Usia menarche sebagai faktor risiko kejadian preeklamsia dan eklamsia

Latar Belakang: Preeklamsia merupakan penyumbang terbesar kedua kematian ibu di Indonesia. Di Amerika Serikat sejak tahun 1998 sampai 2005, Berg (2010) melaporkan bahwa sebesar 12,3% dari 4693 ibu hamil yang meninggal disebabkan karena preeklamsia atau eklampsia. Penyebab preeklamsia masih belum diketahui dengan pasti oleh karena itu preeklampsia disebut sebagai “diseases of theory”. Faktor risiko dari preeklamsia sangat banyak, sebuah penelitian menjelaskan bahwa usia menarche yang dini dapat meningkatkan risiko preeklamsia. Tujuan Penelitian: Tujuan umum dari penelitian ini adalah untuk mengetahui pengaruh usia menarche terhadap kejadian preeklamsia dan eklamsia.Metode Penelitian: Jumlah sampel total yang diambil adalah 90 responden dengan masing-masing kasus dan kontrol 45 responden. Jenis penelitian observasional dengan rancangan case control. Instrumen untuk mengukur usia menarche dengan kejadian preeklamsia mengadopsi dari data SKRT dan jurnal BMI as a modifying factor in the relations between age at menarche, menstrual cycle characteristics, and risk of preeclampsia. Analisis data menggunakan analisis univariabel, bivariabel dengan T-test untuk data numerik kategorik dan McNemar untuk data kategorik kategorik sedangkan analisis multivariabel dengan menggunakan conditional logistic regression.Hasil: Rata-rata usia menarche pada kelompok preeklamsia lebih muda satu tahun dibandingkan dengan kelompok non preeklamsia. Berdasarkan data perhitungan multivariabel setiap kenaikan satu tahun usia menarche menurunkan risiko preeklamsia/eklamsia sebesar 78%. Faktor risiko terjadinya preeklamsia meningkat pada ibu yang hamil di usia > 35 tahun dan memiliki indeks massa tubuh sebelum hamil > 25 kg/m2.Kesimpulan: Terdapat hubungan yang signifikan antara usia menarche dengan kejadian preeklamsia/eklamsia. Indeks masa tubuh sebelum hamil merupakan variabel perancu hubungan antara usia menarche dengan kejadian preeklamsia/eklamsia.Age of menarche as a risk factor for preeclampsia and eclampsiaPurposeThe purpose of this study is to determine the effect of menarche age on the incidence of preeclampsia and eclampsia.MethodThe observational study with the case-control design was conducted involving 90 pregnant and postpartum women. The bivariable analysis used T-test and McNemar test, while multivariable analysis using conditional logistic regression. Results The average age of menarche in the preeclampsia group was one year younger than the non-preeclampsia group. Any increase in one year of age of menarche lowers the risk of preeclampsia and eclampsia by 78%. Risk factors for preeclampsia are increased in pregnant women at age> 35 years and have body mass index before pregnancy> 25 kg/m2.ConclusionThere is a significant relationship between age of menarche and the incidence of preeclampsia and eclampsia. Body mass index before pregnancy is a confounding factor of the association between age of menarche and the incidence of preeclampsia and eclampsia

Two Group A Streptococcal Peptide Pheromones Act through Opposing Rgg Regulators to Control Biofilm Development

Streptococcus pyogenes (Group A Streptococcus, GAS) is an important human commensal that occasionally causes localized infections and less frequently causes severe invasive disease with high mortality rates. How GAS regulates expression of factors used to colonize the host and avoid immune responses remains poorly understood. Intercellular communication is an important means by which bacteria coordinate gene expression to defend against host assaults and competing bacteria, yet no conserved cell-to-cell signaling system has been elucidated in GAS. Encoded within the GAS genome are four rgg-like genes, two of which (rgg2 and rgg3) have no previously described function. We tested the hypothesis that rgg2 or rgg3 rely on extracellular peptides to control target-gene regulation. We found that Rgg2 and Rgg3 together tightly regulate two linked genes encoding new peptide pheromones. Rgg2 activates transcription of and is required for full induction of the pheromone genes, while Rgg3 plays an antagonistic role and represses pheromone expression. The active pheromone signals, termed SHP2 and SHP3, are short and hydrophobic (DI[I/L]IIVGG), and, though highly similar in sequence, their ability to disrupt Rgg3-DNA complexes were observed to be different, indicating that specificity and differential activation of promoters are characteristics of the Rgg2/3 regulatory circuit. SHP-pheromone signaling requires an intact oligopeptide permease (opp) and a metalloprotease (eep), supporting the model that pro-peptides are secreted, processed to the mature form, and subsequently imported to the cytoplasm to interact directly with the Rgg receptors. At least one consequence of pheromone stimulation of the Rgg2/3 pathway is increased biogenesis of biofilms, which counteracts negative regulation of biofilms by RopB (Rgg1). These data provide the first demonstration that Rgg-dependent quorum sensing functions in GAS and substantiate the role that Rggs play as peptide receptors across the Firmicute phylum

Use of Zebrafish to Probe the Divergent Virulence Potentials and Toxin Requirements of Extraintestinal Pathogenic Escherichia coli

Extraintestinal pathogenic E. coli (ExPEC) cause an array of diseases, including sepsis, neonatal meningitis, and urinary tract infections. Many putative virulence factors that might modulate ExPEC pathogenesis have been identified through sequencing efforts, epidemiology, and gene expression profiling, but few of these genes have been assigned clearly defined functional roles during infection. Using zebrafish embryos as surrogate hosts, we have developed a model system with the ability to resolve diverse virulence phenotypes and niche-specific restrictions among closely related ExPEC isolates during either localized or systemic infections. In side-by-side comparisons of prototypic ExPEC isolates, we observed an unexpectedly high degree of phenotypic diversity that is not readily apparent using more traditional animal hosts. In particular, the capacity of different ExPEC isolates to persist and multiply within the zebrafish host and cause disease was shown to be variably dependent upon two secreted toxins, α-hemolysin and cytotoxic necrotizing factor. Both of these toxins appear to function primarily in the neutralization of phagocytes, which are recruited in high numbers to sites of infection where they act as an essential host defense against ExPEC as well as less virulent E. coli strains. These results establish zebrafish as a valuable tool for the elucidation and functional analysis of both ExPEC virulence factors and host defense mechanisms