Investigation of Bacteria from Spoiled Bottled Salad Dressing Leading to Gas Explosion

Background: In 2020, an incident involving spoiled salad dressing from a commercial source occurred. Upon opening the bottle, the contents exploded from gas that seemed to have fermented inside the bottle. For safety concerns, we sought to investigate the bacteria from the salad dressing in order to notify the company that made the product and relevant authorities. Methods: Anaerobic and carbon dioxide culture methods were used. To determine species of colonies, MALDI-TOF-MS and 16S rRNA whole sequencing were performed. Results: There were no colonies grown in anaerobic condition; however, we obtained three colonies from the carbon dioxide atmosphere. We determined the first colony as Alkalihalobacillus clausii (Bacillus clausii), the second as Bacillus spp. such as B. australimaris, B. safensis or B. safensis subsp. osmophilus and the third as B. paralicheniformis. Phylogenic tree analysis using the16S rRNA sequence revealed these colonies to be in a proximity of known gas-producing species. The NCBI database search revealed that a key gas production pathway gene, pyruvate formate-lyase (pfl), of which the gene product catalyzes pyruvate to formate conversion, exists in B. paralicheniformis. Formate dehydrogenase (FdhH) produces CO2 from formate that the coding gene fdhF positive bacteria can participate in gas production when formate is present in the culture. And we found fdhF from A. clausii, B. australimaris/B. safensis and B. paralicheniformis. Furthermore, under butanediol producing pathway, genes coding two enzymes involved in CO2 production, namely als and ald, existed in B. australimaris/B. safensis and B paralicheniformis, whereas A. clausii possessed als. Conclusion: Candidate species A. clausii, B. australimaris/B. safensis and B. paralicheniformis from spoiled salad dressing were thought to produce CO2 gas each from their own enzymes, or in combination, which caused the explosion upon opening. The endospore forming nature of Bacillus should alert us to be cautious when considering food producing process regulations where we need to thoroughly heat any product during manufacture in order to inactivate any bacteria as there is the possibility of this type of dangerous occurrence

