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[PMID]:27172284
[Au] Autor:Richman SH; Razzano AJ; Morscher MA; Riley PM
[Ad] Endereço:*Cleveland Clinic Foundation, Cleveland, OH †Spectrum Orthopaedics, North Canton, OH ‡Akron Children's Hospital, Akron, OH.
[Ti] Título:Metallosis Presenting as a Progressive Neurologic Deficit Four Years After a Posterior Spinal Fusion for Adolescent Idiopathic Scoliosis: A Case Report.
[So] Source:Spine (Phila Pa 1976);42(1):E56-E59, 2017 Jan 01.
[Is] ISSN:1528-1159
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:STUDY DESIGN: A case report. OBJECTIVE: The aim of this study was to report a case of progressive pain and paraparesis secondary to metallosis four years after a pediatric posterior spinal fusion (PSF). SUMMARY OF BACKGROUND DATA: Metallosis as a late complication of pediatric spinal surgery is rarely reported. Myelographic computed tomography (CT) can be helpful in establishing the diagnosis. The use of serum chromium levels as a means of definitive diagnosis has been suggested, but has only been reported retrospectively. METHODS: A 19-year-old male presented four years after PSF for adolescent idiopathic scoliosis with sudden onset of pain and neurologic deficits. Radiographs and CT scan suggested infection. Intraoperatively, no purulent material was noted, but black and yellowish corrosive debris was found around the right L1 pedicle screw, so it was removed and the cavity packed with tobramycin impregnated calcium sulfate beads. After surgery, neurologic deficits worsened. CT myelogram showed irregular opacification of the thecal sac at the level of the conus. A posterior laminectomy and decompression was performed with removal of all debris and spinal instrumentation. Metallosis within the spinal canal was noted and serum chromium levels were obtained. RESULTS: The patient was discharged one week after admission with improvement of pain and gradual improvement in neurologic examination. Three years postdischarge, the patient is asymptomatic and examination shows bilateral clonus. Serum chromium levels declined from a high of 4.5 µg/L operatively to 0.8 at final follow-up (normal: 0.2-0.6 µg/L). CONCLUSION: Although uncommon, metallosis should be considered in the differential diagnosis of any late presenting case of pain, infection-like symptoms, or neurologic deficits after pediatric PSF. CT myelography and serum chromium levels may help guide diagnosis; however, surgical exploration is needed for definitive diagnosis and treatment. LEVEL OF EVIDENCE: 4.
[Mh] Termos MeSH primário: Cromo/toxicidade
Intoxicação do Sistema Nervoso por Metais Pesados/etiologia
Dor Pós-Operatória/etiologia
Paraparesia/etiologia
Complicações Pós-Operatórias/etiologia
Escoliose/cirurgia
Fusão Vertebral/efeitos adversos
[Mh] Termos MeSH secundário: Adolescente
Cromo/sangue
Descompressão Cirúrgica
Intoxicação do Sistema Nervoso por Metais Pesados/sangue
Seres Humanos
Laminectomia
Masculino
Mielografia
Dor Pós-Operatória/sangue
Paraparesia/sangue
Adulto Jovem
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0R0008Q3JB (Chromium)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170817
[Lr] Data última revisão:
170817
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160513
[St] Status:MEDLINE
[do] DOI:10.1097/BRS.0000000000001685


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[PMID]:27816841
[Au] Autor:Karri V; Schuhmacher M; Kumar V
[Ad] Endereço:Center of Environmental Food and Toxicological Technology (TecnATox), Departament d'Enginyeria Química, Universitat Rovira i Virgili, Tarragona, Catalonia, Spain.
[Ti] Título:Heavy metals (Pb, Cd, As and MeHg) as risk factors for cognitive dysfunction: A general review of metal mixture mechanism in brain.
[So] Source:Environ Toxicol Pharmacol;48:203-213, 2016 Dec.
