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Physical exercise has been described as an important tool in the prevention and treatment of numerous diseases as it promotes a range of responses and adaptations in several biological systems, including the immune system. Studies on the effect of exercise on the immune system could play a critical role in improving public health. Current literature suggests that moderate intensity exercise can modulate the Th1/Th2 dichotomy directing the immune system to a Th1 cellular immune response, which favors the resolution of infections caused by intracellular microorganisms. Leishmaniasis is a group of diseases presenting a wide spectrum of clinical manifestations that range from self-limiting lesions to visceral injuries whose severity can lead to death. The etiological agents responsible for this group of diseases are protozoa of the genus Leishmania. Infections by the parasite Leishmania major in mice (Balb/c) provide a prototype model for the polarization of CD4+ T cell responses of both Th1 (resistance) or Th2 (susceptibility), which determines the progression of infections. The aim of this study was to evaluate the effect of exercise on the development of L. major experimental infections by scanning the pattern of immune response caused by exercise. Groups of Balb/c mice infected with L. major were divided into groups that preformed a physical exercise of swimming three times a week or were sedentary along with treatment or not with the reference drug, meglumine antimoniate. Animals in groups submitted to physical exercise did not appear to develop lesions and presented a significantly lower parasite load independent of drug treatment. They also showed a positive delayed hypersensitivity response to a specific Leishmania antigen compared to control animals. The IFN-γ/IL-4 and IFN-γ/IL10 ratios in trained animals were clearly tilted to a Th1 response in lymph node cells. These data suggest that moderate intensity exercise is able to modulate the Th1 response that provides a protective effect against the development of leishmanial lesions.

To demonstrate the usefulness of complementary next-generation sequencing (NGS) and immunohistochemistry (IHC) counting, we analyzed 196 patients with non-small cell lung cancer who underwent surgical resection and adjuvant chemotherapy. Formalin-fixed, paraffin-embedded samples of adenocarcinoma (ADC), squamous cell carcinoma, and large cell carcinoma were used to prepare tissue microarrays and were examined by protein H-score IHC image analysis and NGS for oncogenes and proto-oncogenes and genes of tumor suppressors, immune checkpoints, epithelial-mesenchymal transition factors, tyrosine kinase receptors, and vascular endothelial growth factors. In patients with brain metastases, primary tumors expressed lower PIK3CA protein levels. Overexpression of p53 and a higher PD-L1 protein H-score were detected in patients who underwent surgical treatment followed by chemotherapy as compared with those who underwent only surgical treatment The absence of brain metastases was associated with wild-type sequences of genes EGFR, CD267, CTLA-4, and ZEB1. The combination of protein overexpression according to IHC and mutation according to NGS was rare (ie, represented by a very low percentage of concordant cases), except for p53 and vascular endothelial growth factor. Our data suggest that protein levels detected by IHC may be a useful complementary tool when mutations are not detected by NGS and also support the idea to expand this approach beyond ADC to include squamous cell carcinoma and even large cell carcinoma, particularly for patients with unusual clinical characteristics. Conversely, well-pronounced immunogenotypic features seemed to predict the clinical outcome after univariate and multivariate analyses. Patients with a solid ADC subtype and mutated genes EGFR, CTLA4, PDCD1LG2, or ZEB1 complemented with PD-L1 or p53 protein lower expression that only underwent surgical treatment who develop brain metastases may have the worst prognosis., (Copyright © 2018 Elsevier Inc. All rights reserved.)

Behind each eye of the chicken resides a unique lymph tissue, the Harderian gland, for which RNA sequencing (RNA-seq) analysis is novel. We characterized the response of this tissue to Newcastle disease virus (NDV) in two inbred lines with different susceptibility to NDV across three time points. Three-week-old relatively resistant (Fayoumi) and relatively susceptible (Leghorn) birds were inoculated with a high-titered (10 7 EID 50 ) La Sota strain of NDV via an oculonasal route. At 2, 6, and 10 days post infection (dpi) Harderian glands were collected and analyzed via RNA-seq. The Fayoumi had significantly more detectable viral transcripts in the Harderian gland at 2 dpi than the Leghorn, but cleared the virus by 6 dpi. At all three time points, few genes were declared differentially expressed (DE) between the challenged and nonchallenged birds, except for the Leghorns at 6 dpi, and these DE genes were predicted to activate an adaptive immune response. Relative to the Leghorn, the Fayoumi was predicted to activate more immune pathways in both challenged and nonchallenged birds suggesting a more elevated immune system in the Fayoumis under homeostatic conditions. Overall, this study helped characterize the function of this important tissue and its response to NDV.

