Lääkkeiden aiheuttamat ihoreaktiot

Vertaisarvioitu.• Lääkkeet voivat aiheuttaa välittömiä tai viiveellä tulevia yliherkkyysreaktioita. • Akuutissa vaiheessa tulisi erityisesti kiinnittää huomiota vaikeiden iho-oireiden hälytysmerkkeihin, koska niihin liittyy huono ennuste. • Allergologisissa selvittelyissä korostuu huolellinen anamneesi, jossa potilaskertomusmerkinnät ja valokuvat ihoreaktiosta ovat keskeisiä. • Selvittelyt ovat tarpeen, mikäli reaktio on ollut vaikea, potilaalta on kielletty hänelle tärkeä lääke tai kiellossa on useampia lääkkeitä, mikä voi vaikeuttaa potilaan jatkohoitoa.Peer reviewe

Pistiäisallergian siedätyshoito on turvallista ja tehokasta

• Ampiainen aiheuttaa Suomessa suurimman osan pistiäisen pistoihin liittyvistä anafylaksioista. • Diagnostiikka on tärkeää sekä pistiäisen tunnistamiseksi että herkistymisen osoittamiseksi. • Allergian osoittamiseen käytetään immunoglobuliini E -luokan vasta-aineita ampiaisen ja mehiläisen myrkylle sekä niiden allergeenikomponenteille. • Kaikilta yleisreaktion saaneilta tutkitaan seerumin tryptaasin perustaso mastosytoosin poissulkemiseksi. • Siedätyshoitoa suositellaan niille, jotka ovat saaneet piston yhteydessä yleistyneen allergisen reaktion.</p

Pistiäisallergian siedätyshoito on turvallista ja tehokasta

VertaisarvioituAmpiainen aiheuttaa Suomessa suurimman osan pistiäisen pistoihin liittyvistä anafylaksioista. Diagnostiikka on tärkeää sekä pistiäisen tunnistamiseksi että herkistymisen osoittamiseksi. Allergian osoittamiseen käytetään immunoglobuliini E -luokan vasta-aineita ampiaisen ja mehiläisen myrkylle sekä niiden allergeenikomponenteille. Kaikilta yleisreaktion saaneilta tutkitaan seerumin tryptaasin perustaso mastosytoosin poissulkemiseksi. Siedätyshoitoa suositellaan niille, jotka ovat saaneet piston yhteydessä yleistyneen allergisen reaktion.Peer reviewe

Pilot study in human healthy volunteers on the use of magnetohydrodynamics in needle-free continuous glucose monitoring

The benefits of continuous glucose monitoring (CGM) in diabetes management are extensively documented. Yet, the broader adoption of CGM systems is limited by their cost and invasiveness. Current CGM devices, requiring implantation or the use of hypodermic needles, fail to offer a convenient solution. We have demonstrated that magnetohydrodynamics (MHD) is effective at extracting dermal interstitial fluid (ISF) containing glucose, without the use of needles. Here we present the first study of ISF sampling with MHD for glucose monitoring in humans. We conducted 10 glucose tolerance tests on 5 healthy volunteers and obtained a significant correlation between the concentration of glucose in ISF samples extracted with MHD and capillary blood glucose samples. Upon calibration and time lag removal, the data indicate a Mean Absolute Relative Difference (MARD) of 12.9% and Precision Absolute Relative Difference of 13.1%. In view of these results, we discuss the potential value and limitations of MHD in needle-free glucose monitoring.Peer reviewe

Sampling of fluid through skin with magnetohydrodynamics for noninvasive glucose monitoring

Out of 463 million people currently with diabetes, 232 million remain undiagnosed. Diabetes is a threat to human health, which could be mitigated via continuous self-monitoring of glucose. In addition to blood, interstitial fluid is considered to be a representative sample for glucose monitoring, which makes it highly attractive for wearable on-body sensing. However, new technologies are needed for efficient and noninvasive sampling of interstitial fluid through the skin. In this report, we introduce the use of Lorentz force and magnetohydrodynamics to noninvasively extract dermal interstitial fluid. Using porcine skin as an ex-vivo model, we demonstrate that the extraction rate of magnetohydrodynamics is superior to that of reverse iontophoresis. This work seeks to provide a safe, effective, and noninvasive sampling method to unlock the potential of wearable sensors in needle-free continuous glucose monitoring devices that can benefit people living with diabetes.Peer reviewe

