Terveyspalveluiden alueelliset kustannuserot:tarkastelussa Kainuun perusterveydenhuollon avohoidon kustannukset vuosilta 2015–2018

Tiivistelmä. Tutkielman tavoitteena on selvittää, esiintyykö Kainuussa eroja perusterveydenhuollon avohoidon kustannuksissa kuntien välillä ja tilastollisten kuntaryhmien välillä. Kustannuksia tarkastellaan perusterveydenhuollon avohoidon kokonaiskustannusten osalta sekä palvelumuotokohtaisesti. Aiheen tarkastelu on ajankohtaista, sillä Suomen terveydenhuoltojärjestelmä on murroksessa 2023 alkuvuodesta tapahtuneen soteuudistuksen myötä. Terveydenhuollon kustannusten kasvu on tunnistettu kansainvälisessä kirjallisuudessa länsimaita koskevaksi ongelmaksi. Terveydenhuollon kustannuksiin vaikuttavat lukuisat tekijät ja ne voidaan jakaa altistaviin, mahdollistaviin ja tarvetekijöihin Andersenin mallia mukaillen. Tutkielman aineistona on käytetty Avohilmo-rekisteriaineistoa vuosilta 2015–2018 Kainuun osalta. Aineiston perusteella laskettiin kunnille sekä kuntaryhmille keskimääräiset potilaskohtaiset kustannukset, käyntikohtaiset kustannukset sekä käyntien määrä potilasta kohden. Aineiston perusteella Kainuussa on eroja perusterveydenhuollon avohoidon kustannuksissa sekä kuntien että tilastollisten kuntaryhmien kohdalla. Erot potilaskohtaisissa kustannuksissa vaikuttavat pääosin johtuvan eroista käyntien määrissä. Poikkeuksena tästä on palvelumuodoista terapiapalvelut, jonka käyntikohtaisissa kustannuksissa oli havaittavissa eroavaisuuksia. Jatkossa olisi hyvä selvittää, mitkä tekijät vaikuttavat terveydenhuollon käyntimäärien eroihin Kainuussa

Interaction between parental psychosis and early motor development and the risk of schizophrenia in a general population birth cohort.

BACKGROUND: Delayed motor development in infancy and family history of psychosis are both associated with increased risk of schizophrenia, but their interaction is largely unstudied. AIM: To investigate the association of the age of achieving motor milestones and parental psychosis and their interaction in respect to risk of schizophrenia. METHODS: We used data from the general population-based prospective Northern Finland Birth Cohort 1966 (n=10,283). Developmental information of the cohort members was gathered during regular visits to Finnish child welfare clinics. Several registers were used to determine the diagnosis of schizophrenia among the cohort members and psychosis among the parents. Altogether 152 (1.5%) individuals had schizophrenia by the age of 46 years, with 23 (15.1%) of them having a parent with psychosis. Cox regression analysis was used in analyses. RESULTS: Parental psychosis was associated (P<0.05) with later achievement of holding the head up, grabbing an object, and walking without support. In the parental psychosis group, the risk for schizophrenia was increased if holding the head up (hazard ratio [HR]: 2.46; degrees of freedom [df]=1; 95% confidence interval [95% CI]: 1.07-5.66) and touching the thumb with the index finger (HR: 1.84; df=1; 95% CI: 1.11-3.06) was later. In the group without parental psychosis, a delay in the following milestones increased the risk of schizophrenia: standing without support and walking without support. Parental psychosis had an interaction with delayed touching thumb with index finger (HR: 1.87; df=1; 95% CI: 1.08-3.25) when risk of schizophrenia was investigated. CONCLUSIONS: Parental psychosis was associated with achieving motor milestones later in infancy, particularly the milestones that appear early in a child's life. Parental psychosis and touching the thumb with the index finger had a significant interaction on risk of schizophrenia. Genetic risk for psychosis may interact with delayed development to raise future risk of schizophrenia, or delayed development may be a marker of other risk processes that interact with genetic liability to cause later schizophrenia.This study was supported by grants from the Brain and Behavior Research Foundation, Northern Finland Health Care Support Foundation, Sigrid Jusélius Foundation, and the Signe and Ane Gyllenberg Foundation, Finland. NFBC 1966 received financial support from the Academy of Finland (104781, 120315, 129269, 1114194, 24300796, 268336, 278286), Center of Excellence in Complex Disease Genetics and SALVE, Oulu University Hospital, Oulu, Finland, Biocenter of Oulu, Finland, University of Oulu, Finland (75617, 24002054, 2400692), Ministry of Social Affairs and Health (50459, 50691, 50842, 2749, 2465), NHLBI grant 5R01HL087679-02 through the STAMPEED program (1RL1MH083268-01), NIH/NIMH (5R01MH63706:02), ENGAGE project and grant agreement HEALTH-F4-2007-(201413), EU FP7 EurHEALTHAgeing (277849), EU FP7 EurHealth Epi-Migrant (279143), European Regional Development Fund 537/2010 (24300936) and the Medical Research Council, UK (G0500539, G0600705, G1002319, PrevMetSyn/SALVE).This is the final version of the article. It first appeared from Elsevier via http://dx.doi.org/10.1016/j.eurpsy.2015.04.00