Enhancing genetic resistance of chickens to Newcastle Disease Virus (NDV) provides a promising way to improve poultry health, and to alleviate poverty and food insecurity in developing countries. In this study, two inbred chicken lines with different responses to NDV, Fayoumi and Leghorn, were challenged with LaSota NDV strain at 21 days of age. Through transcriptome analysis, gene expression in spleen at 2 and 6 days post-inoculation was compared between NDV-infected and control groups, as well as between chicken lines. At a false discovery rate <0.05, Fayoumi chickens, which are relatively more resistant to NDV, showed fewer differentially expressed genes (DEGs) than Leghorn chickens. Several interferon-stimulated genes were identified as important DEGs regulating immune response to NDV in chicken. Pathways predicted by IPA analysis, such as "EIF-signaling", "actin cytoskeleton organization nitric oxide production" and "coagulation system" may contribute to resistance to NDV in Fayoumi chickens. The identified DEGs and predicted pathways may contribute to differential responses to NDV between the two chicken lines and provide potential targets for breeding chickens that are more resistant to NDV.

Background: Inflammatory cytokines and acute phase proteins increase with aging, promoting a chronic low-grade inflammation. Studies have shown a positive effect of exercise on inflammatory markers in older persons. Interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), and C-reactive protein (CRP) are the main biomarkers investigated. However, it is unclear if exercise could decrease all these biomarkers., Purpose: The aim was to analyze the effect of chronic exercise on IL-6, TNF-α, and CRP levels in older persons., Methods: Preferred Reporting Items in Systematic Reviews and Meta-analyses guidelines were adopted. Original articles that investigated the effect of chronic exercise on inflammatory profile of the elderly persons were eligible for this review. The databases PubMed, PEDro, EBSCO, and BioMed Central were searched. Three reviewers evaluated each publication for reducing bias. Data about IL-6, TNF-α, and CRP were collected and analyzed. A standardized mean difference based on estimated pooled effect size was calculated considering heterogeneity index (I 2 ) and random effect., Results: Seventy-six studies were retrieved from databases, and 8 of them were analyzed. IL-6 and CRP levels decreased after chronic exercise (overall effect P < .05)., Conclusion: Regular exercise decreases IL-6 and CRP levels in older persons. The effect of exercise on TNF-α remains unclear.

Inhibitors of DNA binding/inhibitors of differentiation (Id) protein family have been shown to be involved in carcinogenesis. However, the roles of Id during lung adenocarcinoma (ADC) progression remain unclear. Eighty-eight ADC samples were evaluated for Id-1,2,3 level and angiogenesis (CD 34 and VEGF microvessel density) by immunohistochemistry and morphometry. The impact of these markers was tested on follow-up until death or recurrence. A significant difference between tumor and normal tissue was found for Id-1,2,3 expression (P < 0.01). In addition, high levels of nuclear Id-1 were associated with higher angiogenesis in the tumor stroma (P < 0.01). Equally significant was the association between patients in T1-stage and low cytoplasmic Id-2, as well as patients in stage-IIb and low Id-3. High cytoplasm Id-3 expression was also directly associated to lymph nodes metastasis (P = 0.05). Patients at stages I to III, with low Id-1 and Id-3 cytoplasm histoscores showed significant long metastasis-free survival time than those with high Id-1 or Id-3 expression (P = 0.04). Furthermore, high MVD-CD34 and MVD-VEGF expression were associated with short recurrence-free survival compared to low MVD-CD34 and MVD-VEGF expressions (P = 0.04). Cox model analyses controlled for age, lymph node metastasis, and adjuvant treatments showed that nuclear Id-1, cytoplasmic Id-3, and MVD-CD34 were significantly associated with survival time. Median score for nuclear Id-1 and cytoplasmic Id-3 divided patients in two groups, being that those with increased Id-1 and Id-3 presented higher risk of death. Ids showed an independent prognostic value in patients with lung ADC, regardless of disease stage. Id-1 and Id-3 should be considered new target candidates in the development of personalized therapy in lung ADC., (© 2016 by the Society for Experimental Biology and Medicine.)

