ABSTRACT
In this study, a new approach to optimize the cellulose nanocrystals (CNCs) extraction using acidic natural deep eutectic solvents (NADES) was introduced using, for the first time, design of experiment method. Choline chloride:oxalic acid dihydrate with a molar ratio of 1:1 was used to extract CNCs. Then, three most important parameters were varied to design the experiment: (i) cotton fibre concentrations, (ii) temperature and (iii) treatment time. Two outcomes were studied: the CNC yield and the crystallinity. The mathematical model for crystallinity perfectly described the experiments, while the model for CNC yield provided only a tendency. For a reaction time of 6â¯h at 95⯰C with a fibre concentration of 2 %, the expected optimum CNC yield was approximately 35.5⯱â¯2.7 % with a crystallinity index of 80⯱â¯1 %. The obtained experimental results confirmed the models with 43.6⯱â¯1.9 % and 81⯱â¯1 % for the CNC yield and the crystallinity index, respectively. This study shows that it is possible to predict the CNC yield CNC and their crystallinity thanks to predictive mathematical models, which gives a great advantage to consider in the near future a scale up of the extraction of cellulose nanocrystals using this original family of green solvents.
ABSTRACT
BACKGROUND AND PURPOSE: Despite recent advances in neurogenetics that have facilitated the identification of a number of dystonia genes, many familial dystonia syndromes remain without known cause. The aim of the study was to identify the cause of autosomal dominant tremulous myoclonus-dystonia in a UK kindred with affected individuals in three generations. METHODS: Known genetic causes of myoclonus-dystonia were excluded. We combined clinical and electrophysiological phenotyping with whole-exome sequencing and Sanger sequencing to identify candidate causal variants in a family with tremulous myoclonus-dystonia. RESULTS: The core phenotype consisted of childhood-onset dystonia predominantly affecting hands and neck, with a fast tremor with superimposed myoclonus and, in some individuals, subtle cerebellar signs. We identified a novel missense variant in potassium calcium-activated channel subfamily N member 2 (KCNN2) [NM_021614:c.1112G>A:p.(Gly371Glu)], which was the only variant that we were able to identify as segregating with the phenotype over three generations. This variant, which is absent from the most recent version of gnomAD, was predicted to be deleterious by SIFT and PolyPhen-2 and had an overall CADD score of 29.7. CONCLUSIONS: KCNN2, a member of the KCNN family of potassium channel genes, is highly conserved across species and in humans is highly expressed in the brain, particularly the cerebellum. KCNN2 mutations have never been described as pathological in human disease, but are recognized abnormalities in two rodent models of fast, jerky tremor. Segregation, absence of the variant in the normal population and in-silico prediction of a deleterious effect together with animal models compatible with the clinical phenotype are all in line with KCNN2 mutations being a plausible cause underlying myoclonus-dystonia.
Subject(s)
Dystonia , Dystonic Disorders , Myoclonus , Small-Conductance Calcium-Activated Potassium Channels/genetics , Animals , Child , Dystonic Disorders/genetics , Humans , Mutation , Phenotype , TremorABSTRACT
The EUREQUA project raises the issue of the definition and evaluation of the environmental quality of neighbourhoods. The approach consists of integrating and cross-referencing observable data characterising the physical environment and people's perception of their quality of life. The study area is a neighbourhood in Toulouse (France) with high social and typo-morphological diversity, subject to noise and air pollution nuisances. Three 3-day field campaigns were organised in January, April, and June 2014. Instrumented and commented walks took place three times per day. For each one, measurements of physical environmental parameters and surveys were performed simultaneously at six locations in the neighbourhood. The study focuses on microclimate and thermal comfort issues. It aims to compare in situ meteorological data of air temperature, humidity, wind speed, and mean radiant temperature, with quantitative results rating human perception of heat, humidity, wind, and thermal comfort. The variability in perception and measurements is mainly driven by seasonal effects, especially for heat and humidity, and, to a lesser extent, for wind. Wind perception and measurement also vary spatially, thus highlighting site effects. Linear models indicate a positive link between heat perception and mean radiant temperature, as well as between wind perception and mean and standard deviation of wind speed (with a higher sensitivity of people to wind under winter climate conditions). Finally, it is found that perception of thermal comfort is only slightly linked to the different microclimate dimensions, and is rather driven by other appreciation factors and emotional criteria related to the general environmental quality of the study area.