分子生物学的手法を用いた腸炎ビブリオ食中毒の疫学的解析に関する研究

腸炎ビブリオ(Vibrio parahaemolyticus)は、好塩性の細菌で、海水、なかでも沿岸海域や汽水域に生息しており、魚介類を生食する習慣のあるわが国においては代表的な食中毒起因菌の一つである。本菌による集団食中毒は、毎年上位を占めていたが、1996年以降さらに著しく増加した。その原因については明確ではない。　一方、腸炎ビブリオの病原因子としては耐熱性溶血毒(Thermostable direct hemolysin ; TDH、または神奈川溶血毒)と耐熱性溶血毒類似毒(TDH-related hemolysin ; TRH)が知られている。腸炎ビブリオ食中毒の発生時に、患者ふん便から分離される菌は、TDH(稀にTRH)産生株であるのに対し、食品や環境から分離される腸炎ビブリオは溶血毒非産生株のみである。原因食品を喫食後に発症した患者由来のTDH産生株と同じTDH産生株が食品や環境から分離されない原因については、本菌の病原因子が解明された1970年代以降の課題であった。　最近、細菌検査に遺伝子増幅法であるPCR(Polymerase chain reaction)法や、パルスフィールドゲル電気泳動(Pulsed-field gel electrophoresis, PFGE)法が広く応用され、分子疫学的解析が可能となってきた。　今回は、腸炎ビブリオ食中毒の増加の原因を明らかにする目的で、発生状況及び原因菌について疫学的解析を行うとともに、食品からTDH産生株を検出するための方法について検討を行ったところ、以下の結果を得た。1)　東京都内で1989～2004年の16年間に発生した腸炎ビブリオ食中毒の発生状況について調査したところ、腸炎ビブリオ食中毒事例として872事例(行政的には有症苦情事例等として処理された事例を含む)が認められた。その発生年次別では、1989年が55事例、1990年が75事例であったが、その後減少し、1993年が24事例とこの期間では最も少なかった。それ以降増加傾向を示し、1998年が最も多く107事例であったが、それ以降は2001年が33事例、2002年が49事例、2003年が29事例、2004年が51事例と増減を繰り返している傾向が明らかになった。2)　食中毒の月別における発生状況では、8月の発生が最も多く393件(45.1%)であった。また、7～9月の3ヶ月間において発生が全体の89%を占めていることが明らかになった。さらにその前後の月をあわせた6～10月の5ヶ月間に全体の99%の事例が発生していた。しかし、今回の調査で、通常では腸炎ビブリオ食中毒の発生が認められない11～2月にも6事例が発生していることが明らかになった。次に7～9月の東京の平均気温と本菌食中毒発生状況を比較検討した結果、1994年までは腸炎ビブリオ食中毒事例数と気温との間にほぼ相関性が認められた。しかしそれ以降は、発生事例数の著しい増加から、気温との相関は認められなかったが、その増加の要因として血清型O3:K6菌による食中毒の増加と一致していることが明らかとなった。3)　1989～1998年の10年間に発生した216事例の本菌食中毒の原因食品について調査したところ、最も多かったものは会食料理で25%、次に寿司類17%、刺身類8%、魚介類の調理品5%の順であった。なお、会食料理は主に飲食店や寿司屋などで刺身や寿司などの魚介類を喫食したものであった。4)　1995～1997年の3年間に発生した39事例についてその発生要因を詳細に調べた結果、原材料間の相互汚染や調理器具を介した二次汚染が34.8%と最も多く、次に室温で解凍するなど不適当な温度保存(28.8%)、長時間の保存(18.2%)、原材料の汚染(10.6%)などの順であった。事例別の発生要因では、単独の要因による発生事例は少なく、2つ以上の複数の要因が重なった場合に発生していることが明らかになった。さらに、食中毒の原因としては、原材料汚染に加え、二次汚染や低温管理の不備による菌の増殖が原因である事を明らかにした。5)　本菌食中毒から分離された菌株について、血清型別を行ったところ、O4:K8やO3:K6などの血清型が高頻度に認められたが、数年毎に異なる血清型の流行が認められた。その年別における菌株の中で最も多く検出された血清型は、1989年ではO4:K4、1990年および1991年ではO4:K8、1992年ではO1:K56、1993～1995年では再びO4:K8であった。しかし、1996年以降はそれ以前にほとんど認められなかったO3:K6が急増の傾向を示し、なかでも2000年では本血清型菌が最も多くを占め、65事例中57事例(87.7%)であった。この傾向は、2005年に至っても継続しており、最近の本菌食中毒菌の血清型はO3:K6が大半を占めていることが明らかとなった。6)　1998年には食中毒の原因菌として既知の血清型ではなく、新たな血清型O4:K68が関与していることを明らかにした。この血清型菌は従来から知られている抗原表にはないOK不一致の新しいタイプの菌であった。7)　食品からTDH産生菌を効率よく分離する方法として、食品の増菌培養液を対象にTDH産生に関与するtdh遺伝子をPCR法を用いてスクリーニングし、さらに性質の異なる2種類の分離培地(最近開発された酵素基質培地と従来から繁用されているTCBS寒天)を用い、画線-ストリップ法等を組み合わせることにより、TDH産生菌を効率的に分離できる方法を開発した。8)　2000～2004年の5年間に発生した腸炎ビブリオ食中毒227事例の内67事例の食品検体(残品、参考品、同一品および検食)を対象に、著者らが開発した上述の方法を用いてTDH産生菌の分離を試みた。その結果、TDH産生性の腸炎ビブリオが分離された食品は11事例(16.4%)に由来する23検体から認められた。それらの食品の内訳は青柳、寿司および生はまぐりなどの生鮮魚介類、その他に煮物、ナムル、玉子焼きなどの加熱調理後に二次汚染したと推定される食品もあった。9)　TDH産生菌を分離するために検討した1検体あたりの集落数は10集落以下が12件、11～100集落が6件、101～200集落が5件であった。食品中のTDH産生菌の検出頻度は、食品によってかなり差異が認められ、腸炎ビブリオ菌数とTDH産生菌数には相関性が無いことが明らかとなった。10)　スクリーニング検査のPCR法でtdh遺伝子が陽性でありながら、最高250集落を釣菌して検討を行ったが、菌を分離することができない食品が16件もあった。その原因としては、(1)加熱により菌は生残しないが遺伝子のみが残っていた、(2)菌は生きているが培養できないVNC(Viable but nonculturable)状態になっていた、(3)さらに多くの集落について検討する必要があったことなどが考えられた。11)　11事例に由来する食品検体から検出されたTDH産生菌の血清型はO3:K6(10検体)、O3:K5(6)、O1:K25(4)、O3:K29(2)、O4:K8(1)、O4:K11(1)で、全事例で患者由来株と同じ血清型のTDH産生菌が分離された。中には2種類のTDH産生菌(血清型O1:K25、O4:K11)が検出された食品(煮物)もあった。さらに1食中毒事例では患者由来株と同一血清型のTDH産生菌が6検体の食品から検出された。12)　食品からTDH産生性腸炎ビブリオが検出された11食中毒事例を対象に、分離された患者および食品由来のTDH産生株についてPFGE法を用いて分子疫学的解析を行った。