In the ligand channel of the cytochrome c oxidase from Rhodobacter sphaeroides (Rs aa3 ) W172 and F282 have been proposed to generate a constriction that may slow ligand access to and from the active site. To explore this issue, the tryptophan and phenylalanine residues in Rs aa3 were mutated to the less bulky tyrosine and threonine residues, respectively, which occupy these sites in Thermus thermophilus (Tt) ba3 cytochrome oxidase. The CO photolysis and recombination dynamics of the reduced wild-type Rs aa3 and the W172Y/F282T mutant were investigated using time-resolved optical absorption spectroscopy. The spectral changes associated with the multiple processes are attributed to different conformers. The major CO recombination process (44 μs) in the W172Y/F282T mutant is ~500 times faster than the predominant CO recombination process in the wild-type enzyme (~23 ms). Classical dynamic simulations of the wild-type enzyme and double mutant showed significant structural changes at the active site in the mutant, including movement of the heme a3 ring-D propionate toward CuB and reduced binuclear center cavity volume. These structural changes effectively close the ligand exit pathway from the binuclear center, providing a basis for the faster CO recombination in the double mutant., (© 2016 The American Society of Photobiology.)

The intracellular protozoa Leishmania spp. and Trypanosoma cruzi and the causative agents of Leishmaniasis and Chagas disease, respectively, belong to the Trypanosomatidae family. Together, these two neglected tropical diseases affect approximately 25 million people worldwide. Whether the host can control the infection or develops disease depends on the complex interaction between parasite and host. Parasite surface and secreted molecules are involved in triggering specific signaling pathways essential for parasite entry and intracellular survival. The recognition of the parasite antigens by host immune cells generates a specific immune response. Leishmania spp. and T. cruzi have a multifaceted repertoire of strategies to evade or subvert the immune system by interfering with a range of signal transduction pathways in host cells, which causes the inhibition of the protective response and contributes to their persistence in the host. The current therapeutic strategies in leishmaniasis and trypanosomiasis are very limited. Efficacy is variable, toxicity is high, and the emergence of resistance is increasingly common. In this review, we discuss the molecular basis of the host-parasite interaction of Leishmania and Trypanosoma cruzi infection and their mechanisms of subverting the immune response and how this knowledge can be used as a tool for the development of new drugs.

Our earlier study revealed that STRA6 (stimulated by retinoic acid gene 6) was up-regulated within 3 h of TCR stimulation. STRA6 is the high-affinity receptor for plasma retinol-binding protein (RBP) and mediates cellular vitamin A uptake. We generated STRA6 knockout (KO) mice to assess whether such up-regulation was critical for T-cell activation, differentiation and function. STRA6 KO mice under vitamin A sufficient conditions were fertile without apparent anomalies upon visual inspection. The size, cellularity and lymphocyte subpopulations of STRA6 KO thymus and spleen were comparable to those of their wild type (WT) controls. KO and WT T cells were similar in terms of TCR-stimulated proliferation in vitro and homeostatic expansion in vivo. Naive KO CD4 cells differentiated in vitro into Th1, Th2, Th17 as well as regulatory T cells in an analogous manner as their WT counterparts. In vivo experiments revealed that anti-viral immune responses to lymphocytic choriomeningitis virus in KO mice were comparable to those of WT controls. We also demonstrated that STRA6 KO and WT mice had similar glucose tolerance. Total vitamin A levels are dramatically lower in the eyes of KO mice as compared to those of WT mice, but the levels in other organs were not significantly affected after STRA6 deletion under vitamin A sufficient conditions, indicating that the eye is the mouse organ most sensitive to the loss of STRA6. Our results demonstrate that 1) in vitamin A sufficiency, the deletion of STRA6 in T cells does no affect the T-cell immune responses so-far tested, including those depend on STAT5 signaling; 2) STRA6-independent vitamin A uptake compensated the lack of STRA6 in lymphoid organs under vitamin A sufficient conditions in mice; 3) STRA6 is critical for vitamin A uptake in the eyes even in vitamin A sufficiency.

