Kalvo-oikomishoidon mahdollisuuksia ja rajoitteita

Tiivistelmä. Syventävän tutkielman aiheena on kalvo-oikomishoito. Tavoitteena on selvittää, millaisia tutkimustuloksia kirjallisuudessa on erilaisista hampaiden siirroista kalvoilla. Tutkielmassa käsitellään myös kalvojen valmistusta ja biomekaniikkaa, vaikutuksia suun terveyteen, hoidon kestoa ja kustannuksia sekä hoitoa vaihduntahampaistossa. Kirjallisuuskatsauksen lähteenä on käytetty Pubmed-tietokannasta haettuja ajankohtaisia tieteellisiä artikkeleita. Kalvo-oikomishoito on esteettisyytensä vuoksi suosittu hoitomuoto kuluttajien keskuudessa. Kalvohoidon haitalliset vaikutukset parodontiumin terveyteen lyhyellä aikavälillä ovat vähäisemmät verrattuna kiinteäkojehoitoon. Juuriresorptioiden ilmaantuvuudessa ei ole eroa eri kojeiden välillä; tärkeämpiä tekijöitä ovat hoitoon kulunut aika ja siinä käytetyt voimat. Hoidosta aiheutuva kipu on ensimmäisten päivien aikana alhaisempi kalvo-oikomispotilailla kuin kiinteäkojepotilailla. Kalvohoidon tehokkuutta halutun lopputuloksen saavuttamisessa on tutkittu vertaamalla tuloksia kiinteäkojehoitoon. Tutkimusten mukaan kalvohoidolla ei saavuteta yhtä tarkasti haluttuja lopputuloksia kuin kiinteäkojehoidolla, jossa hoitoon kuuluu viimeistelyvaihe. Kalvohoitoon kuluva aika ilman poistoja tehtävässä hoidossa on lyhyempi verrattuna kiinteäkojehoitoon, mikä niin ikään saattaa johtua erillisen viimeistelyvaiheen puuttumisesta. Kalvohoidon materiaalikustannukset ovat huomattavasti korkeammat kuin kiinteäkojehoidossa. Toisaalta vastaanottokäyntejä kalvohoidossa on vähemmän. Kalvohoitoa vaihduntahampaistossa on tutkittu vielä melko vähän. Yläleuan levitys kalvoilla onnistuu tutkimusten mukaan vaihduntahampaistossa. Kalvojen kyky intrusoida hampaita on verrattavissa kiinteisiin kojeisiin. Ekstruusion toteuttaminen kalvoilla on haastavaa ilman hampaan tahatonta kallistamista. Okklusaalisesti pyöreiden hampaiden rotaatio on myös kalvoilla haastavaa toteuttaa puutteellisen retention vuoksi. Kontrolloimattomat hampaan labio-linguaali- tai bukko-linguaalisuuntaiset kallistukset onnistuvat kalvoilla hyvin. Laajajuuristen hampaiden siirtäminen yhdensuuntaisina mesio-distaalisuunnassa on haastavaa. Juurten liikkeiden kontrollointi ei ole edelleenkään verrattavissa kiinteäkojehoitoon, mutta on helpottunut kalvojen kehittyessä. Yläleuan molaarien distaalinen siirto 2–3mm onnistuu kalvoilla hyvin, eikä aiheuta muutoksia kasvojen vertikaalisiin suhteisiin. Kalvohoitoa tekevän kliinikon kokemus ja perehtyminen oikomishoitoon ovat tärkeitä potilasvalinnan ja hoitosuunnitelmien onnistumiseksi

Effects of empagliflozin on blood pressure and markers of arterial stiffness and vascular resistance in patients with type 2 diabetes

Peer reviewe

Increased myeloid cell hypoxia-inducible factor-1 delays obliterative airway disease in the mouse

