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Background Halicephalobus gingivalis is a nematode with zoonotic potential which can cause fatal opportunistic infections in various mammals. The parasite has never been diagnosed in Sweden, in any species, prior to the presented case. Case presentation An imported 21-year-old Icelandic mare developed severe neurological signs. The horse was eventually euthanized and submitted for post-mortem examination where severe lesions in the kidneys were noted. Histopathology revealed the presence of H. gingivalis in both kidneys and the brain. Phylogenetic analysis of the parasite determined it to belong to Lineage 1. Conclusions With the occurrence of H. gingivalis in Sweden, the disease should be added to the list of differential diagnoses in cases with acute onset of neurological disease in both horses and other mammals including humans.

Background:Halicephalobus gingivalis is a nematode with zoonotic potential which can cause fatal opportunistic infections in a wide variety of mammals. The parasite has never been diagnosed in Sweden, in any species, prior to the presented case.Case presentation:An imported 21-year-old Icelandic mare developed severe neurological symptoms. The horse was eventually euthanized and submitted for post-mortem examination where severe lesions in the kidneys was noted. Samples for histological examination were submitted, which revealed the presence of H. gingivalis in both renal and brain tissue. Phylogenetic analysis of the parasite determined it to belong to Linage 1.Conclusions:With the occurrence of H. gingivalis in Sweden, the disease should be added to the list of differential diagnoses in cases with acute onset of neurological disease in both horses and mammals including humans.

The first case of African swine fever (ASF) was confirmed in Sweden in September 2023. This article describes the local epidemiology, including the spatiotemporal dynamics of the outbreak and some of the factors that may have contributed to its apparently successful eradication. Upon detection of the outbreak, strict control measures were put in place in a preliminarily defined infected zone. A carcass search, including geo‐localisation, removal, sampling, and destruction of found carcasses, was initiated and a preliminary core area was defined based on the results. Six months after confirmation of the first case, 93 wild boar carcasses had been found in the infected zone, of which 62 tested positive for ASF virus (ASFV). All ASFV‐positive carcasses were found inside the core area. Based on two taphonomy methods, it was assumed that the infection was introduced between early May and late June 2023. The data also indicated that the epidemic curve peaked between mid‐August and mid‐September, with the last death occurring in late September 2023. Based on the average estimated time of death, geo‐localisation of carcasses and two‐dimensional kernel density estimation, clustering in space and time was identified. An online questionnaire with questions about hunting and the wild boar population was sent to all leaders of hunting groups in the infected zone. The results showed that the wild boar population had increased in the last 10 years but with large variations and geographical heterogeneity in space use. Disease introduction through natural wild boar movements was excluded and it was assumed that the long‐distance translocation of the virus had occurred through human activities. A municipal waste collection centre without wild boar‐proof fencing is located close to the epicentre of the outbreak, attracting many wild boar and contributing to the spread of the virus once it had been introduced to the population.

Background An estimated 1.1 million children and adolescents aged under 20 years have type 1 diabetes worldwide. Principal investigators from seven well‐established longitudinal pediatric diabetes registries and the SWEET initiative have come together to provide an international collaborative perspective and comparison of the registries. Work Flow Information and data including registry characteristics, pediatric participant clinical characteristics, data availability and data completeness from the Australasian Diabetes Data Network (ADDN), Danish Registry of Childhood and Adolescent Diabetes (DanDiabKids), Diabetes prospective follow‐up registry (DPV), Norwegian Childhood Diabetes Registry (NCDR), National Paediatric Diabetes Audit (NPDA), Swedish Childhood Diabetes Registry (Swediabkids), T1D Exchange Quality Improvement Collaborative (T1DX‐QI), and the SWEET initiative was extracted up until 31 December 2020. Registry Objectives and Outcomes The seven diabetes registries and the SWEET initiative collectively show data of more than 900 centers and around 100,000 pediatric patients, the majority with type 1 diabetes. All share the common objectives of monitoring treatment and longitudinal outcomes, promoting quality improvement and equality in diabetes care and enabling clinical research. All generate regular benchmark reports. Main differences were observed in the definition of the pediatric population, the inclusion of adults, documentation of CGM metrics and collection of raw data files as well as linkage to other data sources. The open benchmarking and access to regularly updated data may prove to be the most important contribution from registries. This study describes aspects of the registries to enable future collaborations and to encourage the development of new registries where they do not exist.

Extensive angiogenesis, formation of new capillaries from pre-existing blood vessels, is an important feature of malignant glioma. Several antiangiogenic drugs targeting vascular endothelial growth factor (VEGF) or its receptors are currently in clinical trials as therapy for high-grade glioma and bevacizumab was recently approved by the FDA for treatment of recurrent glioblastoma. However, the modest efficacy of these drugs and emerging problems with anti-VEGF treatment resistance welcome the development of alternative antiangiogenic therapies. One potential candidate is histidine-rich glycoprotein (HRG), a plasma protein with antiangiogenic properties that can inhibit endothelial cell adhesion and migration. We have used the RCAS/TV-A mouse model for gliomas to investigate the effect of HRG on brain tumor development. Tumors were induced with platelet-derived growth factor-B (PDGF-B), in the presence or absence of HRG. We found that HRG had little effect on tumor incidence but could significantly inhibit the development of malignant glioma and completely prevent the occurrence of grade IV tumors (glioblastoma).

