Performance of calves born in different periods of the calving season in intensive beef cattle farming / [Desempenho em pecuária de corte intensiva de progênies nascidas em diferentes períodos da estação de parição]

The objective of this study was to evaluate, for two years, the performance of 124 female and 105 male Braford calves born during the first and second halves of the same calving season and the effects of birth period on the development of males until slaughter, as yearlings, and of females until calving, after having mated at 13-15 months of age. Early-born females were heavier than those born late at weaning (119.3 vs 109.9kg; P<0.05), at the start of the breeding season (275.0 vs 263.0kg; P<0.05), and at the end of the breeding season (300.0 vs 289.5kg; P<0.05), in addition to being more fertile (70 vs 50% pregnancy rate). There was no difference (P>0.05) in the development of males born early in relation to those born late, except for weaning weight, which was higher in the former. Steers born early were ready for slaughter at a younger age (459.6 vs 490.1 days; P<0.05), and both groups (early- and late-born) had a body condition classified as fat (4.21 points). In intensive production systems, both male and female calves perform better if they are born during the first half of the calving season.(AU)

O objetivo deste estudo foi avaliar, por dois anos, o desempenho de 124 bezerras e 105 bezerros Braford nascidos durante a primeira e segunda metades da mesma estação, bem como os efeitos do período de nascimento no desenvolvimento dos machos até o abate e das fêmeas até o primeiro parto, após serem acasalados entre 13/15 meses de idade. As fêmeas nascidas precocemente foram mais pesadas do que as nascidas tardiamente ao desmame quando bezerras (119,3 vs. 109,9kg; P<0,05), no início da estação reprodutiva (275,0 vs. 263,0kg; P<0,05) e no final da estação reprodutiva (300,0 vs. 289,5kg; P<0,05), além de terem maior fertilidade (taxa de prenhez 70 vs. 50%). Não houve diferença (P>0,05) no desenvolvimento de bezerros nascidos precocemente em relação aos nascidos mais tardiamente, exceto no peso ao desmame, com superioridade dos primeiros. Os novilhos nascidos mais cedo ficaram prontos para o abate à idade mais jovem (459,6 vs. 490,1 dias; P<0,05), e ambos os grupos (nascidos precoce e tardiamente) tinham uma condição corporal classificada como gordura (4,21 pontos). Em sistemas de produção intensiva, os bezerros machos e fêmeas nascidos precocemente, na primeira metade da estação de parição, possuem melhor desempenho.(AU)

18F-FDG PET/CT images defined the true extent of a urothelial bladder carcinoma.

A patient was referred, after neoadjuvant chemotherapy, for pre-surgical evaluation of urothelial bladder carcinoma (single lesion). Two thickenings in the left ureter wall identified on the CT scan were equivocal for malignancy. 18F-FDG PET/CT with delayed pelvic images, hyperhydration, and furosemide showed hypermetabolic ureteral metastases and multifocal bladder tumors. There were no lymph nodes or distant metastases. These 18F-FDG PET/CT findings completely altered the surgical treatment. The patient underwent left nephroureterectomy, radical cystoprostatectomy, and lymphadenectomy, followed by a urinary transit reconstruction. Histopathology confirmed multifocal high-grade urothelial carcinoma in the bladder walls and left ureter and benign lymph nodes.

Desempenho de bezerras de corte em pastagem de azevém recebendo farelo de arroz com ou sem monensina / Beef heifers performance in ryegrass pasture supplemented with rice bran with or without monensin

Foi estudado o desempenho de bezerras de corte em pastagem de azevém (Lolium multiflorum Lam.), com animais exclusivamente em pastejo ou recebendo farelo de arroz integral (FAI) em nível de 0,8% do peso corporal, associado ou não à monensina. O método de pastejo foi contínuo com número variável de animais. O delineamento experimental foi o inteiramente ao acaso, com medidas repetidas no tempo, com três tratamentos e três repetições de área. O uso de FAI associado ou não à monensina não expressou alteração na área pélvica das bezerras, na taxa de lotação e no ganho de peso por área. As bezerras que receberam FAI, com ou sem monensina, apresentaram maior ganho diário de peso corporal, peso corporal, escore de condição corporal e relação peso corporal:altura. O fornecimento de suplementação energética para bezerras de corte é uma alternativa viável em sistemas de produção que visam à redução da idade ao primeiro acasalamento.(AU)

