Graphene is a single-atom-thick two-dimensional graphitic carbon material, which possesses extraordinary

large surface area and chemical stability [14]. Recently, graphene has been used as an excellent substance to acquire variously functional nanomaterials, including graphene-silver nanoparticles [15], graphene-gold nanoparticles [16], graphene-TiO2 nanomaterials [17], and graphene-palladium nanoparticles [18]. Recently, some works have reported about synthetizing and studying the electrochemical performance of graphene mixed Ku-0059436 chemical structure with Ge nanomaterials [19–23]. For instance, Cheng and Du [22] reported the synthesis of graphene-Ge nanocomposites from expensive GeCl4 and graphene oxide as precursor. Although the nanocomposites exhibited a high specific capacity as anode materials for lithium ion batteries (LIBs), this strategy did not acquire a material with long cycle life. Ren et al. [23] reported Navitoclax in vivo the synthesis of graphene-Ge nanocomposite by chemical vapor deposition (CVD),

which exhibited a good capacity retention behavior and long cycle life as anode materials. However, the strategy did not provide a facile route for synthesis. Moreover, the loss of stability and electrochemical properties often inevitably occurred due to irreversible agglomeration and poor dispersions of graphene-Ge nanocomposites in aqueous solution. Therefore, it was important to find a new synthesized method to prepare water-dispersable Ge nanocomposites with excellent electrical properties. Herein, we demonstrate a simple and mild method to fabricate the RGO-GeNPs in aqueous solution. Stable aqueous dispersions of nanocomposites were synthesized by the reduction of exfoliated graphite oxide and GeO2 precursor.

Poly(sodium 4-styrenesulfonate) (PSS) was employed to obtain aqueous dispersibility of PSS-RGO-GeNPs, which was hopeful to further improve its electrochemical properties. The study provided a strategy to synthetize RGO-GeNPs which could be served as promising anode materials for LIBs. Methods Materials All reagents in this work were of analytical grade and were used as received without further purification. GeO2, PSS (analytically pure), and graphite powders (spectral pure) were purchased from Sinopharm Chemical Reagent Beijing Co. NaBH4, the reducing agent, was obtained from Aladdin Chemical Co., Ltd. (China). All the aqueous Alectinib mouse solutions were prepared with double-distilled water. Preparation of RGO-GeNPs and PSS-RGO-GeNPs Graphene oxide (GO) was prepared by oxidizing natural graphite powder based on a modified Hummers and Offeman method [24] as originally presented by Kovtyukhova et al. [25]. The RGO-GeNPs were synthesized by the following method:10 mL of as-prepared GO supernatant (20 mg/mL) was distributed in 40 mL of ultrapure water to obtain a homogeneous, stable dispersion with the aid of ultrasonication in a water bath (KQ218, 60 W), named ‘A solution’. A 0.08 g GeO2 was dissolved completely in 10 mL 0.

Nobile et al.[30] found that the expression of Hwp1 in Saccharomyces cerevisiae permits adherence to wild-type C. albicans but not an als1Δ/als1Δ als3Δ/als3Δ double RAD001 mutant. In addition, a TDH3-HWP1 hybrid gene could not promote biofilm formation in the als1Δ/als1Δ als3Δ/als3Δ background in vitro or in vivo. Our study revealed that human serum decreased the expression level

of ALS1 and ALS3, so overexpression of HWP1 failed to save the adhesion and biofilm formation of C. albicans. ECE1 was regarded as a hyphal-induced gene, although its mechanism of action is uncertain. Our study showed that hyphae were significantly greater in the presence of serum than in the control group, especially in the mature biofilm stage (data not shown). This may be due to the increase of ECE1 and HWP1[23]. In this study, we also tested the expression of adhesion-related genes in biofilms grown for 24 h and found that the expression trend of related genes at this time was similar to the adhesion phase, both in the reduction of ALS1 and ALS3 and the up-regulation of HWP1 and ECE1. The expression of the BCR1 gene, however, was significantly inhibited. 5-Fluoracil in vitro Its level was far lower than that of the control group. All in all, the serum reduces BCR1 gene expression,

and that might be a reason for biofilm inhibition. Conclusion In summary, our study demonstrated that human serum may reduce the biofilm formation of C. albicans by inhibiting the adhesion. This inhibition is partly due to the down-regulation of adhesion-related genes, including ALS1, ALS3 and BCR1. Meanwhile, the inhibitory effect of human serum is caused by non-protein