Subject(s)
Microclimate , Thermosensing , France , Humans , Humidity , Quality of Life , Temperature , WindABSTRACT
Depression is a highly prevalent psychiatric condition, with over 300 million sufferers, and is an important comorbidity for other conditions, like cardiovascular disorders or diabetes. Therapy is largely based on psychotherapy and/or pharmacological intervention, particularly aimed at altering neurotransmitter levels in the central nervous system, but inadequate response to treatment remains a significant clinical problem. Herein, evidence supporting a molecular link between inflammation and depression will be discussed, particularly the increased prevalence of depression in chronic inflammatory diseases and the evidence on the use of anti-inflammatory drugs to treat depression. Moreover, the potential for the levels of peripheral inflammatory molecules to act as depression biomarkers, in the diagnosis and monitoring of depression will be examined, considering clinical- and animal model-based evidence.
Subject(s)
Biomarkers , Depressive Disorder/etiology , Depressive Disorder/metabolism , Disease Models, Animal , Inflammation Mediators/metabolism , Animals , Anti-Inflammatory Agents/pharmacology , Anti-Inflammatory Agents/therapeutic use , Clinical Studies as Topic , Cytokines , Depression , Depressive Disorder/diagnosis , Depressive Disorder/therapy , Humans , Inflammation/complications , Inflammation/drug therapy , Inflammation/etiology , Inflammation/metabolism , Treatment OutcomeABSTRACT
Correction to:Neth Heart J 2018 https://doi.org/10.1007/s12471-018-1152-y In the version of the article originally published online, there was an error in the 'Methods and results' section of the Abstract. It is stated that 'In the 10-14 year group, hypertrophic cardiomyopathy (nâ¯= 1) and ruptured .
Subject(s)
Alzheimer Disease , Apolipoprotein E4 , Humans , Membrane Glycoproteins , Receptors, ImmunologicABSTRACT
BACKGROUND: Little is known about the causes of unexpected death in minors (0-17 years). In young adults an important cause is cardiovascular disease, with primary arrhythmogenic disorders, atherosclerotic events, cardiomyopathies and myocarditis as main contributors. The aim of this autopsy study was to determine the contribution of cardiovascular disease to unexpected death in minors. METHODS AND RESULTS: In the Netherlands, systematic investigation of all cases of unexplained death in minors was compulsory in a nationwide governmental project during a 15-month period. Autopsies were performed according to a standardised protocol (autopsy rate 85%). A cardiovascular cause of death was found in 13/56 cases (23%). In the group <1 year, the main cardiovascular causes were various congenital defects (nâ¯= 3) and myocarditis (nâ¯= 2). In the 1-9 year group, no cardiovascular causes were found. In the 10-14 year group, coronary anomalies (nâ¯= 2) and arrhythmogenic cardiomyopathy (nâ¯= 1) were observed. In the 1517 year group, hypertrophic cardiomyopathy (nâ¯= 1) and ruptured ascending aortic aneurysm (nâ¯= 1) were among the observed cardiovascular causes [corrected]. In 14/56 (25%) cases autopsy revealed no structural abnormalities that could explain the sudden death, mostly in the group <1 year. CONCLUSION: This national cohort with a high autopsy rate reveals a high incidence (23%) of cardiovascular diseases as the pathological substrate of sudden unexpected death in children. Another high percentage of minors (25%) showed no structural abnormalities, with the possibility of a genetic arrhythmia. These findings underline the importance of systematic autopsy in sudden death in minors, with implications for cardiogenetic screening of relatives.
ABSTRACT
AIM: Late-onset Alzheimer's disease (LOAD) accounts for 95% of all Alzheimer's cases and is genetically complex in nature. Overlapping clinical and neuropathological features between AD, FTD and Parkinson's disease highlight the potential role of genetic pleiotropy across diseases. Recent genome-wide association studies (GWASs) have uncovered 20 new loci for AD risk; however, these exhibit small effect sizes. Using NGS, here we perform association analyses using exome-wide and candidate-gene-driven approaches. METHODS: Whole-exome sequencing was performed on 132 AD cases and 53 control samples. Exome-wide single-variant association and gene burden tests were performed for 76 640 nonsingleton variants. Samples were also screened for known causative mutations in familial genes in AD and other dementias. Single-variant association and burden analysis was also carried out on variants in known AD and other neurological dementia genes. RESULTS: Tentative single-variant and burden associations were seen in several genes with kinase and protease activity. Exome-wide burden analysis also revealed significant burden of variants in PILRA (P = 3.4 × 10-5 ), which has previously been linked to AD via GWAS, hit ZCWPW1. Screening for causative mutations in familial AD and other dementia genes revealed no pathogenic variants. Variants identified in ABCA7, SLC24A4, CD33 and LRRK2 were nominally associated with disease (P < 0.05) but did not withstand correction for multiple testing. APOE (P = 0.02) and CLU (P = 0.04) variants showed significant burden on AD. CONCLUSIONS: In addition, polygenic risk scores (PRS) were able to distinguish between cases and controls with 83.8% accuracy using 3268 variants, sex, age at death and APOE ε4 and ε2 status as predictors.
