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1.
PLoS One ; 18(5): e0284697, 2023.
Artigo em Inglês | MEDLINE | ID: mdl-37134097

RESUMO

BACKGROUND: Apolipoprotein E is involved in lipid transport and clearance of lipoprotein through low-density lipoprotein receptors (LDLR). ApoE variation has been linked to cardiovascular disease (CVD) risk. There are 3 isoforms of ApoE which originate from two non-synonymous single nucleotide polymorphisms denoted as ε2, ε3 and ε4. The ε2 isoform is implicated in higher levels of atherogenic lipoprotein with the ε4 isoform causing LDLR downregulation. This leads to variable effects and differential CVD risk. Malaria and HIV are life-threatening diseases affecting several countries globally especially in sub-Saharan Africa. Parasite and viral activities have been implicated in lipid dysregulation leading to dyslipidaemia. This study examined ApoE variation and CVD risk assessment in malaria and HIV patients. METHODS: We compared 76 malaria-only, 33 malaria-HIV coinfected, 21-HIV-only and 31 controls from a tertiary health facility in Ghana. Fasting venous blood samples were taken for ApoE genotyping and lipid measurements. Clinical and laboratory data were collected with ApoE genotyping performed using Iplex Gold microarray and PCR-RFLP. Cardiovascular disease risk was calculated using the Framingham BMI and cholesterol risk and Qrisk3 tools. RESULTS: The frequency of C/C genotype for rs429358 was 9.32%, whiles T/T genotype for rs7412 was found in 2.48% of all participants. ε3/ε3 was the most distributed ApoE genotype accounting for 51.55% of the total participants whiles ε2/ε2 was found in 2.48% of participants, with 1 in malaria-only and 3 in HIV-only patients. There was a significant association between ε4+ and high TG (OR = 0.20, CI; 0.05-0.73; p = 0.015), whiles ε2+ was significantly associated with higher BMI (OR; 0.24, CI; 0.06-0.87; p = 0.030) and higher Castelli Risk Index II in females (OR = 11.26, CI; 1.37-92.30; p = 0.024). A higher proportion of malaria-only participants had a moderate to high 10-year CVD risk. CONCLUSION: Overall malaria patients seem to have a higher CVD risk though the means through which this occurs may be poorly understood. ε2/ε2 genotypes was observed in our population at a lower frequency. Further studies are vital to determine CVD risk in malaria and how this occurs.


Assuntos
Aterosclerose , Doenças Cardiovasculares , Infecções por HIV , Malária , Feminino , Humanos , Infecções por HIV/complicações , Infecções por HIV/epidemiologia , Infecções por HIV/genética , Gana/epidemiologia , Doenças Cardiovasculares/epidemiologia , Doenças Cardiovasculares/genética , Apolipoproteínas E/genética , Genótipo , Polimorfismo de Nucleotídeo Único , Malária/complicações , Malária/epidemiologia , Malária/genética , Medição de Risco , Predisposição Genética para Doença , Apolipoproteína E2/genética , Apolipoproteína E4/genética
2.
Malar J ; 21(1): 314, 2022 Nov 04.
Artigo em Inglês | MEDLINE | ID: mdl-36333802

RESUMO

The global burden of malaria continues to be a significant public health concern. Despite advances made in therapeutics for malaria, there continues to be high morbidity and mortality associated with this infectious disease. Sub-Saharan Africa continues to be the most affected by the disease, but unfortunately the region is burdened with indigent health systems. With the recent increase in lifestyle diseases, the region is currently in a health transition, complicating the situation by posing a double challenge to the already ailing health sector. In answer to the continuous challenge of malaria, the African Union has started a "zero malaria starts with me" campaign that seeks to personalize malaria prevention and bring it down to the grass-root level. This review discusses the contribution of sub-Saharan Africa, whose population is in a health transition, to malaria elimination. In addition, the review explores the challenges that health systems in these countries face, that may hinder the attainment of a zero-malaria goal.


