| 1. |
- Robinson, Yohan, 1977, et al.
(författare)
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Erythropoiesis in multiply injured patients.
- 2006
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Ingår i: The Journal of trauma. - : Ovid Technologies (Wolters Kluwer Health). - 0022-5282 .- 1529-8809. ; 61:5, s. 1285-91
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Forskningsöversikt (refereegranskat)abstract
- Posttraumatic anemia in multiply injured patients is caused by hemorrhage, reduced red blood cell survival, and impaired erythropoiesis. Trauma-induced hyperinflammation causes impaired bone-marrow function by means of blunted erythropoietin (EPO) response, reduced iron availability, suppression and egress of erythroid progenitor cells. To treat posttraumatic anemia in severely injured patients, symptomatic therapy by blood transfusion is not sufficient. Furthermore, EPO, iron, and the use of red cell substitutes should be considered. The posttraumatic systemic inflammatory response syndrome (SIRS) induces posttraumatic anemia. Thus, a worsening of SIRS by a "second-hit" through blood transfusion ought to be avoided.
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| 2. |
- Robinson, Yohan, 1977, et al.
(författare)
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Postoperative multisegmental lumbar discitis treated by staged ventrodorsoventral intervention.
- 2007
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Ingår i: Surgical infections. - : Mary Ann Liebert Inc. - 1096-2964 .- 1557-8674. ; 8:5, s. 529-34
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Forskningsöversikt (refereegranskat)abstract
- Postoperative spinal infections are relatively rare. They can become life-threatening.A 56-year-old man developed multisegmental spinal infection with methicillin-resistant Staphylococcus aureus after discectomy at L3/4. A staged ventrodorsoventral intervention was needed for radical debridement and stabilization. After femoral head necrosis developed as a result of the infection, a Girdlestone hip was maintained until the joint was aseptic and a hip prosthesis could be implanted. Two years postoperatively, the patient remained free of infection recurrence.Radical debridement and a tightly controlled antibiotic regimen are necessary for the management of postoperative spinal infections. This should include staged interventions until recovery from infection is possible. Early intervention can prevent systemic sepsis caused by widespread bacterial dissemination.
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| 3. |
- Birgander, Mats, et al.
(författare)
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Relationship Between Mild Primary Hyperparathyroidism and Left Ventricular Structure and Diastolic Performance
- 2009
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Ingår i: The Endocrinologist. - 1539-9192. ; 19:4, s. 187-191
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Forskningsöversikt (refereegranskat)abstract
- Aim: This study aims to investigate cardiac structure and function in patients with asymptomatic primary hyperparathyroidism (pHPT) and if there is any relation to severity regarding serum levels of calcium (Ca) and parathyroid hormone. Methods and Results: We consecutively included 50 patients (mean age 62.9 +/- 11 years, 45 women) with clinically diagnosed pHPT. We prospectively recruited 50 healthy control subjects, matched for age and sex. Standard transthoracic echocardiographic examination was performed using the 4 standard views and structural parameters as well as left ventricular (LV) systolic and diastolic function was determined. Mean LV ejection fraction and atrioventricular plane displacement were on average normal and did not differ between patients and controls. However, pHPT patients had significantly greater LV mass (148 +/- 37 vs. 127 +/- 29 g, P = 0.002), LV end diastolic area (81 +/- 20 vs. 68 +/- 18 cm(2), p = 0.003), LV posterior wall diameter (8.9 +/- 1 vs. 8.1 +/- 1 min, P = 0.006), and LA size (21 +/- 3 vs. 19 +/- 2 mm, P < 0.001). A moderate to severe LV diastolic filling impairment was present in substantially more pHPT patients, compared with control subjects (36% vs. 4%, P < 0:001). Conclusion: Patients with asymptomatic pHPT showed LV structural changes and impaired LV diastolic function.
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| 4. |
- Halgamuge, Malka N., et al.
