6 In the United States, Nutlin-3 molecular weight only four cases were reported between 1992 (when vaccine was licensed) and 2008, with two additional cases in 2010.1 To our knowledge, there has been only one possible case reported in a Canadian traveler, who visited Manchuria

in 1982.7 The incidence appears to be higher in those travelers who reside in rural zones for longer periods, estimated at 5 to 50 cases per 100,000.5 In endemic areas, the majority of infections are asymptomatic or mild, with less than 1% presenting with serious neurological symptoms.8 Therefore, the incidence in travelers is likely to be higher than suggested by the reported cases. Although the risk of exposure to JEV infection increases with the duration of stay in endemic areas, one-third of reported cases traveled for less than 1 month, and several traveled for 2 weeks or less to beach resorts in Thailand selleck kinase inhibitor and Bali.6,9,10 Despite these very low risks, the US Advisory Committee on Immunization

Practices and the Public Health Agency of Canada similarly recommend vaccination for travelers staying 30 days or more in an endemic region or for travelers with high risk activities who spend shorter periods of time.11,12 Our patient met the latter criterion. Recent expert opinion underlines the importance of weighting the benefits of JE vaccination on time, place, and host as well as behavioral factors.13 Our report underlines the potential for serious sequelae of JE, and the importance of vaccination, in adventurous young travelers with high-risk activities. Several vaccines are available globally. However, only one inactivated vaccine is available in North America. It requires two doses 4 weeks apart. Single standard dose is poorly immunogenic and short-term seroconversion at 1 month is only 40%.14 There is no good data on doses closer together. This means that Loperamide the traveler must come to clinic at least 5 to 6 weeks before entry into a risk area. Higher risk young

“spontaneous” adult travelers are less likely to comply because of their commonly unpredictable itineraries and activities. In most Western countries the cost of a full course (two doses) of vaccine is between $400 and $600 USD. This financial aversion increases the low likelihood of young adult adventurers to afford vaccination and seek pretravel information on protective measures at the same time. Development of a single-dose, affordable, and immunogenic vaccine would represent an important asset for this expanding category of travelers. We thank The Laboratoire de Santé Publique du Québec (LSPQ), The National Microbiology Laboratory (NML) of Canada, The Canadian Food Inspection Agency, Centre of Expertise (COFE) for Rabies, and The Atlanta National B Virus Resource Center for performing the various serologic analyses. The expert technical assistance provided by K. Makowski and M. Andonova for the flavivirus serology performed during this case investigation is particularly acknowledged.

, 2002; Gonzalez Barrios et al., 2006). Escherichia coli O157:H7 harbors QS-regulated virulence genes on a pathogenicity island termed the locus of enterocyte effacement (LEE) (Surette & Bassler, 1998) that is organized mainly into the five polycistronic operons LEE1–LEE5 (Kaper et al., 2004). The first gene in LEE1, LEE-encoded regulator (ler), produces the principal transcriptional activator of the LEE genes (Elliott et al., 2000) and its expression was reported to be positively regulated by both AI-3 and norepinephrine (Sperandio et al., 2003; Jelcic et al., 2008). In patients with E. coli O157:H7 infection,

antibiotic use is generally limited because bacterial cells lysed by antibiotic treatment release find more an excessive quantity of Shiga toxin, thereby aggravating the patient’s state and resulting in HUS (Wong et al., 2000). To avoid this risk, an antimicrobial treatment that involves attenuation of bacterial virulence by inhibiting QS has been proposed (Ren et al., 2004). Halogenated furanone compounds as QS inhibitors were isolated from marine macroalga, Delisea pulchra (Givskov et al., 1996). Many of the synthesized furanone

derivatives have also been identified as QS inhibitors both in vitro (Martinelli et al., 2004) and in vivo (Wu et al., 2004). However, most of the characterized QS inhibitors have not yet been qualified as chemotherapeutic agents because they are composed PARP inhibitor of halogens that exert toxic effects in humans. Thus, more efforts should be made to develop safer QS inhibitors from natural products. As a soluble fiber, broccoli (Brassica oleracea) contains a large amount of vitamin C and multiple PRKACG nutrients with potent anticancer properties (Vasanthi et al., 2009). However, the effect of broccoli against infection by pathogenic bacteria has never been reported. In this study, we demonstrate the inhibitory effects of broccoli extract (BE) on bacterial QS using E. coli O157:H7 as a model organism. The in vivo effects of the BE against E. coli O157:H7 infection were also elucidated in a Caenorhabditis elegans killing

