr. The average stump pressure of group 1(40 torr) was significantly lower than that of group 2 (75 torr), and was also lower than that of patients with severe contralateral stenosis (35 patients, 76 torr). Perioperative stroke rates were identical in both groups (2.1%). CONCLUSION: Since ICO patients are at a high risk for brain ischemia during ICA clamping, they require shunt insertion frequently. Patients with no contralateral occlusion require shunting at a much lower rate - even in the presence of severe contralateral stenosis. Regional anesthesia allows for early detection of brain ischemia and therefore, the perioperative results in both groups are similar.

Aged↗

The epic project: developing national evidence-based guidelines for preventing healthcare associated infections. Phase I: Guidelines for preventing hospital-acquired infections. Department of Health (England).

In 1998, the Department of Health (England) commissioned the first phase of national evidence-based guidelines for preventing healthcare associated infections. These focused on developing a set of standard principles for preventing infections in hospitals together with guidelines for preventing hospital-acquired infections (HAI) associated with the use of short-term indwelling ureteral catheters in acute care and with central venous catheters in acute care. These guidelines are systematically developed broad statements (principles) of good practice that all practitioners can use and which can be incorporated into local protocols. A nurse-led, multi-professional team composed of infection prevention practitioners, clinical microbiologists/retrovirologist, epidemiologists, and researchers developed the guidelines. A rigorous guideline development process was used to inform the systematic reviews, the clinical and critical appraisal of relevant evidence, and linking that evidence to evolving guidelines. Both general and specialist clinical practitioners were involved in all stages of developing these guidelines, as were representatives from relevant Royal Colleges, learned societies, other professional organisations and key stakeholders. The introduction to these guidelines describes a robust and validated guideline development model that can be used by others to develop future guidelines. This model is described in more detail in the associated technical reports that can be found on the project web site http://www.epic.tvu.ac.uk. Locating and appropriately using good quality evidence to inform guideline development in this field is challenging. Evidence from rigorously conducted experimental studies was frequently limited and consequently a range of other types of evidence were systematically retrieved and carefully appraised. The concluding discussion on implementation highlights potential issues for clinical governance and areas for future research and suggests issues that need to be addressed to allow practitioners to successfully incorporate these guidelines into routine clinical practice.

Acute Disease↗

Myopathy with trabecular muscle fibers.

A systematic review of muscle biopsies over a 15 year period in a large neurological hospital revealed 21 cases (7% of the total of non-inflammatory myopathies) with a distinctive pattern of myopathology and a limb-girdle clinical phenotype. The muscle pathology was dominated by a large prevalence (20-90%) of trabecular or lobulated fibers in which maldistribution of intermyofibrillar mitochondria produced a lobulated pattern of oxidative enzyme activity on transverse sections. The clinical picture was characterized by adult onset, slowly progressive muscle weakness affecting mainly proximal limb musculature, although mild distal weakness was also present in 60% of the cases. The trabecular pattern of oxidative enzyme reaction reflects maldistribution of the intermyofibrillar mitochondria; this may be caused by malfunction of a putative anchoring mechanism. While trabecular fibers can occur as a nonspecific alteration of muscle fibers in many diverse myopathies, the high prevalence of trabecular fibers as the dominant pathology in trabecular fiber myopathy makes it a distinctive (though not necessarily etiologically homogeneous) clinico-pathological entity.

Adolescent↗

[Diagnosis of cerebral embolism by transesophageal echocardiography].

Cerebrovascular events have high mortality and morbidity, especially in the elderly. Ischemia is the main cause and 30% of the ischemic events are embolic and of cardiac origin. The clinical picture is not always typical of the type of stroke, but diagnosis of the mechanism of the event determines treatment. Transesophageal echocardiography (TEE) is a sensitive procedure more appropriate for diagnosing emboli of cardiac origin than transthoracic echocardiography (TTE). We therefore compared TEE and TTE in the determination of the source of emboli in 65 patients with ischemic stroke but without significant atherosclerotic changes in their carotid arteries, and compared these findings with those in 50 patients without stroke. 68% of the patients had potential sources of emboli according to TEE, compared to only 15% according to TTE. In the control group only 24% had potential sources of emboli by TEE. The findings were: clots in the left atrium, severe aortic atheroma, patent foramen ovale with paradoxical shunt, spontaneous echocardiography contrast, vegetations and mitral valve prolapse. The study showed that TEE is better than TTE in detecting the etiology of embolic stroke in those with normal carotid arteries, thus determining appropriate management.