患者と食品由来株のPFGEパターンにおいて、11事例中7事例は完全に一致、残りの4事例についてもほぼ一致(1～数本異なる)しており、11事例の食中毒事例において患者由来株と食品由来株が同一起源に由来することを明らかにした。13)　血清型ごとのPFGEパターンの比較では、O3:K6株とO1:K25株のPFGEパターンは類似し、どちらもI型に分類されたが、それ以外の血清型ではO4:K8株はII型、O4:K11株はIII型、O3:K29株はIV型、O3:K5株はV型と血清型毎に異なるパターンを示した。各血清型の中でさらに詳細に比較すると、O4:K11株は患者由来株と食品由来株が同一パターンを示したが、それ以外の血清型株ではバンドの数が1～数本異なるもの(サブタイプ : a～g)が認められることを明らかにした。　以上の様に1989～2004年の16年間における腸炎ビブリオ食中毒の発生動向の解析を行ったところ、原因菌の血清型が年々変化していることが明らかになった。また、1996年以降、本菌食中毒事例数が著しく増加した原因は明確ではないが、1995年に血清型O3:K6が突然出現し、その後本血清型が急増したことによるものであることを明らかにした。そして、それ以降もO3:K6菌が大半を占める傾向が認められ、2005年に至っても続いていることを明らかにした。さらに1998年以降には新しい血清型O4:K68菌による食中毒が発生したことを明らかにした。次に、分子生物学的手法を応用した腸炎ビブリオ検査法を開発し、これまで検出できないと考えられていた食品からのTDH産生菌の分離に成功し、TDH産生菌の食品汚染状況を明らかにした。さらにPFGE法を用いた解析により、11事例の食中毒事例において患者由来株と食品由来株が同一起源であることを明らかにした。Vibrio parahaemolyticus is a hemophilic bacterium occurs in estuarine waters through the world and is easily isolated from coastal waters and various fish and shellfish. V. parahaemolyticus is a common food-borne disease bacterium in Japan where we often eat raw fish and shellfish. Food-borne outbreaks of V. parahaemolyticus occur very often in Japan. In addition, the number of V. parahaemolyticus food-borne outbreaks has increased remarkably since 1996 when the situation of V. parahaemolyticus food-borne outbreaks in Tokyo was demonstrated. The producibility of thermostable direct hemolysin (TDH) or TDH-related hemolysin (TRH) is the most important pathogenic factor in V. parahaemolyticus. In particular, it must be emphasized that TDH(+) strains of V. parahaemolyticus are of prime importance in human disease. By contrast, TDH(+) strains constitute a very small percentage (typically <1%) of isolates found in aquatic environments and seafood. It was not clear after the 1970\u27s when TDH was discovered as the most important pathogenic factor in human disease why the TDH(+) strain was not isolated from aquatic environments and seafood as well as patients. Recently, the PCR (polymerase chain reaction) method, a gene amplification method, and PFGE (pulsed field gel electrophoresis) have been applied in molecular epidemiology. In this study, the occurrence and cause of V. parahaemolyticus food-borne outbreaks in Tokyo were analyzed epidemiologically and bacteriologically to clarify the cause of increased outbreaks, the isolation method of TDH(+) strains from foods was studied, and the following results were obtained.1) There were 872 food-borne outbreaks due to V. parahaemolyticus in Tokyo between 1989 and 2004. The number of outbreaks per year was 55 in 1989, 75 in 1990, with a gradual decrease to 24 outbreaks in 1993, which was the lowest number during these 16 years. Subsequently, an increasing tendency is shown, and the number of outbreaks increased dramatically year by year until 1998 (107 outbreaks) . They then decreased to 33 in 2001, 49 in 2002, 29 in 2003, and 51 in 2004. Increasing and decreasing trends were shown year after year.2) The monthly incidence of V. parahaemolyticus food-borne outbreaks peaked in August (393 outbreaks, 45.1%) . Moreover, it accounted for 89% of all outbreaks during the 3 months from July to September. In addition, 99% of outbreaks occurred during the 5 months from June to October. However, these were 6 outbreaks in