The relationship between internalizing and externalizing symptoms and cultural resilience factors in Indigenous Sami youth from Arctic Norway

The accepted manuscript version of this article is part of Margrethe Bals' doctoral thesis, which is available in Munin at http://hdl.handle.net/10037/2934Objectives. To examine whether enculturation factors, like cultural activities, ethnic pride and native language competence, are related to decreased internalizing and externalizing symptoms in Indigenous Sami youth from Arctic Norway. The impact of self-efficacy on the relationship between enculturation factors and mental health problems was also examined. Study design. Population-based, cross-sectional questionnaire study. Methods. The Norwegian Arctic Adolescent Health Study was conducted among 10th graders in junior high schools in north Norway during 2003–2005. The study sample consisted of 450 Indigenous Sami youth, aged 15–16 years. Internalizing symptoms were measured with the Hopkins Symptom Check List- 10 (HSCL-10), while externalizing symptoms were measured by two subscales of the Strengths and Difficulties Questionnaire (SDQ). Results. For boys, self-efficacy and participation in cultural activities were associated with decreased internalizing symptoms. Additionally, self-efficacy interacted with Sami language competence and cultural activities: when self-efficacy increased, these enculturation factors were related to symptom reduction. For girls, self-efficacy had an independent effect on internalizing symptoms and also strengthened the relationship between participation in cultural activities and reduced externalizing symptoms. Sami language competence was related to the reduction of both internalizing and externalizing symptoms in girls. Conclusions. In the present study, several enculturation factors as well as self-efficacy were identified as potential protective factors against mental health problems. In order to develop theoretical models that explain the mechanisms between cultural resilience and mental health, there is a need for both qualitative studies and longitudinal studies

MFN2 point mutations occur in 3.4% of Charcot-Marie-Tooth families. An investigation of 232 Norwegian CMT families

Background Point mutations in the mitofusin 2 (MFN2) gene has been identified exclusively in Charcot-Marie-Tooth type 2 (CMT2), and in a single family with intermediate CMT. MFN2 point mutations are probably the most common cause of CMT2. Methods Two-hundred and thirty-two consecutive unselected and unrelated CMT families with available DNA from all regions in Norway were included. We screened for point mutations in the MFN2 gene. Results We identified four known and three novel point mutations in 8 unrelated CMT families. The novel point mutations were not found in 100 healthy controls. This corresponds to 3.4% (8/232) of CMT families have point mutations in the MFN2 gene. The phenotypes were compatible with CMT1 in two families, CMT2 in four families, intermediate CMT in one family and distal Hereditary Motor Neuropathy (dHMN) in one family. This corresponds to 2.3% of CMT1, 5.5% of CMT2, 12.5% of intermediate CMT and 6.7% of dHMN families have a point mutation in the MFN2 gene. Point mutations in the MFN2 gene is likely to be the fourth most common cause to CMT after duplication of the peripheral myelin protein 22 (PMP22) gene, and point mutations in the Connexin32 (Cx32) and myelin protein zero (MPZ) genes. Conclusions The identified known and novel point mutations in the MFN2 gene expand the clinical spectrum from CMT2 and intermediate CMT to also include possibly CMT1 and the dHMN phenotypes. Thus, genetic analyses of the MFN2 gene should not be restricted to persons with CMT2

Two novel connexin32 mutations cause early onset X-linked Charcot-Marie-Tooth disease

<p>Abstract</p> <p>Background</p> <p>X-linked Charcot-Marie Tooth (CMT) is caused by mutations in the connexin32 gene that encodes a polypeptide which is arranged in hexameric array and form gap junctions.</p> <p>Methods</p> <p>We describe two novel mutations in the connexin32 gene in two Norwegian families.</p> <p>Results</p> <p>Family 1 had a c.225delG (R75fsX83) which causes a frameshift and premature stop codon at position 247. This probably results in a shorter non-functional protein structure. Affected individuals had an early age at onset usually in the first decade. The symptoms were more severe in men than women. All had severe muscle weakness in the legs. Several abortions were observed in this family. Family 2 had a c.536 G>A (C179Y) transition which causes a change of the highly conserved cysteine residue, i.e. disruption of at least one of three disulfide bridges. The mean age at onset was in the first decade. Muscle wasting was severe and correlated with muscle weakness in legs. The men and one woman also had symptom from their hands.</p> <p>The neuropathy is demyelinating and the nerve conduction velocities were in the intermediate range (25–49 m/s). Affected individuals had symmetrical clinical findings, while the neurophysiology revealed minor asymmetrical findings in nerve conduction velocity in 6 of 10 affected individuals.</p> <p>Conclusion</p> <p>The two novel mutations in the connexin32 gene are more severe than the majority of previously described mutations possibly due to the severe structural change of the gap junction they encode.</p