Brain Ischemia↗

Dermatomyositis and nasopharyngeal carcinoma.

A nasopharyngeal carcinoma was diagnosed in a 37-year-old man with a two year history of dermatomyositis. The physical and laboratory examinations excluded further medical problems. To our knowledge, this is the first case of dermatomyositis associated with nasopharyngeal carcinoma in a white Israeli Jewish patient.

Adult↗

High association of anticardiolipin antibodies with psychosis.

BACKGROUND: Lupus anticoagulant (LA) and anticardiolipin antibodies (aCL) are autoantibodies that can be detected in plasma or serum of patients with autoimmune-related diseases. The presence of these autoantibodies has been associated with recurrent arterial and/or venous thromboembolism as well as with recurrent fetal loss and thrombocytopenia. In recent years, other medical conditions such as dementia, chorea, psychosis, migraine, and peripheral neuropathy have been associated with these autoantibodies. An adverse response to neuroleptic treatment was reported to be associated with the presence of autoantibodies, but these patients rarely developed clinical vascular manifestations. METHOD: We conducted a study of 34 unmedicated patients admitted to the hospital with acute psychosis in whom aCL and LA were examined before and after neuroleptic treatment to determine the presence of antibodies relative to the treatment condition. RESULTS: 32% (11/34) of the unmedicated psychotic patients had antiphospholipid antibodies: we detected elevated titers of IgG-aCL isotype in 24% (8/34) of unmedicated patients (p < .02 compared with 20 normal controls, none of whom tested positive), and 9% (3/34) had LA. Twenty-two patients were followed up after medication; 31.8% (7/22) of these patients showed moderate titers of IgG-aCL (p < .28), and 18.2% (4/22) were LA positive. Altogether, antiphospholipid antibodies were detected in 40.9% (9/22) of the medicated patients. CONCLUSION: This study shows the increased incidence of LA and aCL antibodies in neuroleptic-treated psychotic patients and the possible association between psychosis and antiphospholipid antibodies.

Acute Disease↗

Interaction between free fatty acids and insulin in the acute control of very low density lipoprotein production in humans.

Changes in VLDL triglyceride and VLDL apo B production were determined semiquantitatively in healthy young men by examining the effect of altering plasma insulin and/or FFA levels on the change in the slopes of the specific activity of VLDL [3H]triglyceride glycerol or the 131I-VLDL apo B versus time curves. In one study (n = 8) insulin was infused for 5 h using the euglycemic hyperinsulinemic clamp technique. Plasma FFA levels declined by approximately 80% (0.52 +/- 0.01 to 0.11 +/- 0.02 mmol/liter), VLDL triglyceride production decreased by 66.7 +/- 4.2% (P = 0.0001) and VLDL apo B production decreased by 51.7 +/- 10.6% (P = 0.003). In a second study (n = 8) heparin and Intralipid (Baxter Corp., Toronto, Canada) were infused with insulin to prevent the insulin-mediated fall in plasma FFA levels. Plasma FFA increased approximately twofold (0.43 +/- 0.05 to 0.82 + 0.13 mmol/liter), VLDL triglyceride production decreased to a lesser extent than with insulin alone (P = 0.006) (-31.8 +/- 9.5%, decrease from baseline P = 0.03) and VLDL apo B production did not decrease significantly (-6.3 +/- 13.6%, P = NS). In a third study (n = 8) when heparin and Intralipid were infused without insulin, FFA levels rose approximately twofold (0.53 +/- 0.04 to 0.85 +/- 0.1 mmol/liter), VLDL triglyceride production increased by 180.1 +/- 45.7% (P = 0.008) and VLDL apo B production increased by 94.2 +/- 28.7% (P = 0.05). We confirm our previous observation that acute hyperinsulinemia suppresses VLDL triglyceride and VLDL apo B production in healthy humans. In addition, we have demonstrated that elevation of plasma FFA levels acutely stimulates VLDL production in vivo in healthy young males. Elevating plasma FFA during hyperinsulinemia attenuates but does not completely abolish the suppressive effect of insulin on VLDL production, at least with respect to VLDL triglycerides. Therefore, in normal individuals the acute inhibition of VLDL production by insulin in vivo is only partly due to the suppression of plasma FFA, and may also be due to an FFA-independent process.

Adult↗

VLDL production is decreased to a similar extent by acute portal vs. peripheral venous insulin.

