In AFM images, we measured three surface morphology parameters of the sample:

the ten-point height value given as the difference between five maximal peaks and five minimal hollows, average height value, and RMS roughness. In spite of LN2 cooling, both the granularity and roughness of the silver film remained nearly the same and the temperature change did not cause any cracks. Effect of cooling substrates While thermal expansion of materials involved in the deposition process has a negligible influence on Ag film roughness, we decide to cool down the substrates and thus GSK2879552 ic50 reduce the surface diffusivity of adatoms. The diffusivity of Ag adatoms was preliminarily reduced due to an intermediate 1-nm-thick wetting layer of germanium [15]. In the vacuum chamber during the deposition process, the specific humidity (defined as the ratio of mass of water vapor to unit mass of dry air) is kept constant in spite of the pressure decrease. However, when the substrate is rapidly cooled with LN2, this specific humidity considerably decreases because most of the water vapor condenses on cooled parts and freezes forming ice crystals of a size reaching single nanometers. selleck chemicals In our custom-made substrate holder module, most of the residual humidity did not deposit on the substrates with controlled temperature but on the walls of the LN2 vessel, which was the coldest element in the vacuum chamber

and Quinapyramine worked as a cold trap. Nevertheless, silver was deposited on the ice crystal-covered substrate, which no longer has flatness RMS = 0.2 nm. Now, we look for the optimum temperature of depositing 30-nm-thick Ag films at temperatures from the range 90 to 400 K. Figure 1 shows AFM images scanned on 9 × 9 μm areas of 30-nm-thick Ag films deposited at temperatures 295, 170, 140, and 90 K. Surface morphology parameters of the samples are given in Table 1. Films deposited at two high temperatures have comparable surface quality (Figure 1a, b); however, the ten-point height value

is lowest in the sample deposited at ambient temperature (Figure 1a). The morphology parameters of the samples evaporated at the two low temperatures are poorer. Figure 1d shows that the silver film was deposited on water ice crystals. After melting of the crystals, some silver flakes are only loosely connected with the substrate. The rift valleys shown in Figure 1d are micrometers long and their deep end reaches the substrate. Figure 1 AFM images of 30-nm-thick Ag films scanned at RT. Samples deposited at (a) 295 K and (b) 170 K – the surface smoothness is influenced solely by thermal MK 8931 clinical trial migration of atoms leading to continuous and almost uniform layers, (c) at 140 K – islands due to atom migration and deposition onto sapphire substrate covered with water ice nanocrystals are more pronounced, and (d) at 90 K – the surface smoothness is deteriorated by cracks that result from water ice crystal melting.

Figure 1 Genetic organization and the predicted primary structure of CB-839 chemical structure PnxIIIA in P. pneumotropica ATCC 35149. (A) AR-13324 molecular weight Schematic representation of the pnxIII operon genetic map and the functions of each gene. Circles represent potential transcriptional termination loops. Predicted functions determined by the protein database are indicated below the gray boxes. (B) Schematic representation of probable domains that were identified by comparing with the HMM database. The numbers represent the regions containing a large repeat sequence.

Arrowheads below the number box represent the position of sequence alignment in Additional file 1. The pnxIIIE gene product contains the OmpA domain (Pfam reference: accession no. PF00691) in the selleck compound C-terminus and is 54% similar to the OM protein A of Cardiobacterium hominis ATCC 15826 (ZP_05705729), with 84% coverage. Although the protein BLAST search yielded no highly similar proteins, the deduced amino

acid sequence of pnxIIIA was partially similar (46%) to the RTX family exoprotein of uropathogenic E. coli (UPEC) CFT073 [29] (NP_752300), i.e., 59% coverage. PnxIIIA is believed to be an essential cytotoxic protein of the structural RTX toxin. Figure 1B shows the putative domains and repeat sequence in the primary structure of PnxIIIA. PnxIIIA did not have any significant identical conserved domains in the Pfam database; however, several partial sequences that