components in the serum. Therefore, biofilm formation in vivo may be “selected for” (possibly by immune pressure and sheer forces) rather than “induced” by serum at the level of transcription. Methods Ethics Statement This study was approved by the Medical Ethics Committee of Beijing Friendship Hospital, Capital Medical University, Beijing, China (approval #BJFH-EC/2013-014), and individual informed consent was waived. Organisms Four Candida albicans strains (laboratory strain ATCC90028 and three clinical isolates of C. albicans: 9079, y2991, 31448) were tested in this study. The three C. albicans bloodstream isolates were collected from three different intensive care patients admitted to the Beijing Friendship Hospital and were confirmed according to standard mycological methods, such as the germ tube test in serum, growth on CHROMagar Candida medium, and API testing methods. All isolates were stored in skim milk at -80°C until use. Medium and growth conditions Prior to each experiment, C. albicans strains were subcultured on Sabouraud’s Agar (SDA) at 35°C for 24 h.

9%~79.8%[3]. Che Xiaoming et al achieved similar outcomes by colony selection with the selleck products use of limited dilution, and harvested about 82% cells that have the proliferation capacity[2]. We obtained highly purified BTSCs by their method. As is known to all, EGF and bFGF, as powerful promoters of cell division, are essential key components in stem cell culture medium, and enable stem cells to proliferate continuously. Through MTT experiment,

we have found that ATRA alone can promote the proliferation of BTSCs, but the promoting effect is weaker than EGF+bFGF, and there is no obvious synergistic or antagonistic effect between ATRA and EGF+bFGF. Previous researches have showed that ATRA can inhibit the proliferation of ordinary glioma cells cultured in serum-containing medium, promoting apoptosis of the glioma cells. We have observed that BTSCs in the control group grew as suspended spheres when cultured in the medium without serum and growth

factors. Similar to the control group, BTSCs in the ATRA group were not adherent, but the formed spheres were larger and the proliferation was more rapid, indicating that ATRA did not induce the DNA Damage inhibitor differentiation of the suspended BTSCs, but promote the proliferation of BTSCs. The reason may be as mentioned below. In the serum-free medium, BTSCs can achieve continuous self renewal and proliferation through symmetric division, retaining the stem cell characteristics; and in the serum-containing click here medium, because of the influence of certain substance in the serum, BTSCs can retain their existence through asymmetric division, and produce a great number of comparatively

mature progeny cells, which differentiate into ordinary tumor cells ultimately, so there is only a small percentage of BTSCs in the whole cell population. The targets of ATRA’s effect of differentiation induction are cells in the process of differentiation. For BTSCs in the stem cell state, ATRA has a promoting effect on their proliferation. So ATRA exerts opposite effects on BTSCs at different stages of differentiation, the mechanism of which needs further clarification. Clinical trials of differentiation of brain glioma cells induced by ATRA showed that the differentiation effect of ATRA alone was weak, with insignificant curative efficacy[8, 9]. We speculate that the application of ATRA alone can induce the differentiation and apoptosis of most ordinary glioma cells, but promote the proliferation of a minority of BTSCs that does not experience differentiation, that is to say, the “”seeds”" resulting in the formation, development and relapse of tumors do not decrease but increase, which may be exactly the major reason for the poor therapeutic effect. Research of Singh et al revealed that only CD133 positive cells had the stem cell characteristics of self-renewal, unlimited proliferation and multilineage parent differentiation[3]. These days, CD133 has been recognized as the marker to isolate and identify BTSCs.

GcrA also activates genes required for polar development (including pleC and podJ, both of which Palbociclib order are also activated by DnaA [3, 4]). CtrA, in turn, regulates at least 95 genes in 55 operons: some are repressed (for example gcrA and podJ[4, 6]) whereas others are activated (such as the pilin subunit gene pilA, flagellum synthesis cascade initiation, and the holdfast anchor operon [7]). Additionally, CtrA binds to the chromosome at the origin of replication where it represses the initiation of DNA replication [8]. Furthermore, CtrA both activates and represses its own promoters. The ctrA gene has two promoters: P1 and P2 [9]. The weaker upstream P1 promoter is activated first. P1 activation

