The Level of Physical Fitness and Everyday Activities vs. Sensory Integration Processing Disorders in Preschool Children – Preliminary Findings

Introduction: Sensory integration processing is defined as organization and interpretation of stimuli reaching the organism. The correctly functioning nervous system interprets sensory impressions, which enables development of awareness of one’s own body and of the surrounding environment. Sensory processing disorders can have a significant impact on the child’s functioning. Aim: The objective of the research was to answer the question whether sensory integration processing disorders in preschool children have an influence on their physical fitness and everyday activities. The research covered a group of 60 preschool children. The studied group comprised 30 children with diagnosed sensory processing disorders, while the control group consisted of 30 children with no disorders diagnosed. Results: The results achieved demonstrate lower physical fitness of children from the studied group and problems with performing everyday activities. The tasks connected with speed and agility were the most problematic. Among everyday activities, the most difficult were: cycling, ball catching, getting dressed and descending stairs. Knowledge of sensory integration processing disorders helps understand problems in the child’s functioning and provides an opportunity to intervene in the form of the sensory integration therapy

High fat mixed meal tolerance test leads to suppression of osteocalcin decrease in obese insulin resistant subjects compared to healthy adults

Nutrients influence bone turnover. Carboxylated osteocalcin (Gla-OC) participates in bone formation whereas its undercarboxylated form (Glu-OC) acts as a hormone in glucose metabolism. The aim of the study was to determine the responses of Gla-OC, Glu-OC, and total-OC (calculated as the sum of Gla-OC and Glu-OC) to a high fat mixed meal tolerance test (HFMTT) in non-obese (body mass index (BMI) < 30 kg/m2, n = 24) and obese subjects (30 < BMI < 40 kg/m2, n = 70) (both sexes, aged 25⁻65 years). Serum Gla-OC and Glu-OC were measured at baseline as well as at 2 and 6 h during a HFMTT by enzyme-linked immunosorbent assay (ELISA). Baseline Gla-OC, Glu-OC, and total-OC levels were lower in obese individuals compared to non-obese participants (p = 0.037, p = 0.016 and p = 0.005, respectively). The decrease in Gla-OC and total-OC, but not in Glu-OC, concentrations during the HFMTT was suppressed in obese, but not in non-obese controls (p < 0.05, p < 0.01, p = 0.08, respectively). Subjects with the highest homeostatic model assessment for insulin resistance (HOMA-IR) index values had a less pronounced decrease in total-OC compared to patients with values of HOMA-IR index in the 1st quartile (p < 0.05). Net incremental area under Gla-OC inversely correlated with adiponectin (rho = −0.35, p = 0.001). Increase in insulin sensitivity and adiponectin level in obese subjects could beneficially influence postprandial bone turnover expressed by osteocalcin concentration

Evidence for a relatively high proportion of DM2 mutations in a large group of Polish patients

Introduction: Myotonic dystrophies (DMs) type 1 (DM1) and type 2 (DM2) are autosomal dominant, multisystem disorders, considered the most common dystrophies in adults. DM1 and DM2 are caused by dynamic mutations in the DMPK and CNBP genes, respectively. Methods: Molecular analyses were performed by PCR and the modified RP-PCR in patients, in their at-risk relatives and prenatal cases. Results: The analysis of Polish controls revealed the range of 5-31 CTG repeats for DM1 and 110-228 bp alleles for DM2. Among 318 confirmed probands - 196 (62%) were DM1 and 122 (38%) – DM2. Within DM1families, 10 subjects carried a low expanded CTG tract (< 100 repeats), which resulted in a full mutation in subsequent generations. Two related individuals had unstable alleles–188 bp and 196 bp without common interruptions. Conclusion: The relative frequencies of DM1/DM2 among Polish patients were 68% and 32%, respectively, with a relatively high proportion of DM2 mutations (1.6:1)

Carboxylated and undercarboxylated osteocalcin in metabolic complications of human obesity and prediabetes

Background Carboxylated osteocalcin (Gla‐OC) participates in bone remodeling, whereas the undercarboxylated form (Glu‐OC) takes part in energy metabolism. This study was undertaken to compare the blood levels of Glu‐OC and Gla‐OC in nonobese, healthy obese, and prediabetic volunteers and correlate it with the metabolic markers of insulin resistance and early markers of inflammation. Methods Nonobese (body mass index [BMI] <30 kg/m2 ; n = 34) and obese subjects (30 <BMI <40 kg/m2 ; n = 98), both sexes, aged 25 to 65 years, were divided into healthy control, normal weight subjects, healthy obese, and obese with biochemical markers of prediabetes. The subgroups with obesity and low or high Gla‐OC or Glu‐OC were also considered for statistical analysis. After 2 weeks of diet standardization, venous blood was sampled for the determination of Gla‐OC, Glu‐OC, lipid profile, parameters of inflammation (hsCRP, interleukin 6, sE‐selectin, sPECAM‐1, and monocyte chemoattractant protein 1), and adipokines (leptin, adiponectin, visfatin, and resistin). Results Gla‐OC in obese patients was significantly lower compared to nonobese ones (11.36 ± 0.39 vs 12.69 ± 0.90 ng/mL, P = .048) and weakly correlated with hsCRP (r = −0.18, P = .042), visfatin concentration (r = −0.19, P = .033), and BMI (r = −0.17, P = .047). Glu‐OC was negatively associated with fasting insulin levels (r = −0.18, P = .049) and reduced in prediabetic individuals compared with healthy obese volunteers (3.04 ± 0.28 vs 4.48 ± 0.57, P = .025). Conclusions Decreased blood concentration of Glu‐OC may be a selective early symptom of insulin resistance in obesity, whereas the decreased level of Gla‐OC seems to be associated with the appearance of early markers of low grade inflammation accompanying obesity