The factor structure and psychometric properties of the Clinical Outcomes in Routine Evaluation - Outcome Measure (CORE-OM) in Norwegian clinical and non-clinical samples

Background The Clinical Outcomes in Routine Evaluation - Outcome Measure (CORE-OM) is a 34-item instrument developed to monitor clinically significant change in out-patients. The CORE-OM covers four domains: well-being, problems/symptoms, functioning and risk, and sums up in two total scores: the mean of All items, and the mean of All non-risk items. The aim of this study was to examine the psychometric properties of the Norwegian translation of the CORE-OM. Methods A clinical sample of 527 out-patients from North Norwegian specialist psychiatric services, and a non-clinical sample of 464 persons were obtained. The non-clinical sample was a convenience sample consisting of friends and family of health personnel, and of students of medicine and clinical psychology. Students also reported psychological stress. Exploratory factor analysis (EFA) was employed in half the clinical sample. Confirmatory (CFA) factor analyses modelling the theoretical sub-domains were performed in the remaining half of the clinical sample. Internal consistency, means, and gender and age differences were studied by comparing the clinical and non-clinical samples. Stability, effect of language (Norwegian versus English), and of psychological stress was studied in the sub-sample of students. Finally, cut-off scores were calculated, and distributions of scores were compared between clinical and non-clinical samples, and between students reporting stress or no stress. Results The results indicate that the CORE-OM both measures general (g) psychological distress and sub-domains, of which risk of harm separates most clearly from the g factor. Internal consistency, stability and cut-off scores compared well with the original English version. No, or only negligible, language effects were found. Gender differences were only found for the well-being domain in the non-clinical sample and for the risk domain in the clinical sample. Current patient status explained differences between clinical and non-clinical samples, also when gender and age were controlled for. Students reporting psychological distress during last week scored significantly higher than students reporting no stress. These results further validate the recommended cut-off point of 1 between clinical and non-clinical populations. Conclusions The CORE-OM in Norwegian has psychometric properties at the same level as the English original, and could be recommended for general clinical use. A cut-off point of 1 is recommended for both genders

Classification of bipolar disorder in psychiatric hospital. a prospective cohort study

<p>Abstract</p> <p>Background</p> <p>This study has explored the classification of bipolar disorder in psychiatric hospital. A review of the literature reveals that there is a need for studies using stringent methodological approaches.</p> <p>Methods</p> <p>480 first-time admitted patients to psychiatric hospital were found eligible and 271 of these gave written informed consent. The study sample was comprised of 250 patients (52%) with hospital diagnoses. For the study, expert diagnoses were given on the basis of a structured diagnostic interview (M.I.N.I.PLUS) and retrospective review of patient records.</p> <p>Results</p> <p>Agreement between the expert's and the clinicians' diagnoses was estimated using Cohen's kappa statistics. 76% of the primary diagnoses given by the expert were in the affective spectrum. Agreement concerning these disorders was moderate (kappa ranging from 0.41 to 0.47). Of 58 patients with bipolar disorder, only 17 received this diagnosis in the clinic. Almost all patients with a current manic episode were classified as currently manic by the clinicians. Forty percent diagnosed as bipolar by the expert, received a diagnosis of unipolar depression by the clinician. Fifteen patients (26%) were not given a diagnosis of affective disorder at all.</p> <p>Conclusions</p> <p>Our results indicate a considerable misclassification of bipolar disorder in psychiatric hospital, mainly in patients currently depressed. The importance of correctly diagnosing bipolar disorder should be emphasized both for clinical, administrative and research purposes. The findings questions the validity of psychiatric case registers. There are potential benefits in structuring the diagnostic process better in the clinic.</p

Two novel missense mutations in the myelin protein zero gene causes Charcot-Marie-Tooth type 2 and Déjérine-Sottas syndrome

<p>Abstract</p> <p>Background</p> <p>The Charcot-Marie-Tooth (CMT) phenotype caused by mutation in the <it>myelin protein zero (MPZ) </it>gene varies considerably, from early onset and severe forms to late onset and milder forms. The mechanism is not well understood. The myelin protein zero (P₀) mediates adhesion in the spiral wraps of the Schwann cell's myelin sheath. The crystalline structure of the extracellular domain of the myelin protein zero (P₀ex) is known, while the transmembrane and intracellular structure is unknown.</p> <p>Findings</p> <p>One novel missense mutation caused a milder late onset CMT type 2, while the second missense mutation caused a severe early onset phenotype compatible with Déjérine-Sottas syndrome.</p> <p>Conclusions</p> <p>The phenotypic variation caused by different missense mutations in the <it>MPZ </it>gene is likely caused by different conformational changes of the MPZ protein which affects the functional tetramers. Severe changes of the MPZ protein cause dysfunctional tetramers and predominantly uncompacted myelin, i.e. the severe phenotypes congenital hypomyelinating neuropathy and Déjérine-Sottas syndrome, while milder changes cause the phenotypes CMT type 1 and 2.</p