BACKGROUND: Obliterative bronchiolitis after lung transplantation is characterized by chronic airway inflammation leading to the obliteration of small airways. Hypoxia-inducible factor-1 (HIF-1) is a master regulator of cellular responses to hypoxia and inflammation. The Von Hippel-Lindau protein (pVHL) drives the degradation of oxygen-sensitive subunit HIF-1 alpha that controls the activity of HIF-1. We investigated the effect of myeloid cell targeted gene deletion of HIF-1 alpha or its negative regulator pVHL on the development of obliterative airway disease (OAD) in the recipients of tracheal allografts, a mouse model for obliterative bronchiolitis after lung transplantation. METHODS: Tracheal allografts were heterotopically transplanted from BALB/c donor mice to fully major histocompatibility complex mismatched recipient mice with HIF-1 alpha or VHL gene deletion in myeloid cells. The recipients were left non-immunosuppressed or received tacrolimus daily. Histologic, immunohistochemical, and real-time reverse transcription polymerase chain reaction analyses were performed at 3, 10, and 30 days. RESULTS: In the absence of immunosuppression, myeloid cell-specific VHL deficiency of the recipient mice improved epithelial recovery, decreased inflammatory cell infiltration and expression of pro-inflammatory cytokines, increased regulatory forkhead box P3 messenger RNA expression, and reduced OAD development in tracheal allografts. In the presence of tacrolimus immunosuppression, loss of HIF-1 alpha activity in myeloid cells of the recipient by HIF-1 alpha gene deletion accelerated OAD development in mouse tracheal allografts. CONCLUSIONS: Activity of the HIF-pathway affects the development of allograft rejection, and our results suggest that myeloid cell-specific VHL-deficiency that potentially increases HIF-activity decreases allograft inflammation and the subsequent development of OAD in mouse tracheal allografts. (C) 2016 International Society for Heart and Lung Transplantation. All rights reserved.Peer reviewe

Improving the surface structure of high quality Sr2FeMoO6 thin films for multilayer structures

Two sets of Sr2FeMoO6 thin films were prepared with pulsed laser deposition and the effect of the laserfluence and the deposition temperature was investigated. The Sr2FeMoO6 thin films showed clear evi-dence of impurity phases when the laser fluence was altered. Phase pure films resulted through thewhole temperature range between 900 ◦C and 1050 ◦C when a proper laser fluence was used. Films fabri-cated at lower deposition temperatures resulted with smaller surface roughnesses around 5 nm, higherCurie temperatures and with relatively high saturation magnetization values. The Curie temperaturewas determined from the minimum of the first order derivative and results showed the highest values of350 K and above. The films with the highest Curie temperature reached zero magnetization above 400 K.The results indicate that both high microstructural and high magnetic quality Sr2FeMoO6 thin films canbe obtained with a deposition temperature between 900 ◦C and 950 ◦C. This provides better fabricationparameters for the upcoming SFMO multilayer structures.</p

Pooled analysis of Phase III trials indicate contrasting influences of renal function on blood pressure, body weight, and HbA1c reductions with empagliflozin

Sodium glucose cotransporter 2 (SGLT2) inhibitors reduce HbA1c, blood pressure, and weight in patients with type 2 diabetes. To investigate the effect of renal function on reductions in these parameters with the SGLT2 inhibitor empagliflozin, we assessed subgroups by baseline estimated glomerular filtration rate (eGFR; Modification of Diet in Renal Disease) in pooled data from five 24-week trials of 2286 patients with type 2 diabetes randomized to empagliflozin or placebo. Reductions in HbA1c with empagliflozin versus placebo significantly diminished with decreasing baseline eGFR. Reductions in systolic blood pressure (SBP) with empagliflozin were maintained in patients with lower eGFR. The mean placebo-corrected changes from baseline in systolic blood pressure at week 24 with empagliflozin were -3.2 (95% confidence interval -4.9,-1.5) mmHg, -4.0 (-5.4, -2.6) mmHg, -5.5 (-7.6, -3.4) mmHg, and -6.6 (-11.4, -1.8) mmHg in patients with an eGFR of 90 or more, 60 to 89, 30 to 59, and under 30 ml/min/1.73m(2), respectively. Similar trends were observed for diastolic blood pressure. Weight loss with empagliflozin versus placebo tended to be attenuated in patients with a lower eGFR. Results were consistent in a 12-week ambulatory blood pressure monitoring trial in 823 patients with type 2 diabetes and hypertension. Thus, unlike HbA1c reductions, systolic blood pressure and weight reductions with empagliflozin are generally preserved in patients with chronic kidney disease.Peer reviewe