Neutral fluorescence probe with strong ratiometric response to surface charge of phospholipid membranes

AbstractWe report on dramatic differences in fluorescence spectra of 4′-dimethylamino-3-hydroxyflavone (probe F) studied in phospholipid membranes of different charge (phosphatidyl glycerol, phosphatidylcholine (PC), their mixture and the mixture of PC with a cationic lipid). The effect consists in variations of relative intensities at two well-separated band maxima at 520 and 570 nm belonging to normal (N*) and tautomer (T*) excited states of flavone chromophore. Based on these studies we propose a new approach to measure electrostatic potential at the surface layer of phospholipid membranes, which is based on potential-dependent changes of bilayer hydration and involves very sensitive and convenient ratiometric measurements in fluorescence emission

Specificity of cholesterol and analogs to modulate BK channels points to direct sterol–channel protein interactions

The activity (Po) of large-conductance voltage/Ca2+-gated K+ (BK) channels is blunted by cholesterol levels within the range found in natural membranes. We probed BK channel–forming α (cbv1) subunits in phospholipid bilayers with cholesterol and related monohydroxysterols and performed computational dynamics to pinpoint the structural requirements for monohydroxysterols to reduce BK Po and obtain insights into cholesterol’s mechanism of action. Cholesterol, cholestanol, and coprostanol reduced Po by shortening mean open and lengthening mean closed times, whereas epicholesterol, epicholestanol, epicoprostanol, and cholesterol trisnorcholenic acid were ineffective. Thus, channel inhibition by monohydroxysterols requires the β configuration of the C3 hydroxyl and is favored by the hydrophobic nature of the side chain, while having lax requirements on the sterol A/B ring fusion. Destabilization of BK channel open state(s) has been previously interpreted as reflecting increased bilayer lateral stress by cholesterol. Lateral stress is controlled by the sterol molecular area and lipid monolayer lateral tension, the latter being related to the sterol ability to adopt a planar conformation in lipid media. However, we found that the differential efficacies of monohydroxysterols to reduce Po (cholesterol≥coprostanol≥cholestanol>>>epicholesterol) did not follow molecular area rank (coprostanol>>epicholesterol>cholesterol>cholestanol). In addition, computationally predicted energies for cholesterol (effective BK inhibitor) and epicholesterol (ineffective) to adopt a planar conformation were similar. Finally, cholesterol and coprostanol reduced Po, yet these sterols have opposite effects on tight lipid packing and, likely, on lateral stress. Collectively, these findings suggest that an increase in bilayer lateral stress is unlikely to underlie the differential ability of cholesterol and related steroids to inhibit BK channels. Remarkably, ent-cholesterol (cholesterol mirror image) failed to reduce Po, indicating that cholesterol efficacy requires sterol stereospecific recognition by a protein surface. The BK channel phenotype resembled that of α homotetramers. Thus, we hypothesize that a cholesterol-recognizing protein surface resides at the BK α subunit itself

Enantioselective Protein-Sterol Interactions Mediate Regulation of Both Prokaryotic and Eukaryotic Inward Rectifier K+ Channels by Cholesterol

Cholesterol is the major sterol component of all mammalian cell plasma membranes and plays a critical role in cell function and growth. Previous studies have shown that cholesterol inhibits inward rectifier K+ (Kir) channels, but have not distinguished whether this is due directly to protein-sterol interactions or indirectly to changes in the physical properties of the lipid bilayer. Using purified bacterial and eukaryotic Kir channels reconstituted into liposomes of controlled lipid composition, we demonstrate by 86Rb+ influx assays that bacterial Kir channels (KirBac1.1 and KirBac3.1) and human Kir2.1 are all inhibited by cholesterol, most likely by locking the channels into prolonged closed states, whereas the enantiomer, ent-cholesterol, does not inhibit these channels. These data indicate that cholesterol regulates Kir channels through direct protein-sterol interactions likely taking advantage of an evolutionarily conserved binding pocket