Biological Sampling and Physical Habitat Assessment Standard Operating Procedure for Iowa Wadeable Streams and Rivers, July 24, 2015

The Iowa Department of Natural Resources uses benthic macroinvertebrate and fish sampling data to assess stream biological condition and the support status of designated aquatic life uses (Wilton 2004; IDNR 2013). Stream physical habitat data assist with the interpretation of biological sampling results by quantifying important physical characteristics that influence a stream’s ability to support a healthy aquatic community (Heitke et al., 2006; Rowe et al. 2009; Sindt et al., 2012). This document describes aquatic community sampling and physical habitat assessment procedures currently followed in the Iowa stream biological assessment program. Standardized biological sampling and physical habitat assessment procedures were first established following a pilot sampling study in 1994 (IDNR 1994a, 1994b). The procedure documents were last updated in 2001 (IDNR 2001a; 2001b). The biological sampling and physical habitat assessment procedures described below are evaluated on a continual basis. Revision of this working document will occur periodically to reflect additional changes.

Revealing a subclinical salt-losing phenotype in heterozygous carriers of the novel S562P mutation in the alpha subunit of the epithelial sodium channel.

OBJECTIVE: Pseudohypoaldosteronism type I (PHA1) is a rare inborn disease causing severe salt loss. Mutations in the three coding genes of the epithelial sodium channel (ENaC) are responsible for the systemic autosomal recessive form. So far, no phenotype has been reported in heterozygous carriers. PATIENTS: A consanguineous family from Somalia giving birth to a neonate suffering from PHA1 was studied including clinical and hormonal characteristics of the family, mutational analysis of the SCNN1A, SCNN1B, SCNN1G and CFTR genes and in vitro analysis of the functional consequences of a mutant ENaC channel. RESULTS: CFTR mutations have been excluded. SCNN1A gene analysis revealed a novel homozygous c.1684T > C mutation resulting in a S562P substitution in the alphaENaC protein of the patient. Functional analysis showed a significantly reduced S562P channel function compared to ENaC wild type. Protein synthesis and channel subunit assembly were not altered by the S562P mutation. Co-expression of mutant and wild-type channels revealed a dominant negative effect. In heterozygote carriers, sweat sodium and chloride concentrations were increased without additional hormonal or clinical phenotypes. CONCLUSION: Hence, the novel mutation S562P is causing systemic PHA1 in the homozygous state. A thorough clinical investigation of the heterozygote SCNN1A mutation carriers revealed increased sweat sodium and chloride levels consistent with a dominant effect of the mutant S562P allele. Whether this subclinical phenotype is of any consequence for the otherwise asymptomatic heterozygous carriers has to be elucidated.

Monday Morning Eye Opener, August 24, 2015

Weekly Newsletter from the Northwest District Office for libraries containing programs, activities, classes for the upcoming week.

