Does physical activity at a younger age reduce the likelihood of falls in seniors? / by Cindy Sabolic.

Purpose: Falls are a significant cause of death and disability and have a serious impact to the psychological and physical health of the elderly. The purpose of this research study was to determine if physical activity reduces the likelihood of falls in seniors living in long term care facility. The main objective of the study was to examine the association between an individual’s history of physical activity throughout their pastime, to determine whether involvement in physical activity at a younger age can be a determinant of the likelihood to incur a debilitating fall at an older age. The research was conducted on seniors currently aged seventy and older who reside at the Specialty Care Mississauga Road long term care center located in Mississauga, Ontario. Methods: This study used a retrospective cohort approach to determine the association between the physical activity at younger age and incidence of falls as documented in the fall risk assessment tool. A mail-out questionnaire was used to collect information on levels of past physical activity, periods of involvement in sport, and specific lifestyle behaviors. One hundred and sixty resident family members were asked to complete the questionnaire, providing specific information based on their loved one’s history. A total of 84 questionnaires were completed and returned. Data Analysis: The data that were collected from the fall risk assessment and questionnaire were entered into standard database for subsequent statistical analysis. The information from the two data sets (i.e retrospective physical activity profile and the falls risk assessment) were merged together to evaluate the research question using correlation procedures. Results: Pearson product moment correlation coefficient scores were computed using SAS to determine the relationship between the physical activity scores and fall risk assessment scores. The results indicated that there was no correlation between the two scores, in either the total group or the separate sub-groups created for age

Surgical Treatment of a Seven-Year-Old Boy with Refractory Epilepsy Due to Focal Cortical Dysplasia, Case Report

The most common developmental malformation encountered in patients with refractory epilepsy is Focal Cortical Dysplasia (FCD). Malformations of cortical development, in particular FCDs are identified in 20–25% of patients with focal epilepsy, and approximately 76% of these patients are supposed to suffer from drug-resistant epilepsy. A promising therapy option for these patients could be surgical treatment. We present a seven-year-old child with drug-resistant epilepsy, who underwent surgical treatment that had an excellent outcome. Throughout the period of five years, the index patient was admitted several times to the Department of Neurology at the University Pediatrics Clinic-Skopje. He was initially admitted at the age of two years, because of his first episode of febrile seizures accompanied by diarrhea. In the following period, during the hospitalization, febrile seizures also developed. CT findings showed a slight degree of front parietal cortical reduction, while the first MRI showed a slight dysmorphia at the frontal gyri, yet no focal abnormalities. The initial EEG revealed a bihemispheric epileptogenic focus. The reason for constant treatment alterations was drug-resistance. Although some encephalographic stabilization had been achieved, a full clinical response had never been obtained for a prolonged period. At the age of seven years, a pediatric epilepsy surgical team at the University School of Medicine–ACIBADEM, Turkey, evaluated the patient. The conclusion of the team was that the child is a candidate for surgical treatment of epilepsy. The child underwent surgery at the age of eight years and has been seizure free since.Keywords: Focal Cortical Dysplasia, Epilepsy, Surgery

MEDICAL CANNABIS IN PEDIATRICS (MYTH OR REAL POSSIBILITY)

The public interest in cannabis for medical use is acknowledged, and anecdotal reports of effectiveness in individual patients are compelling. Our objective isto make overview of the current scientific papers for medicinal cannabis use in paediatric population. Literature review was conducted utilizing, PubMed, Medline, and Google Scholar. Cannabis based product have promising potential for add-on treatment of certain conditions in paediatrics. Well-designed Randomized Clinical Trials (RCTs) with sufficient number of patients are imperative to demonstrate benefit of therapeutic use. In paediatrics, the greatest evidence for medicinal cannabis useis for seizure disorders. RCTs have demonstrated the safety and efficacy of oral Cannabidiol (CBD) for treatment of seizures associated with Lennox-Gastaut or Dravet syndrome.Keywords:  cannabinoids, medical marijuana, pediatrics

Effect of neonatal exposure to estrogenic compounds on development of the excurrent ducts of the rat testis through puberty to adulthood.