[Is] ISSN:1872-7077
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Human exposure to toxic heavy metals is a global challenge. Concurrent exposure of heavy metals, such as lead (Pb), cadmium (Cd), arsenic (As) and methylmercury (MeHg) are particularly important due to their long lasting effects on the brain. The exact toxicological mechanisms invoked by exposure to mixtures of the metals Pb, Cd, As and MeHg are still unclear, however they share many common pathways for causing cognitive dysfunction. The combination of metals may produce additive/synergetic effects due to their common binding affinity with NMDA receptor (Pb, As, MeHg), Na - K ATP-ase pump (Cd, MeHg), biological Ca (Pb, Cd, MeHg), Glu neurotransmitter (Pb, MeHg), which can lead to imbalance between the pro-oxidant elements (ROS) and the antioxidants (reducing elements). In this process, ROS dominates the antioxidants factors such as GPx, GS, GSH, MT-III, Catalase, SOD, BDNF, and CERB, and finally leads to cognitive dysfunction. The present review illustrates an account of the current knowledge about the individual metal induced cognitive dysfunction mechanisms and analyse common Mode of Actions (MOAs) of quaternary metal mixture (Pb, Cd, As, MeHg). This review aims to help advancement in mixture toxicology and development of next generation predictive model (such as PBPK/PD) combining both kinetic and dynamic interactions of metals.
[Mh] Termos MeSH primário: Disfunção Cognitiva/induzido quimicamente
Misturas Complexas/toxicidade
Poluentes Ambientais/toxicidade
Intoxicação do Sistema Nervoso por Metais Pesados/etiologia
Hipocampo/efeitos dos fármacos
Metais Pesados/toxicidade
[Mh] Termos MeSH secundário: Animais
Arsênico/farmacocinética
Arsênico/toxicidade
Ligação Competitiva
Cádmio/farmacocinética
Cádmio/toxicidade
Cálcio/metabolismo
Disfunção Cognitiva/metabolismo
Misturas Complexas/farmacocinética
Poluentes Ambientais/farmacocinética
Ácido Glutâmico/metabolismo
Intoxicação do Sistema Nervoso por Metais Pesados/metabolismo
Hipocampo/metabolismo
Seres Humanos
Chumbo/farmacocinética
Chumbo/toxicidade
Compostos de Metilmercúrio/farmacocinética
Compostos de Metilmercúrio/toxicidade
Modelos Biológicos
Ligação Proteica
Receptores de N-Metil-D-Aspartato/metabolismo
Fatores de Risco
ATPase Trocadora de Sódio-Potássio/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Complex Mixtures); 0 (Environmental Pollutants); 0 (Metals, Heavy); 0 (Methylmercury Compounds); 0 (Receptors, N-Methyl-D-Aspartate); 00BH33GNGH (Cadmium); 2P299V784P (Lead); 3KX376GY7L (Glutamic Acid); EC 3.6.3.9 (Sodium-Potassium-Exchanging ATPase); N712M78A8G (Arsenic); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:170916
[Lr] Data última revisão:
170916
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161107
[St] Status:MEDLINE


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[PMID]:27692615
[Au] Autor:Kuroda H; Mukai Y; Nishiyama S; Takeshita T; Tateyama M; Takeda A; Aoki M
[Ad] Endereço:Department of Neurology, Tohoku University Graduate School of Medicine, Sendai, Japan. Electronic address: dakuro@med.tohoku.ac.jp.
[Ti] Título:Tardily accelerated neurologic deterioration in two-step thallium intoxication.
[So] Source:J Clin Neurosci;34:234-236, 2016 Dec.