Acute changes in very low-density lipoprotein (VLDL) triglyceride (TG) and VLDL apolipoprotein (apo) B production were examined in 11 healthy young males in response to insulin delivered either by the peripheral venous route or secreted directly by the pancreas. Steady rates of pancreatic insulin secretion were achieved for 5 h by a programmed intravenous tolbutamide infusion, while euglycemia was maintained with a dextrose infusion. Insulin secretory rate was calculated from peripheral C-peptide levels by deconvolution, and, in a subsequent study, exogenous insulin was infused peripherally to match this pancreatic insulin secretory rate in each subject. Changes in VLDL TG and VLDL apo B production were determined semiquantitatively on each occasion by examining the change in slope of the specific activity (SA) of 3H-labeled triglyceride glycerol ([3H]TGG) and 131I-VLDL apo B vs. time curves, respectively, occurring with acute hyperinsulinemia. Plasma-free fatty acids (FFA), TG, apo B, and VLDL TG/VLDL apo B ratio decreased to a similar extent in both studies after the onset of hyperinsulinemia. VLDL TG production decreased significantly in both the tolbutamide (-47.1 +/- 7.3%, P < 0.002) and the exogenous insulin infusion study (-52.8 +/- 12.4%, P < 0.005). VLDL apo B production also decreased significantly in both studies (-58.9 +/- 7.5%, P = 0.0007 and -52.1 +/- 6.8%, P < 0.006, respectively), and there were no significant differences between studies. Tolbutamide was shown to have no independent effect on VLDL TG or VLDL apo B production in four insulin-deficient diabetic subjects.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

A new method for comparing portal and peripheral venous insulin delivery in humans: tolbutamide versus insulin infusion.

We describe a new noninvasive method for comparing insulin secreted acutely by the pancreas vs. a matched peripheral venous insulin infusion in humans. An intravenous tolbutamide infusion algorithm was developed that produced sustained steady rates of portal insulin secretion over 5 h in 11 healthy young men. Plasma glucose levels were maintained in the euglycemic range by adjusting the rate of an iv dextrose (20%) infusion. The pancreatic insulin secretory rate was calculated from peripheral C-peptide levels by deconvolution using standard parameters for a two-compartment mathematical model for C-peptide distribution and metabolism. On a subsequent occasion in the same subject, exogenous insulin was infused peripherally at a rate that matched the earlier tolbutamide-induced pancreatic insulin secretory rate, and euglycemia was maintained with a variable 20% dextrose infusion. The assumption that tolbutamide, when used in this fashion, has no independent insulin-like or insulin-potentiating effect at either low or high levels of peripheral insulinemia, does not affect insulin clearance, and does not suppress peripheral glucagon levels was validated in four patients with insulin-dependent diabetes mellitus. Mean peripheral immunoreactive insulin was significantly higher in the insulin infusion study than in the tolbutamide study (286 +/- 31 vs. 156 +/- 21 pmol/L; P = 0.0001). The dextrose infusion rates required to maintain euglycemia were also higher in the insulin infusion study (0.44 +/- 0.03 vs. 0.32 +/- 0.03 mmol/kg.min; P = 0.003). The MCR of insulin was greater in the tolbutamide infusion vs. the exogenous insulin infusion study (32.6 +/- 2.9 vs. 19.8 +/- 2.2 mL/kg.min; P = 0.0003), probably due to the hepatic first pass effect on insulin clearance when insulin is delivered by the portal route. This noninvasive method can be used in future studies to examine the relative importance of direct hepatic vs. peripheral effects of insulin in controlling hepatic glucose and lipid production.

Adult↗

[Idiopathic intracranial hypertension and tetracycline].

Idiopathic intracranial hypertension (IIH, pseudotumor cerebri) was diagnosed in 4 patients who had been treated with tetracycline. The main symptom was headache, and in all there was papilledema. Symptoms and signs improved after tetracycline was discontinued and acetazolamide treatment started. When a patient receiving tetracycline develops IIH, the medication should be stopped as it may be the cause of the IIH, as appeared to be the case in our 4 patients.

Acetazolamide↗

Familial inclusion body myositis among Kurdish-Iranian Jews.