assay. Finally, we tested three different flavonoid compounds (quercetin, kaempferol and myricetin) reported to be present in BE (He et al., 2008; Schmidt et al., 2010) in order to gain better insight into the active inhibitory compound in BE. An E. coli O157:H7 strain ATCC 43894 producing Shiga toxins I and II, an avirulent E. coli OP50 strain and Chromobacterium violaceum CV026 were grown in Luria–Bertani broth (LB, 10 g tryptone, 5 g NaCl, 5 g yeast extract L−1) at 37 °C. Vibrio harveyi BB170, an AI-2 reporter strain, was grown at 30 °C with agitation (175 r.p.m.) in the AB medium (Fong et al., 2001). The AB medium consisted of 10 mM potassium phosphate (pH 7.0), 0.3 M NaCl, 0.05 M MgSO4, 0.2% Casamino acids (Difco), 2% glycerol, 1 mM l-arginine, 1 μg mL−1 of thiamine, and 0.01 μg mL−1 of riboflavin. Quercetin, kaempferol and myricetin were purchased from Sigma-Aldridge (St.

The growth of the two bacteria in the absence of

atrazine was better than in the presence of atrazine. As shown in Fig. 2, SOD activities of E. coli K12 and B. subtilis B19 were increased after 6 h compared with at the beginning, and reached the highest levels of 148.72 and 85.99 U mg protein−1 at a Talazoparib in vivo concentration of 800 μg L−1, respectively. SOD activities in E. coli K12 started to decrease at 12 h and further decreased at 24 h, dropping gradually to a level lower than that at the beginning, showing inhibition. SOD activities in B. subtilis B19 exposed to high concentrations of atrazine (500, 800 and 1000 μg L−1) showed dramatic stimulation compared with the activities at the beginning, indicating that further increasing concentrations of atrazine may cause greater oxidative stress in B. subtilis B19. As shown in Fig. 3, CAT activities in two bacteria reached the highest levels of 1.88 and 1.48 U mg protein−1 at concentration of 800 μg L−1 at 6 h. A similar trend in E. coli K12 was shown at 12 h with increasing concentrations of atrazine. CAT activities

in E. coli K12 were inhibited at 24 h. A relatively small change of CAT activity was observed in B. subtilis B19. This indicates that CAT could assume up a crucial position in the resistance to atrazine stress in E. coli K12, whereas it had a limited role in the defense against atrazine stress in B. subtilis B19. As shown in Fig. 4, there were fluctuations of GST activities in E. coli K12 and B. subtilis B19 with increasing concentrations of atrazine. GST activity in E. coli K12 reached Veliparib concentration very the highest level of 80.56 U mg protein−1 at concentration of 800 μg L−1 at 6 h and was stimulated continuously at 12 h, and then dropped down at 24 h. GST activity in B. subtilis

B19 was significantly activated with increasing concentrations of atrazine during the whole time. At 12 and 24 h, GST activities had the highest values at concentrations of 200 and 800 μg L−1 in E. coli K12 and at concentration of 800 μg L−1 in B. subtilis B19. As shown in Fig. 5, T-AOC in E. coli K12 was significantly activated at 6 h. There was another stimulation at 12 h, which then dropped down at 24 h, denoting that a long exposure affected T-AOC in E. coli K12. The highest T-AOC in E. coli K12 was observed at a concentration of 500 μg L−1 at 12 and 24 h. T-AOC in B. subtilis B19 was significantly stimulated at 6 h and was elevated continuously at 12 and 24 h. The highest T-AOC in B. subtilis B19 was observed at concentrations of 800 μg L−1 at 12 and 24 h. The same chemical compound can result in a distinct response in Gram-positive and Gram-negative bacteria and the complex mechanism is still not very clear (Buurman et al., 2006). As can been seen, the antioxidant enzyme levels differ greatly between Gram-negative and Gram-positive strains. SOD of B. subtilis B19 exposed to low concentrations and CAT of B.