Antigen targeting to endosomal pathway in dendritic cell vaccination activates regulatory T cells and attenuates tumor immunity

Lymphoma cells are malignant cells of the T- or B-cell lineage that often express many surface markers inappropriately, yet are not recognized as abnormal by the immune system. We modeled this situation by inoculating ovalbumin-expressing E.G7-OVA lymphoma cells into mice that expressed ovalbumin as a self antigen in pancreatic islets, and investigated the efficacy of dendritic cell (DC) vaccination in these mice. Although vaccination with DC-expressing ovalbumin induced strong cytotoxic T-cell immunity, which led to clearance of E.G7-OVA lymphoma cells in naive C57BL/6 mice, DC vaccination was ineffective in mice expressing ovalbumin as a self antigen. Antigen modification to increase its processing via the endosomal processing pathway dramatically increased CD4 T-cell activation but paradoxically, impaired the protective effect of DC vaccination even in naive mice. Depletion of CD25(+) T cells (regulatory T cells [Tregs]) prior to vaccination restored the efficacy of DC vaccination and allowed eradication of lymphoma also in mice expressing ovalbumin as a self antigen. We conclude that lymphoma cells may be eradicated using DC vaccination if activation of CD25(+) Tregs is simultaneously inhibited, and that intentionally enhanced endosomal antigen processing in DC vaccines may shift the balance from CD4 T-cell help toward stimulation of Tregs.</p

Living on social assistance with chronic illness: Buffering and undermining features to well-being

<p>Abstract</p> <p>Background</p> <p>In Sweden, the social security and sickness insurance systems are comprehensive and aim to provide people whose illness prevents them from earning their own living, with either sickness benefits or disability pension. Some, however, are not entitled to these benefits or receive social insurance benefits at a level too low for subsistence, and are referred to social assistance. The purpose of this study was to explore in depth how social assistance recipients with chronic illness perceive and respond to the experience of living on social assistance.</p> <p>Methods</p> <p>Seventeen in-depth interviews were carried out with chronically ill people who had received social assistance for several years. Grounded theory informed the design of the study.</p> <p>Results</p> <p>The study showed that different strategies (living one day at a time, taking steps forwards and backwards and making attempts to find ways out of the situation) were employed by social assistance recipients to maintain or improve their well-being. Contextual features like the prevailing welfare system, public services and the local neighbourhood could buffer or undermine these strategies and their overall well-being. These features together influenced how interviewees perceived their situation, the possible ways out of the situation and the consequences for their well-being.</p> <p>Conclusion</p> <p>From this study it is evident that the way in which individuals on social assistance interact with services and how they are treated by professionals plays an important role in their well-being, in combination with what kind of help and support is available for recipients through the welfare system. In this respect, persons living on social assistance with chronic illness are particularly vulnerable. This study suggests that more effort should be made to find long term solutions concerning income support, rehabilitation and other services provided to this group.</p

Mutation update and genotype-phenotype correlations of novel and previously described mutations in TPM2 and TPM3 causing congenital myopathies

Mutations affecting skeletal muscle isoforms of the tropomyosin genes may cause nemaline myopathy, cap myopathy, core-rod myopathy, congenital fiber-type disproportion, distal arthrogryposes, and Escobar syndrome. We correlate the clinical picture of these diseases with novel (19) and previously reported (31) mutations of the TPM2 and TPM3 genes. Included are altogether 93 families: 53 with TPM2 mutations and 40 with TPM3 mutations. Thirty distinct pathogenic variants of TPM2 and 20 of TPM3 have been published or listed in the Leiden Open Variant Database (http://www.dmd.nl/). Most are heterozygous changes associated with autosomal-dominant disease. Patients with TPM2 mutations tended to present with milder symptoms than those with TPM3 mutations, DA being present only in the TPM2 group. Previous studies have shown that five of the mutations in TPM2 and one in TPM3 cause increased Ca2+ sensitivity resulting in a hypercontractile molecular phenotype. Patients with hypercontractile phenotype more often had contractures of the limb joints (18/19) and jaw (6/19) than those with nonhypercontractile ones (2/22 and 1/22), whereas patients with the non-hypercontractile molecular phenotype more often (19/22) had axial contractures than the hypercontractile group (7/19). Our in silico predictions show that most mutations affect tropomyosin–actin association or tropomyosin head-to-tail binding