Neonatal exposure to diethylstilbestrol (DES) can alter the structure of the testicular excurrent ducts in rats. We characterized these changes according to dose and time posttreatment and established whether potent estrogens (ethinyl estradiol), environmental estrogens (genistein, octylphenol, bisphenol A, parabens), and tamoxifen induce such changes. Rats were administered these compounds neonatally and assessed at several time points during (day 10, or day 18 for some treatments) and after (days 18, 25, 35, and 75) the treatment period to detect any changes in testis weight, distension of the rete testis and efferent ducts, epithelial cell height in the efferent ducts, and immunoexpression of the water channel aquaporin-1 (AQP-1). Treatment with DES (10, 1, or 0.1 microg/injection; equivalent to 0.37, 0.037, or 0.0037 mg/kg/day, respectively) induced dose-dependent changes in testis weight and all parameters. These effects were most pronounced at days 18 and 25 and appeared to lessen with time, although some persisted into adulthood. Neonatal treatment with ethinyl estradiol (10 microg/injection; equivalent to 0.37 mg/kg/day) caused changes broadly similar to those induced by 10 mg DES. Administration of tamoxifen (2 mg/kg/day) caused changes at 18 days that were similar to those induced by 1 microg DES. Treatment with genistein (4 mg/kg/day), octylphenol (2 mg/injection; equivalent to 150 mg/kg/day), or bisphenol A (0.5 mg/injection; equivalent to 37 mg/kg/day) caused minor but significant (p<0.05) decreases in epithelial cell height of the efferent ducts at days 18 and/or 25. In animals that were followed through to 35 days and/or adulthood, these changes were no longer obvious; other parameters were either unaffected or were affected only marginally and transiently. Administration of parabens (2 mg/kg/day) had no detectable effect on any parameter at day 18. To establish whether these effects of estrogens were direct or indirect (i.e., resulting from reduced follicle-stimulating hormone/luteinizing hormone secretion), the above end points were assessed in animals in which gonadotropin secretion was suppressed neonatally by administration of a gonadotropin-releasing hormone antagonist. This treatment permanently reduced testis weight, but did not affect any of the other end points, apart from a minor transient reduction in efferent duct epithelial cell height at 18 days. This study suggests that structural and functional (expression of AQP-1) development of the excurrent ducts is susceptible to impairment by neonatal estrogen exposure, probably as a consequence of direct effects. The magnitude and duration of adverse changes induced by treatment with a range of estrogenic compounds was broadly comparable to their estrogenic potencies reported from in vitro assays

Cisplatin administration influences on toxic and non-essential element metabolism in rats

Nowadays several papers deal with the effectiveness and side effects of metal complexes, especially cisplatin, in cancer therapy. The excretion of essential metal elements from the body is a serious problem in the treatment, but there are no data concerning the distribution and metabolism of toxic and nonessential elements. Therefore our aim was to study the concentration of some of these elements after treatment with cisplatin. Male Wistar rats (n=20, 175-190 g) were randomly divided into 2 groups (n=10/group). The control group received 1% (w/v) methyl cellulose at 10 mL/kg body weight, p.o. by gastric gavage twice daily for 14 days, while cisplatin was injected i.p. in a single dose of 6.5 mg/kg body weight. Inductively coupled plasma optical emission spectrometry (ICP-OES) was used for measuring Al, B, Ba, Cr, Li, Ni, Pb, Pt, Sb, Si, Sn, Sr and V content in plasma, liver and kidney. Liver total scavenger capacity, diene conjugate content and malondialdehyde concentration were also determined. Cisplatin elevated the free radical reactions in the liver, although redox balance did not change significantly. According to the study it seems that the metabolism of Al, Ba, Cr, Ni, Pb, Sr were changed by the effect of cisplatin, and the most notable alterations were found for Al and Pb. Therefore, besides the toxic effect of and free radical induction by Pt, the side effects of increased levels of other toxic and non-essential elements have to be taken into consideration

Novel polymorphic AluYb8 insertion in the WNK1 gene is associated with blood pressure variation in Europeans