Subject(s)
Alzheimer Disease/genetics , Exome Sequencing/methods , Genetic Predisposition to Disease/genetics , Membrane Glycoproteins/genetics , Receptors, Immunologic/genetics , Aged , Aged, 80 and over , Cohort Studies , Female , High-Throughput Nucleotide Sequencing/methods , Humans , Male , Multifactorial InheritanceABSTRACT
OBJECTIVES: Primary familial brain calcification (PFBC) is a rare neurological disease often inherited as a dominant trait. Mutations in four genes (SLC20A2, PDGFB, PDGFRB, and XPR1) have been reported in patients with PFBC. Of these, point mutations or small deletions in SLC20A2 are most common. Thus far, only one large deletion covering entire SLC20A2 and several smaller, exonic deletions of SLC20A2 have been reported. The aim of this study was to identify the causative gene defect in a Finnish PFBC family with three affected patients. MATERIALS AND METHODS: A Finnish family with three PFBC patients and five unaffected subjects was studied. Sanger sequencing was used to exclude mutations in the coding and splice site regions of SLC20A2, PDGFRB, and PDGFB. Whole-exome (WES) and whole-genome sequencing (WGS) were performed to identify the causative mutation. A SNP array was used in segregation analysis. RESULTS: Copy number analysis of the WGS data revealed a heterozygous deletion of ~578 kb on chromosome 8. The deletion removes the 5' UTR region, the noncoding exon 1 and the putative promoter region of SLC20A2 as well as the coding regions of six other genes. CONCLUSIONS: Our results support haploinsufficiency of SLC20A2 as a pathogenetic mechanism in PFBC. Analysis of copy number variations (CNVs) is emerging as a crucial step in the molecular genetic diagnostics of PFBC, and it should not be limited to coding regions, as causative variants may reside in the noncoding parts of known disease-associated genes.
Subject(s)
Brain Diseases/genetics , Calcinosis/genetics , Gene Deletion , Sodium-Phosphate Cotransporter Proteins, Type III/genetics , 5' Flanking Region , Brain Diseases/diagnosis , Calcinosis/diagnosis , DNA Copy Number Variations , Exome , Female , Heterozygote , Humans , Male , Pedigree , Point Mutation , Xenotropic and Polytropic Retrovirus ReceptorABSTRACT
Current investigations deal with new surface functionalization strategy of nanocrystalline cellulose-based substrates to impart active molecule release properties. In this study, cellulose nanocrystals (CNC) were surface-functionalized with ß-cyclodextrin (ß-CD) using succinic acid (SA) and fumaric acid (FA) as bridging agents. The main objective of this surface modification performed only in aqueous media was to obtain new active materials able to release antibacterial molecules over a prolonged period of time. The reactions were conducted by immersing the CNC film into a solution composed of ß-CD, SA and FA, leading to CNC grafting. The materials were characterized by infrared spectroscopy (FT-IR), Quartz crystal microbalance-dissipation (QCM-D), AFM and phenolphthalein (PhP) was used to determine the efficiency of CNC grafting with ß-CD. The results indicated that ß-CD was successfully attached to the CNC backbone through the formation of ester bonds. Furthermore, carvacrol was entrapped by the attached ß-CD and a prolonged release was confirmed. In particular, CNC grafted to ß-CD in the presence of FA was selected as the best solution. The antibacterial activity and the controlled release were studied for this sample. Considerably longer bacterial activity against B. subtilis was observed for CNC grafted to ß-CD compared to CNC and CNC-FA, confirming the promising impact of the present strategy.