Biofilms of microbial cells encased in an exopolymeric matrix can form on solid surfaces, but how bacteria sense a solid surface and upregulate biofilm genes is largely unknown. We investigated the role of the Bacillus subtilis signal peptidase, SipW, which has a unique role in forming biofilms on a solid surface and is not required at an air-liquid interface. Surprisingly, we found that the signal peptidase activity of SipW was not required for solid-surface biofilms. Furthermore, a SipW mutant protein was constructed that lacks the ability to form a solid-surface biofilm but still retains signal peptidase activity. Through genetic and gene expression tests, the non-signal peptidase role of SipW was found to activate biofilm matrix genes specifically when cells were on a solid surface. These data provide the first evidence that a signal peptidase is bifunctional and that SipW has a regulatory role in addition to its role as a signal peptidase.

Leishmaniasis is a neglected tropical disease with no effective vaccines. Actin, microtubules and the actin-based molecular motor myosin Va were investigated for their involvement in Leishmania braziliensis macrophage interactions. Results showed a decrease in the association index when macrophages were without F-actin or microtubules regardless of the activation state of the macrophage. In the absence of F-actin, the production of NO in non-activated cells increased, while in activated cells, the production of NO was reduced independent of parasites. The opposite effect of an increased NO production was observed in the absence of microtubules. In activated cells, the loss of cytoskeletal components inhibited the release of IL-10 during parasite interactions. The production of IL-10 also decreased in the absence of actin or microtubules in non-activated macrophages. Only the disruption of actin altered the production of TNF-α in activated macrophages. The expression of myosin Va tail resulted in an acute decrease in the association index between transfected macrophages and L. braziliensis promastigotes. These data reveal the importance of F-actin, microtubules, and myosin-Va suggesting that modulation of the cytoskeleton may be a mechanism used by L. braziliensis to overcome the natural responses of macrophages to establish infections.

Erythropoietin-producing hepatocellular kinases (Eph kinases) constitute the largest family of cell membrane receptor tyrosine kinases, and their ligand ephrins are also cell surface molecules. Because of promiscuous interaction between Ephs and ephrins, there is considerable redundancy in this system, reflecting the essential roles of these molecules in the biological system through evolution. In this study, both Efnb1 and Efnb2 were null-mutated in the T cell compartment of mice through loxP-mediated gene deletion. Mice with this double conditional mutation (double KO mice) showed reduced thymus and spleen size and cellularity. There was a significant decrease in the DN4, double positive, and single positive thymocyte subpopulations and mature CD4 and CD8 cells in the periphery. dKO thymocytes and peripheral T cells failed to compete with their WT counterparts in irradiated recipients, and the T cells showed compromised ability of homeostatic expansion. dKO naive T cells were inferior in differentiating into Th1 and Th17 effectors in vitro. The dKO mice showed diminished immune response against LCMV infection. Mechanistic studies revealed that IL-6 signaling in dKO T cells was compromised, in terms of abated induction of STAT3 phosphorylation upon IL-6 stimulation. This defect likely contributed to the observed in vitro and in vivo phenotype in dKO mice. This study revealed novel roles of Efnb1 and Efnb2 in T cell development and function.

A questionnaire assessing the satisfaction of children with their hospital stay has been developed and tested with 136 children (aged 6-12 years) at 2 Swiss hospital sites. Three out of 4 children were satisfied overall with their hospital stay. Their relationships with the professional medical staff, explanations they received, games they played, and environment, all received positive evaluations. The most critical points were pain, fear, and the absence of relatives. Ninety percent of the children appreciated that their opinions were sought. These results reinforce the importance of having questionnaires available for the children to consider their opinions to enhance the quality of care.

The tick Rhipicephalus (Boophilus) microplus is a hematophagous ectoparasite that causes considerable economic losses to cattle breeding. Although R. microplus saliva contains several molecules that interfere with the blood coagulation process, so far the systemic alterations in the host hemostatic system have not been described. This study aims to determine if R. microplus infestation induces any disturbance to the host's hemostatic system. To address these questions, six calves were experimentally infested with 20,000 R. microplus larvae and their blood was collected before and 7, 14 and 21 days post-infestation. Collagen and ADP-induced platelet aggregation as well as coagulation (activated partial thromboplastin time and prothrombin time) decreased in infested bovines. Platelet blood count and fibrinogen increased during the course of infestation, probably as a compensatory response. These alterations may play a role in host health status, and show that the host cannot fully counteract the tick anti-hemostatic mechanisms.