The experiment was carried out with the objective of evaluating beef cattle heifer performance when exclusively grazing Italian ryegrass (Lolium multiflorum Lam.) pasture or supplemented with whole rice bran (WRB), equivalent to 0.8% of body weight, associated or not with monensin. The grazing method was "put-and-take" stocking, in a completely randomized experimental design, with replicated measures over time, with three treatments and three replications of area. The use of WRB, associated or not with monensin, did not affect heifers' pelvic area, stocking rate and area weight gain. Animals fed WRB, with or without monensin, showed greater average daily gain, body weight, body condition score, and body weight:height ratio. Energetic supplementation for beef heifers is one viable option in production systems seeking age reduction at the first mating.(AU)

Recommendations on breast cancer screening and prevention in the context of implementing risk stratification: impending changes to current policies.

In recent years, risk stratification has sparked interest as an innovative approach to disease screening and prevention. The approach effectively personalizes individual risk, opening the way to screening and prevention interventions that are adapted to subpopulations. The international perspective project, which is developing risk stratification for breast cancer, aims to support the integration of its screening approach into clinical practice through comprehensive tool-building. Policies and guidelines for risk stratification-unlike those for population screening programs, which are currently well regulated-are still under development. Indeed, the development of guidelines for risk stratification reflects the translational aspects of perspective. Here, we describe the risk stratification process that was devised in the context of perspective, and we then explain the consensus-based method used to develop recommendations for breast cancer screening and prevention in a risk-stratification approach. Lastly, we discuss how the recommendations might affect current screening policies.

Padrões de deslocamento de bezerras de corte que receberam suplementos isolipídicos em pastagem de azevém / Displacement patterns of beef heifers receiving iso lipidic supplements on ryegrass pasture

Foram avaliados o uso de estações alimentares, o deslocamento e a taxa de bocado de bezerras de corte que foram mantidas exclusivamente em pastagem de azevém (Lolium multiflorum Lam.) ou receberam suplementos (grão de milho ou gordura). O método de pastejo foi contínuo, com número variável de animais. O delineamento experimental foi inteiramente ao acaso, com medidas repetidas no tempo. O número de bocados realizados por estação alimentar é similar quando as bezerras recebem suplemento ou não. As equações de predição mostram que a massa de lâminas foliares exerce maior influência no tempo por estação alimentar quando as bezerras permanecem exclusivamente em pastejo de azevém ou recebem grão de milho como suplemento, enquanto para bezerras que recebem gordura, essa variável é influenciada pela oferta de forragem. O deslocamento (passos entre estações e passos por minuto) de bezerras exclusivamente em pastejo e que recebem grão de milho é influenciado pela estrutura e qualidade do pasto. A taxa de bocado dos animais suplementados com grão de milho e gordura é influenciada pela proporção de lâminas foliares no dossel. Equações de regressão múltipla, considerando-se os atributos do pasto e da pastagem, podem ser utilizadas como modelos preditores do uso de estações alimentares, deslocamento e taxa de bocado de bezerras de corte...

The use of feeding stations, displacement patterns and bite rate of beef heifers kept exclusively on Italian ryegrass (Lolium multiflorum Lam) or receiving supplements (corn grain or fat) were evaluated. The grazing method was continuous with a variable number of animals. The experimental design was a completely randomized design with repeated time measures. The number of bites per feeding station is similar when heifers receive supplement or not. The prediction equations show that the mass of leaf lamina has greater influence on the time per feeding station when heifers remain exclusively grazing ryegrass or receive corn grain as a supplement, while for calves that receive fat this variable is influenced by forage allowance. The displacement (steps between stations and steps per minute) of heifers exclusively on ryegrass or receiving corn grain is influenced by the structure and quality of grass. The bite rate of heifers supplemented with corn grain and fat is influenced by the proportion of leaf lamina in the sward. Multiple regression equations considering the attributes of grass and pasture can be used as models to predict the use of feeding stations, displacement and bite rate of beef heifers...