CARDIAC AND MUSCLE CHANNELOPATHIES: ROLES AND REGULATION OF VOLTAGE-GATED SODIUM CHANNELS

Abstract :The contraction of the heart or skeletal muscles is mainly due to the propagation, through excitable cells, of an electrical influx called action potential (AP). The AP results from the sequential opening of ion channels that generate inward or outward currents through the cell membrane. Among all the channels involved, the voltage-gated sodium channel is responsible for the rising phase of the action potential. Ten genes encode the different isoforms of these channels (from Nav1.1 to Nav1.9 and an atypical channel named NavX). Nav1.4 and Nav1.5 are the main skeletal muscle and cardiac sodium channels respectively. Their importance for muscle and heart function has been highlighted by the description of mutations in their encoding genes SCN4A and SCNSA. They lead respectively to neuromuscular disorders such as myotonia or paralysis (for Nav1.4), and to cardiac arrhythmias that can deteriorate into sudden cardiac death (for Nav1.5).The general aim of my PhD work has been to study diseases linked with channels dysfunction, also called channelopathies. In that purpose, I investigated the function and the regulation of the muscle and cardiac voltage-gated sodium channels. During the two first studies, I characterized the effects of two mutations affecting Nav1.4 and Nav1.5 function. I used the HEK293 model cells to express wild-type or mutant channels and then studied their biophysical properties with the patch-clamp technique, in whole cell configuration. We found that the SCN4A mutation produced complex alterations of the muscle sodium channel function, that could explain the myotonic phenotype described in patients carrying the mutation. In the second study, the index case was an heterozygous carrier of a SCNSA mutation that leads to a "loss of function" of the channel. The decreased sodium current measured with mutated Nay 1.5 channels, at physiological temperature, was a one of the factors that could explain the observed Brugada syndrome. The last project aimed at identifying a new potential protein interacting with the cardiac sodium channel. We found that the protein SAP97 binds the three last amino-acids of the C-terminus of Na,, 1.5. Our results also indicated that silencing the expression of SAP97 in HEK293 cells decreased the sodium current. Sodium channels lacking their three last residues also produced a reduced INa. These preliminary results suggest that SAP97 is implicated in the regulation of sodium channel. Whether this effect is direct or imply the action of an adaptor protein remains to be investigated. Moreover, our group has previously shown that Nav1.5 channels are localized to lateral membranes of cardiomyocytes by the dystrophin multiprotein complex (DMC). This suggests that sodium channels are distributed in, at least, two different pools: one targeted at lateral membranes by DMC and the other at intercalated discs by another protein such as SAP97.These studies reveal that cardiac and muscle diseases may result from ion channel mutations but also from regulatory proteins affecting their regulation.Résumé :La contraction des muscles et du coeur est principalement due à la propagation, à travers les cellules excitables, d'un stimulus électrique appelé potentiel d'action (PA). C'est l'ouverture séquentielle de plusieurs canaux ioniques transmembranaires, permettant l'entrée ou la sortie d'ions dans la cellule, qui est à l'origine de ce PA. Parmi tous les canaux ioniques impliqués dans ce processus, les canaux sodiques dépendant du voltage sont responsables de la première phase du potentiel d'action. Les différentes isoformes de ces canaux (de Nav1.1 à Nav1.9 et NavX) sont codées par dix gènes distincts. Nav1.4 et Nav1.5 sont les principaux variants exprimés respectivement dans le muscle et le coeur. Plusieurs mutations ont été décrites dans les gènes qui codent pour ces deux canaux: SCN4A (pour Nav1.4) et SCNSA (pour Nav1.5). Elles sont impliquées dans des pathologies neuromusculaires telles que des paralysies ou myotonies (SCN4A) ou des arythmies cardiaques pouvant conduire à la mort subite cardiaque (SCNSA).Mon travail de thèse a consisté à étudier les maladies liées aux dysfonctionnements de ces canaux, aussi appelées canalopathies. J'ai ainsi analysé la fonction et la régulation des canaux sodiques dépendant du voltage dans le muscle squelettique et le coeur. A travers les deux premières études, j'ai ainsi pu examiner les conséquences de deux mutations affectant respectivement les canaux Nav1.4 et Nav1.5. Les canaux sauvages ou mutants ont été exprimés dans des cellules HEK293 afin de caractériser leurs propriétés biophysiques par la technique du patch clamp en configuration cellule entière. Nous avons pu déterminer que la mutation trouvée dans le gène SCN4A engendrait des modifications importantes de la fonction du canal musculaire. Ces altérations fournissent des indications nous permettant d'expliquer certains aspects de la myotonie observée chez les membres de la famille étudiée. Le patient présenté dans la deuxième étude était hétérozygote pour la mutation identifiée dans le gène SCNSA. La perte de fonction des canaux Nav1.5 ainsi engendrée, a été observée lors d'analyses à températures physiologiques. Elle représente l'un des éléments pouvant potentiellement expliquer le syndrome de Brugada du patient. La dernière étude a consisté à identifier une nouvelle protéine impliquée dans la régulation du canal sodique cardiaque. Nos expériences ont démontré que les trois derniers acides aminés de la partie C-terminale de Nav1.5 pouvaient interagir avec la protéine SAP97. Lorsque que l'expression de la SAP97 est réduite dans les cellules HEK293, cela induit une baisse importante du courant sodique. De même, les canaux tronqués de leurs trois derniers acides aminés génèrent un flux ionique réduit. Ces résultats préliminaires suggèrent que SAP97 est peut-être impliquée dans la régulation du canal Na,,1.5. Des expériences complémentaires permettront de déterminer si ces deux protéines interagissent directement ou si une protéine adaptatrice est nécessaire. De plus, nous avons préalablement montré que les canaux Nav1.5 étaient localisés au niveau de la membrane latérale des cardiomyocytes par le complexe multiprotéique de la dystrophine (DMC). Ceci suggère que les canaux sodiques peuvent être distribués dans un minimum de deux pools, l'un ciblé aux membranes latérales pax le DMC et l'autre dirigé vers les disques intercalaires par des protéines telles que SAP97.L'ensemble de ces études met en évidence que certaines maladies musculaires et cardiaques peuvent être la conséquence directe de mutations de canaux ioniques, mais que l'action de protéines auxiliaires peut aussi affecter leur fonction.

Relationships among endogenous ouabain, alpha-adducin polymorphisms and renal sodium handling in primary hypertension.