Assuntos
Transição Epidemiológica , Malária , Humanos , África Subsaariana/epidemiologia , Malária/prevenção & controle , Saúde Pública
3.
OMICS ; 26(11): 583-585, 2022 11.
Artigo em Inglês | MEDLINE | ID: mdl-36269614

RESUMO

The current pandemic has markedly shifted the focus of the global research and development ecosystem toward infectious agents such as SARS-CoV-2, the causative agent for COVID-19. A case in point is the chronic liver disease associated with hepatitis B virus (HBV) infection that continues to be a leading cause of severe liver disease and death globally. The burden of HBV infection is highest in the World Health Organization designated western Pacific and Africa regions. Tenofovir disoproxil fumarate (TDF) is a nucleoside analogue used in treatment of HBV infection but carries a potential for kidney toxicity. TDF is not metabolized by the cytochrome P450 enzymes and, therefore, its clearance in the proximal tubule of the renal nephron is controlled mostly by membrane transport proteins. Clinical pharmacogenomics of TDF with a focus on drug transporters, discussed in this perspective article, offers a timely example where resource-limited countries and regions of the world with high prevalence of HBV can strengthen the collective efforts to fight both COVID-19 and liver diseases impacting public health. We argue that precision/personalized medicine is invaluable to guide this line of research inquiry. In all, our experience in Ghana tells us that it is important not to forget the burden of chronic diseases while advancing research on infectious diseases such as COVID-19. For the long game with COVID-19, we need to address the public health burden of infectious agents and chronic diseases in tandem.


Assuntos
COVID-19 , Hepatite B Crônica , Hepatite B , Humanos , Tenofovir/efeitos adversos , Vírus da Hepatite B/genética , Hepatite B Crônica/tratamento farmacológico , Farmacogenética , Ecossistema , Antivirais/efeitos adversos , DNA Viral/uso terapêutico , SARS-CoV-2 , Hepatite B/complicações , Hepatite B/genética , Rim , Gana
4.
Int J Breast Cancer ; 2018: 2539056, 2018.
Artigo em Inglês | MEDLINE | ID: mdl-29850258

RESUMO

BACKGROUND: What cheaper alternative breast screening procedures are available to younger women in addition to clinical breast examination (CBE) in Sub-Saharan countries? In 2009, we first described BreastLight for screening and reported high sensitivity at detecting breast cancer. Due to limitations of BreastLight, we have since 2014 been using the more technologically advanced Breast-i to screen 2204 women to find cheaper screening alternatives. METHODOLOGY: First, the participant lies down for CBE and then, in a darkened room, Breast-i was placed underneath each breast and trained personnel confirm vein pattern and look out for dark spot(s) to ascertain the presence of suspicious angiogenic lesion(s). RESULTS: CBE detected 153 palpable breast masses and Breast-i, which detects angiogenesis, confirmed 136. However, Breast-i detected 22 more cases of which 7 had angiogenesis but were not palpable and 15 were missed by CBE due to large breast size. Overall confirmed cases were 26, with Breast-i detecting 7 cases missed by CBE. Breast-i and CBE gave sensitivities of 92.3% and 73%, respectively. CONCLUSION: Breast-i with its high sensitivity to angiogenesis, reliability, and affordability will be an effective adjunct detection device that can be used effectively to increase early detection in younger women, thereby increasing treatment success.

5.
Int J Breast Cancer ; 2016: 3645308, 2016.
Artigo em Inglês | MEDLINE | ID: mdl-27635263

RESUMO

Background. Nearly 70% of women diagnosed with breast cancer in Ghana are in advanced stages of the disease due especially to low awareness, resulting in limited treatment success and high death rate. With limited epidemiological studies on breast cancer in Ghana, the aim of this study is to assess and understand the pattern of breast cancer distribution for enhancing early detection and treatment. Methods. We randomly selected and screened 3000 women for clinical palpable breast lumps and used univariate and bivariate analysis for description and exploration of variables, respectively, in relation to incidence of breast cancer. Results. We diagnosed 23 (0.76%) breast cancer cases out of 194 (6.46%) participants with clinically palpable breast lumps. Seventeen out of these 23 (0.56%) were premenopausal (<46.6 years) with 7 (0.23%) being below 35 years. With an overall breast cancer incidence of 0.76% in this study, our observation that about 30% of these cancer cases were below 35 years may indicate a relative possible shift of cancer burden to women in their early thirties in Ghana, compared to Western countries. Conclusion. These results suggest an age adjustment for breast cancer screening to early twenties for Ghanaian women and the need for a nationwide breast cancer screening to understand completely the pattern of breast cancer distribution in Ghana.