this investigation in the winter season between January and February when V. parahaemolyticus food-borne outbreaks are not usually reported. A correlation was almost confirmed before 1994 between the number of V. parahaemolyticus food-borne outbreaks from July-September and environmental temperature; however, there were no such correlation depending on a remarkable increase in the number of outbreaks due to serotype O3:K6 after 1995.3) As a result of investigating 216 outbreaks between 1989 and 1998, the vehicle food was mixed dishes (25%), sushi (17%), raw fish (sashimi, 8%), cooked fish (5%) . The mixed dishes which included raw fish, sushi and so on, were eaten at restaurants or sushi restaurants.4) The risk factors of 39 food-borne outbreaks from 1995 through 1997 were cross contamination (34.8%) between food staff and cooking utensils, failure to control the temperature of food (28.8%) , keeping food at room temperature for a long time (18.2%), contaminations of food staff (10.6%). More than 2 types of failure of those risk factors were described in many outbreaks. This suggested that the most important risk factors were not only the contamination of food staff but also cross contamination and failure to control the temperature of food.5) The most prevalent serotype of V. parahaemolyticus also changed from 1989 through 2005. The most prevalent was O4:K4 in 1989, O4:K8 during 1990 and 1991, O1:K56 in 1992, and O4:K8 from 1993 through 1995. Serotype O3:K6 became the most prevalent in 1996, and this trend has continued. In 2000, 57 (87.7%) of 65 outbreaks were due to serotype O3:K6 and this continued until 2005, when half of all causal organisms in food-borne outbreaks were serotype O3: K6. Thus, the trends of V. parahaemolyticus food-borne outbreaks during the 12 years to 2005 in Tokyo showed various characteristics and dramatic changes in causal organisms.6) In addition, it was clarified that a new serotype, O4:K68 was also a causal organisms in 1998.7) A new effective method for isolating TDH(+) V. parahaemolyticus from food samples was developed, involving of several steps. The first was screening using PCR to detect the tdh gene. The 2nd step was the isolation of V. parahaemolyticus using 2 kinds of isolation agar plates such as enzymatic chromogenic substrate media (CHROMagar Vibrio, OXOID) and traditional media (TCBS) . The 3rd step was to detect V. parahaemolyticus using the new detection method, \u27the stroke-stripping method\u27.8) V. parahaemolyticus was isolated from food samples related to 67 of 227 V. parahaemolyticus food-borne outbreaks in the 5 years from 2000 to 2004, in Tokyo. In these outbreaks, TDH(+) strains were also isolated using our newly developed method. As a result, TDH(+) strains of the same serotype as patients were isolated from 23 food samples related to 11 outbreaks (16.4%) . The foods from which TDH(+) strains were isolated were fresh seafood such as shellfish (Aoyagi, clams), sushi, and cooked foods such as boiled vegetables, boiled carrots and the boiled bean sprouts (Namuru), omelet, etc. The cooked foods were suspected to have been cross-contaminated with V. parahaemolyticus.9) The isolation rate of the TDH(+) strain from the enrichment broth cultures