AN EXPLORATION OF HEALTH AND SAFETY MANAGEMENT ISSUES IN NIGERIA’S EFFORT TO INDUSTRIALIZE

All organizations have a duty of care to ensure that employees and other persons who may be affected by the company’s undertakings remain safe at all times. This paper examines the background of occupational health and safety (OHS) practices in Nigeria, and highlights the importance of mitigating the OHS challenges identified from the moral, legal, financial and other dimensions. In the Nigerian context, the need to reinforce health and safety management (HSM) issues is exemplified from the unsavory recurrent reports of plane crashes in the aviation industry, high rates of motor vehicle accidents, numerous cases of death due to poisoning in the solid mineral sector, frequent accounts of disasters in the petroleum sector arising from oil spills, pipeline vandalism as well as accidents involving petroleum tankers. More effective and efficient management of these issues is a sine qua non to the industrialization efforts of an economy. Against the background of extant HS legislation in Nigeria, some reasons for the frequent violations of OHS standards and norms by the operators were identified as bribery and corruption in the system, the ‘Nigerian Factor’, inadequate funding of monitoring institutions, low level of education of employees as well as problems of persistent unemployment in the country. While recommending ways to mitigate the OHS flaws in Nigerian institutions, the relative duties and responsibilities of stakeholders in the OHS business were identified. The paper concludes by noting the importance of a virile HSM environment to the overall economic development and industrialization of the nation

Importância do dismorfismo eritrocitário na investigação da origem da hematúria: revisão da literatura The importance of the dysmorphic erythrocyte for investigation of the source of hematuria: literature review

As hematúrias são achados comuns nos exames de urina de rotina e nem sempre são sinais de doenças. A presença de hematúria associada a outras alterações urinárias, especialmente a proteinúria, sugere comprometimento do trato urinário e merece investigação. Na literatura são inúmeros os trabalhos que valorizam a sedimentoscopia urinária, principalmente a morfologia das hemácias, como indicativo do local do sangramento: se glomerular ou não-glomerular. Neste artigo, os autores revisam o estudo do dismorfismo eritrocitário, enfatizando a definição, a fisiopatologia, os métodos, os valores de referência e as limitações apontadas na literatura. As comparações com demais marcadores de hemorragia glomerular também foram discutidas. No final, os autores relatam como a literatura interpreta e utiliza os resultados da pesquisa do dismorfismo eritrocitário para guiar a propedêutica complementar na investigação da origem da hematúria.<br>The hematurias are a frequent finding in urinary routine exams and do not necessarily indicate illness. The presence of hematuria associated with other urinary disturbances, especially proteinuria, indicates urinary tract pathology and should be investigated. In the literature, several studies point out the importance of urinary sedimentoscopy, specially the red cells morphology, to determine the source of bleeding: glomerular or non-glomerular. In this article, the authors review the dysmorphic erythrocyte, emphasizing on the meaning, the physiopathology, the methods, the cut-of values, and the limitations according to the literature. The comparisons with other markers of glomerular bleeding were also discussed. At the end, the authors exposed how the literature analyses and applies the dysmorphic erythrocyte results to guide the complementary research for investigation the source of urinary bleeding

Urolitíase pediátrica: experiência de um hospital infantil de cuidados terciários

Resumo Introdução: A urolitíase pediátrica tornou-se mais prevalente nas últimas décadas, com altas taxas de recorrência e considerável morbidade. A maioria das crianças com urolitíase idiopática tem uma anormalidade metabólica subjacente e a investigação adequada permite intervenções terapêuticas para reduzir a formação de novos cálculos e suas complicações. Objetivos: Identificar características demográficas e clínicas da urolitíase pediátrica, a etiologia, condutas terapêuticas, recidiva da doença e evolução dos pacientes em um hospital infantil de cuidados terciários. Métodos: Estudo descritivo e retrospectivo com pacientes pediátricos internados no Hospital Infantil Joana de Gusmão, Florianópolis, SC, Brasil, com diagnóstico de urolitíase, no período de janeiro 2002 a dezembro de 2012. Dados foram obtidos dos prontuários e foram incluídos aqueles com diagnóstico confirmado por exame de imagem e urina 24h ou amostra única urinária. Resultados: Foram avaliados 106 pacientes (65%M) pediátricos. Idade média ao diagnóstico 8,0 ± 4,2 e 85% tinham história familiar positiva para urolitíase. Dor abdominal, cólica nefrética clássica e infecção urinária foram as principais manifestações. 93,2% tinham alteração metabólica, sendo a hipercalciúria a mais comum. Tratamento farmacológico foi instituído em 78% dos casos. Utilizou-se citrato de potássio e hidroclorotiazida. Tratamento cirúrgico foi realizado em 38% dos pacientes. Houve resposta ao tratamento em 39% deles, com recidiva da urolitíase em 34,2%. Apenas 4,7% dos pacientes continuaram acompanhamento, 6,6% foram encaminhados para outros serviços, 8,5% receberam alta e 73,8% perderam acompanhamento. Conclusão: A urolitíase pediátrica merece avaliação metabólica detalhada após sua apresentação inicial para tratamento, acompanhamento e prevenção da formação lítica e de suas complicações