Urinary Biomarkers Indicative of Apoptosis and Acute Kidney Injury in the Critically Ill

BackgroundApoptosis is a key mechanism involved in ischemic acute kidney injury (AKI), but its role in septic AKI is controversial. Biomarkers indicative of apoptosis could potentially detect developing AKI prior to its clinical diagnosis.MethodsAs a part of the multicenter, observational FINNAKI study, we performed a pilot study among critically ill patients who developed AKI (n = 30) matched to critically ill patients without AKI (n = 30). We explored the urine and plasma levels of cytokeratin-18 neoepitope M30 (CK-18 M30), cell-free DNA, and heat shock protein 70 (HSP70) at intensive care unit (ICU) admission and 24h thereafter, before the clinical diagnosis of AKI defined by the Kidney Disease: Improving Global Outcomes - creatinine and urine output criteria. Furthermore, we performed a validation study in 197 consecutive patients in the FINNAKI cohort and analyzed the urine sample at ICU admission for CK-18 M30 levels.ResultsIn the pilot study, the urine or plasma levels of measured biomarkers at ICU admission, at 24h, or their maximum value did not differ significantly between AKI and non-AKI patients. Among 20 AKI patients without severe sepsis, the urine CK-18 M30 levels were significantly higher at 24h (median 116.0, IQR [32.3-233.0] U/L) than among those 20 patients who did not develop AKI (46.0 [0.0-54.0] U/L), P = 0.020. Neither urine cell-free DNA nor HSP70 levels significantly differed between AKI and non-AKI patients regardless of the presence of severe sepsis. In the validation study, urine CK-18 M30 level at ICU admission was not significantly higher among patients developing AKI compared to non-AKI patients regardless of the presence of severe sepsis or CKD.ConclusionsOur findings do not support that apoptosis detected with CK-18 M30 level would be useful in assessing the development of AKI in the critically ill. Urine HSP or cell-free DNA levels did not differ between AKI and non-AKI patients

Response to letter on use of functional imaging by 11C-metomidate PET for primary aldosteronism subtyping

Non peer reviewe

Alterations of Cardiac Protein Kinases in Cyclic Nucleotide-Dependent Signaling Pathways in Human Ischemic Heart Failure

ObjectivesImpaired protein kinase signaling is a hallmark of ischemic heart disease (IHD). Inadequate understanding of the pathological mechanisms limits the development of therapeutic approaches. We aimed to identify the key cardiac kinases and signaling pathways in patients with IHD with an effort to discover potential therapeutic strategies.MethodsCardiac kinase activity in IHD left ventricle (LV) and the related signaling pathways were investigated by kinomics, transcriptomics, proteomics, and integrated multi-omics approach.ResultsProtein kinase A (PKA) and protein kinase G (PKG) ranked on top in the activity shift among the cardiac kinases. In the IHD LVs, PKA activity decreased markedly compared with that of controls (62% reduction, p = 0.0034), whereas PKG activity remained stable, although the amount of PKG protein increased remarkably (65%, p = 0.003). mRNA levels of adenylate cyclases (ADCY 1, 3, 5, 9) and cAMP-hydrolysing phosphodiesterases (PDE4A, PDE4D) decreased significantly, although no statistically significant alterations were observed in that of PKGs (PRKG1 and PRKG2) and guanylate cyclases (GUCYs). The gene expression of natriuretic peptide CNP decreased remarkably, whereas those of BNP, ANP, and neprilysin increased significantly in the IHD LVs. Proteomics analysis revealed a significant reduction in protein levels of “Energy metabolism” and “Muscle contraction” in the patients. Multi-omics integration highlighted intracellular signaling by second messengers as the top enriched Reactome pathway.ConclusionThe deficiency in cAMP/PKA signaling pathway is strongly implicated in the pathogenesis of IHD. Natriuretic peptide CNP could be a potential therapeutic target for the modulation of cGMP/PKG signaling.Peer reviewe