AO performed the immunohistochemical staining. CW gave technical assistance. GM designed the study, examined histological and immunohistochemical staining, and reviewed the manuscript. All the authors have read and approved the final manuscript.”
“Background Non alcoholic fatty liver disease (NAFLD) involves a spectrum of conditions ranging from simple fat accumulation in the liver to end stage liver failure and cirrhosis. NAFLD can lead into the development of non alcoholic steatohepatitis

(NASH) [1]. NASH is an emerging health concern and it is believed that its prevalence is on the rise due to escalating obesity rates [2]. Estimated NAFLD prevalence in Western countries is between 17-33% [3]. NAFLD accounts for up to 20%, and NASH find more accounts for 2-3% of liver test abnormalities in most developed countries [4]. NASH is typically reported in obese individuals suffering from one

or a combination of type 2 diabetes, insulin resistance and CB-839 ic50 dyslipidaemia, but is not restricted to this group [2]. There is often an increase in aspartate aminotransferase (AST) and alanine aminotransferase (ALT) [5]. Lipid accumulation occurs early in NASH as part of the development of the disease [6]. The two hit disease model postulates that steatosis is a trigger for the establishment of NASH and the increased levels of fat infiltration cause damage to the liver by forming fat droplets within the hepatic tissue, thus setting off the second hit of

the disease by causing lipotoxicity. In addition, cytokines and learn more reactive oxygen species (ROS) create a pro-oxidant state that can activate stellate cells to produce fibrotic scar tissue [7]. Liver fatty acid binding protein (LFABP) accounts for 3-5% of the cytosolic protein content in hepatocytes. N-acetylglucosamine-1-phosphate transferase LFABP is transcriptionaly regulated by the nuclear hormone receptor, peroxisome proliferator-activated protein α (PPAR-α), and is responsible for intracellular trafficking of long chain fatty acids [8]. Rat LFABP has recently been described as an endogenous antioxidant [9], and may be useful in states of extreme oxidative stress when intracellular antioxidants such as superoxide dismutase, glutathione and catalase cannot quench excessive quantities of ROS. This antioxidant characteristic of LFABP is thought to result from the methionine groups located in the cavity of the LFABP binding site [9]. NADPH oxidase (NOX), an enzyme complex responsible for generating superoxide, is activated in rat Kupffer cells in alcoholic liver disease, through induction of transcription factor NF-κβ and TNF-α production [10]. However, administration of a methionine choline deficient (MCD) diet to p47 knockout mice, lacking a critical subunit of the NOX complex, showed that NOX is not an important contributor of oxidative stress generation. The p47 knockout mice on an MCD diet developed NASH with similar pathology as wild type, despite the lack of a functional NOX enzyme [11].

Therefore, we decided to investigate the anatomy of the pelvic organs of a group of human female foetuses, collected at autopsy. Methods We collected at autopsy 36 human female fetuses at different gestational ages, that did not displayed any visible alteration of the pelvic organs. The

characteristics of the fetuses are depicted in Table 1. Pelvic organs were collected en-block, fixed in paraphormaldeyde and included in paraffin. We performed histological analysis of the pelvic organs for each fetus, using Hematoxylin/Eosin and Hematoxylin/Van Gieson staining. For immunohistochemistry 5–7 μm specimen sections embedded in paraffin, were cut, mounted on glass and selleckchem dried overnight at 37°C. All sections were then deparaffinized in xylene, rehydrated through a graded alcohol series and washed in phosphate-buffered Savolitinib datasheet saline (PBS). PBS was used for all subsequent

washes and for antiserum dilution. AZD8931 concentration Tissue sections were quenched sequentially in 3% hydrogen peroxide in aqueous solution and blocked with PBS-6% non-fat dry milk (Biorad, Hercules, CA, U.S.A.) for 1 h at room temperature. Slides were then incubated at 4°C overnight at 1:100 dilution with the following antibodies: the affinity-purified rabbit antibody ERα for the oestrogen receptor (Santa Cruz, Santa Cruz, CA, USA; cat. # sc-542) and the mouse monoclonal antibody M11 for CA125(Dako Laboratories, Carpinteria, CA, USA).