were not significantly similar to conserved domains were identified in the HMM database. In brief, several groups of bacterial immunoglobulin (Ig)-like domains (Pfam reference: accession no. PF05345, PF02369, PF02368, PF07532, and PF10648) and a hemagglutinin repeat (PF05594) were scattered in the primary sequence of PnxIIIA, and a hemolysin-type calcium-binding PIK3C2G repeat (PF00353) identical to nonapeptides of the RTX repeat sequence in the C-terminal half was present (Figure 1B). In particular, only 1 copy of amino acid residues in position 2319-2327 (LDGGDGNDT) was found to be identical to the RTX sequence; otherwise, 2 RTX-like sequences were found in positions 2114-2122 (NFGGMGVSN; alternate amino acid residues are italicized) and 2377-2384 (IKGGT-NDT; the missing amino acid residue is indicated with a hyphen). PnxIIIA was also found to have a unique feature: 3 regions with large repeat sequences existed, and the amino acid sequences in these regions were similar to the repeat sequences of the extracellular protein toxin identified in various prokaryotes, including important pathogens (see multiple alignments in Additional file 1). Of these, except for the unknown function of the RTX exoprotein and hemolysin-type calcium-binding protein, almost similar proteins were predicted to be localized in the OM fraction and to function as adhesive proteins.

To check

the crystallization kinetics, electrical resistivity was in situ measured with increasing temperature with various heating rates dT/dt. Applying Kissinger’s analysis which relates the transition temperature T c, the rate of heating (dT/dt), and the activation energy (E a) for crystallization by the formula below: (1) where C is click here a constant, k B is the Boltzmann constant, a plot of ln[(dT/dt)/T c 2 against 1/T c yields a straight line with slope, -E a/k B. From the Kissinger plot shown in Figure 2b, the activation energy for crystallization of AST was determined to be about 3.55 eV which is higher than that of GST films (approximately 2.01 eV) [22]. It has to be noted that the high crystallization temperature and high activation energy of AST offer a large benefit ITF2357 for a stable operation of the PCM device because the cells in the amorphous state tend to switch to the crystalline state due to cross talk, i.e., the heat dissipation from other cells. Figure 2 Sheet resistance change and Kissinger plot. (a) Temperature dependence of the sheet resistance of AST films and (b) Kissinger plot from which the E a of the amorphous to crystalline transition

at T c of AST films are determined. The bright-field TEM was used to study the structure of thin films. Figure 3 shows the TEM image of AST film after a 2-min heating at 400°C in Ar atmosphere; nanocrystals (dark spots) were observed. Peng et al. reported that an embedded crystal structure of hexagonal (Sb2Te) and monoclinic (Al2Te3) phases can be found in AST materials [10]. The black area in the image results from an GDC-0449 concentration overlap of Sb2Te and Al2Te3 crystalline grains. The overlap of grains will lead Celecoxib to a larger local density, and the incident electrons will be more scattered

by these areas. Figure 3 TEM image of AST film after a 2-min heating at 400°C. The phase transition of PCM cell can be characterized from the relation between the cell resistance and the corresponding amplitude of voltage pulse or current pulse (so called R-V or R-I curve). The measured R-V curves for AST PCM cells with different pulse width are shown in Figure 4a. Reversible phase-change process has been observed. As revealed, once the programming voltage increases beyond the threshold voltage, the cell resistance starts to drop due to the crystallization of AST alloy and then reaches a minimum, which is corresponding to the set resistance. When the voltage is further increased, the resistance again rises and then returns to the reset state. It is clear that the set resistance decreases with the pulse width. The higher set resistance resulted from a shorter pulse implies that incomplete crystallization states are formed after set programming. It can be seen from Figure 4a the resistance of the AST devices dramatically increased by two orders of magnitude at a reset voltage of around 4.1 V (at 50 ns).

Peridium of locules two-layered, outer layer composed of dark brown or brown thick-walled cells of textura angularis, inner layer composed

of hyaline thin-walled cells of textura angularis lining the locule. Pseudoparaphyses 2–4 μm wide, hyphae-like, septate. Asci 63–125 × 16–20 μm, 8–spored, bitunicate, fissitunicate, clavate, short pedicellate, apically rounded with a small ocular chamber. Ascospores 20–25 × 7–9 μm, biseriate, hyaline, aseptate, fusoid to ovoid, sometimes with tapered ends giving a spindle shaped appearance, smooth with granular contents. Conidiomata pycnidial in nature. Conidiogenous cells 6–20 × 2–5 μm, holoblastic, hyaline, subcylindrical, proliferating percurrently with 1–2 proliferations and periclinical thickening. Conidia (17-)18–20(−22) × 4–5 μm \( \left( ]# \times 4.8\,\upmu \mathrmm,\mathrmn f–i Asci. j–l Ascospores. m Ascospore with India ink showing learn more sheath.