Subject(s)
Carboxylic Acids/chemistry , Cellulose/chemistry , Monoterpenes/pharmacology , Nanoparticles/chemistry , beta-Cyclodextrins/chemistry , Anti-Bacterial Agents/pharmacology , Bacillus subtilis/drug effects , Cymenes , Delayed-Action Preparations , Drug Liberation , Microscopy, Atomic Force , Molecular Weight , Phenolphthalein/chemistry , Quartz Crystal Microbalance Techniques , Spectroscopy, Fourier Transform Infrared , TemperatureABSTRACT
A shared genetic susceptibility between cutaneous malignant melanoma (CMM) and Parkinson's disease (PD) has been suggested. We investigated this by assessing the contribution of rare variants in genes involved in CMM to PD risk. We studied rare variation across 29 CMM risk genes using high-quality genotype data in 6875 PD cases and 6065 controls and sought to replicate findings using whole-exome sequencing data from a second independent cohort totaling 1255 PD cases and 473 controls. No statistically significant enrichment of rare variants across all genes, per gene, or for any individual variant was detected in either cohort. There were nonsignificant trends toward different carrier frequencies between PD cases and controls, under different inheritance models, in the following CMM risk genes: BAP1, DCC, ERBB4, KIT, MAPK2, MITF, PTEN, and TP53. The very rare TYR p.V275F variant, which is a pathogenic allele for recessive albinism, was more common in PD cases than controls in 3 independent cohorts. Tyrosinase, encoded by TYR, is the rate-limiting enzyme for the production of neuromelanin, and has a role in the production of dopamine. These results suggest a possible role for another gene in the dopamine-biosynthetic pathway in susceptibility to neurodegenerative Parkinsonism, but further studies in larger PD cohorts are needed to accurately determine the role of these genes/variants in disease pathogenesis.
Subject(s)
Genetic Association Studies , Genetic Predisposition to Disease/genetics , Genetic Variation/genetics , Melanoma/genetics , Parkinson Disease/genetics , Skin Neoplasms/genetics , Cohort Studies , DCC Receptor , Dopamine/biosynthesis , Genotype , Humans , Melanins/biosynthesis , Membrane Glycoproteins/genetics , Monophenol Monooxygenase , Oxidoreductases/genetics , Pigmentation/genetics , Receptor, ErbB-4/genetics , Receptors, Cell Surface/genetics , Risk , Tumor Suppressor Proteins/genetics , Ubiquitin Thiolesterase/geneticsABSTRACT
Pseudohypoparathyroidism type 1b (PHP1b) is characterized by hypocalcemia, hyperphosphatemia, increased levels of circulating parathyroid hormone (PTH), and no skeletal or developmental abnormalities. The goal of this study was to perform a full characterization of a familial case of PHP1b with neurological involvement and to identify the genetic cause of disease. The initial laboratory profile of the proband showed severe hypocalcemia, hyperphosphatemia and normal levels of PTH, which was considered to be compatible with primary hypoparathyroidism. With disease progression the patient developed cognitive disturbance, PTH levels were found to be slightly elevated and a picture of PTH resistance syndrome seemed more probable. The diagnosis of PHP1b was established after the study of family members and blunted urinary cAMP results were obtained in a PTH stimulation test. Integration of whole genome genotyping and exome sequencing data supported this diagnosis by revealing a novel homozygous missense mutation in PTH1R (p.Arg186His) completely segregating with the disease. Here, we demonstrate segregation of a novel mutation in PTH1R with a phenotype of PHP1b presenting with neurological symptoms, but no bone defects. This case represents the extreme end of the spectrum of cognitive impairment in PTH dysfunction and defines a possible novel form of PHP1b resulting from the impaired interaction between PTH and PTH1R.
Subject(s)
Mutation , Pseudohypoparathyroidism/genetics , Receptor, Parathyroid Hormone, Type 1/genetics , Aged , Aged, 80 and over , Female , Genome , Homozygote , Humans , Hyperphosphatemia/genetics , Hypocalcemia/genetics , Male , Middle Aged , Parathyroid Hormone/genetics , Parathyroid Hormone/metabolism , Pedigree , Pseudohypoparathyroidism/blood , Pseudohypoparathyroidism/metabolism , Receptor, Parathyroid Hormone, Type 1/metabolism , PseudohypoparathyroidismABSTRACT
Cellulose nanocrystals (CNC) and starch nanocrystals (SNC) were grafted by ozone-initiated free-radical polymerisation of styrene in a heterogeneous medium. Surface functionalisation was confirmed by infrared spectroscopy, contact angle measurements, and thermogravimetric and elemental analysis. X-ray diffraction and scanning electron microscopy showed that there was no significant change in the morphology or crystallinity of the nanoparticles following ozonolysis. The grafting efficiency, quantified by (13)C NMR, was greater for SNC, with a styrene/anhydroglucose ratio of 1.56 compared to 0.25 for CNC. The thermal stability improved by 100°C. The contact angles were 97° and 78° following the SNC and CNC grafting, respectively, demonstrating the efficiency of the grafting in changing the surface properties even at low levels of surface substitution. The grafting increased the compatibility with the polylactide, and produced nanocomposites with improved water vapour barrier properties. Ozone-mediated grafting is thus a promising approach for surface functionalisation of polysaccharide nanocrystals.