After three washes in PBS to remove the excess of antiserum, the slides were incubated with Alectinib diluted goat anti-rabbit or anti-mouse biotinylated antibodies (Vector Laboratories, Burlingame, CA, U.S.A.) at 1:200 dilution in PBS-3% non-fat dry milk (Biorad) for 1 h. All the slides were then processed by the ABC method (Vector Laboratories) for 30 min at room temperature. Diaminobenzidine (Vector Laboratories) was used as the final chromogen and haematoxylin was used as the nuclear counterstaining. Negative controls for each tissue section were prepared by leaving out the primary antiserum. Positive controls constituted of tumour tissues expressing either the oestrogen receptor or CA125, were run at the same time. All samples were processed under the same conditions.

“
“Review Background Strongly correlated-electron materials, such as the rare-earth PLX3397 order perovskite oxide manganites having a general formula R1-x AxMnO3, where R is a trivalent rare-earth element (e.g., La, Pr, Sm) and A is a divalent alkaline-earth element such as Ca, Sr, and Ba, have been attracting much attention because of their unusual electron-transport and magnetic properties, e.g., colossal magnetoresistance (CMR) effect [1–3], a sharp metal-insulator transition

(MIT) as a function of temperature, electric field, magnetic field, light, hydrostatic pressure, strain, etc. [4–6]. Such MIT is also accompanied by a paramagnetic to ferromagnetic transition as the temperature is lowered. The competition selleck between several interactions in the rare-earth perovskite oxide manganites makes that only small energy differences exist between

the different possible phases of the system. As a result, the phase of the material can be tuned by various external perturbations, such as magnetic and electric fields, strain, and disorder. These perturbations may lead to the CMR effect and can be used for electronic phase control in manganite devices. Recently, there is strong experimental evidence to indicate that the rare-earth perovskite oxide manganites are electronically inhomogeneous, which consist of different spatial regions with different electronic orders [7–10], a phenomenon that is named as electronic phase separation (EPS). As an inherent electronic inhomogeneity, BEZ235 purchase EPS has been widely reported in the rare-earth perovskite oxide manganites, and its size varies from nano to mesoscopic scales [11–15]. It has been recognized to be crucial for the CMR effect and the MIT in manganites, leading to the new applications of spintronics [9]. However, the presence of EPS raises many intriguing questions, e.g., what is the microscopic nature of the EPS? Why does it have such a large range of length scales from nanometers to

micrometers? More importantly, is it responsible for the related physical properties such as CMR and high-Tc superconducting exhibited by Molecular motor the manganites and related oxide materials? Therefore, EPS is getting recognized as a phenomenon of importance in understanding the magnetic and electron transport properties of perovskite oxide manganites [16, 17]. Recent advances in science and technology of perovskite oxide manganites have resulted in the feature sizes of the microelectronic devices based on perovskite oxide manganites entering into nanoscale dimensions. At nanoscale, perovskite oxide manganites exhibit a pronounced size effect manifesting itself in a significant deviation of the properties of low-dimensional structures from their bulk and film counterparts.

The risk of enterotomy can be reduced if meticulous care is taken in the use of atraumatic graspers only and if the manipulation of friable, distended bowel is minimized by handling the mesentery of the bowel whenever possible [74]. In fact to handle dilated and edematous bowel during adhesiolysis is dangerous and the risk increases with a long lasting obstruction; this is the reason why early operation is advisable as one multicenter study showed: the success rate for early laparoscopic intervention for acute SBO is significantly higher after a shorter duration

of symptoms (24 h vs 48 h) [75]. After trocar placement, the initial goal is to this website expose the collapsed distal bowel [74]. This is facilitated with the use of angled telescopes and maximal tilting/rotating of the surgical table. It may also be necessary to move the laparoscope to different trocars to improve visualization. Only pathologic adhesions should be lysed. Additional adhesiolysis only adds to the operative time and to the risks of surgery without benefit. The area lysed should be thoroughly inspected AZD5363 solubility dmso for possible bleeding and bowel injury. In AP26113 purchase conclusion, careful selection criteria for laparoscopy [76] may

be: (1) Hemodynamic stability and patient not in shock, (2) absence of peritonitis or severe intra-abdominal sepsis, (3) proximal i.e. SB obstruction, (4) localized distension on radiography, and/or (5) absence of severe abdominal distension, (6) anticipated single band, (7) low or intermediate predicted PAI score in < = 3 abdominal quadrants, and last but not least (8) the experience and laparoscopic skills of the surgeon. A partial obstruction is better first approached with a non-operative challenge with hyperosmolar water soluble contrast medium with both therapeutic and diagnostic purposes. A complete SB obstruction