Scale bars: a = 500 μm, b = 200 μm, c–e = 50 μm, f–i = 20 μm, j–m = 10 μm ≡ Physalospora agaves Henn., Bot. Jb. 34: 51 (1905) Hemibiotrophic or saprobic on leaves. Ascostromata 140–260 μm high (excluding the papilla), 600–880 μm diam, circular, blackened areas on host tissue, immersed to erumpent on host tissue, visible as minute black dots or papilla on host tissue, uni to multi loculate, gregarious, individually globose to subglobose. Ostiole circular, central, papillate. Locules 120–200 μm high, 140–250 μm diam. Peridium of locules up to 19–50 μm wide, comprising several layers of brown to dark brown walled cells of textura angularis, broader at the base. Pseudoparaphyses 3–5 μm wide, hyphae-like, aseptate, numerous. Asci 90.5–122 × 27–38 μm \( \left( \overline x = 105.5 \times 31\,\upmu \mathrmm,\mathrmn = 20 \right) \), 8–spored, bitunicate, fissitunicate, clavate to cylindro-clavate, short pedicellate, apically rounded with an ocular chamber (7–9 μm wide, n = 10). Ascospores 21–43× 8–12 μm \( \left( \overline x = 28 \times 10\,\upmu \mathrmm,\mathrmn = 30 \right) \), 2(−3) –seriate at the ascus apex, 1–seriate at the base, hyaline, aseptate, ellipsoidal, fusiform, or inequilateral, usually wider in the middle, wall rough, surrounded by a mucilaginous sheath. Asexual state not established.

We carried out an extensive selleck compound review of the English-language literature and found that there was little high-level evidence Pifithrin-�� manufacturer in this field, and no systematically described practical manual for the field. Most importantly, there are no standardized diagnostic criteria and therapeutic management guidelines for ASBO, therefore, we would like to establish standards for these items. The Bologna Guidelines include evidence-based

medicine and reflect the international consensus obtained through earnest discussions among professionals in the field on 1-3 July, 2010, at the Belmeloro Convention Center, Bologna, Italy. Notes on the use of the Guidelines The Guidelines are evidence-based, with the grade of recommendation also based on the evidence. The Guidelines present the diagnostic and therapeutic methods for optimal management and prevention of ASBO. The practice

Guidelines promulgated in this work do not represent a standard of practice. They are suggested plans of care, based on best available evidence and the consensus of experts, but they do not exclude other approaches as being within the standard of practice. For example, they should not be used to compel adherence to a given method of medical management, which method should be finally determined after taking account of the conditions at the relevant medical institution (staff levels, experience, equipment, etc.) Eltanexor research buy and the characteristics of the individual patient. However, responsibility for the results of treatment rests with those who are directly engaged therein, and not with the consensus group. Methods – Consensus Development In the Consensus Conference on July 2nd 2010, the expert panel had two meetings and a further plenary session. The aim was to focus and clarify the diagnostic and therapeutic issues of the complex management of ASBO, leading to new clinical guidelines, updated and including a wide range of recommendations, for diagnosis, non operative management, timing for surgery, type of surgery and prevention strategies of peritoneal post-operative adhesions causing small bowel obstruction. Based on the review of the current literature, Ergoloid a panel of worldwide experts were invited to participate

in the development of the new guidelines. All members of the expert panel were asked to define ASBO. For each step of diagnosis, treatment (conservative and surgical) and prevention of ASBO, one expert summarized the current state of the art. From the evidence based presentations and the reported statements as well as from the results of the relevant literature review, a preliminary document with the resume of the Consensus Statements and Recommendations was compiled. For every key statement, the discussion within the expert panel with the involvement of the audience, took place until a 100% consensus within the group and the audience was achieved. Comments from the audience were collected and partly included in the manuscript.