6.
PLoS One ; 8(1): e54456, 2013.
Artigo em Inglês | MEDLINE | ID: mdl-23372726

RESUMO

Enteropathogenic Escherichia coli (EPEC), enterohemorrhagic E. coli (EHEC) and enteroaggregative E. coli (EAEC) are intestinal pathogens that cause food and water-borne disease in humans. Using biochemical methods and NMR-based comparative metabolomics in conjunction with the nematode Caenorhabditis elegans, we developed a bioassay to identify secreted small molecules produced by these pathogens. We identified indole, indole-3-carboxaldehyde (ICA), and indole-3-acetic acid (IAA), as factors that only in combination are sufficient to kill C. elegans. Importantly, although lethal to C. elegans, these molecules downregulate several bacterial processes important for pathogenesis in mammals. These include motility, biofilm formation and production of Shiga toxins. Some pathogenic E. coli strains are known to contain a Locus of Enterocyte Effacement (LEE), which encodes virulence factors that cause "attaching and effacing" (A/E) lesions in mammals, including formation of actin pedestals. We found that these indole derivatives also downregulate production of LEE virulence factors and inhibit pedestal formation on mammalian cells. Finally, upon oral administration, ICA inhibited virulence and promoted survival in a lethal mouse infection model. In summary, the C. elegans model in conjunction with metabolomics has facilitated identification of a family of indole derivatives that broadly regulate physiology in E. coli, and virulence in pathogenic strains. These molecules may enable development of new therapeutics that interfere with bacterial small-molecule signaling.


Assuntos
Escherichia coli Êntero-Hemorrágica/patogenicidade , Escherichia coli Enteropatogênica/patogenicidade , Infecções por Escherichia coli/prevenção & controle , Escherichia coli/patogenicidade , Ácidos Indolacéticos/farmacologia , Indóis/farmacologia , Adesinas Bacterianas/biossíntese , Animais , Aderência Bacteriana/efeitos dos fármacos , Caenorhabditis elegans/efeitos dos fármacos , Caenorhabditis elegans/fisiologia , Escherichia coli Êntero-Hemorrágica/genética , Escherichia coli Êntero-Hemorrágica/isolamento & purificação , Escherichia coli Êntero-Hemorrágica/metabolismo , Escherichia coli Enteropatogênica/genética , Escherichia coli Enteropatogênica/isolamento & purificação , Escherichia coli Enteropatogênica/metabolismo , Escherichia coli/genética , Escherichia coli/isolamento & purificação , Escherichia coli/metabolismo , Infecções por Escherichia coli/microbiologia , Infecções por Escherichia coli/mortalidade , Humanos , Ácidos Indolacéticos/isolamento & purificação , Ácidos Indolacéticos/metabolismo , Indóis/isolamento & purificação , Indóis/metabolismo , Camundongos , Viabilidade Microbiana/efeitos dos fármacos , Toxina Shiga/antagonistas & inibidores , Toxina Shiga/biossíntese , Análise de Sobrevida , Virulência , Fatores de Virulência/antagonistas & inibidores , Fatores de Virulência/biossíntese
7.
J Bacteriol ; 193(17): 4516-22, 2011 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-21705596

RESUMO

Enteropathogenic Escherichia coli(EPEC) requires the tnaA-encoded enzyme tryptophanase and its substrate tryptophan to synthesize diffusible exotoxins that kill the nematode Caenorhabditis elegans. Here, we demonstrate that the RNA-binding protein CsrA and the tryptophan permease TnaB coregulate tryptophanase activity, through mutually exclusive pathways, to stimulate toxin-mediated paralysis and killing of C. elegans.


Assuntos
Sistemas de Transporte de Aminoácidos/metabolismo , Caenorhabditis elegans/microbiologia , Escherichia coli Enteropatogênica/patogenicidade , Proteínas de Escherichia coli/metabolismo , Exotoxinas/metabolismo , Proteínas de Ligação a RNA/metabolismo , Proteínas Repressoras/metabolismo , Triptofanase/genética , Sequência de Aminoácidos , Sistemas de Transporte de Aminoácidos/genética , Animais , Sequência de Bases , Escherichia coli Enteropatogênica/enzimologia , Escherichia coli Enteropatogênica/genética , Proteínas de Escherichia coli/genética , Regulação Bacteriana da Expressão Gênica , Dados de Sequência Molecular , Óperon , Proteínas de Ligação a RNA/genética , Proteínas Repressoras/genética , Triptofano/metabolismo , Triptofanase/metabolismo
8.
Mol Biol Cell ; 20(15): 3608-16, 2009 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-19535455