should no longer be considered an exclusion criteria for laparoscopic approach. The experts panel also agreed, as from the cited studies, that laparoscopic lysis of adhesions should be attempted preferably in case of first episode of SBO and/or anticipated single band adhesion (i.e. SBO after appendectomy or hysterectomy). Previous midline incision is MTMR9 not an absolute exclusion criteria for laparoscopic approach. A multicenter series of 103 patients from the WSES – Iitalian Working Group on peritoneal adhesions and ASBO management, presented at the 2013 Clinical Congress of American College of Surgeons [77], described a safe and effective surgical technique for laparoscopic approach to ASBO and confirmed that laparoscopy should be attempted preferably in case of first episode of SBO and/or anticipated single band adhesion (i.e. SBO after appendectomy or hysterectomy).

This response is typical of the telomere deprotection occurring during cellular senescence Alpelisib or upon the loss of telomeric proteins [34–40]. The ability of G-quadruplex ligands

to uncap telomeres and to possess anti-tumor activity has been already described for other agents, [41–45] reinforcing the notion that these agents can act as inhibitors of a telomere-related process and therefore the rationale for the development of this class of inhibitors as anti-tumor agents must be found elsewhere other than in higher telomerase expression in cancer cells. Taken collectively our results clearly demonstrate that compounds 2 (but less efficiently 3) rapidly disrupt telomere architecture of cells, by delocalizing the telomeric protein POT1, resulting in a potent DNA damage response characterized by the formation of several telomeric foci. Furthermore, it is apparent that the 2-substitued Gemcitabine in vivo quinoacridinium salt 2 more closely mimics the overall pharmaceutical profile of the prototypic compound 1 than the regioisomer 3. Our recent synthetic work has therefore focused on the 2-substituted series and our efforts

to maximize on-target and minimize off-target properties will be reported separately. Conclusions Molecular modification of quinoacridinum salts 1 have shown to reduce undesired cardiotoxic effects while maintaining the on-target features as telomere targeting agents. This findings provide a strong rational for development of this class of compounds

as tools for a G-quadruplex targeted anti-cancer therapy. Electronic supplementary material Additional file 1: Cytotoxicity of 2 and 3 and SPR sensorgrams. (PDF 281 KB) References 1. Hanahan D, Weinberg RA: The hallmarks of cancer. Cell 2000, 100:57–70.PubMedCrossRef 2. Testorelli C: Telomerase and cancer. J Exp Clin Cancer Res 2003, 22:165–169.PubMed 3. Cech TR: Beginning to understand the end of the chromosome. Cell 2004, 116:273–279.PubMedCrossRef 4. Phan AT, Kuryavyi V, Patel DJ: DNA architecture: from G to Z. Curr Opin Struct Biol 2006, 16:288–298.PubMedCrossRef Tolmetin 5. Huppert JL, Subramanian S: Prevalence of quadruplexes in the human genome. Nucleic Acids Res 2005, 33:2908–2916.PubMedCrossRef 6. Garner TP, Williams HEL, Gluszyk KI, Roe S, KU55933 nmr Oldham NJ, Stevens MF, Moses JE, Searle MS: Selectivity of small molecule ligands for parallel and anti-parallel G-quadruplex structures. Org Biomol Chem 2009, 7:4194–4200.PubMedCrossRef 7. Akiyama M, Hideshima T, Munshi NC, Anderson KC: Telomerase inhibitors as anticancer therapy. Curr Med Chem Anticancer Agents 2002, 5:567–575.CrossRef 8. Lai XF, Shen CX, Wen Z, Qian YH, Yu CS, Wang JQ, Zhong PN, Wang HL: PinX1 regulation of telomerase activity and apoptosis in nasopharyngeal carcinoma cells. J Exp Clin Cancer Res 2012, 31:12.PubMedCrossRef 9. Yingying L, Junchao G, Dachuan J, Yanjing G, Mengbiao Y: Inhibition of telomerase activity by HDV ribozyme in cancers.