Canine trypanosomiasis: etiology of infection and implications for public health

Canine trypanosomiasis, caused by protozoans of the genus Trypanosoma, is divided into two primary types: the American form (Chagas disease), due to Trypanosoma cruzi infection, and the African form (sleeping sickness or surra), provoked by Trypanosomaevansi. This disease was originally enzootic and affected only wild animals, including mammals and birds, which served as reservoirs. Later, it spread to domestic animals such as horses, cattle and dogs. The disease became a zoonosis when contact between rural inhabitants and natural Trypanosoma foci occurred, due to ecological imbalances and increasing migration. Dogs are significantly involved in this context, because they are the main domestic animals and participate in the transmission and maintenance cycles of these parasites. This article reports etiological, epidemiological and public health aspects of canine trypanosomiasis, and the most important peculiarities of this zoonosis in dogs.

Further mapping of the Idd5.1 locus for autoimmune diabetes in NOD mice.

The Idd5 locus for autoimmune diabetes in nonobese diabetic (NOD) mice has been mapped to the proximal half of chromosome 1 and appears to include two loci, Idd5.1 and Idd5.2, Idd5.1 being a candidate homolog of the human IDDM12 locus. Using new recombinant congenic lines, we have reduced the Idd5.1 interval to 5 cM at most, between D1Mit279 and D1Mit19 (not included). This interval now excludes the Casp8 and Cflar (Flip) candidate genes. It still retains Cd28 and Ctla4 and also includes Icos (inducible costimulator). The previously reported differential expression of Ctla4, which is induced at a lower level in NOD than in B6-activated T-cells, was found independent of Idd5.1 itself because Ctla4 expression was induced at a low level in T-cells from Idd5.1-congenic mice. The Idd5.1 locus protected against both spontaneous and cyclophosphamide-induced diabetes, but it did not prevent inflammatory infiltration of the islets of Langerhans. Furthermore, diabetogenic precursor spleen cells from prediabetic NOD and Idd5.1-congenic mice were equally capable of transferring diabetes to immunodeficient NOD.scid/scid recipient mice. The Idd5.1 locus might affect a late event of disease development, subsequent to the onset of insulitis and possibly taking place in the islets of Langerhans.

N-terminus cleavage of bcl-2 by a novel cellular non-ICE cysteine proteinase.

The bcl-2 protein plays an essential role in preventing cell death. Its activity is regulated through association with bcl-2 homologous and nonhomologous proteins and also by serine phosphorylation. We now report that bcl-2 can be proteolytically cleaved towards its N-terminus by a cysteine proteinase present in RL-7 lymphoma cell lysates, yielding a major product of apparent MW 20 kDa, different from the products of bcl-2 cleavage by HIV protease. Moreover, bcl-2 proteins mutated for Asp residues at positions 31 and 34 were efficiently cleaved by RL-7 cell lysates, indicating that this proteolytic activity is distinct from the caspase-3 that cleaves bcl-2 at Asp 34. This bcl-2 cleaving activity is inhibited by E-64 and is therefore distinct from the proteinases of the ICE/Ced-3 family (caspases), whereas reciprocally, ICE (caspase-1) is unable to cleave bcl-2. It is optimally active at pH 5, a feature distinguishing it from calpain, another non-ICE cysteine proteinase which has been associated with apoptosis. This novel bcl-2 cleaving protease, although constitutively present in RL-7 cells and resting peripheral blood lymphocytes (PBL) was upregulated following induction of apoptosis in RL-7 cells or mitogen activation in PBL. The N-terminus of bcl-2 which contains the BH4 domain that binds the kinase Raf-1 and the phosphatase calcineurin is essential for anti-apoptotic activity. Its cleavage might provide a novel post-translational mechanism for regulating bcl-2 function and could amplify ongoing programmed cell death.

Resistance of T-cells to apoptosis in autoimmune diabetic (NOD) mice is increased early in life and is associated with dysregulated expression of Bcl-x.

