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The presence of Global Navigation Satellite System (GNSS) interference poses a significant risk to both GNSS and the infrastructures that depend on them. This article describes how an existing GNSS infrastructure, the Swedish Continuously Operating Reference Stations network SWEPOS with more than 500 stations, can be leveraged to control the quality of GNSS signals and to be able to detect interferences in GNSS and adjacent frequency bands. This study introduces a SWEPOS-based automatic system that effectively detects GNSS interference by examining the signal-to-noise ratio (SNR) of Global Positioning System, Globalnaya Navigatsionnaya Sputnikovaya Sistema, Galileo, and BeiDou frequency bands. By comparing the SNR of tracked satellites against historical data, the system detects radio frequency interference (RFI) by statistically characterizing the SNR of simultaneously tracked satellites. Furthermore, based on the SNR characteristics across satellites, the system distinguishes between RFI and non-RFI sources. The effectiveness of the detection system is demonstrated through both simulated signal interference waves and real-world interference events.

Abstract Background Polycystin-2 (PC2), encoded by the gene that is mutated in autosomal dominant polycystic kidney disease (ADPKD), functions as a calcium (Ca2+) permeable ion channel. Considerable controversy remains regarding the subcellular localization and signaling function of PC2 in kidney cells. Methods We investigated the subcellular PC2 localization by immunocytochemistry and confocal microscopy in primary cultures of human and rat proximal tubule cells after stimulating cytosolic Ca2+ signaling. Plasma membrane (PM) Ca2+ permeability was evaluated by Fura-2 manganese quenching using time-lapse fluorescence microscopy. Results We demonstrated that PC2 exhibits a dynamic subcellular localization pattern. In unstimulated human or rat proximal tubule cells, PC2 exhibited a cytosolic/reticular distribution. Treatments with agents that in various ways affect the Ca2+ signaling machinery, those being ATP, bradykinin, ionomycin, CPA or thapsigargin, resulted in increased PC2 immunostaining in the PM. Exposing cells to the steroid hormone ouabain, known to trigger Ca2+ oscillations in kidney cells, caused increased PC2 in the PM and increased PM Ca2+ permeability. Intracellular Ca2+ buffering with BAPTA, inositol 1,4,5-trisphosphate receptor (InsP3R) inhibition with 2-aminoethoxydiphenyl borate (2-APB) or Ca2+/Calmodulin-dependent kinase inhibition with KN-93 completely abolished ouabain-stimulated PC2 translocation to the PM. Conclusions These novel findings demonstrate intracellular Ca2+-dependent PC2 trafficking in human and rat kidney cells, which may provide new insight into cyst formations in ADPKD.

Abstract Background Interleukin-18 is a pro-inflammatory cytokine suspected to be associated with atherosclerosis and its complications. We had previously shown that one single nucleotide polymorphism (SNP) of the IL18 gene was associated with cardiovascular disease (CVD) through an interaction with smoking. As a further step for elucidating the contribution of the IL-18 pathway to the etiology of CVD, we here investigated the association between the genetic variability of two IL-18 receptor genes, IL18R1 and IL18RAP, with the risk of developing CVD. Methods Eleven tagging SNPs, 5 in IL18R1 and 6 in IL18RAP, characterizing the haplotypic variability of the corresponding genes; were genotyped in 5 European prospective CVD cohorts including 1416 cases and 1772 non-cases, as part of the MORGAM project. Both single-locus and haplotypes analyses were carried out to investigate the association of these SNPs with CVD. Results We did not find any significant differences in allele, genotype and haplotype frequencies between cases and non-cases for either of the two genes. Moreover, the search for interactions between SNPs located in different genes, including 5 IL18 SNPs previously studied in the MORGAM project, and between SNPs and environmental factors remained unfruitful. Conclusion Our analysis suggests that the variability of IL18R1 and IL18RAP genes are unlikely to contribute to modulate the risk of CVD.

Iliac crest bone biopsies in patients with chronic renal failure with severely disturbed renal function were measured with regard to osteoclast activity and active and inactive osteoid. In none of the 21 patients had hemodialysis been applied. In uremia cases, as earlier demonstrated in hemodialysis cases, the alkaline phosphatase and the parathyroid hormone activity were the best variables for prediction of bone complications. However, none of the laboratory variables or all taken together could predict the type of bone changes. The osteoclast activity was less than in hemodialysis cases indicating that secondary hyperparathyroidism may be less important in the non-hemodialysed cases.