Applied methods of exercise based therapy for the extension of walking distance in patients with intermittent claudication

Intermittent claudication, according to the Fontaine Classification Scale is a symptom of 2nd degree atherosclerosis of the arteries of the lower limbs. The process of atherosclerosis involves increased narrowing of the blood vessel lumina and their eventual closure. Patients with atherosclerosis often suffer bouts of muscular pain while walking which eventually leads to restricted mobility. The treatment of those affected by furring up of the arteries of the lower limbs includes intravascular procedures, insertion of balloon devices and stents and in severe cases of atherosclerosis surgical intervention is required. The more conservative areas of treatment involve pharmacotherapy, patient participation in educational training sessions, lifestyle changes and appropriate physiotherapy referrals. If applied early on, lifestyle changes such as smoking cessation, an improved diet, as well as targeted training can help avoid the need for surgical intervention. At the moment, the goal of mainstream physiotherapy in the treatment of peripheral artery disease is to determine the most appropriate forms of exercise which can increase the walking distance of patients with intermittent claudication, improve blood-flow in particular to the lower extremities as well as improve patients’ overall quality of life. The purpose of this study is to gather and analyse exercise strategies that result in increased walking distance in intermittent claudication. The best results have been observed in groups who teamed up ambulatory therapy with strength training; Nordic walking therapy along with strength training and finally walking training with upper body aerobic training on the cross-trainer. The variety of training combinations gives us the ability to cater for and accommodate individual patient needs

Identification of genetic variants associated with Huntington's disease progression: a genome-wide association study

Background Huntington's disease is caused by a CAG repeat expansion in the huntingtin gene, HTT. Age at onset has been used as a quantitative phenotype in genetic analysis looking for Huntington's disease modifiers, but is hard to define and not always available. Therefore, we aimed to generate a novel measure of disease progression and to identify genetic markers associated with this progression measure. Methods We generated a progression score on the basis of principal component analysis of prospectively acquired longitudinal changes in motor, cognitive, and imaging measures in the 218 indivduals in the TRACK-HD cohort of Huntington's disease gene mutation carriers (data collected 2008–11). We generated a parallel progression score using data from 1773 previously genotyped participants from the European Huntington's Disease Network REGISTRY study of Huntington's disease mutation carriers (data collected 2003–13). We did a genome-wide association analyses in terms of progression for 216 TRACK-HD participants and 1773 REGISTRY participants, then a meta-analysis of these results was undertaken. Findings Longitudinal motor, cognitive, and imaging scores were correlated with each other in TRACK-HD participants, justifying use of a single, cross-domain measure of disease progression in both studies. The TRACK-HD and REGISTRY progression measures were correlated with each other (r=0·674), and with age at onset (TRACK-HD, r=0·315; REGISTRY, r=0·234). The meta-analysis of progression in TRACK-HD and REGISTRY gave a genome-wide significant signal (p=1·12 × 10−10) on chromosome 5 spanning three genes: MSH3, DHFR, and MTRNR2L2. The genes in this locus were associated with progression in TRACK-HD (MSH3 p=2·94 × 10−8 DHFR p=8·37 × 10−7 MTRNR2L2 p=2·15 × 10−9) and to a lesser extent in REGISTRY (MSH3 p=9·36 × 10−4 DHFR p=8·45 × 10−4 MTRNR2L2 p=1·20 × 10−3). The lead single nucleotide polymorphism (SNP) in TRACK-HD (rs557874766) was genome-wide significant in the meta-analysis (p=1·58 × 10−8), and encodes an aminoacid change (Pro67Ala) in MSH3. In TRACK-HD, each copy of the minor allele at this SNP was associated with a 0·4 units per year (95% CI 0·16–0·66) reduction in the rate of change of the Unified Huntington's Disease Rating Scale (UHDRS) Total Motor Score, and a reduction of 0·12 units per year (95% CI 0·06–0·18) in the rate of change of UHDRS Total Functional Capacity score. These associations remained significant after adjusting for age of onset. Interpretation The multidomain progression measure in TRACK-HD was associated with a functional variant that was genome-wide significant in our meta-analysis. The association in only 216 participants implies that the progression measure is a sensitive reflection of disease burden, that the effect size at this locus is large, or both. Knockout of Msh3 reduces somatic expansion in Huntington's disease mouse models, suggesting this mechanism as an area for future therapeutic investigation

The activity of micafungin against clinical isolates of non-albicans Candida spp.

Infections caused by non-albicans Candida spp. are an important medical problem in people from risk groups, e.g. hematooncological patients. The aim of this paper was to analyse the in vitro activity of micafungin against 30 clinical isolates of non-albicans Candida spp. (C. glabrata, C. famata, C. tropicalis, C. inconspicua, C. lusitaniae, C. parapsilosis, C. krusei) by way of the E-test procedure, allowing determination of minimal inhibitory concentration (MIC). Data presented in this paper indicate that most of the studied clinical isolates - 27 (90%) showed sensitivity to micafungin, with MIC values ranging from 0.004 to 2 mg/l, while 3 (10%) isolates, including 2 isolates of C. tropicalis and 1 isolate of C. famata, were resistant to micafungin, with MIC values > 32 mg/l. The MIC50 and MIC90 values of micafungin, defined as MIC inhibited growth of 50% or 90% of the isolates studied, were 0.008 mg/l or 2 mg/l, respectively. In the case of C. glabrata isolates, MICs ranged from 0.004 to 0.016 mg/l, while MIC50 was 0.004 mg/l and MIC90 - 0.008 mg/l. Our data confirm the utility of micafungin for the therapy of the infections caused by non-albicans Candida spp., especially C. glabrata