RESUMO

In Caenorhabditis elegans two M-line proteins, UNC-98 and UNC-96, are involved in myofibril assembly and/or maintenance, especially myosin thick filaments. We found that CSN-5, a component of the COP9 signalosome complex, binds to UNC-98 and -96 using the yeast two-hybrid method. These interactions were confirmed by biochemical methods. The CSN-5 protein contains a Mov34 domain. Although one other COP9 signalosome component, CSN-6, also has a Mov34 domain, CSN-6 did not interact with UNC-98 or -96. Anti-CSN-5 antibody colocalized with paramyosin at A-bands in wild type and colocalized with abnormal accumulations of paramyosin found in unc-98, -96, and -15 (encodes paramyosin) mutants. Double knockdown of csn-5 and -6 could slightly suppress the unc-96 mutant phenotype. In the double knockdown of csn-5 and -6, the levels of UNC-98 protein were increased and the levels of UNC-96 protein levels were slightly reduced, suggesting that CSN-5 promotes the degradation of UNC-98 and that CSN-5 stabilizes UNC-96. In unc-15 and unc-96 mutants, CSN-5 protein was reduced, implying the existence of feed back regulation from myofibril proteins to CSN-5 protein levels. Taken together, we found that CSN-5 functions in muscle cells to regulate UNC-98 and -96, two M-line proteins.


Assuntos
Proteínas de Caenorhabditis elegans/metabolismo , Proteínas de Transporte/metabolismo , Proteínas Musculares/metabolismo , Músculos/metabolismo , Western Blotting , Complexo do Signalossomo COP9 , Proteínas de Caenorhabditis elegans/genética , Proteínas de Transporte/genética , Imunofluorescência , Complexos Multiproteicos/genética , Complexos Multiproteicos/metabolismo , Proteínas Musculares/genética , Mutação , Peptídeo Hidrolases/genética , Peptídeo Hidrolases/metabolismo , Ligação Proteica , Interferência de RNA , Tropomiosina/genética , Tropomiosina/metabolismo , Técnicas do Sistema de Duplo-Híbrido
9.
Cell Host Microbe ; 5(5): 450-62, 2009 May 08.
Artigo em Inglês | MEDLINE | ID: mdl-19454349

RESUMO

Caenorhabditis elegans exhibits avoidance behavior when presented with diverse bacterial pathogens. We hypothesized that exposure to pathogens might not only cause worms to move away but also simultaneously activate pathways that promote resistance to the pathogen. We show that brief exposure to virulent or avirulent strains of the bacterial pathogen enteropathogenic E. coli (EPEC) "immunizes"C. elegans to survive a subsequent exposure that would otherwise prove lethal, a phenomenon we refer to as "conditioning." Conditioning requires dopaminergic neurons; the p38 MAP kinase pathway, which regulates innate immunity; and the insulin/IGFR pathway, which regulates lifespan. Our findings suggest that the molecular pathways that control innate immunity and lifespan may be regulated or "conditioned" by exposure to pathogens to allow survival in noxious environments.


Assuntos
Proteínas de Caenorhabditis elegans/genética , Caenorhabditis elegans/genética , Caenorhabditis elegans/microbiologia , Modelos Animais de Doenças , Escherichia coli Enteropatogênica/patogenicidade , Imunidade Inata , Longevidade , Animais , Caenorhabditis elegans/imunologia , Caenorhabditis elegans/fisiologia , Proteínas de Caenorhabditis elegans/imunologia , Escherichia coli Enteropatogênica/fisiologia , Interações Hospedeiro-Patógeno , Humanos , Transdução de Sinais , Virulência , Proteínas Quinases p38 Ativadas por Mitógeno/genética , Proteínas Quinases p38 Ativadas por Mitógeno/imunologia
10.
J Mol Biol ; 379(2): 201-11, 2008 May 30.
Artigo em Inglês | MEDLINE | ID: mdl-18448117