The osteoclast activity (number of osteoclasts per surface bone section) and the osteoid abundance (percentage of trabecular bone surface covered with osteoid) were measured in iliac crest biopsies from 38 men with alcoholism. These patients had histories of decades of over-consumption of alcohol and repeated injuries, as well as medical complications. In older individuals, the bone mineral content of the forearms decreased so that the reduction in relation to age was comparable to that of women rather than men. Osteoid seams increased in thickness only in alcoholics who had previously undergone gastric resection. Otherwise, there were no differences in osteoid seams in alcoholics and control nonalcoholism patients. Osteoclasts, however, were more abundant in the iliac crest biopsies from alcoholics than from the nonalcoholic group. Osteoclasts were also more numerous in alcoholics who had undergone gastric resection although, in the other cases, there were also significant increases above normal. In any case, the nutritional effects of alcoholism on the skeleton were relatively slight inasmuch as there was no case of advanced osteomalacia. Nevertheless, alcoholism causes bone changes, both systemic (possibly hormonal) and local in nature, and is characterized by bone resorption.

One hundred and five coniotomies have been carried out, as an alternative to tracheotomy on patients in the ICU, Danderyd Hospital. The procedure is easy to perform, relatively riskfree and is attractive in terms of resources required. However a rather high frequency of voice-changes were found.

Iliac crest biopsies were obtained from 110 women, 62 of whom had been clinically and radiologically classified as osteoporotics. The amount of osteoid surface was measured by a histological planimetrical method. It was demonstrated that the amount of osteoid does not differ between osteoporotic women and control women and that osteomalacia is rare in both groups.

Bone morphological parameters of renal osteodystrophy such as abundance of osteoid surface, osteoid seam width index, calcification fronts, osteoclast activity and trabecular bone volume were studied in 71 patients on maintenance hemodialysis and compared with bone densitometry, laboratory and clinical data. Increased osteoclast activity (hyperparathyroidism) was by far the most common bone morphological finding. Patients with chronic pyelonephritis or polycystic kidney disease had more than double the amount of osteoid than patients with chronic glomerulonephritis. The trabecular bone volume seemed to be increased in most patients in contrast to the cortical bone volume which was decreased, judged from bone densitometry and previously from X-ray. Despite that patients with polycystic kidney disease were older, their trabecular volume was larger than in patients with glomerulonephritis. The bone mineral content evaluated by bone densitometry was low in most patients, and more associated with bone morphological signs of osteomalacia than with secondary hyperparathyroidism. Serum phosphate (S-PO4) and serum parathyroid hormone (S-PTH) seemed to discriminate better between osteomalacia and secondary hyperparathyroidism than serum alkaline phosphatase (S-Alk. phosph.), which was elevated in both groups. Patients who had been bilaterally nephrectomized were no more abnormal than other patients, and they had lower S-Alk. phosph. The abundance of osteoclasts was found to be a predictor of future development of clinical secondary hyperparathyroidism.

A description is given of a modified method of counting osteoclasts both per section area and also relative to the remaining trabeculae surface area in crista biopsies. The material consisted of normal individuals, patients with clinical osteoporosis, and patients with chronic renal failure undergoing haemodialysis. The number of osteoclasts in the biopsies from normal and osteoporotic individuals showed a normal distribution with the same mean. In the haemodialysis patients there was a marked skew distribution. In normal individuals, there was a significant decrease in the number of osteoclasts per section area with age, but this was not significant when calculated relative to the bone surface area.

The Burkhardt instrument is a useful tool for obtaining bone biopsies from the iliac crest in order to study bone tissue. Information on bone mass, however, is rather unreliable and iliac crest biopsy has also a low predictive value for spinal bone mass, whereas estimation of osteoid is more useful and this variable cannot be studied by any other means. Even if the precision is only 20% or even less, the differences between patients are considerable and useful information can therefore be obtained. It was demonstrated in an unselected group of patients that, even if the number of cases which could be classified as osteomalacia was small, there were significant deviations in the amount of osteoid in many groups.

A therapeutical program in pre-eclampsia and eclampsia is presented. The results in 10 patients suggest that the same basic program as is used in the hypoperfusion syndrome can be used in pre-eclampsia and eclampsia: Chlorpromazin to combat vasoconstriction and dilate the vascular bed. Plasma expanders, plasma, albumin and glucose with electrolytes to fill up the dilated vascular bed and restore the tissue perfusion. Buffers to combat acidosis, oxygen to combat hypoxemia, hypertonic Mannitol to mobilize edema. Furosemide to force diuresis.

In 31 epileptics, most of whom had been on anticonvulsive drugs for decades, the amount of osteoid--active and inactive--and the osteoclast activity were measured in iliac crest biopsies and compared with the same variables from a control group. Although falling within normal limits, the amount of osteoid, in particular the inactive osteoid, was significantly increased in the epileptics. The osteoclast activity was also significantly increased in the epileptics.

Altogether 15 partially independent measurements of bone mass in 100 women with clinical and roentgenological signs of osteoporosis were correlated to the alkaline phosphatase activities of the same individuals. There was a slight but significant negative correlation indicating an increasing alkaline phosphatase activity with decreasing bone mass. This correlation was not caused by interaction of age. There was no correlation or morphological signs of osteomalacia. The changes could not be explained by fractures. It is suggested that a slight increase in the alkaline phosphatase activity in women with a more severe osteoporosis is related to bone resorption.