RHO family proteins are important for the function of inflammatory cells. They are modified with a 20-carbon geranylgeranyl lipid in a process catalyzed by protein geranylgeranyltransferase type I (GGTase-I). Geranylgeranylation is viewed as essential for the membrane targeting and activity of RHO proteins. Consequently, inhibiting GGTase-I to interfere with RHO protein activity has been proposed as a strategy to treat inflammatory disorders. However, here we show that mice lacking GGTase-I in macrophages develop severe joint inflammation resembling erosive rheumatoid arthritis. The disease was initiated by the GGTase-I-deficient macrophages and was transplantable and reversible in bone marrow transplantation experiments. The cells accumulated high levels of active GTP-bound RAC1, CDC42, and RHOA, and RAC1 remained associated with the plasma membrane. Moreover, GGTase-I deficiency activated p38 and NF-κB and increased the production of proinflammatory cytokines. The results challenge the view that geranylgeranylation is essential for the activity and localization of RHO family proteins and suggest that reduced geranylgeranylation in macrophages can initiate erosive arthritis.

Background Technetium-labeled agents, which are most often used for assessing myocardial perfusion in myocardial perfusion scintigraphy (MPS), are cleared by the liver and excreted by the biliary system. Spillover from extra-cardiac activity into the myocardium, especially the inferior wall, might conceal defects and lower the diagnostic accuracy of the study. The objective was to determine rules of thumb for when reacquisition is useful due to high extra-cardiac uptake, i.e., when interpretation of the studies was affected by poor image quality. Methods Patients admitted to MPS at any of the three study sites, who also underwent a reacquisition due to high extra-cardiac uptake were included. Image quality was assessed by ten technologists on a scale ranging from 1 to 5. Interpretations regarding the presence/absence of ischemia/infarction, including the certainty of the diagnosis, were made by three physicians. Results There was a statistically significant increase in image quality between the first and the repeated acquisition (1,256 cases of increased quality at the repeated study (66%), 134 cases of decreased quality at the repeated study (7%), 510 cases of unchanged quality (27%) P < 0.0001). The number of equivocal studies, interpreted by physicians, decreased when evaluating the repeated studies compared to the first studies for all physicians, both for the interpretations of ischemia and for infarction. Receiver operating characteristic analyses revealed that for both endpoints (ischemia, infarction) and all physicians, the optimal cutoff point for performing a reacquisition was between quality categories 2 and 3. Conclusion This study indicates that repeat acquisition is useful when (1) the intensity of the extra-cardiac uptake is equal to or higher than the cardiac uptake when there is no separation between the extra-cardiac uptake and the inferior cardiac wall and (2) when the intensity of the extra-cardiac uptake is higher than the cardiac uptake when there is a separation between the extra-cardiac uptake and the inferior wall of less than one cardiac wall.

Wear particles from the bearing surfaces of joint implants are one of the main limiting factors for total implant longevity. Si3N4 is a potential wear resistant alternative for total joint replacements. In this study, SixNy-coatings were deposited on cobalt chromium-discs and Si-wafers by a physical vapour deposition process. The tribological properties, as well as surface appearance, chemical composition, phase composition, structure and hardness of these coatings were analysed. The coatings were found to be amorphous or nanocrystalline, with a hardness and coefficient of friction against Si3N4 similar to that found for bulk Si3N4. The low wear rate of the coatings indicates that they have a potential as bearing surfaces of joint replacements. The adhesion to the substrates remains to be improved.

The structural requirements for generation of amyloid from the plasma protein transthyretin (TTR) are not known, although it is assumed that TTR is partly misfolded in amyloid. In a search for structural determinants important for amyloid formation, we generated a TTR mutant with high potential to form amyloid. We demonstrated that the mutant represents an intermediate in a series of conformational changes leading to amyloid. Two monoclonal antibodies were generated against this mutant; each displayed affinity to ex vivo TTR and TTR mutants with amyloidogenic folding but not to wild-type TTR or mutants exhibiting the wild-type fold. Two cryptic epitopes were mapped to a domain of TTR, where most mutations associated with amyloidosis occur and which we propose is displaced at the initial phase of amyloid formation, opening up new surfaces necessary for autoaggregation of TTR monomers. The results provide direct biochemical evidence for structural changes in an amyloidogenic intermediate of TTR.

The structural requirements for generation of amyloid from the plasma protein transthyretin (TTR) are not known, although it is assumed that TTR is partly misfolded in amyloid. In a search for structural determinants important for amyloid formation, we generated a TTR mutant with high potential to form amyloid. We demonstrated that the mutant represents an intermediate in a series of conformational changes leading to amyloid. Two monoclonal antibodies were generated against this mutant; each displayed affinity to ex vivo TTR and TTR mutants with amyloidogenic folding but not to wild-type TTR or mutants exhibiting the wild-type fold. Two cryptic epitopes were mapped to a domain of TTR, where most mutations associated with amyloidosis occur and which we propose is displaced at the initial phase of amyloid formation, opening up new surfaces necessary for autoaggregation of TTR monomers. The results provide direct biochemical evidence for structural changes in an amyloidogenic intermediate of TTR.