We report two cases of adult-onset, slowly progressive limb-girdle muscle weakness with a remarkable sparing of quadriceps muscles that developed in patients from different families of Iranian-Kurdish-Jewish origin. Each patient had a similarly affected sibling. The findings by means of muscle biopsies showed abnormalities typical of inclusion body myositis, including abundant lined vacuoles and characteristic cytoplasmic inclusions of 15- to 18-nm filaments. Remarkably, many vacuolated muscle fibers showed immunoreactivity to neural cell adhesion molecule, a fetal muscle antigen. The common origin of these patients from an isolated ethnic group with frequent consanguinity and the familial incidence is indicative of a genetic causation or predisposition, probably with an autosomal recessive inheritance. This familial myopathy is one of several clinical syndromes that share the typical pathological findings of inclusion body myositis. The pathogenic relationship between these different familial forms and the more common sporadic form of inclusion body myositis is not known.

Adult↗

Glucocorticoids and immunosuppressants do not change the prevalence of necrosis and regeneration in mdx skeletal muscles.

Therapeutic doses of methylprednisolone, azathioprine, cyclosporin A, and cyclophosphamide administered to mdx mice between 15 and 45 days of age failed to significantly influence the time course and prevalence of necrosis and regeneration or serum creatine kinase activity. This finding contrasts with previously reported findings of beneficial effects of glucocorticoids in Duchenne muscular dystrophy (DMD). This may indicate that, mechanisms upon which beneficial effects of glucocorticoids depend in DMD, do not operate (sufficiently) in mdx mice.

Animals↗

Major alteration of the pathological phenotype in gamma irradiated mdx soleus muscles.

Two thousand rads of gamma irradiation delivered to the lower legs of ten day old normal and x-chromosome linked muscular dystrophy (mdx) mice caused significant inhibition of tibial bone and soleus muscle fiber growth. In the irradiated mdx solei, there was a major loss of muscle fibers, lack of central nucleation, and some endomysial fibrosis. These features were caused by a failure of regeneration of muscle fibers due to impaired proliferative capacity of satellite cells. Gamma irradiation transforms the late pathological phenotype of mdx muscles, so that in one major aspect (muscle fiber loss) they resemble muscles in Duchenne muscular dystrophy. However, extensive endomysial fibrosis which is another characteristic feature of Duchenne muscular dystrophy did not develop. This experimental model could be useful for the functional investigation of possible beneficial effects of therapeutic interventions in mdx dystrophy.

Animals↗

Inhibition of myosatellite cell proliferation by gamma irradiation does not prevent the age-related increase of the number of dystrophin-positive fibers in soleus muscles of mdx female heterozygote mice.

In skeletal muscles of young mdx female heterozygote mice, there is a mosaic of dystrophin-positive and dystrophin-negative fiber segments. In older animals, there is a marked decline in the number of dystrophin-negative fiber segments. This phenomenon might be due to a fusion of dystrophin-competent satellite cells into the originally dystrophin-negative fiber segments during growth. To study this possibility, soleus muscles of 10-day-old mdx female heterozygotes were gamma irradiated (2000 rads) to inhibit subsequent myosatellite cell proliferation and fusion. In the irradiated soleus muscles of animals at 60 days, the relative amount of dystrophin measured by quantitative immunoblots was not significantly different from that of the contralateral nonirradiated muscles. The prevalence of dystrophin-negative fibers in the 60-day-old irradiated solei was not higher than in the nonirradiated contralateral muscles, implying that dystrophin-competent satellite cell fusion was not a significant factor in the observed conversion. A longitudinal expansion of the cytoplasmic domain of the original dystrophin-competent myonuclei during growth could explain the observed conversion phenomenon.

Aging↗

Dystrophin-deficient mdx muscle fibers are preferentially vulnerable to necrosis induced by experimental lengthening contractions.

Lengthening contractions were induced in the right anterior tibialis muscles (ATM) of anaesthetized normal and mdx (dystrophic) mice by supramaximal, nonfatiguing stimulation of the sciatic nerve for 180 min. In the left ATM of the same animals identical stimulation caused shortening contractions because of a prestimulation Achilles tenotomy. The prevalence of recently necrotic fibers was determined in all stimulated ATM by demonstrating the presence of IgG in the necrotic fibers using immunoperoxidase staining of cryostat sections. The results were compared to unstimulated normal and mdx ATM. A significantly higher rate of necrosis was demonstrated after lengthening contractions in the mdx ATM than normal ATM. Unstimulated normal and mdx ATM have either no or extremely infrequent necrotic fibers. We suggest that the enhanced vulnerability of mdx muscle fibers to lengthening contractions is related to the deficiency of dystrophin, which renders the sarcolemma more susceptible to suffer focal breaks. A similar situation may occur in Duchenne muscular dystrophy.

Animals↗