requires that the

promoter be in the hemi-methylated state, meaning that DNA replication has initiated and the replication fork has passed the P1 promoter. The P1 promoter is also directly activated by GcrA [4, 9, 10]. The low level of expression from the GcrA-activated ctrA P1 promoter allows some CtrA protein to accumulate. Once sufficient CtrA has accumulated, it represses the P1 promoter (as well as gcrA expression) and activates check details the strong downstream P2 promoter [9], leading to a burst of CtrA production and activity. The sequential activation of the master regulators forms the timeline by which developmental processes are regulated and coordinated. In particular, GcrA contributes to the Doxacurium chloride expression of the key developmental regulators, the histidine kinase PleC and the polar localization factor PodJ. Loss of either protein causes pleiotropic defects in development. A pleC mutant does not synthesize a stalk, holdfast or pili, and though the flagellum is made, flagellar rotation is not activated and the flagellum is not shed during the swarmer cell differentiation [11–13]. A podJ mutant, like pleC, does not synthesize holdfast or pili or shed its flagellum, but it does synthesize a stalk and activates its flagellum, however its motility is impaired in low-percentage agar as compared to wild type [6, 14, 15]. To further elucidate

the pathways that lead to these pleiotropic phenotypes a genetic approach was used. We conducted a transposon mutagenesis screen, selecting for resistance to phage ΦCbK, which requires pili for infection, and screening for defects in motility and adhesion, which require the flagellum and holdfast respectively. In this work we report the identification of a transposon insertion in the promoter region of ctrA that causes a drastic reduction of CtrA accumulation, resulting in pleiotropic phenotypes bearing similarities to the pleC and podJ phenotypes. Results and discussion A transposon mutation causes a pleiotropic phenotype C. crescentus wild-type strain CB15 was mutagenized with the mariner transposon and mutants resistant to the bacteriophage ΦCbK were isolated to enrich for mutants defective in pilus synthesis.

There is a growing awareness of the need to eliminate such pathogens by disinfecting the water in the aquaculture systems [4, 5]. Disinfection is an effective treatment for many types of pathogenic microorganisms, including viruses, bacteria, fungi and protozoan parasites [6]. However, water disinfection

remains a scientific and technical challenge [7]. The most commonly used techniques for water disinfection are chlorination, membrane filtration and ozone treatment [8] but antibiotics and biocides have also been used. Unfortunately all have disadvantages, particularly in relation to the generation of toxic by-products which may cause health risks to human consumers [9]. Additionally, some viral vaccines see more selleck chemicals have been developed in the past two decades, but these are limited to selected viral pathogens and they are also extremely costly to produce and to administer [10]. Solar radiation is an alternative, low-cost, effective technology for water disinfection [11]. Solar disinfection

normally refers to exposure of contaminated water to natural sunlight for a sufficient length of time to reduce the number of pathogenic microbes below the infective dose [5, 12]. So far the most commonly employed method for solar disinfection is to expose contaminated drinking water kept in transparent plastic containers to full sunlight for at least 6 h [11, 13] which is slow, and is

not always feasible as a result of daily and seasonal variations in weather conditions. Solar disinfection can be enhanced substantially by using certain photocatalysts such as the photoactive semiconductors TiO2, ZnO, Fe2O3, WO3 and CdSe. These photocatalysts produce highly reactive oxygen species (ROS) which destroy microbial pathogens; this is known as solar photocatalytic disinfection [14, 15]. Titanium dioxide (TiO2) is one of the most widely used, stable and active photocatalysts in water disinfection [8]. It has shown its effectiveness not only ifenprodil in small-scale solar disinfection reactors but also in pilot studies of large-scale solar photocatalysis for drinking water and waste water [16–19]. Typically, TiO2 slurries are used for chemical and microbial photodegradation [9, 19]. However, such slurries create problems in separating the photocatalyst from the treated water, leading to the development of reactors containing an immobilised photocatalyst. Different types of solar photocatalytic reactors have been developed for water treatment [20]. The most frequently used types of reactors are: (i) the parabolic trough reactor (PTR), (ii) the double skin sheet reactor (DSSR), (iii) the compound parabolic collecting reactor (CPCR) and (iv) the thin-film fixed-bed reactor (TFFBR).