For example, 25(OH)D3 XAV-939 purchase levels are determined by sun exposure

and diet that may be affected by a range of factors including SEP and outdoor physical activity, which may confound relationships with bone outcomes. Although the association between 25(OH)D3 and endosteal adjusted for periosteal circumference was unaffected by adjusting for observed measurements Sepantronium clinical trial of these additional factors, unmeasured confounders may be important. For example, D2 intake is related to consumption of fruits and vegetables, which is positively associated with childhood BMD as measured by DXA [30]. In addition, fruit and vegetable intake is related to a ‘prudent’ or ‘healthy’ diet [31], of which intake in pregnancy is positively associated with BMD in subsequent childhood [19]. Limitations In terms of limitations of this study, our pQCT measurements comprised a single slice, namely, the 50% mid-tibia, which is unable to provide any information about trabecular bone. In the study of 171 girls aged 9–15 years described Protein Tyrosine Kinase inhibitor above, the relationship between baseline total 25(OH)D and subsequent gain in BMD across puberty was particularly strong at the lumbar spine [16] which is rich in trabecular bone. Whereas

the present study suggests that 25(OH)D status has minimal effects on cortical bone, it may be that stronger effects exist for trabecular bone which we were unable to evaluate here. A further Edoxaban limitation is the relatively long interval between measurement of 25(OH)D and measurement of cortical bone from pQCT scans, which may have reduced the strength of associations observed between these sets of parametres. Finally, the generalisability of our findings is limited by the fact that the subset of 3,579 subjects forming the basis of the present study is likely to differ in important ways from the original cohort drawn from the general population. For example, maternal social class in the subset on which this paper is based was higher compared with those who were not included (P = 0.0001).

In conclusion, we found that in contrast to 25(OH)D2, 25(OH)D3, as measured in childhood, was positively related to BMCC, cortical thickness and resistance to buckling as assessed 5 years later. These different associations suggest that supplementation with vitamin D3 in childhood is likely to prove more beneficial for subsequent cortical bone development compared to vitamin D2, presumably reflecting important differences between the actions of these two isoforms on bone, the basis of which is currently unclear. Interventional studies are justified in which effects of these two forms of vitamin D are directly compared in the same population, in order to test the conclusions from this observational study, given that we are unable to exclude confounding as a possible explanation for our findings.

AUC analysis also demonstrated a significantly greater sodium EPZ015938 manufacturer concentration for T2 compared to all other trials. Table 2 Plasma Lactate, Glucose, Osmolality and Electrolyte Response to Exercise Variable T2 T3 T4 T5   Time Point         Lactate (mmol·L-1) DHY 1.9 ± 0.6 1.9 ± 0.6 2.0 ± 0.6 1.7 ± 0.6   RHY 1.8 ± 0.5 2.1 ± 0.4 2.0 ± 0.5 2.1 ± 0.4   IP* 11.1 ± 2.3 11.9 ± 2.2 9.9 ± 4.2 11.7 ± 2.2 Glucose (mmol·L-1) BL 5.8 ± 1.2 5.8 ± 1.2 5.8 ± 1.2 5.8 ± 1.2   DHY 6.5 ± 1.8 6.4 ± 1.1

6.4 ± 1.4 5.7 ± 1.2   RHY 5.9 ± 1.7 6.2 ± 1.1 6.4 ± 0.9 5.6 ± 1.2   IP* 6.9 ± 1.6 8.6 ± 1.5 8.4 ± 1.9 7.4 ± 2.6 Osmolality (mOsm) BL 295 ± 4 295 ± 4 295 ± 4 295 ± 4   DHY 298 ± 5 298 ± 5 296 ± 4 298 ± 6   RHY 298 ± 6 293 ± 5 292 ± 4 294 ± 4   IP# 308 ± 5 299 ± 4 302 ± 5 303 ± 7 Potassium (mmol·L-1) BL 4.1 ± 0.4 4.1 ± 0.4 4.1 ± 0.4 4.1 ± 0.4   DHY 4.2 ± 0.9 4.0 ± 0.3 4.1 ± 0.3 4.0 ± 0.3   RHY 4.1 ± 0.2 4.3 ± 0.3 4.3 ± 0.6 4.1 ± 0.4   IP* 4.5 ± 0.7 4.5 ± 0.5 4.4 ± 0.4 4.5 ± 0.6 Sodium (mmol·L-1) BL 139.4 ± 1.1 139.4 ± 1.1 139.4 ± 1.1 139.4 ± 1.1   DHY* 141.7 ± 1.1 141.3 ± 1.6 141.1 ± 2.5 141.2 ± 1.4   RHY 141.5 ± Lazertinib 1.5@ 139.6 ± 1.9 138.7 ± 1.9 138.7 ± 1.6   IP# 144.0 ± 2.2@ 140.6 ± 1.8 140.7 ± 2.0 140.2 ± 1.3 * = Significant main Foretinib price effect compared

