Search

In this study, highly porous biocompatible and biodegradable zinc, iron and magnesium alloy foams were fabricated for temporary implant and scaffold applications. Specimens with open porous structure were fabricated by powder metallurgy based space holder method. Mg, Fe and Zn are the main bioabsorable metals. Mg alloys biodegrade too fast with H2 evolution. Biodegradation rate of Fe alloys is too slow, and by-products remain inside the body. Zn alloys show biodegradation rates in the middle of Mg and Fe alloys, and their biodegradation by-products are bioresorbable. Here several Fe, Zn, and Mg alloys were manufactured, and comparatively characterized. Effects of alloying elements on biodegradation, corrosion and mechanical properties were investigated separately. As the mechanical properties of temporary implants must decrease slowly, the variation of mechanical properties with time in the foams was investigated. Corrosion performance was tested in simulated body fluid. Biodegradation rate was investigated by using weight loss and metal ion release measurements. The corrosion and biodegradation rates of Zn specimens were lower than in Mg specimens and higher than in Fe specimens. Fe2+, Zn2+ and Mg2+ ion release amounts were lower than the upper limit for humans. [ABSTRACT FROM AUTHOR]

Background: It has long been known that the majority of patients with multiple sclerosis (MS) display an intrathecal, polyspecific humoral immune response to a broad panel of neurotropic viruses. This response has measles virus, rubella virus and varicella zoster virus as its most frequent constituents and is thus referred to as the MRZ reaction (MRZR). Objective: Re-evaluation of the specificity of MRZR as a marker of MS. Methods: Structured review of the existing English-, German- and Spanish-language literature on MRZR testing, with evaluation of MRZR in a cohort of 43 unselected patients with MS and other neurological diseases as a proof of principle. Results: A positive MRZ reaction, defined as a positive intrathecal response to at least two of the three viral agents, was found in 78% of MS patients but only in 3% of the controls ( p < 0.00001), corresponding to specificity of 97%. Median antibody index values were significantly lower in non-MS patients (measles, p < 0.0001; rubella, p < 0.006; varicella zoster, p < 0.02). The 30 identified original studies on MRZR reported results from 1478 individual MRZR tests. A positive MRZR was reported for 458/724 (63.3%) tests in patients with MS but only for 19/754 (2.5%) tests in control patients ( p < 0.000001), corresponding to cumulative specificity of 97.5% (CI 95% 96-98.4), cumulative sensitivity of 63.3% (CI 95% 59.6-66.8) (or 67.4% [CI 95% 63.5-71.1] in the adult MS subgroup), a positive likelihood ratio of 25.1 (CI 95% 16-39.3) and a negative likelihood ratio of 0.38 (CI 95% 0.34-0.41). Of particular note, MRZR was absent in 52/53 (98.1%) patients with neuromyelitis optica or MOG-IgG-positive encephalomyelitis, two important differential diagnoses of MS. Conclusion: MRZR is the most specific laboratory marker of MS reported to date. If present, MRZR substantially increases the likelihood of the diagnosis of MS. Prospective and systematic studies on the diagnostic and prognostic impact of MRZR testing are highly warranted. [ABSTRACT FROM AUTHOR]

Copyright of Anaesthesist is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

BACKGROUND/OBJECTIVES: Glycogen storage disease type I (GSD I) is an autosomal recessive metabolic disorder caused by defects in the glucose-6-phosphatase complex. Deficient activity in the glucose-6-phosphatase-α catalytic unit characterizes GSD Ia and defects in the glucose-6-phosphate transporter protein characterize GSD Ib. Type Ia involves the liver, kidney and intestine (and Ib also leukocytes), and the clinical manifestations are hepatomegaly, failure to thrive, severe fasting hypoglycemia within 3-4 h after a meal, hyperlactatemia, hyperuricemia and hyperlipidemia. The aim of the present study was to examine the safety and efficacy of a continuous subcutaneous glucose monitoring system to determine the magnitude and significance of hypoglycemia in GSD I and to evaluate the efficacy of the revised dietary treatment. SUBJECTS/METHODS: Sixteen children with GSD I were studied over a 72-h period. Continuous glucose monitoring (CGM) was repeated in all patients 3–6 months after the first monitoring to examine the effects of revised dietary instructions on glycemic control. RESULTS: All the patients completed the study without any major adverse events. Significant periods of asymptomatic hypoglycemia (below 4 mmol/l, 70 mg/dl) were noted. There was a close correlation between CGM sensor and capillary blood glucose values measured by a glucometer. CGM indicated a considerable reduction in duration of hypoglycemia, liver size and improvements in secondary metabolic derangements such as hyperlacticacidemia and hyperlipidemia. CONCLUSIONS: CGM could be applied in the clinical setting to help the physician to identify hypoglycemic events, and repeated CGM may serve as a safe and useful tool for the assessment of the long-term management of patients with GSD I. [ABSTRACT FROM AUTHOR]