, 2008) and reflecting the fact that the agent has not been approved for use in veterinary practice in China. Although phenotypic resistance may be

overestimated in our analysis because isolates showing intermediate susceptibility were considered resistant, we believe that the results reflect the general trend observed Tyrosine Kinase Inhibitor Library concentration with E. coli strains isolated from pigs. Other studies have reported that E. coli isolates from cattle and swine fall into phylogenetic groups A and B1, whereas avian pathogenic E. coli isolates mainly belonged to groups A, D, and B1 (Johnson et al., 2008; Ghanbarpour et al., 2010) and human pathogenic isolates predominantly belonged to phylogenetic groups B2 and D (Johnson et al., 2002, 2003). In agreement with some of these findings, we found that E. coli isolates

from diseased swine were mostly from phylogenetic groups A and B1. Ten VGs associated with swine E. coli were detected in all isolates. The high prevalence of Stx2e (63%) in this study was in agreement with other studies from swine E. coli isolates (da Silva et al., 2001; Fratamico et al., 2004). The prevalence of AIDA-I (9%) and EAST1 (64%) in the study was similar to that in previous studies (Ngeleka et al., 2003; Vu-Khac find more et al., 2007). Both paa and eae play a role in attaching/effacing (AE) adhesion in enteropathogenic E. coli (EPEC) and enterohemorrhagic E. coli (EHEC) (Nataro & Kaper, 1998; Batisson et al., 2003). In pig EPEC O45 strains, paa is associated with the presence of eae and the AE phenotype in vivo and in vitro (An et al., 1999). In agreement, all paa-positive isolates were eae-positive in this study, although the prevalence of paa was somewhat lower.

The relationships of EAST1 with faeG, STa, STb, AIDA-I, and combinations of VGs are easily explained by the clustering of STa, STb, EAST1, and faeG on the pTENT2 plasmid of porcine ETEC from Ontario (Leclerc et al., 2007). These findings suggest that E. coli strains from diseased swine possess a variety of VGs associated with various pathogenic E. coli, such as ETEC, EHEC, STEC, and EPEC. Among all Lepirudin ETEC strains, VGs astA, STa, Stx2e, and F4 were the most frequent, while the prevalence of STb, paa, sepA, and AIDA-I appeared to be lower than has been reported previously from ETEC isolates (Boerlin et al., 2005; Zhang et al., 2007). Resistance to antimicrobials in pathogens is an increasing threat to animal and human health. Compared with their susceptible counterparts, resistant bacterial infections are generally associated with increased morbidity, mortality, and treatment expense (Barza, 2002; Barza & Travers, 2002; Travers & Barza, 2002). Other investigators have also reported more frequent resistance, physical linkages, and statistical associations between resistance and VGs in swine pathogenic E. coli (Boerlin et al., 2005; Travis et al., 2006). In this study, E.

Partially supporting Kennelly et al., Birns and Kalra[24] concluded that the majority of studies showed an association between raised blood pressure and a decline in cognitive function, but that the evidence for improved or maintained cognition after

pharmacological lowering of blood pressure was conflicting. The review by Fournier et al.[25] accepted that antihypertensive drugs prevented the onset of cognitive decline and dementia in patients with hypertension but concluded that calcium-channel blockers (CCBs) and AIIA antihypertensives were more effective than ACEIs and diuretic antihypertensives, which only affected cognition in those patients with a history of stroke. They did, however, report that a small study in Japanese patients suggested that those ACEIs able to penetrate AZD2014 research buy the blood–brain barrier may prevent cognitive decline. Shah et al.[26] reviewed papers up until mid-2009 and similarly concluded that ACEIs, but also

diuretics, were able significantly to reduce the progression to dementia. There have been no randomized, controlled, clinical trials but 18 cohort studies BIBW2992 of hypertension, cognition and antihypertensive therapies published in 2009 and 2010 add to the debate (see Table 1[27–44]). A small study in 782 very elderly Chinese individuals reported that there was no association between blood pressure and cognition,[27] but a much larger study in nearly 20 000 individuals determined that increased blood pressure was associated with impaired cognition;[28] this result was replicated in a study in nearly 2000 individuals over 70 years of age in rural China.[29] Similarly, a study in 73 stroke-free and dementia-free patients showed that increased blood pressure was associated

with decreased Niclosamide cognitive function.[30] There was some suggestion, however, that the association of blood pressure with cognition was dependent on age. Euser et al.[31] studied the association of blood pressure and cognition in over 3000 young and old patients. In the younger individuals there was no association between blood pressure and cognition, but in the 65–74-year age group increased blood pressure was associated with decreased cognition. Paradoxically, in those patients over 75 years, increased blood pressure was associated with increased cognitive ability,[31] highlighting the association of hypotension with cognitive impairment. Independently, a psychometric study in 525 subjects determined that blood pressure was able to account for 11% of the variance in scores on tests of cognition.[32] Several studies considered the association of blood pressure and diagnoses of Alzheimer’s disease or dementia rather than results of tests of cognition. Cherbuin et al.