Role of FGF23 in Pediatric Hypercalciuria

Background. This study explored the possible role of FGF23 in pediatric hypercalciuria. Methods. Plasma FGF23 was measured in 29 controls and 58 children and adolescents with hypercalciuria: 24 before treatment (Pre-Treated) and 34 after 6 months of treatment (Treated). Hypercalciuric patients also measured serum PTH hormone, 25(OH)vitD, phosphate, calcium, creatinine, and 24 h urine calcium, phosphate, and creatinine. Results. There were no differences in age, gender, ethnicity, or body mass index either between controls and patients, or between Pre-Treated and Treated patients. Median plasma FGF23 in controls was 72 compared with all patients, 58 RU/mL (p=0.0019). However, whereas FGF23 in Pre-Treated patients, 73 RU/mL, was not different from controls, in Treated patients it was 50 RU/mL, significantly lower than in both controls (p<0.0001) and Pre-Treated patients (p=0.02). In all patients, there was a correlation between FGF23 and urinary calcium (r=0.325; p=0.0014). Treated patients had significantly lower urinary calcium (p<0.0001), higher TP/GFR (p<0.001), and higher serum phosphate (p=0.007) versus Pre-Treated patients. Conclusions. Pharmacological treatment of hypercalciuric patients resulted in significantly lower urinary calcium excretion, lower serum FGF23, and elevated TP/GFR and serum phosphate concentration, without significant changes in PTH. Further studies are indicated. This trial is registered with Clinical Registration Number RBR 8W27X5

American and Brazilian Children With Primary Urolithiasis

Objectives . Considering the differences in location, socioeconomic background, and cultural background, the aim of this study was to try to identify possible factors associated with the increased incidence of urolithiasis by comparing American and Brazilian children with stones. Methods . Data of 222 American and 190 Brazilian children with urolithiasis were reviewed including age, gender, body mass index, imaging technique used (ultrasound and computed tomography), and 24-hour urine volume and chemistries. Results . There were no differences between age and gender at diagnosis. Brazilian children were leaner but in no population did obesity rate exceed that of the general population. Ultrasound was most commonly used to diagnose stones, even more so in Brazilians. Decreased urine flow was more common among Americans ( P = .004), hypercalciuria among Brazilians ( P = .001), and elevated Ca/citrate ratio among Americans ( P = .009). There were no differences between the groups in the frequency of hypocitraturia, hyperuricosuria, absorptive hyperoxaluria, and cystinuria. Conclusions . Despite some differences between the populations, the leading causes of urolithiasis among both were “oliguria,” hypercalciuria, and high Ca/citrate ratio. In neither country was obesity the reason for the increase in incidence of urolithiasis, nor was the use of computed tomography. The similarities between the 2 populations call for combining efforts in addressing the leading causes of pediatric urolithiasis

Hereditary fructose intolerance in Brazilian patients

Introduction: Hereditary fructose intolerance (HFI) is a rare inborn error of carbohydrate metabolism, autosomal recessive, caused by mutations in the gene ALDOB, leading to deficiency of aldolase B. Symptoms begin in the first months of life with the introduction of complementary foods containing fructose, sucrose or sorbitol, often with vomiting, feeding problems and failure to thrive. Prolonged exposure may cause liver and kidney failure, which can lead to death. Treatment consists in removing the toxic sugars of diet. Materials and methods: Clinical and molecular characterization of four unrelated patients from the State of Minas Gerais, Brazil, all children from non-consanguineous parents. Results and discussion: Age at diagnosis was between 10 and 32 months and the severity of the disease correlated with the increasing of age at diagnosis. The predominant symptoms were vomiting, weight loss, and hepatomegaly. Severe renal tubular acidosis manifested in one child. All patients had remission of symptoms after dietary modification. The sequencing of the ALDOB gene identified one homozygous patient for the mutation c.524C>A (p.A175D), while the others were compound heterozygous for c.360_363delCAAA (p.N120KfsX32), c.178C>T (p.R60X) mutations, c.448G>C (p.A150P) and c.524C>A (p.A175D). Clinical improvement of patients after dietary treatment is suggestive of the diagnosis, confirmed by molecular analysis. The prevalence of mutations found in our Brazilian patients is different from those of international literature