RESUMO

Gene regulation during development is an important biological activity that leads to synthesis of biomolecules at specific locations and specific times. The single tropomyosin gene of Caenorhabditis elegans, tmy-1/lev-11, produces four isoforms of protein: two from the external promoter and two from the internal promoter. We investigated the internal promoter of tropomyosin to identify sequences that regulate expression of tmy-1 in the pharynx and intestine. By promoter deletion of tmy-1 reporters as well as by database analyses, a 100-bp fragment that contained binding sequences for a GATA factor, for a chicken CdxA homolog, and for a forkhead factor was identified. Both the forkhead and CdxA binding sequences contributed to pharyngeal and intestinal expression. In addition, the GATA site also influenced intestinal expression of tmy-1 reporter. We showed that ELT-2 and PHA-4 proteins interact directly with the GATA and forkhead binding sequences, respectively, in gel mobility shift assays. RNA interference knockdown of elt-2 diminished tmy-1::gfp expression in the intestine. In contrast to RNA interference knockdown of pha-4, expression of tmy-1::gfp in pha-4;smg-1 mutants was slightly weaker than that of the wild type. Ectopic expression of PHA-4 and ELT-2 by heat shock was sufficient to elicit widespread expression of tmy-1::lacZ reporter in embryos. We found no indication of a synergistic relation between ELT-2 and PHA-4. Based on our data, PHA-4 and CdxA function as general transcription factors for pharyngeal and intestinal regulation of tmy-1. We present models by which ELT-2, PHA-4, and CdxA orchestrate expression from the internal promoter of tmy-1.


Assuntos
Proteínas de Caenorhabditis elegans/metabolismo , Caenorhabditis elegans , Fatores de Transcrição GATA/metabolismo , Regulação da Expressão Gênica no Desenvolvimento , Intestinos/fisiologia , Faringe/fisiologia , Transativadores/metabolismo , Tropomiosina , Animais , Animais Geneticamente Modificados , Proteínas Aviárias/genética , Proteínas Aviárias/metabolismo , Sequência de Bases , Caenorhabditis elegans/anatomia & histologia , Caenorhabditis elegans/embriologia , Caenorhabditis elegans/fisiologia , Proteínas de Caenorhabditis elegans/genética , Linhagem da Célula , Galinhas , Fatores de Transcrição GATA/genética , Genes Reporter , Proteínas de Homeodomínio/genética , Proteínas de Homeodomínio/metabolismo , Intestinos/anatomia & histologia , Dados de Sequência Molecular , Faringe/anatomia & histologia , Regiões Promotoras Genéticas , Isoformas de Proteínas/genética , Isoformas de Proteínas/metabolismo , Interferência de RNA , Proteínas Recombinantes de Fusão/genética , Proteínas Recombinantes de Fusão/metabolismo , Transativadores/genética , Tropomiosina/genética , Tropomiosina/metabolismo
11.
Mol Microbiol ; 57(4): 988-1007, 2005 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-16091039

RESUMO

Pathogenic Escherichia coli, including enteropathogenic E. coli (EPEC), enterohaemorrhagic E. coli (EHEC), enteroinvasive E. coli (EIEC) and enterotoxigenic E. coli (ETEC) are major causes of food and water-borne disease. We have developed a genetically tractable model of pathogenic E. coli virulence based on our observation that these bacteria paralyse and kill the nematode Caenorhabditis elegans. Paralysis and killing of C. elegans by EPEC did not require direct contact, suggesting that a secreted toxin mediates the effect. Virulence against C. elegans required tryptophan and bacterial tryptophanase, the enzyme catalysing the production of indole and other molecules from tryptophan. Thus, lack of tryptophan in growth media or deletion of tryptophanase gene failed to paralyse or kill C. elegans. While known tryptophan metabolites failed to complement an EPEC tryptophanase mutant when presented extracellularly, complementation was achieved with the enzyme itself expressed either within the pathogen or within a cocultured K12 strains. Thus, an unknown metabolite of tryptophanase, derived from EPEC or from commensal non-pathogenic strains, appears to directly or indirectly regulate toxin production within EPEC. EPEC strains containing mutations in the locus of enterocyte effacement (LEE), a pathogenicity island required for virulence in humans, also displayed attenuated capacity to paralyse and kill nematodes. Furthermore, tryptophanase activity was required for full activation of the LEE1 promoter, and for efficient formation of actin-filled membranous protrusions (attaching and effacing lesions) that form on the surface of mammalian epithelial cells following attachment and which depends on LEE genes. Finally, several C. elegans genes, including hif-1 and egl-9, rendered C. elegans less susceptible to EPEC when mutated, suggesting their involvement in mediating toxin effects. Other genes including sek-1, mek-1, mev-1, pgp-1,3 and vhl-1, rendered C. elegans more susceptible to EPEC effects when mutated, suggesting their involvement in protecting the worms. Moreover we have found that C. elegans genes controlling lifespan (daf-2, age-1 and daf-16), also mediate susceptibility to EPEC. Together, these data suggest that this C. elegans/EPEC system will be valuable in elucidating novel factors relevant to human disease that regulate virulence in the pathogen or susceptibility to infection in the host.