OBJECTIVE: The basolateral Na pump drives renotubular reabsorption. In cultured renal cells, mutant adducins, as well as sub-nanomolar ouabain concentrations, stimulate the Na-K pump. METHODS: To determine whether these factors interact and affect Na handling and blood pressure (BP) in vivo, we studied 155 untreated hypertensive patients subdivided on the basis of their plasma endogenous ouabain or alpha-adducin genotype (ADD1 Gly460Trp-rs4961). RESULTS: Under basal conditions, proximal tubular reabsorption and plasma Na were higher in patients with mutated Trp ADD1 or increased endogenous ouabain (P = 0.002 and 0.05, respectively). BPs were higher in the high plasma endogenous ouabain group (P = 0.001). Following volume loading, the increment in BP (7.73 vs. 4.81 mmHg) and the slopes of the relationship between BP and Na excretion were greater [0.017 +/- 0.002 vs. 0.009 +/- 0.003 mmHg/(muEq min)] in ADD1 Trp vs. ADD1 Gly carriers (P < 0.05). BP changes were similar, whereas the slopes of the relationship between BP and Na excretion were lower [0.016 +/- 0.003 vs. 0.008 +/- 0.002 mmHg/(muEq min)] in patients with low vs. high endogenous ouabain (P < 0.05). In patients with high endogenous ouabain, volume loading increased the BP in the ADD1 Trp group but not in the Gly group (P < 0.05). Thus, patients with ADD1 Trp alleles are sensitive to salt and tubular Na reabsorption remains elevated after volume expansion. CONCLUSION: With saline loading, BP changes are similar in high and low endogenous ouabain patients, whereas tubular Na reabsorption increases in the high endogenous ouabain group. Saline loading unmasks differences in renal Na handling in patients with mutant adducin or high endogenous ouabain and exposes an interaction of endogenous ouabain and Trp alleles on BP.

Iowa Crop Progress & Condition, August 24, 2015

Report produced by the The Department of Agriculture and Land Stewardship, Climatology Bureau. Weather report released by the USDA National Agricultural Statistical Service. The report is released weekly from April through October. Formally titled: Iowa Crop and Weather Report

Trayectorias docentes e investigadoras en la universidad. 24 historias de vida profesional. Los efectos de los cambios en el trabajo y la vida profesional de los docentes universitarios

[spa] Este texto forma parte de un proyecto de investigación Los efectos de los cambios sociales en el trabajo y la vida profesional de los docentes universitarios, parcialmente financiado por el Ministerio de Ciencia e Innovación (SEJ2006-01876), en el que nos planteamos explorar los cambios los ámbitos de la legislación, laorganización institucional, la investigación, la gestión y la docencia en los últimos treinta años. El principal objetivo del estudio era profundizar en nuestra comprensión sobre el impacto del cambio económico, social, cultural, tecnológico y laboral que están experimentando las universidades españolas en la vida y la identidad profesional del personal docente e investigador, teniendo en cuenta el contexto nacional y europeo. Estapublicación recoge la 24 historias de vida profesional realizas con o sobre otros tantos docentes universitarios. Sus relatos analizados y contextualizados, significan una contribución significativa al conocimiento basado en la investigación sobre el saber profesional y la experiencia laboral en las universidades españolas, y en consecuencia, a nuestra comprensión sobre cómo los académicos se están enfrentando con los cambios actuales.

Trayectorias docentes e investigadoras en la universidad. 24 historias de vida profesional. Los efectos de los cambios en el trabajo y la vida profesional de los docentes universitarios

[spa] Este texto forma parte de un proyecto de investigación Los efectos de los cambios sociales en el trabajo y la vida profesional de los docentes universitarios, parcialmente financiado por el Ministerio de Ciencia e Innovación (SEJ2006-01876), en el que nos planteamos explorar los cambios los ámbitos de la legislación, laorganización institucional, la investigación, la gestión y la docencia en los últimos treinta años. El principal objetivo del estudio era profundizar en nuestra comprensión sobre el impacto del cambio económico, social, cultural, tecnológico y laboral que están experimentando las universidades españolas en la vida y la identidad profesional del personal docente e investigador, teniendo en cuenta el contexto nacional y europeo. Estapublicación recoge la 24 historias de vida profesional realizas con o sobre otros tantos docentes universitarios. Sus relatos analizados y contextualizados, significan una contribución significativa al conocimiento basado en la investigación sobre el saber profesional y la experiencia laboral en las universidades españolas, y en consecuencia, a nuestra comprensión sobre cómo los académicos se están enfrentando con los cambios actuales.