Cerebral venous thrombosis (CVT) is caused by various etiologies. In Mediterranean and Middle Eastern countries, Behçet’s disease (BD) is one of the leading causes of CVT. We aimed to evaluate any differences in CVT patients with and without BD. All registered patients with CVT were evaluated retrospectively. Clinical, neuroradiological findings and follow-up data were compared between patients with BD and patients with other etiologies. There were 36 patients with CVT and BD, and 32 patients with CVT related to other etiological causes. BD patients were younger (median age at onset 26 vs. 39 years; P < 0.001), and there was a male preponderance (28 males, 8 females) as compared to the non-BD group (10 males, 22 females; P < 0.001). Onset was frequently acute in the non-BD group, and it was subacute or chronic in the BD group. Hemi/quadriparesis, aphasia and seizures were significantly more common ( P < 0.001) in the non-BD group. In the BD group 94% of the patients presented with symptoms of isolated intracranial hypertension ( P < 0.001). Venous infarcts were observed in 63% of the patients with other causes and in 6% of the patients with BD ( P < 0.001). At admission 97% of the patients in the BD group and 41% of the patients in the non-BD group had a modified Rankin score of 0–2. Outcome was good in all of the patients with BD and in 91% of patients with other causes. Clinical recurrences were seen in six patients with BD and in one patient without BD. CVT associated with BD has a subacute onset, mostly presents with signs of isolated intracranial hypertension and venous infarction rarely develops; these features distinguish CVT due to BD from those with other causes. [ABSTRACT FROM AUTHOR]

Two observers, blinded to the patient’s neurological status, reviewed 134 MRI studies of 98 consecutive patients with Behçet’s disease (BD), to define imaging patterns and to look for any relationship between the MRI findings and the timing of the examination in patients with differing courses of disease. There were 43 patients with overt parenchymal central nervous system (CNS) involvement, 22 with attacks and remissions, 15 with secondary progressive and six with primary progressive disease; 14 had raised intracranial pressure (RICP). Of the remaining 41 patients without specific neurological complaints, 16 had abnormalities on examination (silent CNS involvement) and 25 did not. During an acute CNS attack, the most common finding was a large lesion in the brain-stem or basal ganglia, extending to the diencephalon. On MRI performed after remission of an acute attack or during secondary progression, the same sites were affected, but the lesions were smaller or scattered, with less clearly defined margins. In primary progressive disease or silent CNS involvement, the cerebral white matter was most commonly involved, but almost half the MRI studies were normal. The brain parenchyma was abnormal in only one of the patients with RICP. MRI was normal in all but three patients without clinical CNS involvement, in whom it showed a few millimetric white-matter lesions. Brain-stem atrophy was seen in 15 patients examined >1 year after an initial parenchymal CNS episode, with secondary progressive cases predominating. [ABSTRACT FROM AUTHOR]

Anemia is a frequent complication of cancer and its treatment. A defect in erythropoietin production has been advocated as being the main cause of anemia in cancer patients. We studied serum erythropoietin levels in 74 patients with solid tumors and in a control group consisting of 20 otherwise healthy individuals without any malignancy, who have only iron deficiency anemia. Serum erythropoietin levels were measured by enzyme immunoassay in cancer patients without anemia (n=34), and in anemic cancer patients (n=40); either receiving chemotherapy (n=21) or not (n=19). Anemic cancer patients were found to have decreased response of erythropoietin for a given hemoglobin level (mean, 40.1+/-34.7 u/ml), compared with the patients having only iron deficiency anemia (mean, 69.7+/-68.6 u/ml) (P<0.05). In patients with iron deficiency anemia having no malignancy, erythropoietin response was remarkably high and inversely correlated with the level of hemoglobin (r=-0.69; P=0. 05). Although there was no correlation between hemoglobin and erythropoietin response in cancer anemia (r=-0.07), serum levels of erythropoietin were found to be higher in anemic cancer patients (mean, 40.1+/-34.7 u/ml), compared with cancer patients with normal hemoglobin values (mean, 19.96+/-18.4 u/ml). There was not any statistically significant difference between erythropoietin levels in anemic cancer patients with or without chemotherapy (mean, 43. 7+/-37.7 u/ml and 41.9+/-30.08 u/ml respectively; P>0.05). No difference in serum erythropoietin levels were noted in patients treated with cisplatin or non-cisplatin containing regimens (mean, 48.36+/-33.12 u/ml and 38.55+/-43.52 u/ml, respectively; P>0.05). In this study, we demonstrated that anemia in cancer patients was caused by blunted erythropoietin response, rather than its quantitative deficiency. Serial measurements, however, should be considered in patients receiving chemotherapy. [ABSTRACT FROM AUTHOR]