Assuntos
Toxinas Bacterianas/genética , Caenorhabditis elegans/microbiologia , Proteínas de Escherichia coli/genética , Escherichia coli/enzimologia , Escherichia coli/patogenicidade , Triptofanase/genética , Animais , Toxinas Bacterianas/metabolismo , Transporte Biológico , Caenorhabditis elegans/genética , Caenorhabditis elegans/metabolismo , Escherichia coli/genética , Proteínas de Escherichia coli/metabolismo , Indóis/farmacologia , Mutação , Fosfoproteínas/genética , Regiões Promotoras Genéticas/efeitos dos fármacos , Triptofano/metabolismo , Triptofano/farmacologia , Triptofanase/metabolismo , Virulência
12.
J Cell Biol ; 167(4): 639-47, 2004 Nov 22.
Artigo em Inglês | MEDLINE | ID: mdl-15545320

RESUMO

Tissue-specific alternative pre-mRNA splicing is essential for increasing diversity of functionally different gene products. In Caenorhabditis elegans, UNC-60A and UNC-60B, nonmuscle and muscle isoforms of actin depolymerizing factor (ADF)/cofilin, are expressed by alternative splicing of unc-60 and regulate distinct actin-dependent developmental processes. We report that SUP-12, a member of a new family of RNA recognition motif (RRM) proteins, including SEB-4, regulates muscle-specific splicing of unc-60. In sup-12 mutants, expression of UNC-60B is decreased, whereas UNC-60A is up-regulated in muscle. sup-12 mutations strongly suppress muscle defects in unc-60B mutants by allowing expression of UNC-60A in muscle that can substitute for UNC-60B, thus unmasking their functional redundancy. SUP-12 is expressed in muscle and localized to the nuclei in a speckled pattern. The RRM domain of SUP-12 binds to several sites of the unc-60 pre-mRNA including the UG repeats near the 3'-splice site in the first intron. Our results suggest that SUP-12 is a novel tissue-specific splicing factor and regulates functional redundancy among ADF/cofilin isoforms.


Assuntos
Caenorhabditis elegans/metabolismo , Proteínas dos Microfilamentos/metabolismo , Desenvolvimento Muscular/genética , Músculos/metabolismo , Precursores de RNA/metabolismo , Proteínas de Ligação a RNA/metabolismo , Fatores de Despolimerização de Actina , Actinas/metabolismo , Processamento Alternativo/genética , Sequência de Aminoácidos/genética , Animais , Sequência de Bases/genética , Sítios de Ligação/genética , Caenorhabditis elegans/genética , Proteínas de Caenorhabditis elegans/genética , Proteínas de Caenorhabditis elegans/isolamento & purificação , Proteínas de Caenorhabditis elegans/metabolismo , Núcleo Celular/genética , Núcleo Celular/metabolismo , DNA Complementar/análise , DNA Complementar/genética , Destrina , Proteínas dos Microfilamentos/genética , Dados de Sequência Molecular , Músculos/citologia , Mutação/genética , Isoformas de Proteínas/genética , Isoformas de Proteínas/metabolismo , Estrutura Terciária de Proteína/genética , Precursores de RNA/genética , Sítios de Splice de RNA/genética , Proteínas de Ligação a RNA/genética , Proteínas de Ligação a RNA/isolamento & purificação , Regulação para Cima/genética
13.
Afr J Health Sci ; 2(4): 388-391, 1995 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-12160428

RESUMO

In a 12 month study of children with acute diarrhoea seeking medical care in 2 hospitals in Accra, Ghana, 16.3% were found to be infected with human rotaviruses (HRV). Vomiting and diarrhoea were the main symptoms observed. HRV infection was frequently associated with severe diarrhoea. Vomiting was however less frequent in HRV associated diarrhoea than in non HRV diarrhoea. No significant association was observed between the severity of dehydration and HRV infection. Subgroup II HRV was the predominant subgroup identified with the dominant serotypes being HRV serotypes 1 and 4. Poly-acrylamide gel electrophoresis of HRV RNAs isolated from 40 positive stool samples revealed the existence of 7 distinct electrophoretic migration patterns in the study population.

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