[Is] ISSN:1532-2653
[Cp] País de publicação:Scotland
[La] Idioma:eng
[Ab] Resumo:Thallium intoxication was reported in cases with accidental ingestion, suicide attempt, and criminal adulteration. Reported cases were mostly one-time ingestion, therefore, the clinical course of divisional ingestion has not been fully known. Here, we report a case with two-step thallium intoxication manifesting as tardily accelerated neurologic deterioration. A 16-year-old adolescent was cryptically poisoned with thallium sulfate twice at an interval of 52days. After the first ingestion, neurologic symptoms including visual loss, myalgia, and weakness in legs developed about 40days after the development of acute gastrointestinal symptoms and alopecia. After the second ingestion, neurologic symptoms deteriorated rapidly and severely without gastrointestinal or cutaneous symptoms. Brain magnetic resonance imaging exhibited bilateral optic nerve atrophy. Nerve conduction studies revealed severe peripheral neuropathies in legs. Thallium intoxication was confirmed by an increase in urine thallium egestion. Most of the neurologic manifestations ameliorated in two years, but the visual loss persisted. The source of thallium ingestion was unraveled afterward because a murder suspect in another homicidal assault confessed the forepast adulteration. This discriminating clinical course may be attributable to the cumulative neurotoxicity due to the longer washout-time of thallium in the nervous system than other organs. It is noteworthy that the divisional thallium intoxication may manifest as progressive optic and peripheral neuropathy without gastrointestinal or cutaneous symptoms.
[Mh] Termos MeSH primário: Intoxicação do Sistema Nervoso por Metais Pesados/diagnóstico
Doenças do Nervo Óptico/induzido quimicamente
Doenças do Sistema Nervoso Periférico/induzido quimicamente
Rodenticidas/envenenamento
Tálio/envenenamento
[Mh] Termos MeSH secundário: Adolescente
Alopecia/induzido quimicamente
Seres Humanos
Masculino
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Rodenticides); AD84R52XLF (Thallium); U9F9QIR12T (thallium sulfate)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:170213
[Lr] Data última revisão:
170213
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161004
[St] Status:MEDLINE


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[PMID]:25923962
[Au] Autor:Go J; Kim JE; Kwak MH; Koh EK; Song SH; Sung JE; Kim DS; Hong JT; Hwang DY
[Ad] Endereço:a Department of Biomaterials Science, College of Natural Resources and Life Science/Life and Industry Convergence Research Institute , Pusan National University , Miryang , Korea.
[Ti] Título:Neuroprotective effects of fermented soybean products (Cheonggukjang) manufactured by mixed culture of Bacillus subtilis MC31 and Lactobacillus sakei 383 on trimethyltin-induced cognitive defects mice.
[So] Source:Nutr Neurosci;19(6):247-59, 2016 Jul.
[Is] ISSN:1476-8305
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:OBJECTIVES: This study aimed to investigate the beneficial effects of Cheonggukjang (CGK) manufactured by mixed culture of Bacillus subtilis MC31 and Lactobacillus sakei 383 on neurotoxic damages. METHODS: The specific aspects of brain functions were measured in Institute for Cancer Research (ICR) mice that had been pretreated for 4 weeks with three difference doses of CGK before trimethyltin (TMT) treatment. RESULTS: The short- and long-term memory loss induced by TMT treatment was significantly improved in the CGK-pretreated group in a dose-dependent manner. The number of dead cells in the granule cell layer of the dentate gyrus was decreased in the TMT/CGK-cotreated group relative to the TMT/vehicle-treated group, whereas significant suppression of acetylcholinesterase (AChE) activity was observed in the same group. Additionally, a dose-dependent increase in nerve growth factor (NGF) concentration, activation of the NGF receptor signaling pathway including the TrkA high affinity receptor and p75(NTR) low affinity receptor, and decline in Bax/Bcl-2 level was measured in all TMT/CGK-treated groups, although a decrease in the active form of caspase-3 was observed in the TMT/H-CGK-treated group. Furthermore, superoxide dismutase (SOD) activity was enhanced in the TMT/CGK-treated group, whereas the level of malondialdehyde (MDA), a marker of lipid peroxidation, was 43-58% lower in the TMT/CGK-treated group than the TMT/vehicle-treated group. DISCUSSION: These results demonstrate that CGK fermented by mixed culture of B. subtilis and L. sakei could exert a wide range of beneficial activities for neurodegenerative diseases, including Alzheimer, Parkinson, and Huntington disease.