Enteritidis, S. Typhimurium, S. Albany, S. Derby, S. Anatum and S. Havana were common in both hosts (Table 5). MI-503 However, these serovars shares same antigens: g complex; i; and z4,z24 of H1 antigen and 1 complex and – of H2 antigens (Table 5), implying these antigens may be important for Salmonella transmission between chicken and human. Prevalent serogroups and serovars are related to chicken lines (Table 1)[9, 10] and ages [15]. In layer, age-related prevalence was reported earlier

[15] and no Salmonella was isolated from 1-year-old layers in the present study (Table 1). Such age-associated clearance may be due to stronger antigen-specific T-cell response in older chicken [41] and not related to B-cell response [42]. Age-related serovars were also identified in Taiwan broiler chickens (Table 2). Almost all isolates were S. Choleraesuis and non-typable Salmonella (possibly monophasic S. Choleraesuis) of serogroup C1 in Chick PF-01367338 solubility dmso group and S. Mons of serogroup B in NHC group (Table 2). As swine-adapted pathogen, S. Cholearesuis has

seldom reported from chicken. However, S. Choleraesuis in 1-day-old chicks may be contaminated from the hatchery, particular from eggshell membrane; in which S. Typhimurium, not S. Choleraesuis, is main serovar [43]. If highly invasive S. Choleraesuis could infect chicks and use the chicken as reservoir, it will lead to a public problem of circulating such high invasive serovar in animals. In broiler, prevalence of Salmonella differed between chicken parts (2.36% for legs and 4.25% for breasts of broiler) [19]. Further, Tacrolimus (FK506) prevalent serovars differ between sampling sources e.g. the S. Anatum and S. Rissen in chicken meat [44] and S. Blockley, S. Hadar and S. Bredeney in the

cecal samples (24). Several methods have been developed to differentiate clinical isolates. In this study, PFGE patterns almost matched serotypes, although S. Albany and S. Havana appeared multiple genotypes with highly similar banding patterns (Table 2). Therefore, PFGE typing is a useful tool to assist serotyping of Salmonella isolates before doing traditional serotypes [2, 27]. In contrast to PFGE type, plasmid analysis is the most convenient method for subtyping [15, 45]. In this study, plasmid variations were more diverse than genomic variations; however, S. Albany and S. Havana with highly genomic variations lacked plasmid (Table 2). These results may imply that recent evolution of Salmonella might be mainly through plasmid acquisition to introduce beneficial genes for host serovar to survival. Antimicrobial susceptibility of Salmonella can be used to monitor drug abuse in different regions (Table 2) [46] and animal sources [44, 47]. Early study reported that Salmonella from chicken, not from human, pig and cattle, was less resistance to A, C, and Sxt [47]. Nevertheless, resistance to T was frequently found in chicken isolates [48]. Since discovery of ACSSuT-resistant region in SGI of S.

BLAST analysis of these four genome sequences revealed a type b capsule locus in each case and all four strains were recorded as being isolated from CSF, or click here were associated with meningitis. We suppose that loss, or reduction, of type b capsule expression in these strains may have occurred during isolation and/or culture in the laboratory. Based on the output from Mauve analysis, we selected Hib strains to analyse, in more depth, the differences in genome content that shape this level of diversity within the species. We used read-mapping by MAQ to investigate single nucleotide polymorphisms

(SNPs) between 18 Hib strains included in our genome sequence database and a common reference (Table  1, Figure  2). Strain RM7018, originally designated non-typeable was excluded ICG-001 cost as it was not a member of this Hib group based on Mauve analysis (Figure  1). Conversely, we included strain PLMIOG2822H-L, a type b strain that had been wrongly classified as H. haemolyticus. Sequence reads were mapped onto a complete reference Hib genome sequence (strain 10810; Genbank FQ312006.1) and used to identify SNPs for all Hib strains. The Hib groupings observed (Figure  2) were essentially the same as those observed by Mauve analysis (Figure  1). Based on the location and number of SNPs, the β1 strains can be sub-grouped into β1a-β1e, and strain

RM7598 contains sufficient differences to constitute a separate group (ψ) from the β2 strains (Figure  2). Genome sequence data provides greater resolution in characterising divergence of strains that share identical or similar MLST profiles. For example, when we compared the patterns of SNPs of the sub-grouped β1a-β1e strains to their respective MLSTs, we found that strains RM7578 and DC800 shared similar blocks of SNPs when compared to strain 10810, in a pattern indicative of a common vertical inheritance. Strains RM7578 and DC800 had differed by two MLST alleles (Figure  2). Strains RM7122 and Eagan also differed by two MLST alleles but differed

by 4,853 SNPs in comparison to strain 10810. Figure 2 SNPs of H. influenzae type b strain sequences when compared with Hib strain 10810. The complete genome sequence of the Hib strain 10810 was used as a reference against which the sequence Docetaxel molecular weight reads of each strain were mapped using MAQ. Each vertical black line represents the location of a SNP. The equivalent groupings to those identified in Figure  1 are labelled on the right hand side. Regions marked at the bottom of the figure represent genome segments which are present in the reference strain 10810 but that may not be found in all other strains. The brackets on the left hand side of the figure indicate the number of MLST alleles shared between the pairs of genomes indicated; the sequence type (ST) of each strain is indicated to the right of its name.