Comparison of Variable-Number Tandem-Repeat Markers typing and IS1245 Restriction Fragment Length Polymorphism fingerprinting of Mycobacterium avium subsp hominissuis from human and porcine origins

Peer reviewe

Quantifying groundwater fluxes from an aapa mire to a riverside esker formation

Water flows in peatland margins is an under-researched topic. This study examines recharge from a peatland to an esker aquifer in an aapa mire complex of northern Finland. Our objective was to study how the aapa mire margin is hydrogeologically connected to the riverside aquifer and spatial and temporal variations in the recharge of peatland water to groundwater (GW). Following geophysical studies and monitoring of the saturated zone, a GW model (MODFLOW) was used in combination with stable isotopes to quantify GW flow volumes and directions. Peatland water recharge to the sandy aquifer indicated a strong connection at the peatland–aquifer boundary. Recharge volumes from peatland to esker were high and rather constant (873 m3 d−1) and dominated esker recharge at the study site. The peat water recharging the esker boundary was rich in dissolved organic carbon (DOC). Stable isotope studies on water (δ18O, δ2H, and d-excess) from GW wells verified the recharge of DOC-rich water from peatlands to mineral soil esker. Biogeochemical analysis revealed changes from DOC to dissolved inorganic carbon in the flow pathway from peatland margin to the river Kitinen. This study highlights the importance of careful investigation of aapa mire margin areas and their potential role in regional GW recharge patterns. HIGHLIGHTS Peatland water recharge to aquifer showed connection at the peatland–aquifer boundary.; Analysis revealed changes from dissolved organic carbon to dissolved inorganic carbon in groundwater flow pathway from peatland.; Connection between an aapa mire margin and riverside esker was documented.

NMR metabolomic modeling of age and lifespan: A multicohort analysis.

Metabolomic age models have been proposed for the study of biological aging, however, they have not been widely validated. We aimed to assess the performance of newly developed and existing nuclear magnetic resonance spectroscopy (NMR) metabolomic age models for prediction of chronological age (CA), mortality, and age-related disease. Ninety-eight metabolic variables were measured in blood from nine UK and Finnish cohort studies (N ≈31,000 individuals, age range 24-86 years). We used nonlinear and penalized regression to model CA and time to all-cause mortality. We examined associations of four new and two previously published metabolomic age models, with aging risk factors and phenotypes. Within the UK Biobank (N ≈102,000), we tested prediction of CA, incident disease (cardiovascular disease (CVD), type-2 diabetes mellitus, cancer, dementia, and chronic obstructive pulmonary disease), and all-cause mortality. Seven-fold cross-validated Pearson's r between metabolomic age models and CA ranged between 0.47 and 0.65 in the training cohort set (mean absolute error: 8-9 years). Metabolomic age models, adjusted for CA, were associated with C-reactive protein, and inversely associated with glomerular filtration rate. Positively associated risk factors included obesity, diabetes, smoking, and physical inactivity. In UK Biobank, correlations of metabolomic age with CA were modest (r = 0.29-0.33), yet all metabolomic model scores predicted mortality (hazard ratios of 1.01 to 1.06/metabolomic age year) and CVD, after adjustment for CA. While metabolomic age models were only moderately associated with CA in an independent population, they provided additional prediction of morbidity and mortality over CA itself, suggesting their wider applicability

Respiratory symptoms among infants at risk for asthma: association with surfactant protein A haplotypes

BACKGROUND: We examined the association between single nucleotide polymorphisms (SNPs) in loci encoding surfactant protein A (SFTPA) and risk of wheeze and persistent cough during the first year of life among a cohort of infants at risk for developing asthma. METHODS: Between September 1996 and December 1998, mothers of newborn infants were invited to participate if they had an older child with clinician-diagnosed asthma. Each mother was given a standardized questionnaire within 4 months of her infant's birth. Infant respiratory symptoms were collected during quarterly telephone interviews at 6, 9 and 12 months of age. Due to the association of SFTPA polymorphisms and race/ethnicity, analyses were restricted to 221 white infants for whom whole blood and respiratory data were available. Ordered logistic regression models were used to examine the association between respiratory symptom frequency and SFTPA haplotypes. RESULTS: The 6A allele haplotype of SFTPA1, with an estimated frequency of 6% among our study infants, was associated with an increased risk of persistent cough (OR 3.69, 95% CI 1.71, 7.98) and wheeze (OR 4.72, 95% CI 2.20, 10.11). The 6A/1A haplotype of SFTPA, found among approximately 5% of the infants, was associated with an increased risk of persistent cough (OR 3.20, 95% CI 1.39, 7.36) and wheeze (OR 3.25, 95% CI 1.43, 7.37). CONCLUSION: Polymorphisms within SFTPA loci may be associated with wheeze and persistent cough in white infants at risk for asthma. These associations require replication and exploration in other ethnic/racial groups