[Mh] Termos MeSH primário: Bacillus subtilis/metabolismo
Transtornos Cognitivos/prevenção & controle
Suplementos Nutricionais
Lactobacillus sakei/metabolismo
Fármacos Neuroprotetores/uso terapêutico
Extratos Vegetais/uso terapêutico
Alimentos de Soja/análise
[Mh] Termos MeSH secundário: Animais
Biomarcadores/metabolismo
Transtornos Cognitivos/etiologia
Transtornos Cognitivos/metabolismo
Transtornos Cognitivos/patologia
Giro Denteado/efeitos dos fármacos
Giro Denteado/enzimologia
Giro Denteado/patologia
Suplementos Nutricionais/análise
Fermentação
Alimento Funcional/análise
Alimento Funcional/microbiologia
Intoxicação do Sistema Nervoso por Metais Pesados/fisiopatologia
Peroxidação de Lipídeos/efeitos dos fármacos
Masculino
Transtornos da Memória/etiologia
Transtornos da Memória/metabolismo
Transtornos da Memória/patologia
Transtornos da Memória/prevenção & controle
Camundongos
Camundongos Endogâmicos ICR
Proteínas do Tecido Nervoso/agonistas
Proteínas do Tecido Nervoso/antagonistas & inibidores
Proteínas do Tecido Nervoso/metabolismo
Neurônios/efeitos dos fármacos
Neurônios/enzimologia
Neurônios/patologia
Fármacos Neuroprotetores/química
Extratos Vegetais/química
Organismos Livres de Patógenos Específicos
Compostos de Trimetilestanho/toxicidade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Nerve Tissue Proteins); 0 (Neuroprotective Agents); 0 (Plant Extracts); 0 (Trimethyltin Compounds); 1631-73-8 (trimethyltin)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170310
[Lr] Data última revisão:
170310
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150430
[St] Status:MEDLINE
[do] DOI:10.1179/1476830515Y.0000000025


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[PMID]:26604027
[Au] Autor:Cavaleri F
[Ti] Título:Review of Amyotrophic Lateral Sclerosis, Parkinson's and Alzheimer's diseases helps further define pathology of the novel paradigm for Alzheimer's with heavy metals as primary disease cause.
[So] Source:Med Hypotheses;85(6):779-90, 2015 Dec.
[Is] ISSN:1532-2777
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Pathologies of neurological diseases are increasingly recognized to have common structural and molecular events that can fit, sometimes loosely, into a central pathological theme. A better understanding of the genetic, proteomic and metabolic similarities between three common neurodegenerative diseases - Amyotrophic Lateral Sclerosis (ALS), Parkinson's disease (PD) and Alzheimer's disease (AD) - and how these similarities relate to their unique pathological features may shed more light on the underlying pathology of each. These are complex multigenic neuroinflammatory diseases caused by a combined action by multiple genetic mutations, lifestyle factors and environmental elements including a proposed contribution by transition metals. This comprehensive dynamic makes disease decoding and treatment difficult. One case of ALS, for example, can manifest from a very different pool of genetic mutations than another. In the case of ALS multiple genes in addition to SOD1 are implicated in the pathogenesis of both sporadic and familial variants of the disease. These genes play different roles in the processing and trafficking of signalling, metabolic and structural proteins. However, many of these genetic mutations or the cellular machinery they regulate can play a role in one form or another in PD and AD as well. In addition, the more recent understanding of how TREM-2 mutations factor into inflammatory response has shed new light on how chronic inflammatory activity can escalate to uncontrolled systemic levels in a variety of inflammatory diseases from neurodegenerative, auto-inflammatory and autoimmune diseases. TREM-2 mutations represent yet another complicating element in these multigenic disease pathologies. This review takes us one step back to discuss basic pathological features of these neurodegenerative diseases known to us for some time. However, the objective is to discuss the possibility of related or linked mechanisms that may exist through these basic disease hallmarks that we often classify as absolute signatures of one disease. These new perspectives will be discussed in the context of a new paradigm for Alzheimer's disease that implicates heavy metals as a primary cause. Plausible links between these distinctly different pathologies are presented showing intersections of their distinct pathologies that hinge on metal interactions.