In the thymus, 2 types of Lin-Sca-1+ (lineage-negative stem cell antigen-1-positive) progenitors can generate T-lineage cells: c-Kit(hi) interleukin-7 receptor alpha-negative (c-Kit(hi)IL-7Ralpha-) and c-Kit(lo)IL-7Ralpha+. While c-Kit(hi)IL-7Ralpha- progenitors are absent, c-Kit(lo)IL-7Ralpha+ progenitors are abundant in the lymph nodes (LNs). c-Kit(lo)IL-7Ralpha+ progenitors undergo abortive T-cell commitment in the LNs and become arrested in the G1 phase of the cell cycle because they fail both to up-regulate c-myb, c-myc, and cyclin D2 and to repress junB, p16(INK4a), and p21(Cip1/WAF). As a result, development of LN c-Kit(lo)IL-7Ralpha+ progenitors is blocked at an intermediate CD44+CD25lo development stage in vivo, and LN-derived progenitors fail to generate mature T cells when cultured with OP9-DL1 stromal cells. LN stroma can provide key signals for T-cell development including IL-7, Kit ligand, and Delta-like-1 but lacks Wnt4 and Wnt7b transcripts. LN c-Kit(lo)IL-7Ralpha+ progenitors are able to generate mature T cells when cultured with stromal cells producing wingless-related MMTV integration site 4 (Wnt4) or upon in vivo exposure to oncostatin M whose signaling pathway intersects with Wnt. Thus, supplying Wnt signals to c-Kit(lo)IL-7Ralpha+ progenitors may be sufficient to transform the LN into a primary T-lymphoid organ. These data provide unique insights into the essence of a primary T-lymphoid organ and into how a cryptic extrathymic T-cell development pathway can be amplified.

The human-specific p35 isoform of the invariant chain (Ii) includes an R-X-R endoplasmic reticulum (ER) retention motif that is inactivated upon HLA-DR binding. Although the masking is assumed to involve the cytoplasmic tails of class II molecules, the mechanism underlying this function remains to be investigated. Moreover, in light of the polymorphic nature of the class II cytosolic tails, little is known about the capacity of various isotypes or alleles to overcome the retention signal of Iip35. To gain further insights into these issues, we first addressed the proposed role of the HLA-DR cytoplasmic tails. As shown by flow cytometry, the presence of Iip35 in transfected HeLa cells prevented surface expression of HLA-DR molecules lacking their cytoplasmic tails (DRalphaTM/betaTM). These truncated class II molecules and Iip35 accumulated in the ER, and co-localized with calnexin, as determined by confocal microscopy. Sensitivity of DRalphaTM/betaTM to endoglycosidase H treatment confirmed that these molecules do not reach the trans-Golgi network when associated with Iip35. Further characterization revealed that the beta chain cytosolic tail is critical for efficient ER egress of class II/Iip35 complexes. Interestingly, our results clearly demonstrate for the first time that DP and DQ isotypes can also overcome the retention motif of Iip35 through a mechanism involving their very distinctive polymorphic beta chain cytoplasmic tails. Altogether, these results further dissect the masking of di-basic retention signals, and emphasize the interplay between class II molecules and Ii for the transport of the complex to the endocytic pathway.

TWEAK is a new TNF family member with proinflammatory and proliferative effects on different cell types, mediated by the recently identified Fn14 receptor. TWEAK expression was analyzed on mouse microglial cells and astrocytes. Both cell types express TWEAK mRNA. Astrocytes expressed Fn14 and proliferated in the presence of rTWEAK. TWEAK mRNA is expressed in normal CNS and its steady state level increases in spinal cord during EAE. Finally, EAE severity is enhanced in soluble TWEAK-overexpressing transgenic mice. These results support the contention that TWEAK is involved in CNS inflammation.