differed with samples. In 12 food samples, TDH(+) strains were isolated easily by examining less than 10 colonies. The examination of 11-100 colonies was needed to isolate the TDH(+) strain in 6 samples, and 101-200 colonies in 5 samples. No correlation was seen between the number of V. parahaemolyticus and the isolation rate of TDH(+) strains in food samples.10) In several samples, TDH(+) strains were isolated easily by examining only 3 colonies, but no TDH(+) strains were isolated in spite of the examination of 250 colonies. As many as 16 foods were tdh (+) -positive in the PCR screening test although the TDH(+) strain could not be isolated in spite of examining 250 colonies. In those cases, various reasons were considered, (1) after boiling to prepare the template for PCR, the organisms had already died and only the DNA gene remained, (2) organisms were VNC (viable but not culturable), (3) more than 250 colonies should be examined.11) The serotypes of V. parahaemolyticus isolated from food samples related to 11 outbreaks were O3:K6 (10 samples), O3:K5 (6 samples), O1:K25 (4 samples), O3:K29 (2 samples), O4:K8 (1 sample), and O4:K11 (1 sample). The same serotypes of organisms were isolated both from food samples and patients in each food-borne outbreak. Moreover, two kinds of serotypes (O1:K25 and O4:K11) was detected in a food sample (boiled vegetable). The same serotype of TDH(+) organisms was isolated both from 6 food samples and patients in a food-borne outbreak.12) TDH(+) strains isolated from food and patients in 11 food-borne outbreaks were also analyzed by molecular epidemiology using the PFGE method. Among 7 outbreaks, the PFGE patterns of those isolates from food and patients were not distinguishable, and in 4 outbreaks, only a few bands were different, but were very similar. These results showed that those TDH(+) organisms from patients and food had the same origin in each food-borne outbreak.13) When PFGE patterns of each serotypes were compared, both PFGE patterns of O3:K6 and O1:K25 were similar, and were classified into type I, O4:K8 were type II, O4:K11 were type III, O3:K29 were type IV, O3:K5 were type V. Some subtypes (a-g) were also observed. In conclusion, when the generation trend of V. parahaemolyticus food-borne outbreaks in Tokyo from 1989 through 2004 was analyzed, it was clarified that the serotypes of the causal organisms changed every year. Moreover, the remarkably increased number of V. parahaemolyticus outbreaks after 1996 was clarified by the sudden appearance of serotype O3:K6 in 1995, the subsequent rapid increase of this serotype, and its persistence, with its tendency to dominate continuing until 2005. In addition, many food-borne outbreaks after 1998 were confirmed as a new serotype, O4:K68. Next, a new method to isolate V. parahaemolyticus from food samples using a molecular biology technique was developed, and succeeded in isolating TDH(+) strains from food that had been thought very difficult up to now. Using this method, the food contamination situation of TDH(+) organisms was clarified. In addition, it was clarified that the patient organism and the food organism had the same origin in 11 food-borne outbreaks by analysis using the PFGE method.博士(学術）麻布大