[Mh] Termos MeSH primário: Encéfalo/efeitos dos fármacos
Encéfalo/fisiopatologia
Intoxicação do Sistema Nervoso por Metais Pesados/fisiopatologia
Metais/envenenamento
Modelos Neurológicos
Doenças Neurodegenerativas/fisiopatologia
[Mh] Termos MeSH secundário: Progressão da Doença
Medicina Baseada em Evidências
Intoxicação do Sistema Nervoso por Metais Pesados/complicações
Seres Humanos
Doenças Neurodegenerativas/etiologia
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Metals)
[Em] Mês de entrada:1608
[Cu] Atualização por classe:160217
[Lr] Data última revisão:
160217
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151126
[St] Status:MEDLINE


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[PMID]:26454485
[Au] Autor:Sojáková M; Zigrai M; Karaman A; Placková S; Klepancová P; Hrusovský S
[Ad] Endereço:1st Department of Internal Medicine, Faculty of Medicine, Slovak Medical University in Bratislava and University Hospital in Bratislava, Slovakia.
[Ti] Título:Thallium intoxication. Case Report.
[So] Source:Neuro Endocrinol Lett;36(4):311-5, 2015.
[Is] ISSN:0172-780X
[Cp] País de publicação:Sweden
[La] Idioma:eng
[Ab] Resumo:We report a rare case of serious voluntary intoxication by laboratory thallium monobromate combined with alcohol intake by a 24-years old man. The diagnosis of thallium intoxication was based on history, nonspecific but typical clinical symptoms including gastrointestinal complaints, painful polyneuropathy, alopecia, and confirmed by the finding of increased thallium concentration in the urine. The treatment, performed at the due time, consisted of decontamination of the stomach by irrigation, administration of active charcoal and Prussian blue, correction of water and mineral dysbalance, symptomatic treatment, and led to complete recovery.
[Mh] Termos MeSH primário: Intoxicação do Sistema Nervoso por Metais Pesados/complicações
Intoxicação por Metais Pesados
Envenenamento/complicações
Comportamento Autodestrutivo/complicações
Tálio/envenenamento
[Mh] Termos MeSH secundário: Intoxicação do Sistema Nervoso por Metais Pesados/tratamento farmacológico
Seres Humanos
Masculino
Envenenamento/tratamento farmacológico
Adulto Jovem
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
AD84R52XLF (Thallium)
[Em] Mês de entrada:1603
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151012
[St] Status:MEDLINE


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[PMID]:23719850
[Au] Autor:Lung S; Li H; Bondy SC; Campbell A
[Ad] Endereço:Department of Pharmaceutical Sciences, College of Pharmacy, Western University of Health Sciences, Pomona, CA, USA.
[Ti] Título:Low concentrations of copper in drinking water increase AP-1 binding in the brain.
[So] Source:Toxicol Ind Health;31(12):1178-84, 2015 Dec.
[Is] ISSN:1477-0393
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Copper (Cu) in trace amounts is essential for biological organisms. However, dysregulation of the redox-active metal has been implicated in different neurological disorders such as Wilson's, Menkes', Alzheimer's, and Parkinson's diseases. Since many households use Cu tubing in the plumbing system, and corrosion causes the metal to leach into the drinking water, there may be adverse effects on the central nervous system connected with low-level chronic exposure. The present study demonstrates that treatment with a biologically relevant concentration of Cu for 3 months significantly increases activation of the redox-modulated transcription factor AP-1 in mouse brains. This was independent of an upstream kinase indicated in AP-1 activation. Another redox-active transcription factor, NF-κB, was not significantly modified by the Cu exposure. These results indicate that the effect of Cu on AP-1 is unique and may involve direct modulation of DNA binding.