This study further showed that tumors excised from the EA-treated mice revealed increased inhibitory phosphorylation of the insulin receptor substrate 1 (IRS1) and decreased activity of the Cytoskeletal Signaling inhibitor PI3/AKT pathway, in line with our in vitro results in A498 cells. Based on their in vitro results, the authors of this study concluded that EA bound and activated PKCθ to inhibit insulin signaling while, concurrently, activating HSF1, a known inducer of selleck chemicals glucose dependence,

thus, starving cells of glucose while promoting glucose addiction. However, because the in vitro binding studies with EA and PKCθ were indirect without any binding kinetic analyses, it is unclear if PKCθ is a primary target of EA. Furthermore, the experiments demonstrating inhibition of glucose uptake by EA were performed using EA at 10 μM, a concentration of EA approximately 200-fold higher than its IC50. It is well established that when cells are starved, the energy sensor, AMP-activated protein kinase, becomes activated by phosphorylation resulting in the induction of autophagy. If EA inhibits glucose uptake, it would be expected to result in a higher ADP/ATP and AMP/ATP ratio and consequent activation of AMPK. Our results, however, did not reveal activation of AMPK by EA at a concentration of 100 nM, a concentration that is highly cytotoxic to A498 cells. Hence, it is possible that the effects

of EA on glucose uptake may occur at micro molar concentrations that are much higher than required for cell death (nanomolar) and could represent off-target effects. Moreover, as a natural product, EA would be expected to have multiple VX-661 mw targets and most likely has targets in addition to PKCθ. Such targets may include those associated with the ER stress since it is well established that ER stress results in the induction of cell death and autophagy [49]. An example

of agent that induces autophagy and cell death by inducing ER stress in RCC includes STF-62247 which targets VHL-deficient RCC [50]. EA may target proteins within the Golgi complex analogous oxyclozanide to carminomycin I, a natural product with selective toxicity to VHL-deficient CC-RCC [51]. In conclusion, EA induces cell death via multiple mechanisms and likely has multiple cellular targets. The identification of these targets and pathways affected by this unique agent will be invaluable in understanding the high RCC- selectivity of EA and allow development of highly effective chemotherapeutics for the treatment of metastatic RCC, a highly treatment resistant cancer. Acknowledgment We gratefully acknowledge Dr. Stoyan Dimitrov for his assistance with the flow cytometry studies. This work was supported by a fund from Academia Sinica (A. L. Yu) and, in part, by an NIH grant (CA 133002) awarded to Emmanuel Theodorakis. References 1. Nguyen MM, Gill IS, Ellison LM: The evolving presentation of renal carcinoma in the United States: trends from the Surveillance, Epidemiology, and End Results program.

The first nested PCR consisted of 30 ng of genomic DNA, 0.05 μl of Hot start taq (5 unit/μl, Promega), 1 mM of each dNTP,

4 μl of reaction buffer (Promega), 1 μl of each Vorinostat mouse forward and reverse primers (5 μM) and 11.5 μl of molecular grade water. Cycling started with an initial denaturation and hot start activation of 10 min at 95°C followed by a low number of 16 cycles of 30 s denaturation at 95°C, 30 s at 50°C and 90 s at 72°C and a final extension of 10 min at 72°C. One μl of each PCR product was then diluted in 99 μl of molecular grade water before the internal stretch was Tucidinostat chemical structure amplified for 454 sequencing. Here, each individual microbiome was tagged by a unique combination of multiplex identifiers (MID, Roche, Basel, CH) integrated into forward and reverse primers [37, 38]. We used a total of 20 tagged primers consisting of the Titanium B sequencing adaptor (Roche, Basel), the 454 sequencing key, a MID tag and the gene-specific sequence. Hence, an example of a forward primer would have the following sequence: 5′-CCATCTCATCCCTGCGTGTCTCCGAC TCAG ACGAGTGCGT CCACGAGCCGCGGTAAT -3′ and a reverse primer: 5′-CCTATCCCCTGTGTGCCTTGGCAGTCTCAG TCAG ACGAGTGCGT CCGTCAATTCMTTTAAGTTT-3′, with the 454 sequencing key in italics, the MID tag in bold and gene specific sequence

underlined. Combinations of forward and reverse MIDs were random with respect to VS-4718 cost treatment and oyster bed. Therefore any amplification bias introduced by the MID will be randomly distributed among groups. After mafosfamide amplification single PCR reactions were purified using the MinElute 96