Nphs1 gene mutations confirm congenital nephrotic syndrome in four Brazilian cases: a novel mutation is described

FAPESP - FUNDAÇÃO DE AMPARO À PESQUISA DO ESTADO DE SÃO PAULOCNPQ – CONSELHO NACIONAL DE DESENVOLVIMENTO CIENTÍFICO E TECNOLÓGICOAutosomal recessive mutations in NPHS1 gene are a common cause of congenital nephrotic syndrome (CNS). The disorder is characterized by massive proteinuria that manifests in utero or in the neonatal period during the first 3 months of life. NPHS1 encodes nephrin, a member of the immunoglobulin family of cell adhesion molecules and the main protein expressed at the renal slit diaphragm. Currently, there are approximately 250 mutations described in NPHS1 gene distributed among all nephrin domains. The main objective of this study was to perform the analysis of NPHS1 gene in patients with congenital nephrotic syndrome in order to determine the molecular cause of the disease. We performed direct sequencing of NPHS1 gene in four children. Each patient was heterozygous for two pathogenic mutations disclosing the molecular cause of the disease in 100% of the cases. We identified six different mutations, consisting of one in-frame deletion, one frameshift, and four missense substitutions. The p.Val736Met mutation that is described here for the first time was considered pathogenic by different mutation predictive algorithms. Regardless of the type of mutation, three patients had a bad outcome and died. Despite the small size of the cohort, this study contributed to the increasing number of deleterious mutations in the NPHS1 gene by describing a new mutation. Also, since we identified NPHS1 pathogenic mutations as the cause of the disease in all cases analyzed, it might be a frequent cause of CNS in South Eastern region of Brazil, although the analysis of a larger sample is required to obtain more indicative epidemiological data.Autosomal recessive mutations inNPHS1geneareacommoncauseofcongenital nephrotic syndrome (CNS). The disorder is characterized by massiveproteinuria that manifestsin uteroor in the neonatal period during thefirst3months of life.NPHS1encodes nephrin, a member of the immunoglobulin fam-ily of cell adhesion molecules and the main protein expressed at the renal slitdiaphragm. Currently, there are approximately 250 mutations described in theNPHS1gene distributed among all nephrin domains. The main objective of thisstudy was to perform the analysis of theNPHS1gene in patients with congenitalnephrotic syndrome in order to determine the molecular cause of the disease.Methods:Direct sequencing ofNPHS1gene in four children was performed.Results:Each patient was heterozygous for twopathogenic mutations disclosingthemolecularcauseofthediseasein100%ofthecases.Weidentified six differ-ent mutations, consisting of one in-framedeletion, one frameshift, and four mis-sense substitutions. The p.Val736Met mutation that is described here for thefirsttime was considered pathogenic by different mutation predictive algorithms.Regardless of the type of mutation, three patients had a bad outcome and diedConclusions:Despite the small size of the cohort, this study contributed to theincreasing number of deleterious mutations in theNPHS1gene by describing anew mutation. Also, since we identifiedNPHS1pathogenic mutations as thecause of the disease in all cases analyzed, it might be a frequent cause of CNSin the South Eastern region of Brazil, although the analysis of a larger sampleis required to obtain more indicative epidemiological data219753757FAPESP - FUNDAÇÃO DE AMPARO À PESQUISA DO ESTADO DE SÃO PAULOCNPQ – CONSELHO NACIONAL DE DESENVOLVIMENTO CIENTÍFICO E TECNOLÓGICOFAPESP - FUNDAÇÃO DE AMPARO À PESQUISA DO ESTADO DE SÃO PAULOCNPQ – CONSELHO NACIONAL DE DESENVOLVIMENTO CIENTÍFICO E TECNOLÓGICO2012/51109-0478444/08-7; 141072/201