[Mh] Termos MeSH primário: Encéfalo/efeitos dos fármacos
Cobre/envenenamento
Intoxicação do Sistema Nervoso por Metais Pesados/metabolismo
Proteínas do Tecido Nervoso/metabolismo
Neurônios/efeitos dos fármacos
Fator de Transcrição AP-1/metabolismo
Poluição Química da Água/efeitos adversos
[Mh] Termos MeSH secundário: Animais
Encéfalo/metabolismo
Sulfato de Cobre/administração & dosagem
Cruzamentos Genéticos
DNA/metabolismo
Ensaio de Desvio de Mobilidade Eletroforética
Masculino
Camundongos Endogâmicos C3H
Camundongos Endogâmicos C57BL
Neurônios/metabolismo
Concentração Osmolar
Estresse Oxidativo
Testes de Toxicidade Crônica
Regulação para Cima/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Nerve Tissue Proteins); 0 (Transcription Factor AP-1); 789U1901C5 (Copper); 9007-49-2 (DNA); LRX7AJ16DT (Copper Sulfate)
[Em] Mês de entrada:1609
[Cu] Atualização por classe:151128
[Lr] Data última revisão:
151128
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:130531
[St] Status:MEDLINE
[do] DOI:10.1177/0748233713491805


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[PMID]:25451971
[Au] Autor:Liu W; Huo X; Liu D; Zeng X; Zhang Y; Xu X
[Ad] Endereço:Laboratory of Environmental Medicine and Developmental Toxicology, and Provincial Key Laboratory of Infectious Diseases and Molecular Immunopathology, Shantou University Medical College, Shantou 515041, Guangdong, China.
[Ti] Título:S100ß in heavy metal-related child attention-deficit hyperactivity disorder in an informal e-waste recycling area.
[So] Source:Neurotoxicology;45:185-91, 2014 Dec.
[Is] ISSN:1872-9711
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Exposure to lead even at low levels correlates with attention-deficit/hyperactivity disorder (ADHD). However, lead-contaminated environments are often contaminated with other heavy metals that could exacerbate lead-induced ADHD. We conducted this study to evaluate the relationship between multiple heavy metals and child behaviors, and the involvement of S100 calcium-binding protein ß (S100ß) expression in child ADHD in Guiyu, an internationally-known e-waste contaminated recycling town. Two hundred and forty kindergarten children, 3- to 7-years of age, who lived in Guiyu, were recruited for this study. Child behavioral assessment was derived from parent and teacher ratings. Serum S100ß was assayed by an enzyme-linked immunosorbent assay (ELISA). Lead (Pb), cadmium (Cd) and manganese (Mn) levels in whole blood were measured using graphite furnace atomic absorption spectrometry (GFAAS). The prevalence of children with ADHD symptoms in Guiyu was 18.6%, with the percentage of children suspected to have behavior problems being 46.2% or 46.5%, based on the Rutter parents' or teachers' scale scores, respectively. Child blood levels of Pb, Cd, and Mn correlated with certain behavioral abnormalities, such as conduct problems and antisocial behavior. Serum S100ß levels were associated with heavy metal levels in blood, and certain behavioral abnormalities. These findings suggest that exposure to various environmental heavy metals in Guiyu might result in child behavior disorders. Results also indicate that S100ß may provide information for laboratory evaluation of neurotoxicity.
[Mh] Termos MeSH primário: Transtorno do Deficit de Atenção com Hiperatividade/induzido quimicamente
Exposição Ambiental
Intoxicação do Sistema Nervoso por Metais Pesados/sangue
Intoxicação do Sistema Nervoso por Metais Pesados/psicologia
Subunidade beta da Proteína Ligante de Cálcio S100/sangue
[Mh] Termos MeSH secundário: Intoxicação por Cádmio/sangue
Criança
Pré-Escolar
Feminino
Seres Humanos
Intoxicação por Chumbo/sangue
Masculino
Intoxicação por Manganês/sangue
Reciclagem
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (S100 Calcium Binding Protein beta Subunit); 0 (S100B protein, human)
[Em] Mês de entrada:1510
[Cu] Atualização por classe:141216
[Lr] Data última revisão:
141216
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:141203
[St] Status:MEDLINE


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[PMID]:25096449
[Au] Autor:van Lingen CP; Ettema HB; Van Der Straeten C; Kollen BJ; Verheyen CC
[Ad] Endereço:1 Department of Orthopaedic Surgery and Traumatology, Isala Clinics, Zwolle - The Netherlands.