kit (Qiagen, Hilden) before 2 μl of each elution was used for pooling. To eliminate remaining primer-dimer both pools were purified again using Wizard PCR clean-up system (Promega, Mannheim) following the manufacturer’s instructions. After confirming the sole presence of the desired PCR product without any traces of primer by gel electrophoresis, the pool of individually barcoded PCR reactions were sequenced on the 454 FLX genome sequencer (Roche, Basel, CH) using Titanium chemistry. Sequencing was performed by GATC Biotech (Konstanz, Germany). Data analysis Assignment of reads to individual PCRs was done using modified python scripts from the cogent package. In short, within each raw read we looked for the presence of both primers ensuring complete sequencing of the PCR product. Afterwards, we identified individuals by determining combinations of MID tags allowing for a maximum hemming distance of one in each MID tag. After correct assignment of single reads to an individual oysters, we used the AmpliconNoise pipeline [39] to remove pyrosequencing and PCR noise and Perseus to remove chimeric sequences using default parameters except for alpha and beta values for false discovery detection in Perseus, which were set to −7.5 and 0.5, respectively. Reads were trimmed by cutting off their forward and reverse primers. We used scripts from the Qiime package [40] for the analysis of microbial diversity.

Using cloned pigs in obesity-related studies could provide a more homogenous experimental model, hence the cloning in this study was performed to minimize genetic influences and thereby reduce inter-individual variation [9]. One of the main focuses of obesity-related gut microbial studies have been to identify groups of bacteria that are correlated with the obese state, and initially the relative abundance of Bacteroidetes and Firmicutes in the gut microbiota was linked to obesity. In pigs, as in humans [10] and other mammals [11], the two main phyla of bacteria in the gut microbiota are Bacteroidetes and

Firmicutes[12, 13]. Previous studies have reported a greater proportion of Firmicutes in obese mice [14] when compared PF-01367338 with their leaner counterparts and a reduced ratio of Firmicutes to Bacteroidetes in a small group of obese humans on a weight loss regimen [15]. A similar result in a study of lean and obese pigs revealed a negative correlation between percentage of Bacteroidetes and body-weight [16]. Furthermore, a fluorescence in situ hybridization

(FISH)-based study on obese adolescents during weight loss regimens showed a decrease in the phylum Firmicutes[17]. However several studies suggest a decrease in ratio of Firmicutes to Bacteroidetes in obese and overweight subjects [18] and suggest diet to be a contributing factor in shaping the gut microbial community and not the bacterial proportions [19, 20]. Other observations in humans, NCT-501 suggest obesity to be associated with a lower bacterial diversity [3], while other studies showed no difference in the abundance of bacteria in the gut microbiota between lean and obese individuals that were on weight maintaining diet [21]. Hence this putative relationship between obesity, diet and specific phyla of bacteria in the gut microbiota is still controversial and there are few studies on the association between the gut microbiota and obesity during the development of obesity. Therefore, the focus of this paper was to investigate the gut microbiota

in cloned pigs compared with non-cloned Clomifene control pigs and to further elucidate if diet-induced obesity over time is associated with changes in the gut microbiota. We hypothesized that the composition of the gut microbiota would be more similar among the cloned pigs compared to non-cloned controls. The second hypothesis was that weight-gain would be related to an increase in the ratio of Firmicutes to Bacteroidetes as well as a decrease in the diversity of the gut microbiota. We therefore investigated the changes in the gut microbiota of cloned and control pigs beginning with lean pigs during a period of 136 days on a high-fat/high-caloric (HF/high-caloric) diet. Methods Animals The animals for this experiment were pigs of similar genotype of Danish AZD1480 Landrace and Yorkshire.

A third cluster of freshwater sequences (2p), entirely composed of sequences sampled from a glacier in Svalbard, belonged to TEL 2. This cluster was distantly related

to the other freshwater group (2e) and was embedded in a large assembly of Arctic and Antarctic sequences, although this relationship was weakly supported (Figure 1). T. subtilis is commonly observed inhabiting the sea-ice in the Baltic Sea [49] and it is therefore possible that these sequences originate from a marine species transported onto the glacier from marine waters by aerosols or other vectors. On the other mTOR inhibitor hand, if these represent an actual freshwater species this would be a second freshwater species within TEL 2, distantly related to the Bayelva River sequences. It remains to be verified that these are actually living cells and whether these have been transported from freshwater sources or dispersed on to the glacier from