The direct conversion of H2 (or formate) + CO2 to methane is catalysed by hydrogenotrophic methanogens. The acetate conversion to methane Wee1 inhibitor and CO2 can be performed through two alternative pathways. The first pathway, catalysed by acetoclastic methanogens (species of Methanosarcina or Methanosaeta), is a cleavage of the methyl and carboxyl groups from acetate producing methane and

CO2, respectively. The second possible pathway relies on the syntrophic association between acetate oxidizing bacteria and hydrogenotrophic methanogens: the formers convert acetate into H2 and CO2, which are then used by the hydrogenotrophic methanogens to produce methane (Schink & Stams, 2006). Regardless of the environmental conditions and of the predominance of either acetoclastic or hydrogenotrophic pathways, methanogenic Archaea, as the terminal oxidizers of the community, play a key role. As a consequence, developing new and rapid methods to elucidate the identity and diversity of methanogens would be useful for the global understanding of the complex

process of methanogenesis. The methyl-coenzyme-M reductase enzyme complex (MCR), composed of two alpha, beta and gamma subunits, catalyses methane formation and is ubiquitous in methanogens (Thauer, 1998). MCR is unique to methanogens, with the exception of the methane-oxidizing Archaea (Hallam et al., 2003). In addition, 4��8C a few members of the Methanomicrobiales and Methanococcales also possess a type II isoenzyme Nutlin-3 solubility dmso (Mrt) (Lehmacher & Klenk, 1994). On the basis of the comparison of available 16S rRNA and mcrA gene sequences of methanogens, the mcrA gene was demonstrated to be an alternative phylogenetic marker to the 16S rRNA gene (Luton et al., 2002). T-RFLP fingerprints of the mcrA gene have been used for phylogenetic analysis of methanogen populations (Lueders et al., 2001). Our objective in this study was to develop a novel fingerprinting method that distinguishes the methanogenic groups from environmental or engineered systems that should be

less time-consuming, more cost-effective, but as informative as T-RFLP. This methodology, based on the natural length variations of the mcrA gene, originates from the work of Suzuki et al. (1998), who developed the amplicon length heterogeneity PCR method (LH-PCR) based on the natural length variation of the bacterial 16S rRNA gene. In this study, the new methodology we have developed and named amplicon LH-PCR of the mcrA gene (LH-mcrA) is validated using clones from libraries from a plug flow-type bioreactor (PFBR). The PFBR consisting in eight serially linked compartments was operated at 25 °C and fed with liquid swine manure at a rate of 1–2 g chemical oxygen demand (COD) L−1 day−1 and a hydraulic retention time of 60 days, as described in Roy et al. (2009).

106 It may be that at the expense of generating mutations, mammalian cells may use transient up-regulation of Pol ι to deal with replication arrest by DNA damage for survival.107 However, continuous over-expression of such error prone DNA polymerase, for instance by chronic hypoxia, may

result in a high rate of point mutations.108 As mentioned above, germline mutations in NBS1 predispose it to the Nijmegen breakage syndrome. The NBS1 protein forms a complex with MRE11A and RAD50 called MRN, which interacts with double-strand breaks and begins the DNA damage response by recruiting the ATM protein (see above). Inactivation of NBS1 impairs the function of MRN, leading to a high sensitivity to radiation, CIN and defective cell cycle checkpoints. To et al. demonstrated that hypoxia (1% O2 for find more 16 h) down-regulates NBS1 expression at the mRNA and protein levels in cancer cell lines.109 They showed that this down-regulation is

HIF1 but not HIF2 dependent and is mediated by reduction of Sp1-MYC by competing Sp1-HIF1 at the promoter region of the NBS1 locus, similar to the MSH2 locus.86,109 All cancers contain a much greater number of genetic and epigenetic alterations than do corresponding MK-8669 normal cells. At nucleotide levels, these alterations include: substitutions of one base by another,

insertions or deletions of small or large segments of DNA, rearrangements, copy number increases, copy number reductions, acquisition of foreign DNA (virus) in some cases and hypermethylation Sitaxentan or hypomethylation of guanosine residue.3 The cancer genome also shows changes in numbers of whole or parts of chromosomes. It is reasonable to assume that these genetic alterations can be caused in part by exposure to environmental carcinogens. Data from the whole genome sequencing of melanoma showed clearly the contribution of UV radiation to the melanoma genome.110 Interestingly, there is a sign of the second genetic insult after UV damage is detected in the genome and this is characterized by an increase in the frequency of C > A transversions.110 It is tempting to speculate that the second event occurring in the melanoma genome may be associated with H/R. As reviewed in this article, H/R is a strong candidate for induction of genetic alterations and the DNA damage response found in cancer genomes and tissues; however, our insights into H/R on the cellular genome are all based on experiments performed in tissue culture or in animal models. The question is whether H/R really plays the same contributing role for genetic instability in human tumor tissues as observed in experimental systems.