to all other time points. # = Significant main effect compared to BL and RHY. @ = significantly different than T3 – T5. BL = baseline; DHY = dehydration; RHY = rehydration; IP = immediate post-exercise. The ALD response to the experimental trials is presented in Figure 5. A significant main effect for time (p = 0.013) was observed. [ALD] at RHY and IP were significantly lower than that at BL and DHY (Figure 5). No other significant differences were noted and no significant interactions were observed. The plasma AVP responses are shown in Figure Amobarbital 6. A significant main effect for time (p = 0.000) was also observed. AVP

was significantly elevated at DHY (p = 0.000), RHY (p = 0.000) and IP (p = 0.000) compared to BL measures. In addition, AVP concentrations at DHY were significantly higher (p = 0.05) than IP across all trials. There were no significant differences between trials, and no significant interactions between time and trial. Figure 5 Serum Aldosterone Response. # = significant main effect for time between BL and DHY. Figure 6 Arginine Vasopressin. # = significant main effect for time BL versus DHY, RHY and IP.

Thus, general inhibitors of fungi and/or bacteria, selective inhibitors, and a selective fungal growth-promoting strain were chosen. HPLC analyses revealed great differences in substance production. For example, strains 29 and 30 exhibited comparable impacts on fungal growth, yet they differed greatly in the numbers of detected products

(10 vs. 2). The strain producing the most unreported metabolites, AcM29, was characterized by a complex Streptomyces-fungus interaction spectrum. AcM29 had a negative impact on A. muscaria, H. cylindrosporum and L. bicolor but did not inhibit plant pathogenic fungi. Streptomycetes and other tested Gram-positive bacteria were inhibited by AcM29, while Gram-negative bacteria were only slightly influenced. This suggests that in search for Streptomyces

strains producing putatively novel compounds, a preliminary PF-562271 purchase screen should not only target fungi and Gram-negative bacteria, but also the streptomycetes. find more Heterobasidion infects roots in particular by growing over root to root contacts [31], and the roots of their host trees are predominatly mycorrhizal [12]. Cycloheximide producing streptomycetes on the mycorrhizal roots could thus potentially affect root rot development. We observed that the addition of 1 nmol cycloheximide to the culture medium mimicked the impact of cycloheximide producer AcM11 to Heterobasidion NU7026 price species. Neither of the other compounds produced by AcM11 (antibiotic Acta 2930 B1, actiphenol and ferulic acid) affected the growth of H. abietinum

or H. annosum, Roflumilast indicating that cycloheximide is responsible for the observed growth inhibition by AcM11. The role of cycloheximide in the inhibition of Heterobasidion species is supported by our study with another cycloheximide producing streptomycete, Streptomyces sp. A230 from South Brazilian soil. Whereas H. abietinum is killed by A230, H. annosum still retains 30% of its growth rate. Interestingly, A230 not only produces cycloheximide, but also actiphenol, a combination also observed in AcM11 (S.D.S, N.H., A. Zander and L. Braun, unpublished). H. abietinum and H. annosum have been reported to be physiologically and taxonomically distinct species [31]. The data of Lehr et al. [21] indicate that the two species also respond differently to cycloheximide: the levels of gene expression by H. abietinum and H. annosum are highly distinct upon cycloheximide application. Long-term screening of streptomycetes shows that approximately 10% of Streptomyces isolated from soil produce cycloheximide (H.-P. Fiedler, unpublished). It would thus be expected that most fungi have developed resistance or at least tolerance against the antibiotic, since they supposedly regularly encounter cycloheximide producers in the rhizosphere. P. croceum and H.

The present study is the first direct, head-to-head comparison of vaccine formulations using three different adjuvants, BCG, MPL-TDM and cationic liposomes, with the same leishmanial antigen for their

efficacy against L. donovani challenge in BALB/c model. BCG and MPL were chosen as adjuvants in this study as they are human-compatible potent inducer of cell-mediated immunity. BCG, being almost the only adjuvant licensed for human use and effective against intracellular pathogen infections, was extensively used in clinical trials of vaccination against CL and VL [9]. Amongst the adjuvants recently approved for human vaccines is MPL, a potent stimulator of Th1 response, being evaluated in clinical trials against various diseases including malaria, tuberculosis and leishmaniasis [10]. Previous studies from our laboratory established that selleck cationic liposomes is a potent adjuvant as they have the ability to enhance