marine habitats via aerosols or other vectors. So far, we have not detected sequences from the marine samples that are identical to these glacier phylotypes, which could indicate such freshwater dispersal, but as only few samples have been made in these areas we cannot exclude this possibility. Few marine-freshwater cross-colonizations In Figure 1 the freshwater sequences form Selleckchem LY2874455 distinct selleck inhibitor clusters and phylotypes, www.selleck.co.jp/products/Neratinib(HKI-272).html suggesting the existence of several different freshwater species. These are placed within both TEL 1 and TEL 2, demonstrating that relatively distantly related species of Telonemia

exists in freshwater. This diversity is detected even with a very limited number of samples; we therefore expect future surveys of other types of freshwaters at other continents to uncover an even larger diversity. The clustering pattern of the Telonemia sequences is in accordance with recent studies of other protist groups showing that freshwater species form distinct clades in phylogenetic trees, i.e. they are more closely related to each other than to marine species [reviewed in [50]]. Such clustering pattern of freshwater phylotypes has in these studies been interpreted as successful marine-freshwater transitions. These transitions have often been ancient and rare events, resulting in most of the extant species being restricted to either of the two habitats: e.g. in bodonids [51], goniomonas [52], cryptomonads [53], dinoflagellates [54] and Perkinsea [55]. If further examinations of freshwater with the use of Telonemia-specific PCR approaches confirms the clustering pattern shown here (see Figure 1), it would imply that the biogeophysical differences between marine and fresh waters constitutes a significant ecological barrier for dispersal of Telonemia that affects diversification of the lineage.

We examined the five genomes of G. vaginalis available in the NCBI genome database that had spacers targeting coding and non-coding regions on the chromosomes of strains 409–05, 6420B, 315A, 41 V, ATCC14019,

and AMD. We did not find a match between the spacers and the endogenous genomic sequences, except for the sequences located in the CRISPR arrays. We also analysed whether the protospacers located on the G. vaginalis chromosome displayed conserved protospacer adjacent motif (PAM) sequences [41, 42]. We aligned the protospacers with the flanking regions comprising 20 bp on both sides. Alignments were performed for ten AG-120 protospacers sharing 100% identity with the spacers. The conserved motif of two nucleotides (AA) situated immediately upstream of the target region was detected (Figure 5). The PAM signature AA was confirmed for nine protospacers with up to 10% mismatches located distant from the 5′- and 3′-ends of the spacers. Figure 5 WebLogo for the PAM consensus sequence determination. Ten protospacers identical to

spacers were aligned Pexidartinib cost relative to the 5′-end of the protospacer (base 1). Sequences include the protospacer (positive numbers) and 13 nucleotides (negative numbers) upstream of the first base of the protospacer (containing the PAM). Thus, the motifs adjacent to the protospacers located in the G. vaginalis genomic DNA bear the signatures of PAMs. The PLX4032 order orientation of the G. vaginalis PAM is 5′-AA-protospacer-3′, which coincides with the orientation of the PAM identified in E. coli as CRISPR/Cas; both bacteria belong to the same type [41, 42]. Among all of the G. vaginalis CRISPR acetylcholine arrays, the first nucleotide of 97.5% of the spacers was either C or T. Only six spacers started with A or G (2.5%). All of the spacers targeting the protospacers on the G. vaginalis chromosome started with C or T (18:13). Discussion The CRISPR locus of the recently

discovered CRISPR/Cas defence system in prokaryotes protects against invading viruses and plasmids and is a map of the “immunological memory” of the microorganism [25, 26]. The spacer sequences that are incorporated into the CRISPR loci provide a historical view on the exposure of the bacteria to a variety of foreign genetic elements [23]. A recent report on the ability of CRISPR/Cas to prevent natural transformation in Streptococcus pneumoniae enlarged the role of CRISPR in bacterial nucleic acid-based immunity and the impact that CRISPR has on the emergence of bacterial pathogens [43]. In the current study, we analysed the CRISPR arrays in 17 recently characterised G. vaginalis clinical isolates [18] and the genomes of 21 of G. vaginalis strains deposited in the NCBI genome database. We examined the spacer repertoire and evaluated the potential impact of CRISPR/Cas on gene uptake in G. vaginalis. We found that six clinical isolates (35%) and 14 G. vaginalis genomes deposited in the NCBI database (67%) contained CRISPR/Cas loci.