For higher temperatures, the temperature dependence deviates from linearity and fractons cannot be considered as the dominant mechanism. Our experimental results for highly porous Si at temperatures higher than 100 K [18] were fitted by models considering a simplified porous Si structure, as for example the phonon diffusion model by Gesele et al. [17] and the phonon hydrodynamic model by Alvarez et al. [48]. A comparison of our experimental results with the above models was made in [18]. Very good agreement with the phonon diffusion model was obtained for temperatures in the range 200 to 350 K, while a better qualitative description of the temperature dependence

of k in a larger temperature range (100 to 350 K) was obtained with the phonon hydrodynamic approach. We have to note here that discrepancies this website between the experimental results and the different theoretical models as the ones above are

mainly due to the very complicated structure of porous Si, which is not fully taken into account by the models. Nanostructured porous Si is composed of interconnected Si nanowires and nanocrystals, covered by a native oxide shell and separated by voids. The ratio of the native oxide compared to the Si core plays a critical selleck kinase inhibitor role in the determination of the mechanism of thermal conduction in the different temperature ranges, especially at cryogenic temperatures [49]. This is because of the different temperature dependence of vibrational modes in the two systems (the Si backbone and the shell oxide). Conclusions The thermal conductivity of 63% porosity nanostructured porous Si was measured for the first time in the cryogenic temperature range 5 to 20 K. A stable value as low as 0.04 W/m.K was obtained in this temperature range. We attribute the plateau-like behavior of our porous Si material at cryogenic temperatures to the presence of fractons, which are localized anomalous vibrational modes according to the scaling theory pheromone of localization of Rammal and

Toulouse. We discussed in detail the specific fractal geometry of our porous Si system and its fractal dimensionality that supports the adoption of the fracton formalism. Literature results demonstrated the existence of the so-called Boson peak in the micro-Raman spectra of porous Si with a similar porosity than that of the porous Si layer used in this work. The existence of this peak in a material is in general considered as a signature of the presence of localized vibrational modes (‘fractons’ in a fractal lattice). In addition, literature results of Brillouin spectra of porous Si also showed localized vibrational modes that support our interpretation. Above the plateau and up to approximately 100 K, an almost linear increase with temperature was obtained for our highly porous Si material, as that obtained in amorphous materials and attributed to the anharmonic interaction between fractons and phonons.

Otherwise, data were discussed qualitatively, considering all key GSK1120212 characteristics and placing the evidence in light of the study strengths and weaknesses. To best explain the relationship between illness perceptions and work participation,

we made a distinction between studies with a longitudinal design and those with a cross-sectional design. As the design of longitudinal studies carries, in comparison with cross sectional studies, in potential more weight with regard to causality, these are presented first. The results were described by considering both the type of analyses (descriptive analyses or multivariate analyses) and the type of study design (longitudinal or cross-sectional design). Both the longitudinal studies and the cross-sectional studies used descriptive (comparative) analyses by comparing illness perception dimension scores in working versus non-working patients. In addition, both also used multivariate stepwise regression analyses to show the added value of including illness perceptions over and above commonly used health and socio-demographic variables, either in predicting return to work using baseline data (longitudinal studies) or in showing its association with

work participation (cross-sectional studies) at one moment in time. Results Study selection and characteristics The primary search strategy generated 5,163 references. After a first selection on title and abstract, 158 references were left for full-text screening. The majority of find more studies were excluded as they did not include an outcome on the level of work participation. Four studies met all criteria for inclusion and were selected for this review; two small studies using a longitudinal design including Protein kinase N1 72 and 77 patients (Petrie et al. 1996; McCarthy et al. 2003) and two larger survey studies using a cross-sectional design including 552 and 1,121 subjects (Sluiter and Frings-Dresen 2008; Boot et al. 2008). The study populations in the two longitudinal studies by McCarthy et

al. (2003) and Petrie et al. (1996) included, respectively, recent trauma as a result of molar extractions in the past week or recent myocardial infarction in the past 6 weeks. The two cross-sectional survey studies by Boot et al. (2008) and Sluiter and Frings-Dresen (2008) both included chronic populations: one with various chronic diseases (mean duration 8–10 years) (Boot et al. 2008) and the other chronic repetitive strain injury (RSI) (mean pain duration 6 years) (Sluiter and Frings-Dresen 2008) (see Table 1). The outcomes of work participation and definitions differed between studies; i.e., days until back to work, return to work rates at 6 weeks (longitudinal studies), or sick-listed or fully work disabled (cross-sectional studies).