[Ti] Título:Self-reported neurological clinical manifestations of metal toxicity in metal-on-metal hip arthroplasty.
[So] Source:Hip Int;24(6):568-74, 2014 Dec 05.
[Is] ISSN:1724-6067
[Cp] País de publicação:Italy
[La] Idioma:eng
[Ab] Resumo:Adverse reactions to metal particle debris have been increasingly reported as a complication following large head metal-on-metal (MoM) hip arthroplasty. Elevated metal ion levels are a cause for concern. The aim of this study is to evaluate whether exposure to cobalt is associated with patient characteristics and symptoms of neuropathy, representing nervous system dysfunction. A cross-sectional study was conducted comparing patients with a MoM total hip arthroplasty and patients with a conventional hip arthroplasty. They received three questionnaires, one to assess neurotoxic complaints and two standardised self-administered questionnaires to identify symptoms that are suggestive of peripheral neuropathy. Current and historical data were available for whole blood cobalt levels in all patients. We analysed potential predictive factors for cobalt based on five different cut-off levels (0-2, 2-4, 4-10, 10-20, >20 µg/L). We performed 723 MoM total hip arthroplasties in 643 patients in our clinic. The response rate was 89%. Male-female ratio was 236/280, median age 63.6 years (30-72) with a mean follow-up of 50.6 months (20-86). We also sent the questionnaires to 98 patients in the control group. An increase in the incidence of reported symptoms was not consistent with higher serum cobalt levels. Female gender was the only consistent predictive factor for serum cobalt at different cobalt cut-off levels in the multivariate analysis. The study population did not show an increase in reported symptoms with elevated cobalt levels. Neurotoxic symptoms and whole blood cobalt levels did not show a consistent relationship with different dichotomised levels of cobalt exposure.
[Mh] Termos MeSH primário: Cobalto/efeitos adversos
Autoavaliação Diagnóstica
Intoxicação do Sistema Nervoso por Metais Pesados/etiologia
Prótese de Quadril/efeitos adversos
Próteses Articulares Metal-Metal/efeitos adversos
Autorrelato
[Mh] Termos MeSH secundário: Adulto
Idoso
Artroplastia de Quadril/efeitos adversos
Cobalto/sangue
Estudos Transversais
Feminino
Intoxicação do Sistema Nervoso por Metais Pesados/sangue
Seres Humanos
Masculino
Meia-Idade
Desenho de Prótese
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
3G0H8C9362 (Cobalt)
[Em] Mês de entrada:1602
[Cu] Atualização por classe:150821
[Lr] Data última revisão:
150821
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140807
[St] Status:MEDLINE
[do] DOI:10.5301/hipint.5000179


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[PMID]:24880014
[Au] Autor:Pal A; Jayamani J; Prasad R
[Ad] Endereço:Department of Biochemistry, PGIMER, Chandigarh, India.
[Ti] Título:An urgent need to reassess the safe levels of copper in the drinking water: lessons from studies on healthy animals harboring no genetic deficits.
[So] Source:Neurotoxicology;44:58-60, 2014 Sep.
[Is] ISSN:1872-9711
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Recent seminal studies have established neurodegeneration, cognitive waning and/or ß-amyloid deposition due to chronic copper intoxication via drinking water in healthy animals; henceforth, fuelling the debate all again over the safe levels of copper in the drinking water. This review encompasses the contemporary imperative animal studies in which the effect of chronic copper toxicity (especially via drinking water) was evaluated on the central nervous system and memory of uncompromised animals along with discussing the future perspectives.
[Mh] Termos MeSH primário: Cobre/toxicidade
Água Potável/química
Água Potável/normas
[Mh] Termos MeSH secundário: Animais
Água Potável/efeitos adversos
Intoxicação do Sistema Nervoso por Metais Pesados/etiologia
Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; REVIEW
[Nm] Nome de substância:
0 (Drinking Water); 789U1901C5 (Copper)
[Em] Mês de entrada:1505
[Cu] Atualização por classe:140924
[Lr] Data última revisão:
140924
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140601
[St] Status:MEDLINE



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