Mutations in WNK1 and WNK4 cause familial hypertension, the Gordon syndrome. WNK1 and WNK4 conserved noncoding regions were targeted to polymorphism screening using DHPLC and DGGE. The scan identified an undescribed polymorphic AluYb8 insertion in WNK1 intron 10. Screening in primates revealed that this Alu-insertion has probably occurred in human lineage. Genotyping in 18 populations from Europe, Asia, and Africa (n = 854) indicated an expansion of the WNK1 AluYb8 bearing chromosomes out of Africa. The allele frequency in Sub-Saharan Africa was ∼3.3 times lower than in other populations (4.8 vs. 15.8%; P = 9.7 × 10−9). Meta-analysis across three European sample sets (n = 3,494; HYPEST, Estonians; BRIGHT, the British; CADCZ, Czech) detected significant association of the WNK1 AluYb8 insertion with blood pressure (BP; systolic BP, P = 4.03 × 10−3, effect 1.12; diastolic BP, P = 1.21 × 10−2, effect 0.67). Gender-stratified analysis revealed that this effect might be female-specific (n = 2,088; SBP, P = 1.99 × 10−3, effect 1.59; DBP P = 3.64 × 10−4, effect 1.23; resistant to Bonferroni correction), whereas no statistical support was identified for the association with male BP (n = 1,406). In leucocytes, the expressional proportions of the full-length WNK1 transcript and the splice-form skipping exon 11 were significantly shifted in AluYb8 carriers compared to noncarriers. The WNK1 AluYb8 insertion might affect human BP via altering the profile of alternatively spliced transcripts. Hum Mutat 32:1–9, 2011. © 2011 Wiley-Liss, Inc

Na(+)-D-glucose cotransporter SGLT1 is pivotal for intestinal glucose absorption and glucose-dependent incretin secretion.

To clarify the physiological role of Na(+)-D-glucose cotransporter SGLT1 in small intestine and kidney, Sglt1(-/-) mice were generated and characterized phenotypically. After gavage of d-glucose, small intestinal glucose absorption across the brush-border membrane (BBM) via SGLT1 and GLUT2 were analyzed. Glucose-induced secretion of insulinotropic hormone (GIP) and glucagon-like peptide 1 (GLP-1) in wild-type and Sglt1(-/-) mice were compared. The impact of SGLT1 on renal glucose handling was investigated by micropuncture studies. It was observed that Sglt1(-/-) mice developed a glucose-galactose malabsorption syndrome but thrive normally when fed a glucose-galactose-free diet. In wild-type mice, passage of D-glucose across the intestinal BBM was predominantly mediated by SGLT1, independent the glucose load. High glucose concentrations increased the amounts of SGLT1 and GLUT2 in the BBM, and SGLT1 was required for upregulation of GLUT2. SGLT1 was located in luminal membranes of cells immunopositive for GIP and GLP-1, and Sglt1(-/-) mice exhibited reduced glucose-triggered GIP and GLP-1 levels. In the kidney, SGLT1 reabsorbed ∼3% of the filtered glucose under normoglycemic conditions. The data indicate that SGLT1 is 1) pivotal for intestinal mass absorption of d-glucose, 2) triggers the glucose-induced secretion of GIP and GLP-1, and 3) triggers the upregulation of GLUT2

Expression Profile of Nuclear Receptors along Male Mouse Nephron Segments Reveals a Link between ERRβ and Thick Ascending Limb Function

The nuclear receptor family orchestrates many functions related to reproduction, development, metabolism, and adaptation to the circadian cycle. The majority of these receptors are expressed in the kidney, but their exact quantitative localization in this ultrastructured organ remains poorly described, making it difficult to elucidate the renal function of these receptors. In this report, using quantitative PCR on microdissected mouse renal tubules, we established a detailed quantitative expression map of nuclear receptors along the nephron. This map can serve to identify nuclear receptors with specific localization. Thus, we unexpectedly found that the estrogen-related receptor β (ERRβ) is expressed predominantly in the thick ascending limb (TAL) and, to a much lesser extent, in the distal convoluted tubules. In vivo treatment with an ERR inverse agonist (diethylstilbestrol) showed a link between this receptor family and the expression of the Na+,K+-2Cl− cotransporter type 2 (NKCC2), and resulted in phenotype presenting some similarities with the Bartter syndrom (hypokalemia, urinary Na+ loss and volume contraction). Conversely, stimulation of ERRβ with a selective agonist (GSK4716) in a TAL cell line stimulated NKCC2 expression. All together, these results provide broad information regarding the renal expression of all members of the nuclear receptor family and have allowed us to identify a new regulator of ion transport in the TAL segments