5) * According to the third English edition of the Japanese Classification of Gastric Carcinoma [4]. † According to the seventh edition of the International Union Against Cancer TNM guidelines [3]. Relationships between clinicopathological characteristics and nodal metastases are shown https://www.selleckchem.com/autophagy.html in Table 2. The only characteristic significantly associated with nodal metastases was lymphatic invasion in pT1b2 tumors. Table 2 Results of univariate analyses showing relationships between clinicopathological characteristics and lymph node metastases Variables

pT1a tumor (n = 161) pT1b1 tumor (n = 43) pT1b2 tumor (n = 123)   pN(+) p-value pN(+) p-value pN(+) p-value Total 4/161 (2.5%)   4/43 (9.3%)   37/123 (30.1%)      Sex   0.6269   0.2802   0.8309    Male 3/88 (3.4%)   4/28 (14.3%)   26/88 (29.6%)      Female 1/73 (1.4%)   0/15   11/35 (31.4%)   Age   0.6332   0.3449   0.8432    < 65 3/91 (3.3%)   3/21 (14.3%)   16/51 (31.4%)      65 ≤ 1/70 (1.4%)   1/22 (4.6%) Palbociclib ic50   21/72 (29.2%)   Main tumor site   0.1903   0.2707   0.1129    Upper 0/19   0/3   3/21 (14.3%)      Middle 4/89 (4.5%)   4/27 (14.8%)   17/59 (28.8%)      Lower 0/53   0/13   17/43

(39.5%)   Clinical macro type   0.5655   0.5579   0.4764    Depressed or excavated 3/131 (2.3%)   4/33 (12.1%)   27/96 (28.1%)      Flat or elevated 1/30 (3.3%)   0/10   10/27 (37.0%)   Pathological macro type   1.0000   1.0000   0.4764    Depressed 4/139 (2.9%)   4/37 (10.8%)   27/96 (28.1%)      Flat or elevated 0/22   0/6   10/27 (37.0%)   Ulceration   0.1287   0.3235   0.4200    No 0/72   1/23 (4.4%)   21/77 (27.3%)      Yes 4/89 (4.5%)   3/20 (15.0%)   16/46 (34.8%)   Main histologic type   0.1252   0.4672   0.8441    Differentiated 0/74   2/29 (6.9%)   19/66 (28.8%)      Undifferentiated 4/87 (4.6%)   2/14 (14.3%)   18/57 (31.6%)   Pathological tumor size   1.0000   1.0000   0.0589

   ≤20 mm 1/60 (1.7%)   0/7   4/28 (14.3%)      20 mm< 3/101 (2.5%)   4/36 (11.1%)   33/95 (34.7%)   Pathological tumor size   0.3083   1.0000   0.1730    ≤30 mm 1/96 (1.0%)   2/21 (9.5%)   13/55 (23.6%)      30 mm< 3/65 (4.6%)   2/22 (9.1%)   24/68 (35.3%)   Lymphatic invasion †   0.0731 L-NAME HCl   0.5227   < 0.0001**    L0 3/158 (1.9%)   3/36 (8.3%)   4/52 (7.7%)      L1-2 1/3 (33.3%)   1/7 (14.3%)   33/71 (46.5%)   Venous invasion †   1.0000   1.0000   0.4200    V0 4/160 (2.5%)   4/42 (9.5%)   21/77 (27.3%)      V1-3 0/1   0/1   16/46 (34.8%)   ** p < 0.01. † According to the seventh edition of the International Union Against Cancer TNM guidelines [3]. We combined pT1a (m) and pT1b1 (sm1) tumors into one group because the incidence of nodal metastases was under 10% in both, and compared relationships between histological types and nodal metastases in the pT1a-pT1b1 (m-sm1) and pT1b2 (sm2) groups (Table 3). A total of 45 out of 327 patients had nodal metastases, including 8 of the 204 patients in the pT1a-pT1b1 (m-sm1) group.