Heritability of Self-reported Phobic Fear

Twin studies on fear and phobia suggest moderate genetic effects. However, results are inconclusive regarding the presence of dominant genetic effects and sex differences. Using an extended twin design, including male and female twins (n = 5,465) and their siblings (n = 1,624), we examined the genetic and environmental influences on blood-injury, social, and agoraphobic fear and investigated their interaction with sex and age. Data of spouses (n = 708) of twins were used to evaluate assortative mating for the three fear dimensions. Results showed that there was no assortative mating for blood-injury, social and agoraphobic fear. Resemblance between biological relatives could be explained by additive and non-additive genetic effects for blood-injury and agoraphobic fear in all participants, and social fear in participants aged 14–25 years. For social fear in participants aged 26–65 only additive genetic effects were detected. Broad-sense heritability estimates ranged from 36 to 51% and were similar for men and women

The effect of temperature on growth and competition between Sphagnum species

Peat bogs play a large role in the global sequestration of C, and are often dominated by different Sphagnum species. Therefore, it is crucial to understand how Sphagnum vegetation in peat bogs will respond to global warming. We performed a greenhouse experiment to study the effect of four temperature treatments (11.2, 14.7, 18.0 and 21.4°C) on the growth of four Sphagnum species: S. fuscum and S. balticum from a site in northern Sweden and S. magellanicum and S. cuspidatum from a site in southern Sweden. In addition, three combinations of these species were made to study the effect of temperature on competition. We found that all species increased their height increment and biomass production with an increase in temperature, while bulk densities were lower at higher temperatures. The hollow species S. cuspidatum was the least responsive species, whereas the hummock species S. fuscum increased biomass production 13-fold from the lowest to the highest temperature treatment in monocultures. Nutrient concentrations were higher at higher temperatures, especially N concentrations of S. fuscum and S. balticum increased compared to field values. Competition between S. cuspidatum and S. magellanicum was not influenced by temperature. The mixtures of S. balticum with S. fuscum and S. balticum with S. magellanicum showed that S. balticum was the stronger competitor, but it lost competitive advantage in the highest temperature treatment. These findings suggest that species abundances will shift in response to global warming, particularly at northern sites where hollow species will lose competitive strength relative to hummock species and southern species

Speech Graphs Provide a Quantitative Measure of Thought Disorder in Psychosis

Background: Psychosis has various causes, including mania and schizophrenia. Since the differential diagnosis of psychosis is exclusively based on subjective assessments of oral interviews with patients, an objective quantification of the speech disturbances that characterize mania and schizophrenia is in order. In principle, such quantification could be achieved by the analysis of speech graphs. A graph represents a network with nodes connected by edges; in speech graphs, nodes correspond to words and edges correspond to semantic and grammatical relationships. Methodology/Principal Findings: To quantify speech differences related to psychosis, interviews with schizophrenics, manics and normal subjects were recorded and represented as graphs. Manics scored significantly higher than schizophrenics in ten graph measures. Psychopathological symptoms such as logorrhea, poor speech, and flight of thoughts were grasped by the analysis even when verbosity differences were discounted. Binary classifiers based on speech graph measures sorted schizophrenics from manics with up to 93.8% of sensitivity and 93.7% of specificity. In contrast, sorting based on the scores of two standard psychiatric scales (BPRS and PANSS) reached only 62.5% of sensitivity and specificity. Conclusions/Significance: The results demonstrate that alterations of the thought process manifested in the speech of psychotic patients can be objectively measured using graph-theoretical tools, developed to capture specific features of the normal and dysfunctional flow of thought, such as divergence and recurrence. The quantitative analysis of speech graphs is not redundant with standard psychometric scales but rather complementary, as it yields a very accurate sorting of schizophrenics and manics. Overall, the results point to automated psychiatric diagnosis based not on what is said, but on how it is said.FINEP [01.06.1092.00]FINEPCNPq Universal [481506/2007-1]CNPq UniversalCNPqCNPqCapesCAPESad Associacao Alberto Santos Dumont para Apoio a Pesquisa (AASDAP)a'd Associacao Alberto Santos Dumont para Apoio a Pesquisa (AASDAP