A 990-bp PCR fragment containing the 477-bp upstream of the ATG start codon and the 513-bp downstream of the TAA stop codon of ompP2 gene was amplified using overlap PCR with primers (P1 and P4) and subsequently cloned into plasmid pK18mobsacB to create pZB1. Both DNA fragments (upstream and downstream) contained the 9-bp core DNA uptake signal sequence (USS) of 5′-ACCGAACTC (Bigas et al., 2005). Next, an 800-bp gentamicin resistance cassette was amplified from a p34s-Gm plasmid with primers (P5 and P6). Both the pZB1 and the gentamicin resistance cassette were digested with BamHI and SalI and then ligated together to form plasmid pZB2.

A pZB3 plasmid PF-02341066 datasheet contained the entire heptosyltransferase (hep) II gene plus 517-bp upstream of the ATG start codon and 433-bp downstream of the TAA stop codon, and the gentamicin resistance cassette ligated between the hepII gene and the downstream sequence. To obtain plasmid pZB4, a mutation cassette of the OmpP2 gene was amplified from the pZB1 plasmid using primers (P11 and P12) containing AZD3965 a novel putative USS of 5′-ACCGCTTGT. Next, this PCR product was cloned into pK18mobsacB to make pZB4. A 2.32-kb PCR fragment was amplified using overlap PCR with primers (P13 and P16), which contained the complete open reading frame (ORF) of ompP2 gene and the kanamycin resistance cassette. Both

the fragment and the pZB3 plasmid were excised with BamHI and SalI and then ligated together to form plasmid pZB5. All plasmids were mobilized into E. coli DH5α by CaCl2-mediated transformation. A natural transformation assay was performed using the method of Bigas et al. (2005) with some modifications. Recipient bacteria were cultured overnight at 37 °C and resuspended in TSB supplemented with serum and NAD at 5 × 1010 CFU mL−1. A 20-μL aliquot

of the suspension was spotted onto a TSA plate supplemented with serum and Carbohydrate NAD and spread onto a small area. Next, 1 μg of donor DNA plasmid resuspended in TE buffer was added, mixed and incubated for 5 h at 37 °C. Bacterial cells were scraped up and plated on the selective medium and incubated at 37 °C for 2–3 days. Additionally, TE buffer was added to a bacterial spot, instead of donor DNA, as a negative control. To characterize the outer membrane protein (OMP) profiles of the wild-type and mutant strains, OMPs were extracted from H. parasuis according to a previously described method with some modifications (Zhou et al., 2009). Briefly, H. parasuis cultures were harvested by centrifugation for 10 min at 4500 g. The pellet was resuspended in 10 mM HEPES buffer (pH 7.4), and the suspension was subjected to sonication. Cellular debris was removed by centrifugation (10 000 g, 10 min, 4 °C). The supernatant was then removed and centrifuged at 200 000 g for 45 min at 4 °C. The supernatant was discarded, and the pellets were resuspended and washed in 10 mM HEPES buffer (pH 7.

e. characterization of pMMO and sMMO, and acquisition and handling of copper by methanobactin. However, the recent findings of the large complement of c-type cytochromes in

M. capsulatus Bath, their unusual cellular surface localization, and copper-dependent expression and their putative roles in the copper homeostasis and metabolic flexibility, post-translational modifications (exemplified by the formation of kynurenine in MopE), open new fields of research on this model methanotroph. Importantly, searches for surface exposed c-type cytochromes in a broader range of methanotrophic bacteria may aid addressing these emerging questions. For example, is such redox active CX-4945 surface enzymes important for cells to survive in methanotrophic communities distributed in several different redox conditions? Is the presence of such enzymes in methanotrophs linked to the bioavailability of copper, due to the likely limiting copper availability at lower redox conditions which may result in insoluble copper complexes? It has also been shown that c-type cytochromes are involved in the siderophore biosynthesis in other