(författare)
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Comparison Between Two Models for Interactions Between Electric and Magnetic Fields and Proteins in Cell Membranes
- 2009
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Ingår i: Environmental Engineering Science. - : Mary Ann Liebert Inc. - 1092-8758 .- 1557-9018. ; 26:10, s. 1473-1480
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Forskningsöversikt (refereegranskat)abstract
- Investigations on exposure to electromagnetic have generated conflicting results both in epidemiological and laboratory studies, leaving their possible health consequences largely inconclusive. One of the well-reported reasons for the discrepancies is that there is no generally accepted theory to describe the interactions between the very weak electromagnetic fields and the living cells. This work presents a critical evaluation of three theories that describes the effects of weak electromagnetic fields on channel proteins in the cell membrane. The forced ion vibration model appears to explain the opening of ion channel proteins for exposures to low-frequency magnetic fields in the mili-Tesla range. No resonance frequencies or amplitude window effects are predicted in this method. We identify inconsistencies in the forced vibration model and show that the environmental magnetic fields that would be required to elicit opening of channel proteins are much stronger than predicted by the proposers of this model. The Ion Parametric Resonance model predicts a biological response at well-defined resonance frequencies for magnetic fields exceeding about 10 micro-Tesla. The oscillating magnetic field is assumed to act on proteins together with the earth's static magnetic field. This model predicts amplitude windows. We explain how a purely magnetic interaction, where in a two-stage ion magnetic resonance model, the conformation of a protein is changed under the influence of ions attached to its surface, which in turn, changes the function of the protein, can overcome the inherent signal-to-noise problem caused by electric thermal noise. The hydrogen nuclear polarization model predicts a biological response for oscillating magnetic field strengths above 0.1 micro-Tesla. The presence of a static magnetic field is required, and biological effects can be expected for frequencies below a few hundred hertz. All models except the forced vibration model can be applied for amplitude modulated microwaves.
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| 5. |
- Heyde, Christoph-E, et al.
(författare)
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Pitfalls and complications in the treatment of cervical spine fractures in patients with ankylosing spondylitis.
- 2008
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Ingår i: Patient safety in surgery. - : Springer Science and Business Media LLC. - 1754-9493. ; 2
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Forskningsöversikt (refereegranskat)abstract
- Patients with ankylosing spondylitis are at significant risk for sustaining cervical spine injuries following trauma predisposed by kyphosis, stiffness and osteoporotic bone quality of the spine. The risk of sustaining neurological deficits in this patient population is higher than average. The present review article provides an outline on the specific injury patterns in the cervical spine, diagnostic algorithms and specific treatment modalities dictated by the underlying disease in patients with ankylosing spondylitis. An emphasis is placed on the risks and complication patterns in the treatment of these rare, but challenging injuries.
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| 6. |
- Lerner, Ulf H
(författare)
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New molecules in the tumor necrosis factor ligand and receptor superfamilies with importance for physiological and pathological bone resorption
- 2004
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Ingår i: Critical Reviews in Oral Biology and Medicine. - Alexandria : International association for dental research (IADR). - 1045-4411 .- 1544-1113. ; 15:2, s. 64-81
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Forskningsöversikt (refereegranskat)abstract
- Osteoclasts are tissue-specific polykaryon bone-resorbing cells derived from the monocyte/macrophage hematopoietic lineage with specialized functions required for the adhesion of the cells to bone and the subsequent polarization of the cell membrane, secretion of acid to dissolve mineral crystals, and release of proteolytic enzymes to degrade the extracellular matrix proteins. Most pathological conditions in the skeleton lead to loss of bone due to excess osteoclastic bone resorption, including periodontal disease, rheumatoid arthritis, and osteoporosis. In rare cases, most of them genetic, patients with osteopetrosis exhibit sclerotic bone due either to a lack of osteoclasts or to non-functional osteoclasts. Mainly because of phenotypic findings in genetically manipulated mice or due to spontaneous mutations in humans, mice, and rats, several genes have been discovered as being crucial for osteoclast formation and activation. Recent breakthroughs in our understanding of osteoclast biology have revealed the critical roles in osteoclast differentiation played by RANKL, RANK, and OPG, three novel members of the tumor necrosis factor ligand and receptor superfamilies. The further study of these molecules and downstream signaling events are likely to provide a molecular basis for the development of new drugs for the treatment of diseases with excess or deficient osteoclastic bone resorption.
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| 7. |
- Duan, Rui-Dong
(författare)
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Alkaline sphingomyelinase: An old enzyme with novel implications.
- 2006
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Ingår i: Biochimica et Biophysica Acta - Molecular and Cell Biology of Lipids. - : Elsevier BV. - 1388-1981. ; 1761:3, s. 281-291
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Forskningsöversikt (refereegranskat)abstract
- Alkaline sphingomyelinase (alk-SMase) is present in the intestinal tract and additionally human bile. It hydrolyses sphingomyelin in both intestinal lumen and the mucosal membrane in a specific bile salt dependent manner. The enzyme was discovered 36 years ago but got real attention only in the last decade, when sphingomyelin metabolism was realized to be a source of multiple lipid messengers, and when dietary sphingomyelin was found to inhibit colonic tumorigenesis in animals. The enzyme shares no structural similarity with other SMases and belongs to the nucleotide pyrophosphatase/phosphodiesterase family. The enzyme is of specific properties, such as bile salt dependency, trypsin resistance, high stability, and tissue specific expression. In the colon, the enzyme may play antiproliferative and antiinflammatory roles through generating ceramide, reducing the formation of lysophosphatidic acid, and inactivating platelet-activating factor. The enzyme is down regulated in human long-standing ulcerative colitis and colonic adenocarcinoma, and mutation of the enzyme has been found in colon cancer cells. In the small intestine, alk-SMase is the key enzyme for sphingomyelin digestion. The hydrolysis of sphingomyelin may affect the cholesterol uptake and have impact on sphingomyelin levels in plasma lipoproteins. The review summarizes the new information of alk-SMase from biochemical, cell and molecular biological studies in the last decade and evaluates its potential implications in development of colon cancer, inflammatory bowel diseases, and atherosclerosis. (c) 2006 Elsevier B.V. All rights reserved.