Two neuroradiologists reviewed MRI studies of 34 patients with neuro-Behçet's disease (NBD), 22 with multiple sclerosis (MS) and 7 with systemic lupus erythematosus (SLE) with central nervous system involvement, masked to the clinical diagnosis, age and sex of the patients. Of the patients with NBD 12 were in an acute attack; the others had chronic disease. MRI was assessed using a set of criteria, looking at atrophy, the site of discrete parenchymal lesions, regions of predominant involvement and the extent of the lesion(s). The observers also made a guess at the clinical diagnosis. The brain stem and/or basal ganglia were the most predominantly involved sites in all patients with acute NBD; 75 % of these lesions were large and confluent, mainly extending from the brain stem to the diencephalon and basal ganglia. However, in chronic cases, the predominant involvement was in the brain stem and/or basal ganglia in only 36 %, and in cerebral hemisphere white matter in another 36 %; 27 % of these patients showed no parenchymal lesion. Hemisphere white-matter lesions were equally distributed between periventricular and other areas in NBD, while in MS more were periventricular, and in SLE more were nonperiventricular. Brain-stem atrophy was seen in 21 % of patients with NBD, with a specificity of 96.5 %. In the absence of cortical atrophy, its specificity was 100 %. The attempt at making a radiological diagnosis was successful in all cases of acute NBD and 95.5 % of patients with MS, but in only 40 % of patients with chronic NBD. Most of this latter groups MRI studies were interpreted as MS. An extensive lesion involving the brain stem and basal ganglia seemed to be diagnostic of acute NBD. However, hemisphere white-matter lesions could not be differentiated from those in MS. [ABSTRACT FROM AUTHOR]

Subacute sclerosing panencephalitis (SSPE) is a progressive, slow virus infection of the brain, caused by the measles virus, attacking children and young adults. We investigated 15 patients with SSPE by MRI, with 5 normal and 10 pathological results. In the early period, lesions were in the grey matter and subcortical white matter. They were asymmetrical and had a predilection for the posterior parts of the hemispheres. Later, high-signal changes in deep white matter and severe cerebral atrophy were observed. Parenchymal lesions significantly correlated with the duration of disease. A significant relationship between MRI findings and clinical stage was observed in the 1st year of the disease. [ABSTRACT FROM AUTHOR]

Our aim was to test the reliability of interpreting MRI studies in neuro-Behçet's disease (NBD) and to determine the sensitivity and specificity of different MRI findings. We prospectively studied 50 patients: 24 had chronic NBD, 12 multiple sclerosis, 5 vasculitis other than Behçet's disease (BD) and 9 patients had BD without neurological involvement. MRI studies were performed according to a standard protocol with a 0.2 T imager. Two neuroradiologists, blinded to the diagnosis, age and sex of the subjects, reviewed the films independently, twice. Separate assessments were made for a set of items: dural sinus pathology, widening of ventricles and sulci, brain stem atrophy, lesions of the cerebral cortex, discrete lesions of deep white matter, basal ganglia, brain stem and cerebellum and the presence of smooth periventricular high-signal foci. Intraobserver agreement was substantial or better, and interobserver agreement moderate to substantial for most items. In these patients with chronic NBD we found low sensitivity on all assessed items. Dural sinus pathology or brain stem atrophy were highly specific, but parenchymal lesions in different sites had uniformly low specificity. [ABSTRACT FROM AUTHOR]

Anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis has been recently identified as a fulminant encephalopathy, presenting with a variety of symptoms including behavioral change, amnesia and seizures suggesting cortical gray matter involvement. A 42-year-old woman presented with acute-onset clinical and magnetic resonance imaging (MRI) findings indicating brainstem and diencephalon involvement. Her neuropsychological examination revealed mild frontal dysfunction with no memory impairment. Detailed diagnostic workup proved negative except for serum/cerebrospinal fluid (CSF) NMDAR-antibodies and increased activity in inguinal and pelvic lymph nodes on positron-emission tomography (PET) examination. The symptoms and MRI findings completely resolved following steroid treatment. A 38-year-old woman presented with migraine-type headache and episodes of forgetfulness. Her brain MRI and neuropsychological examination were normal and diagnostic workup was unremarkable. N-methyl-D-aspartate receptor antibodies were identified in her sera and her symptoms spontaneously resolved within few months. Our cases suggest that anti-NMDAR encephalitis might present with minimal cognitive impairment, no apparent cortical gray matter involvement, a mild clinical course and without the classical clinical features of the disease. [ABSTRACT FROM AUTHOR]

A 40-year-old man with known definite Behçet's disease (BD) was admitted with confusional state which had started 4 days before admission with an acute headache and vomiting. Neurological examination revealed confusion, stiff neck, right facial weakness, left hemiparesis, dysartria and truncal ataxia. CSF was haemorrhagic and xanthochromic. Cranial CT scans were negative, but MRI showed a right pontine hyperintense lesion on T2-weighted images. Bilateral carotid angiograms were normal. Right vertebral angiogram showed findings consistent with a dissection at the V segment of the artery. At the level of the fifth cervical vertebra, a radiculomedullary branch of the vertebral artery with an ancurysmal dilatation in its intradural portion was notable. This case shows that, in BD, aneurysn formation can also occur in a spinal artery and spontaneous vertebral artery dissection can be seen. [ABSTRACT FROM AUTHOR]