Trayectorias docentes e investigadoras en la universidad. 24 historias de vida profesional. Los efectos de los cambios en el trabajo y la vida profesional de los docentes universitarios

[spa] Este texto forma parte de un proyecto de investigación Los efectos de los cambios sociales en el trabajo y la vida profesional de los docentes universitarios, parcialmente financiado por el Ministerio de Ciencia e Innovación (SEJ2006-01876), en el que nos planteamos explorar los cambios los ámbitos de la legislación, laorganización institucional, la investigación, la gestión y la docencia en los últimos treinta años. El principal objetivo del estudio era profundizar en nuestra comprensión sobre el impacto del cambio económico, social, cultural, tecnológico y laboral que están experimentando las universidades españolas en la vida y la identidad profesional del personal docente e investigador, teniendo en cuenta el contexto nacional y europeo. Estapublicación recoge la 24 historias de vida profesional realizas con o sobre otros tantos docentes universitarios. Sus relatos analizados y contextualizados, significan una contribución significativa al conocimiento basado en la investigación sobre el saber profesional y la experiencia laboral en las universidades españolas, y en consecuencia, a nuestra comprensión sobre cómo los académicos se están enfrentando con los cambios actuales.

Trayectorias docentes e investigadoras en la universidad. 24 historias de vida profesional. Los efectos de los cambios en el trabajo y la vida profesional de los docentes universitarios

[spa] Este texto forma parte de un proyecto de investigación Los efectos de los cambios sociales en el trabajo y la vida profesional de los docentes universitarios, parcialmente financiado por el Ministerio de Ciencia e Innovación (SEJ2006-01876), en el que nos planteamos explorar los cambios los ámbitos de la legislación, laorganización institucional, la investigación, la gestión y la docencia en los últimos treinta años. El principal objetivo del estudio era profundizar en nuestra comprensión sobre el impacto del cambio económico, social, cultural, tecnológico y laboral que están experimentando las universidades españolas en la vida y la identidad profesional del personal docente e investigador, teniendo en cuenta el contexto nacional y europeo. Estapublicación recoge la 24 historias de vida profesional realizas con o sobre otros tantos docentes universitarios. Sus relatos analizados y contextualizados, significan una contribución significativa al conocimiento basado en la investigación sobre el saber profesional y la experiencia laboral en las universidades españolas, y en consecuencia, a nuestra comprensión sobre cómo los académicos se están enfrentando con los cambios actuales.

2012 Community Tree Management Plan, Alburnett, IA, June 24, 2013

This plan was developed to assist Alburnett with the management, budgeting and future planning of their urban forest. Across the state, forestry budgets continue to decrease with more and more of that money spent on tree removal. With the anticipated arrival of Emerald Ash Borer (EAB), an invasive pest that kills native ash trees, it is time to prepare for the increased costs of tree removal and replacement planting. With proper planning and management of the current canopy in Alburnett, these costs can be extended over years and public safety issues from dead and dying ash trees mitigated. Trees are an important component of Alburnett’s infrastructure and one of the greatest assets to the community. The benefits of trees are immense. Trees provide the community with improved air quality, stormwater runoff interception, energy conservation, lower traffic speeds, increased property values, reduced crime, improved mental health and create a desirable place to live, to name just a few benefits. It is essential that these benefits be maintained for the people of Alburnett and future generations through good urban forestry management. Good urban forestry management involves setting goals and developing management strategies to achieve these goals. An essential part of developing management strategies is a comprehensive public tree inventory. The inventory supplies information that will be used for maintenance, removal schedules, tree planting and budgeting. Basing actions on this information will help meet Alburnett’s urban forestry goals.

2012 Community Tree Management Plan, Belle Plaine, IA, June 24, 2013

This plan was developed to assist Belle Plaine with the management, budgeting and future planning of their urban forest. Across the state, forestry budgets continue to decrease with more and more of that money spent on tree removal. With the anticipated arrival of Emerald Ash Borer (EAB), an invasive pest that kills native ash trees, it is time to prepare for the increased costs of tree removal and replacement planting. With proper planning and management of the current canopy in Belle Plaine, these costs can be extended over years and public safety issues from dead and dying ash trees mitigated. Trees are an important component of Belle Plaine’s infrastructure and one of the greatest assets to the community. The benefits of trees are immense. Trees provide the community with improved air quality, stormwater runoff interception, energy conservation, lower traffic speeds, increased property values, reduced crime, improved mental health and create a desirable place to live, to name just a few benefits. It is essential that these benefits be maintained for the people of Belle Plaine and future generations through good urban forestry management. Good urban forestry management involves setting goals and developing management strategies to achieve these goals. An essential part of developing management strategies is a comprehensive public tree inventory. The inventory supplies information that will be used for maintenance, removal schedules, tree planting and budgeting. Basing actions on this information will help meet Belle Plaine’s urban forestry goals.

EPI Update, July 24, 2015

Weekly newsletter for Center For Acute Disease Epidemiology of Iowa Department of Public Health.