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| 8. |
- Ekegren, Titti, et al.
(författare)
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Clinical perspectives of high-resolution mass spectrometry-based proteomics in neuroscience: exemplified in amyotrophic lateral sclerosis biomarker discovery research.
- 2008
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Ingår i: Journal of mass spectrometry : JMS. - : Wiley. - 1076-5174 .- 1096-9888. ; 43:5, s. 559-71
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Forskningsöversikt (refereegranskat)abstract
- Biomarker discovery is a central application in today's proteomic research. There is an urgent need for valid biomarkers to improve diagnostic tools and treatment in many disorders, such as the rapidly progressing neurodegenerative disorder amyotrophic lateral sclerosis (ALS) that has a fatal outcome in about 3 years and yet no curative treatment. Screening for clinically relevant biomarkers puts high demands on high-throughput, rapid and precise proteomic techniques. There is a large variety in the methods of choice involving mainly gel-based approaches as well as chromatographic techniques for multi-dimensional protein and peptide separations followed by mass spectrometry (MS) analysis. This special feature article will discuss some important aspects of MS-based clinical proteomics and biomarker discovery in the field of neurodegenerative diseases and ALS research respectively, with the aim to provide a prospective view on current and future research aspects in the field. Furthermore, examples for application of high-resolution MS-based proteomic strategies for ALS biomarker discovery will be demonstrated with two studies previously reported by our group. These studies include among others, utilization of capillary liquid chromatography-Fourier transform ion cyclotron resonance mass spectrometry (LC-FTICR-MS) for advanced protein pattern classification in cerebrospinal fluid (CSF) samples of ALS patients as well as highly sensitive protein identification in minimal amounts of postmortem spinal cord tissue and laser micro-dissected motor neurons using FT-ICR-MS in conjunction with nanoflow LC coupled to matrix-assisted laser desorption ionization time-of-flight tandem mass spectrometry (LC-MALDI-TOF-TOF-MS).
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| 9. |
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| 10. |
- Ragnarsdottir, Bryndis, et al.
(författare)
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TLR- and CXCR1-dependent innate immunity: insights into the genetics of urinary tract infections.
- 2008
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Ingår i: European Journal of Clinical Investigation. - : Wiley. - 0014-2972 .- 1365-2362. ; 38 Suppl 2, s. 12-20
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Forskningsöversikt (refereegranskat)abstract
- The susceptibility to urinary tract infection (UTI) is controlled by the innate immune response and Toll like receptors (TLRs) are the sentinels of this response. If productive, TLR4 signalling may initiate the symptomatic disease process. In the absence of TLR4 signalling the infected host instead develops an asymptomatic carrier state. The activation of mucosal TLR4 is also influenced by the properties of the infecting strain, and pathogens use their virulence factors to trigger 'pathogen-specific' TLR4 responses in the urinary tract but do not respond to the asymptomatic carrier strains in patients with asymptomatic bacteriuria (ABU). The TLR4 dependence has been demonstrated in mice and the relevance of low TLR4 function for protection for human disease was recently confirmed in children with asymptomatic bacteriuria, who expressed less TLR4 than age matched controls. Functional chemokines and functional chemokine receptors are crucial for neutrophil recruitment, and for the neutrophil dependent bacterial clearance. Interleukin (IL)-8 receptor deficient mice develop acute septic infections and chronic tissue damage, due to aberrant neutrophil function. This mechanism is relevant for human UTI as pyelonephritis prone children express low levels of the human CXCL8 (Il-8) receptor, CXC chemokine receptor 1 (CXCR1) and often have heterozygous CXCR1 polymorphisms. This review illustrates how intimately the innate response and the susceptibility to UTI are linked and sophisticated recognition mechanisms that rely on microbial virulence and on host TLR4 and CXCR1 signalling.
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