bacteria (Yip et al., 2011), and it is at present an open question if such enzymes are involved in the maturation of methanobactin in M. capsulatus Bath. Furthermore, several protein families and proteins (e.g. cytochrome c553o family proteins, ‘MCA0445’, ‘MCA0446’ and ‘MCA0347’ and others) still appear to be unique to this bacterium and of unknown function. Importantly, several of these findings indicate a hitherto unrecognized plasticity of the metabolic pathways in M. capsulatus Bath. This plasticity may be essential to the bacterium to efficiently Selleckchem MK-8669 adapt to a wide variety in copper conditions. In our opinion, many of these observations warrant further research, and have the potential to reveal unanticipated properties important to fully understand the biology and potentials of methanotrophy. This work was supported by the Norwegian Research Council (grant no. 101742). We would like to acknowledge Professor

Johan Lillehaug at the University of Bergen for interesting and useful discussions. “
“Methanotrophs (-)-p-Bromotetramisole Oxalate are a group of phylogenetically diverse microorganisms characterized by their ability to utilize methane as their sole source of carbon and energy. Early studies suggested that growth on methane could be stimulated with the addition of some small organic acids, but initial efforts to find facultative methanotrophs, i.e., methanotrophs able to utilize compounds with carbon–carbon bonds as sole growth substrates were inconclusive. Recently, however, facultative methanotrophs in the genera Methylocella, Methylocapsa, and Methylocystis have been reported that can grow on acetate, as well as on larger organic acids or ethanol for some species. All identified facultative methanotrophs group within the Alphaproteobacteria and utilize the serine cycle for carbon assimilation from formaldehyde.

268 (P = 0.057), respectively. INCB018424 in vivo Sociodemographic factors that correlate with MVFSFI score were: patient’s age (r = 0.520, P < 0.001); duration of marriage (r = −0.355, P = 0.001); husband's age (r = −0.460, P = 0.001); age of oldest child (r = −0.449, P = 0.001); and age of youngest child (r = −0.627, P < 0.001). We found in this study that the prevalence of FSD in rheumatoid arthritis in our centers was 29.4%. Age and family dynamics appear to be more important predictors compared to disease activity. "
“To identify commonly occurring DNA copy number alterations in Korean cervical

cancers. DNA copy number alteration was screened by whole-genome array comparative genomic hybridization (CGH) analysis. For the array CGH discovery, genomic DNA from five cervical cancers and 10 normal cervical tissues were examined. For the independent validation of the most significant chromosomal alteration (1p36.22, PGD gene), 40 formalin-fixed paraffin-embedded cervical tissue samples were collected; 10 of them were used for quantitative polymerase chain reaction and the other 30 samples were used for immunohistochemical analysis. Chromosomal segments

differently distributed between cancers and normal controls were determined to be recurrently altered regions (RAR). A total of 13 RAR (11 RAR losses and two RAR gains) were defined in this study. Of the 13 cervical cancer-specific RAR, RAR gain in the 1p36.22 locus where the PGD gene is located was the most commonly detected in cancers (P = 0.004). In the quantitative selleck kinase inhibitor polymerase chain reaction replication, copy number gain of the PGD gene was consistently identified in cervical cancers but not in the normal tissues (P = 0.02). In immunohistochemical analysis, PGD expression was significantly higher in cervical cancers than normal tissues (P = 0.02). Our results will be helpful to understand cervical carcinogenesis, and the PGD gene can be a useful biomarker of cervical cancer. “
“The activity of the Women’s Health Care Committee for 1 year up to June 2013 includes: (i) guides Mannose-binding protein-associated serine protease for the management of health care in middle-aged

women; (ii) postoperative women’s health care; (iii) survey on the treatment of pelvic organ prolapse; and (iv) survey of postoperative infection in gynecologic surgery. The detailed activity of the four subcommittees is described in the text. Subcommittee on Guides for the Management of Health Care in Middle-aged Women Small chairman: Akihiko Wakatsuki Committee: Kiyoshi Takamastu, Tsutomu Douchi, Yoshiko Mochizuki, Ichiro Iwamoto and Koichi Shinohara The mortality or morbidity rate of cardiovascular disease has been reported to be higher than that of malignant diseases in women. The prevalence of cardiovascular disease begins to increase after menopause, because plasma estrogen decreases. Estrogen has been reported to protect against atherosclerotic diseases.