Separation between primary and secondary lymphoid organs is a universal feature in jawed vertebrates. Strikingly, oncostatin M (OM)-transgenic mice present massive extrathymic T cell development, localized exclusively in the lymph nodes (LN). According to the prevailing paradigm, the thymus is the main source of T lymphocytes in gnathostomes mainly because thymic epithelial cells have a unique ability to support early steps in T cell development. It is therefore remarkable that productive T cell development occurs in the OM(+) LN, despite the absence of epithelial cells. The present study shows that in the OM(+) LN: 1) MHC class I expression strictly on hemopoietic cells is sufficient to support the development of a diversified repertoire of CD8 T cells; 2) the efficiency of positive selection of specific TCR-transgenic T cells is not the same as in the thymus; 3) negative selection is very effective, despite the lack of an organized thymic-like medulla. Furthermore, our data suggest that extrathymic T lymphocytes developing in the OM(+) LN undergo extensive postselection expansion because they live in the microenvironment in which they were positively selected. This work illustrates how the division of labor between primary and secondary lymphoid organs influences the repertoire and homeostasis of T lymphocytes.

Patients with short bowel syndrome (SBS) receiving total parenteral nutrition (TPN) have a high incidence of catheter-related sepsis, one of its major complications. The aim of this study was to correlate the length of remaining small bowel (RSB) with septic episodes related to the central venous catheter in a group of patients with severe SBS with home TPN. The length of the RSB (<50 cm or > or = 50 cm) was related to the frequency of catheter sepsis, time until the first episode, and the agents responsible in eight SBS patients receiving home TPN. There were 13 episodes of catheter infection (0.88 per patient-year). The group with a shorter RSB length (five patients) presented 1.3 to 2.76 infections/year and 2 to 9 months until the first episode, compared to 0 to 0.75 infections/ year (p = 0.0357) and 11 to 65 months until the first episode (p = 0.0332) in the group with the longer RSB. In the first group, the agents isolated were Enterobacteriae (Enterobacter sp., Klebsiella sp., Pseudomonas sp., and Proteus sp.) in eight episodes and Candida sp. in one. In the latter sepsis was caused by Staphylococcus sp. in three episodes and Pseudomonas sp. in one. Therefore patients with remaining small bowel shorter than 50 cm have a higher frequency of catheter-related sepsis, particularly by enteric microorganisms. This might be an evidence of the occurrence of bacterial translocation and its role in the pathogenesis of catheter-related sepsis in patients with an extremely short RSB receiving home TPN.

Enteral nutrition (EN) and total parenteral nutrition (TPN) may provide life-sustaining therapy for surgical patients. The duration of nutritional therapy (enteral or parenteral) implies distinct access routes. We review the main aspects related to access routes for nutrient delivery. The enteral route, whenever feasible, is preferred. For EN lasting less than 6 weeks, nasoenteric tubes are the route of choice. Conversely, enterostomy tubes should be used for longer-term enteral feeding and can be placed surgically or with fluoroscopic and endoscopic assistance. The first choice for patients who will not be submitted to laparotomy is percutaneous endoscopic gastrostomy. Postpyloric access, although not consensual, must be considered when there is a high risk of aspiration. For intravenous delivery of nutrients lasting less than 10 days, the peripheral route can be used. However, because of frequent infusion phlebitis, its role is still in discussion. Central venous catheters (CVCs) for TPN delivery may be (1) nonimplantable, percutaneous, nontunneled-used for a few days to 3 to 4 weeks; (2) partially implantable, percutaneous, tunneled-used for longer periods and permanent access; or (3) totally implantable subcutaneous ports-also used for long-term or permanent access. The subclavian vein is usually the insertion site of choice for central venous catheters. Implantable ports are associated with lower rates of septic complications than percutaneous CVCs. The catheter with the least number of necessary lumens should be applied. Central venous nutrient delivery can also be accomplished through peripherally inserted central catheters, which avoid insertion-related risks.

Surgical trauma induces complex physiologic changes that lead to catabolism and loss of body cell mass. This reaction is usually mild but can be exacerbated by previous malnutrition and postoperative complications. To avoid severe metabolic distress, nutritional therapy may be prescribed, using the enteral route whenever possible. Postoperative total parenteral nutrition (TPN) is indicated for patients already receiving TPN preoperatively, those severely malnourished prior to major surgery, those unable to eat satisfactorily for 7 days, or patients presenting with severe complications. Postoperative TPN should last for at least 7 days. The total energy requirements are between 30 and 35 kcal/kg/day. About 50% to 70% should be provided in the form of carbohydrates, and 20% to 30% in the form of lipids. The optimal input rates for glucose and lipids are 4 to 5 g/kg/day and 80 mg/kg/hr, respectively. The ideal nitrogen administration is 250 to 300 mg/kg/day, and the optimal calorie/nitrogen ratio is 150 to 200. Some specific amino acids can be added as intravenous dipeptides. An adequate follow-up must include clinical and biochemical parameters. Several trials evaluated the impact of TPN in postoperative patients, but further well designed, controlled clinical trials are still necessary to address a great number of unanswered questions.