protective cell-mediated immune response against experimental VL [15–18]. Thus, cationic liposomes was selected to compare its efficacy with two other human-compatible adjuvants BCG and MPL to confer protection against L. donovani infection. Comparison of the vaccine potentiality of cationic liposomal formulation of LAg with BCG+LAg and MPL-TDM+LAg revealed that all the three vaccines afforded significant protection against challenge with L. donovani. However, Inhibitor Library cell line cationic liposome was the most potent of the three adjuvants and conferred protection superior to other two adjuvants. The ability of cationic liposomes to induce significant protection with LAg is entirely consistent with results of our previous studies in mice as well as hamster models of VL [15]. However, the level of Calpain protection afforded by this formulation was lower than mice immunized with SLA (soluble

leishmanial antigens) entrapped in these vesicles or LAg entrapped in neutral and cationic DSPC liposomes [16, 27, 29], suggesting entrapment of more immunogenic antigens or optimization of liposomal formulation could influence the efficacy of cationic liposomes. Cationic liposomes was also shown to be a potent adjuvant to enhance immune response against CL [30]. BCG is the most widely used adjuvant in clinical vaccine trials against leishmaniasis including VL. Although the vaccines were found to be safe and immunogenic, the efficacy was not carried over to a protective effect [31, 32]. Reports on the ability of BCG-vaccine to protect against leishmaniasis even in experimental models vary from effective [33, 34] to partial protection [35, 36]. MPL-SE (stable Selumetinib emulsion) has been found to be safe and efficacious against cutaneous and mucosal leishmaniasis in mice, non-human primates and humans when vaccinated with Leishmania-derived recombinant polyprotein Leish-111f or its component proteins [37–39].

The cells were surface stained with anti-CD3+ and anti-CD4+ antibodies or anti-CD3+ and anti-CD8+ and analyzed by flow cytometry (P < 0.001). Immunofluorescence analysis and histological changes in the livers of recipient mice Immunofluoresence analysis of the liver sections of the transgenic mice showed infiltration of high number of the CFSE labeled cells, when they received transfer from immunized mice (Figure 9a). H&E staining of the liver sections for the same group of recipient mice showed infiltration of lymphocytes beside

the histological changes, AZD6244 such as steatosis, due to the expression of transgenes (Figure 9b). Interestingly, the infiltrated cells were concentrated in the areas where there was steatosis. On the other hand, the transgenic mice receiving cells from non-immunized donors showed few CFSE labeled cells on the liver sections and no cell infiltration was observed in the H&E stained liver section (Figure 10a, b). The non-transgenic mice showed no histological changes and no infiltration of CFSE labeled cells, whether they received donor cells from immunized (Figure 9c,

d) or non-immunized mice (Figure 10c, d). Thus, repetitive transfer of splenocytes from HCV immunized mice into HCV transgenic mice may be needed in order to increase inflammation in the liver. Figure 9 Histological alterations in livers Fosbretabulin research buy from transgenic and non-transgenic mice injected with CFSE-labeled splenocytes from immunized mice. A) Immunofluorescent analysis of frozen liver sections (5 μm thick) of a transgenic mouse showing CFSE labeled cells scattered over all the liver section. The fluorescent cells are selleck indicated by arrows. B) H&E stained liver section of transgenic mouse showing steatosis. There is infiltration

of lymphocytes in the liver which is concentrated close to hepatic steatosis (indicated by arrows). C) Immunofluorescence analysis of frozen liver sections (5 μm thick) of non-transgenic mouse showing no Megestrol Acetate CFSE labeled cells over the liver section. D) H&E staining of liver section of non-transgenic mouse showing normal histology of the liver and no lymphocyte infiltration. Scale bar = 50 μm. Figure 10 Histological alterations in livers from transgenic and non-transgenic mice injected with CFSE-labeled splenocytes from non-immunized mice. A) Immunofluorescent analysis of frozen liver sections (5 μm thick) of a transgenic mouse showing few CFSE labeled cells scattered over all the liver section. B) H&E stained liver section of transgenic mouse showing steatosis. There is no infiltration of lymphocytes in the liver. C) Immunofluorescence analysis of frozen liver sections (5 μm thick) of non-transgenic mouse showing no CFSE labeled cells over the liver section. D) H&E staining of liver sections of non-transgenic mouse showing normal histology of the liver and no lymphocyte infiltration. Scale bar = 50 μm.