Subject(s)
Cellulose/chemistry , Nanocomposites/chemistry , Nanoparticles/chemistry , Ozone/chemistry , Polystyrenes/chemistry , Starch/chemistry , Hydrogen Peroxide/chemistry , PolymerizationABSTRACT
A Revista Médica de Moçambique (RMM) foi a publicação científica oficial do Instituto Nacional de Saúde de Moçambique entre 1982 e 2010. Foi realizado um estudo descritivo retrospectivo dos artigos publicados na RMM com o objectivo de analisar as tendências de publicação em saúde em Moçambique. Metodologia: Para cada número daRMM publicado foram colhidos dadossobre a data de edição, o tipo de artigo, o local em que decorreu a pesquisa, afiliação do primeiro autor, os assuntos abordados por artigo e a forma de financiamento. Foram definidos três períodos: I (1982-1988), II (1993-1999) e III (2003-2010), tendo em conta as interrupções havidas na edição da revista. Resultados: A RMM publicou 28 números dos quais 3 não foram considerados para análise por serem suplementos contendo apenas resumos de comunicações apresentadas em Jornadas Nacionais de Saúde. Os 25 números analisados continham 177 artigos, dos quais 143 (80,7%) eram de pesquisa original. A maior parte dos trabalhos publicados foram realizados na Província de Maputo: 21 artigos no período I, 50 no período II e 12 no período III. Os primeiros autores dos artigos publicados na RMM eram pesquisadores do Ministério da Saúde e do Instituto Nacional de Saúde, também localizados em Maputo, tendo publicado 51 e 50 artigos, respectivamente. Os autores concluem que se registou um predomínio de pesquisas realizadas em Maputo, por autores provenientes de instituições localizadas também nesta Província. Os temas mais abordados foram as doenças parasitárias e a saúde materno-infantil. A RMM foi editada com frequência irregular, tendo o pico de produção ocorrido no período II. De modo a garantir regularidade na edição e qualidade científica os autores recomendam a criação de mecanismos de auto-sustentabilidade da revista
The Mozambican Medical Journal (MMJ) was the official publication of the National Health Institute between 1982 and 2010. We performed a retrospective study to evaluate the trends of health research publication by this journal. For each published journal we collected information on the date of edition, type of articles included, site of research described, affiliation of the first author, subject of research and how the edition was funded. Three periods were defined taking into account interruptions that occurred in the publication of the journal: period I (1982-1988), II (1993-1999) e III (2003-2010). The Mozambican Medical Journal published 28 editions; of these, 3 were not considered for analysis as they were supplements containing only abstracts of communications presented at the National Health Congress. The 25 editions considered for analysis had 177 articles of which 143 (80.7%) presented the results of original research. Maputo Province had the greater number of articles published: 21 during Period I, 50 during Period II and 12 in the last Period. First authors from the National Health Institute and the Ministry of Health, both located in Maputo, were in first and second place, publishing respectively 51 and 50 articles. It is concluded that there was asymmetry of the work published at the Mozambican Medical Journal, regarding authorship and place implementation of research. The vast majority of studies were performed in Maputo Province. Most published articles were the result of studies on parasitic diseases and maternal and child health. The editions of the Journal were irregular; the peak of publications was during Period II. There is need to find mechanisms to achieve regularity of editions and sustainability of this scientific journal.