Poly[[{μ3-tris­[2-(4-phenyl-1,2,3-triazol-1-yl)eth­yl]amine}silver(I)] hexa­fluorido­phosphate]

The title compound, {[Ag(L)]PF6)n {L is tris­[2-(4-phenyl-1,2,3-triazol-1-yl)eth­yl]amine, C30H30N10}, consists of alternating two-dimensional cationic layers of [Ag(L)]+ and anionic PF6 − layers. Each AgI atom is three coordinated in a T-shaped geometry by three N atoms from three ligands. Each ligand links three AgI atoms, generating a two-dimensional network structure with two different metallacycles, A and B. In A, eight coordination units from four ligands connect four AgI atoms, forming a 48-membered ring. In B, four coordination units from two ligands link two AgI atoms, forming a 24-membered ring. Each B ring is surrounded by four A rings, and each A ring has four A and four B rings as neighbours. This cationic layer thus generates a 4.82 topology network, with each AgI centre and ligand acting as a three-connected topological node

選択的セロトニン再取り込み阻害薬とセロトニン4受容体作動薬の直腸吻合部におけるインビボ神経再建に与える効果の比較

It was recently reported that activation of enteric neural 5-HT(4) receptors (SR4) promotes reconstruction of enteric neural circuit injury in distal gut of guinea pigs and that this reconstruction involves neural stem cells. We aimed to explore a novel approach using a selective serotonin reuptake inhibitor (SSRI), which increases endogenous 5-HT, to repair enteric nerve fiber injury in the rat distal gut. Enteric nerve fiber injury was performed by rectal transection and subsequent end-to-end one-layer anastomosis. The SSRI fluvoxamine maleate (100 μmol/l) was applied locally at the anastomotic site to compare with the 5-HT(4) agonist mosapride citrate (100 μmol/l) (applied for patent) applied locally and orally. Unlike mosapride, fluvoxamine failed to promote the regeneration of the nerve fiber tract across the anastomosis. Furthermore, fluvoxamine did not generate anti-distal-less homeobox 2 (DLX2)- and anti-SR4-positive cells (neural stem cells) and/or anti-neurofilament (NF)-positive cells (neural cells) in newly formed granulation tissue at the anastomosis, whereas these cell types were observed in mosapride-treated preparations. In contrast to its effects in guinea pigs, mosapride generated 5-bromo-2'-deoxyuridine (BrdU)-positive neural cells in ganglia sites 3 mm oral and anal from the anastomosis 2 wk after nerve fiber injury. All actions of mosapride were observed after local and or oral applications. These findings indicate that local SSRI treatment does not induce in vivo nerve fiber tract growth across the anastomosis in the rat distal gut. Mosapride induces nerve fiber tract growth across the anastomosis, mediated through enteric neural stem cells possibly from neural crest-derived stem cells or mesenchymal stem cells in the bone marrow.博士（医学）・甲616号・平成26年3月17日発行元の規定により、本文の登録不可。本文は以下のURLを参照 "http://dx.doi.org/10.1152/ajpgi.00284.2011

インビボイメージング法を用いたマウス小腸の肉芽組織深部における腸壁内神経形成の解析

One of the challenges of using imaging techniques as a tool to study cellular physiology has been the inability to resolve structures that are not located near the surface of the preparation. Nonlinear optical microscopy, in particular two photon-excited fluorescence microscopy (2PM), has overcome this limitation, providing deeper optical penetration (several hundred µm) in ex vivo and in vivo preparations. We have used this approach in the gut to achieve the first in vivo imaging of enteric neurons and nerve fibers in the mucosa, submucosa, submucosal and myenteric plexuses, and circular and longitudinal muscles of the small intestine in H-line: Thy1 promoter GFP mice. Moreover, we obtained clear three-dimensional imaging of enteric neurons that were newly generated after gut transection and reanastomosis. Neurogenesis was promoted by oral application of the 5-HT4-receptor agonist, mosapride citrate (MOS). The number of newly generated neurons observed in mice treated with MOS for one week was 421±89 per 864,900 µm2 (n = 5), which was significantly greater than that observed in preparations treated with MOS plus an antagonist (113±76 per 864,900 µm2) or in 4 week vehicle controls (100±34 per 864,900 µm2) (n = 4 both). Most neurons were located within 100 µm of the surface. These results confirm that activation of enteric neural 5-HT4-receptor by MOS promotes formation of new enteric neurons. We conclude that in vivo 2PM imaging made it possible to perform high-resolution deep imaging of the living mouse whole gut and reveal formation of new enteric neurons promoted by 5-HT4-receptor activation.博士（医学）・甲第631号・平成27年3月16日© 2014 Goto Kei et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited

Isolated gestational proteinuria preceding the diagnosis of preeclampsia : an observational study

Introduction. Some pregnant women develop significant proteinuria in the absence of hypertension. However, clinical significance of isolated gestational proteinuria (IGP) is not well understood. This study aimed to determine the prevalence of IGP in singleton pregnancies and the proportion of women with IGP who subsequently developed preeclampsia (IGP-PE) among all PE cases. Material and methods. This was an observational study of 6819 women with singleton pregnancies at 12 centers, including 938 women with at least once determination of protein-to-creatinine ratio (P/Cr). Significant proteinuria in pregnancy (SPIP) was defined as P/Cr (mg/mg) level >0.27. IGP was defined as SPIP in the absence of hypertension. Gestational hypertension (GH) preceding preeclampsia (GH-PE) was defined as preeclampsia (PE) in which GH preceded SPIP. Simultaneous PE (S-PE) was defined as PE in which both SPIP and hypertension occurred simultaneously. Results. IGP and PE were diagnosed in 130 (1.9%) and 158 (2.3%) of 6819 women, respectively. Of 130 women with IGP, 32 (25%) progressed to PE and accounted for 20% of all women with PE. Hence, women with IGP had a relative risk of 13.1 (95% CI; 9.2-18.5) for developing PE compared with those without IGP [25% (32/130) vs. 1.9% (126/6689)]. At diagnosis of SPIP, P/Cr levels already exceeded 1.0 more often in women with S-PE than in those with IGP-PE [67% (33/49) vs. 44% (14/32), respectively, p = 0.031]. Conclusions. IGP is a risk factor for PE, and IGP-PE accounts for a considerable proportion (20%) of all PE

Prenatal Diagnosis of Atrioventricular Block and QT Interval Prolongation by Fetal Magnetocardiography in a Fetus with Trisomy 18 and SCN5A R1193Q Variant

We report a case of fetal trisomy 18 with SCN5A R1193Q variant that presented with sinus bradycardia, 2 : 1 atrioventricular block (AVB), and QT interval prolongation. These complex arrhythmias were diagnosed by fetal magnetocardiography combined with ultrasound findings. Advanced AVB and ventricular arrhythmias were confirmed after birth. Genetic testing of the baby revealed a SCN5A R1193Q variant, which we considered could account for the various arrhythmias in this case

Higher D-dimer level in the early third trimester predicts the occurrence of postpartum hemorrhage

Aims: This study aimed to determine effective predictive factors for primary postpartum hemorrhage (PPH) among clinical blood parameters associated with coagulation and fibrinolysis and demographic characteristics.Methods: We retrospectively studied 1032 women who underwent determinations of clinical blood parameters at gestational week (GW) 29–32 and GW 35–37 and gave birth to singleton infants at our hospital between January 2011 and December 2013. PPH was defined as estimated blood loss ≥700 mL. Multivariate logistic regression analyses were used to determine independent risk factors and odds ratios (OR) for PPH.Results: PPH occurred in 104 of 1032 women (10%). Three blood variables, fibrinogen level 2.7 μg/mL (2.03 [1.29–3.19]) at GW 35–37, and three demographic characteristics, maternal age ≥35 years (1.75 [1.15–2.68]), BMI >28.2 kg/m2 on admission for childbirth (1.95 [1.20–3.16]), and previous cesarean delivery (2.77 [1.31–5.83]), were identified as independent risk factors for PPH.Conclusion: Among blood parameters, higher D-dimer levels and lower levels of antithrombin activity and fibrinogen in late gestation were independent risk factors for PPH