ВажноÑÑ‚ на 6 минутниот теÑÑ‚ на одење во дијагноÑтика на ретка метаболна миопатија – приказ на Ñлучај на карнитин палмитоил транÑфераза 2 дефицит

Diagnosis of rare inherited neuromuscular disorders is sometimes delayed due to variations in time of onset, different clinical appearance and limited diagnostic possibilities. The management of patients  starts  with neurological examination, followed by  specific laboratory tests  and neurophysiologic assessment. In the  era of molecular medicine, molecular biology tools are useful in avoiding some of the invasive investigations such as muscle biopsy. We present a boy with a mild form of metabolic myopathy due to carnitine  palmitoyltransferase  2 deficiency diagnosed upon timed functional assessment. A child had delayed developmental milestones, associated with fatigue and muscle pain during exercising and longer walks. There were no episodes of myoglobinuiria during exercise or during febrile illnesses. Neurological examination reveled proximal muscle weakness. Serum creatine kinase (CK) and serum lactate were above normal limits. Serum acylcarnitine profile was normal. Short timed functional tests such as 10 meters  walk/run test  showed normal results. Nord Star Ambulatory Assessment showed difficulties in balance and jumping. Diagnosis of myopathy was suspected after performance of 6-minute walk test, when the passed distance was 327 meters with slowing and fatigue. EMG and echocardiography were within normal range. Diagnosis was established by sequencing  of the CPT II gene which revealed   c.338C&gt;T (p.Ser113Leu) mutation in homozygous form as characteristic CPT II deficiency profile.Дијагнозата на ретките невромуÑкулни заболувања е понекогаш пролонгирана заради различното вре- ме на почеток на Ñимптомите, различната клиничка Ñлика и ограничените дијагноÑтички можноÑти. Обработката на пациентот започнува Ñо невролошки преглед, по што Ñледат Ñпецифични лаборато- риÑки теÑтови и неврофизиолошки иÑпитувања. Во ера на молекуларната медицина, генетÑката анали- за овозможува да Ñе избегнат некои од инвазивните иÑпитувања, како на пример муÑкулната биопÑија. Прикажуваме момче Ñо блага форма на метаболичка миопатија Ñо карнитин палмитоил транÑфераза 2 (CPT II) дефицит, која е дијагноÑтицирана врз оÑнова на временÑка функционална проценка. Детето имало забавен моторен развој, Ñо замор и муÑкулна болка во тек на вежбање или подолго одење. Ðема- ло епизоди на миоглобинурија во тек на вежбање или во тек на фебрилни болеÑти. Ðевролошкиот пре- глед покажа прокÑимална муÑкулна ÑлабоÑÑ‚. СерумÑката креатин киназа и ÑерумÑкото ниво на лакта- ти беа над нормалните граници. СерумÑкиот профил на ацил карнитини беше нормален. Кратките функционални теÑтови како 10 метри одење/трчање покажаа уредни резултати. Nord Star Ambulatory Assessment  – теÑтирањето покажа потешкотии во рамнотежата и при Ñкокање. Сомнение за вродена миопатија Ñе поÑтави по изведување на подолготраен функционален теÑÑ‚ – 6-минутниот теÑÑ‚ на одење кога поминатата  Ð´Ð¸Ñтанца беше 327 метри Ñо уÑпорување и замор. Електроневромиографијата и ехо- кардиографијата кај детето покажаа нормални наоди. Дијагнозата беше потврдена Ñо Ñеквенциони- рање на CPT II генот Ñо региÑтрирање на c.338C&gt;T (p.Ser113Leu) мутација  Ð²Ð¾ хомозиготна форма која е карактериÑтична за CPT II дефицит