Attempts to reproduce inflammatory colitis have created many experimental models. Since the pioneer work of Morris et al. (1989), trinitrobenzenosulfonic (TNBS) solutions have been used with different dosages. The aims of this work were standardize the induction of colitis, evaluate the clinical and intestinal effects of different doses and verify the reproducibility of the intestinal inflammatory process. Wistar rats were inoculated endo rectally with 2.5 ml solutions of different concentrations of TNBS and ethanol, and the rats were sacrificed after 14 days. According to the solution concentrations of TNBS (mg) and ethanol (%), six groups of animals were established: Control (saline), 30 mg/30%, 30 mg/40%, 30 mg/50%, 50 mg/10% and 50 mg/30%. Statistical analysis of food ingestion showed no differences between groups (p = 0.247). The 30/50 group presented greater weight loss when compared to 50/10 and 50/30 groups (p = 0.012). Groups 30/50 and 30/40 showed greater degrees of macroscopic lesion than control and 50/10 group (p < 0.05). Histologic lesion was not uniform to all rats regardless of the solution employed. Group 50/10 presented the less severe histologic alterations; on the other hand, 30/40 and 30/50 groups had important changes on mucosal thickness, on vascularization and ulceration. The authors conclude that experimental colitis with TNBS 1) cause intestinal lesions that are not uniform to all animals, although they may be reproduced in many of them; 2) with the same doses of TNBS, the increase in ethanol concentrations leads to a greater inflammatory process, intestinal thickness, vascularization, abscess formation and intestinal ulceration; 3) 50/10 and 50/30 solutions make less severe lesions when compared to 30/40 and 30/50 solutions; 4) 30/50 solution was the best one, as it produces inflammation 90% of the animals, increases in wall thickness in 50%, abscess in 70% and ulceration in 38%.

Selenium concentration was measured in paired maternal blood samples and fetal liver specimens collected at a San Joaquin County, Calif, slaughterhouse (beef = 19, dairy = 54) and from bovine aborted fetuses submitted to the California Veterinary Diagnostic Laboratory System (CVDLS; beef = 20, dairy = 20). Of the slaughterhouse samples and specimens, dairy maternal blood selenium concentration was significantly (P < 0.001) higher (mean +/- SD; 0.22 +/- 0.056 microgram/ml) than that for beef breeds (0.137 +/- 0.082 microgram/ml). The CVDLS mean maternal blood selenium concentration for the dairy-breed samples (0.192 +/- 0.028 microgram/ml) was similar to that for the slaughterhouse dairy-breed samples, but was greater than that for the slaughterhouse beef-breed samples. Slaughterhouse mean fetal liver selenium content also was higher (P < 0.001) for the dairy breeds (0.777 +/- 0.408 microgram/g), compared with the beef breeds (0.443 +/- 0.038 microgram/g). Mean fetal liver selenium content for slaughterhouse specimens was higher (P < 0.002) than that for the CVDLS specimens (beef, 0.244 +/- 0.149 microgram/g; dairy, 0.390 +/- 0.165 microgram/g). At the CVDLS, dairy fetal liver content was greater (P < 0.001) than that for beef breeds. Mean ratio of fetal liver selenium content to maternal blood selenium concentration was 3.53 +/- 1.89 for dairy breeds at the slaughterhouse (liver-to-blood correlation [r] = 0.38), and was 2.11 +/- 1.00 for dairy breeds at the CVDLS (r = 0.31) and 3.43 +/- 1.50 for beef breeds (r = 0.58). Both slaughterhouse breed ratios were significantly (P < 0.002) greater than the CVDLS dairy-breed ratio. On the basis of these results, breed and source location should be taken into account when interpreting selenium values. Fetal liver selenium content should only be used as a screening test and combined with whole blood selenium concentration from clinically normal herdmates to evaluate herd selenium status.