Subject(s)
Health Research Policy , Health Research Evaluation , Asymmetry of Information/trends , Ethics Committees, Research , Scientific and Technical Publications , Asymmetry of Information/ethics , MozambiqueABSTRACT
The gene encoding the family 6 carbohydrate-binding module (CtCBM6A) from Clostridium thermocellum, cloned in pET-21a(+) expression vector, was overexpressed using Escherichia coli BL-21(DE3) cells and purified by immobilized metal-ion affinity chromatography. SDS-PAGE analysis of the recombinant CtCBM6A showed molecular size of approximately 15 kDa. Ligand-binding analysis of CtCBM6A with rye arabinoxylan and oat spelt xylan by affinity gel electrophoresis showed low affinity for these ligands (Ka of 40 and 26 liter/g, respectively), and analysis by fluorescence spectroscopy (Ka of 33 and 15 liter/g, respectively) corroborated lower binding affinity with the above soluble ligands. However, CtCBM6A displayed significantly higher ligand-binding affinity with insoluble wheat arabinoxylan with equilibrium association constant Ka of 230 M(-1) and binding capacity (N0) of 11 µmole/g. The protein melting curve of CtCBM6A displayed a peak shift from 53 to 58°C in the presence of Ca2+, indicating that Ca2+ imparts thermal stability to the CtCBM6A structure. Homology modeling of CtCBM6A revealed a characteristic ß-sandwich core structure. The Ramachandran plot of CtCBM6A showed 89% of the residues in the most favorable region, 10% in additionally favored region, and 1% in generously allowed region, indicating that CtCBM6A has a stable conformation.
Subject(s)
Bacterial Proteins/metabolism , Clostridium thermocellum/enzymology , Glycoside Hydrolases/chemistry , Amino Acid Sequence , Bacterial Proteins/chemistry , Bacterial Proteins/genetics , Escherichia coli/metabolism , Glycoside Hydrolases/genetics , Glycoside Hydrolases/metabolism , Ligands , Molecular Sequence Data , Protein Binding , Protein Denaturation , Protein Stability , Protein Structure, Tertiary , Recombinant Proteins/biosynthesis , Recombinant Proteins/chemistry , Recombinant Proteins/isolation & purification , Sequence Alignment , Triticum/metabolism , Xylans/chemistry , Xylans/metabolismABSTRACT
Gastric adenocarcinoma is not uncommon in the adult population, but in the pediatric population it is an extremely rare entity. A 13-year-old boy was referred to a pediatric oncology unit for evaluation of a tumor in the upper abdomen. Further investigation revealed an advanced stage gastric carcinoma with metastases suggestive for a hereditary cause. Awareness for uncommon diagnoses is a key issue in regard of accurate treatment and overall prognosis.
Subject(s)
Adenocarcinoma/diagnosis , Stomach Neoplasms/diagnosis , Adenocarcinoma/drug therapy , Adolescent , Age Distribution , Antineoplastic Combined Chemotherapy Protocols/therapeutic use , Humans , Male , Prognosis , Stomach Neoplasms/drug therapy , Tomography, X-Ray ComputedABSTRACT
OBJECTIVES: To identify independent risk factors of severe falciparum malaria among travelers to endemic regions. MATERIALS AND METHODS: A retrospective study on imported malaria into metropolitan France. The World's Health Organization severity criteria were used to classify malarial episodes. RESULTS: Nine hundred and twenty-one malarial cases were studied; 81 were severe. Independent risk factors of severe malaria were aged above 40 years, high level of parasitized erythrocytes (more than 4%), parasite acquisition in the south-eastern asian region, infection with a chloroquine resistant Plasmodium falciparum (P. falciparum) phenotype and a self administered antimalarial treatment. CONCLUSION: This study points out two particularly interesting results: severe malaria is significantly associated with the infection by a chloroquine resistant P. falciparum phenotype and with the parasite's acquisition in the south-eastern asian region.
Subject(s)
Malaria, Falciparum/epidemiology , Travel , Adolescent , Adult , Age Factors , Antimalarials/therapeutic use , Asia, Southeastern/epidemiology , Child , Child, Preschool , Chloroquine , Drug Resistance , Endemic Diseases , Erythrocytes/parasitology , Female , France/epidemiology , Humans , Infant , Infant, Newborn , Malaria, Falciparum/drug therapy , Malaria, Falciparum/parasitology , Male , Plasmodium falciparum/drug effects , Retrospective Studies , Risk FactorsABSTRACT
Equine dysautonomia, also known as equine grass sickness (EGS), is a well documented disease in several countries. To the authors' knowledge, EGS has not been reported previously in North America. This report describes EGS in a 6-year-old female mule in the USA. Failure initially to consider EGS resulted in a delayed diagnosis. EGS should be considered as a differential diagnosis and appropriate diagnostic tests performed in similar cases in North America.