Activated lymphocytes of autoimmune non-obese diabetic (NOD) mice exhibit an increased resistance to programmed cell death (PCD) following withdrawal of interleukin-2 (IL-2). In the present study, we found that resistance of NOD T lymphocytes to PCD was increased as early as 1 week of age, hence several weeks before the invasion of the pancreas by inflammatory cells, which is compatible with a role of the NOD apoptotic phenotype in the autoimmune susceptibility of this strain. In the thymus, mature single positive but not double positive or double negative thymocytes were more resistant to PCD in NOD compared to B6 mice. Moreover, in both NOD and B6 mice, CD4+ T cells were more resistant to PCD induced by IL-2 deprivation than CD8+ cells. As a result, NOD CD4+ T cells were remarkably resistant to cell death induced in this manner. In relation with this increased resistance to apoptosis, expression of the anti-apoptotic Bcl-x protein was upregulated in activated T cells of NOD mice, most notably after 24 h of IL-2 deprivation. These results should help us to understand the relationship of the NOD apoptotic phenotype to the emergence of the NOD mouse autoimmune disease.

Defective Fc gamma RII gene expression in macrophages of NOD mice: genetic linkage with up-regulation of IgG1 and IgG2b in serum.

A quantitative trait locus for increased IgG serum levels in the NOD mouse strain was mapped to distal chromosome 1, close to the fcgr2 locus encoding the low-affinity type II receptor for the Fc portion of IgG (Fc gamma RII). Expression of membrane-inserted (b2) and soluble (b3) isoforms of Fc gamma RII was strongly decreased in macrophages of NOD compared with C57BL/6 (B6) mice. In contrast, B cell-specific (Fc gamma RIIb1) isoform was only slightly decreased and Fc gamma RIII was not altered. This Fc gamma RII regulatory defect was cis-encoded by fcgr2 or by a closely linked locus, occurred at the mRNA level, and was associated with multiple mutations in the fcgr2 gene promoter. In relation with this defect, binding of IgG1- and IgG2b- but not IgG2a-opsonized RBC by macrophages of NOD and congenic B6.NOD-fcgr2 mice was severely impaired, but was normal in macrophages of NOD.B6-fcgr2 congenic mice, indicating that Fc gamma RII plays a nondispensable role in binding of IgG1 and IgG2b isotypes. Likewise, serum levels of IgG1 and IgG2b but not IgG2a were up-regulated in NOD compared with NOD.B6-fcgr2 congenic mice. These findings indicate that macrophage Fc gamma RII may regulate serum IgG1 and IgG2b through their catabolism, and validate the NOD strain as a model to investigate the functions of Fc gamma RII isoforms.

Genetic analysis of immune dysfunction in non-obese diabetic (NOD) mice: mapping of a susceptibility locus close to the Bcl-2 gene correlates with increased resistance of NOD T cells to apoptosis induction.

The non-obese diabetic (NOD) mouse strain provides a remarkable model for investigating the mechanisms of autoimmunity. Independent genetic analyses of this model have previously shown that chromosome 1-linked loci were involved in the control of periinsulitis and sialitis on the one hand and of insulitis and diabetes on the other hand. In the present work, analysis of a [NOD x (NOD x C57BL/6)F1] backcross progeny allowed us to clearly dissociate two genetic regions: one was associated with periinsulitis and mapped to the middle region of chromosome 1, in the vicinity of the Bcl-2 gene; the other was associated with insulitis and mapped to the proximal part of the chromosome. Three intermediate markers D1Mit18, D1Mit5 and D1Mit19 covering at least 25 centiMorgans between these two regions, were associated with neither periinsulitis nor insulitis. The role of the Bcl-2-linked region in the immune anomalies of NOD mice was further investigated in a (NOD x C57BL/6)F2 cross where the Bcl-2nod haplotype was linked to elevated serum levels of IgG (p < 0.0005). The middle region of chromosome 1 is, therefore, involved in the control of three phenotypes, including periinsulitis, sialitis and hyperIgG, pointing to Bcl-2 as a good candidate for a cause of the NOD mouse disease. Consistent with the anti-apoptotic function of the Bcl-2 gene product, activated T lymphocytes from NOD mice showed a markedly increased resistance to induction of apoptosis following deprivation of interleukin-2 when compared to those from non-autoimmune strains. After the recent observation of the Fas gene alterations in the lpr and lprcg mutations, these findings indicate that deregulation of lymphoid cell apoptosis may be a general pathogenetic mechanism in autoimmune diseases.

Identification and mapping to chromosome 1 of a susceptibility locus for periinsulitis in non-obese diabetic mice.

Insulin-dependent diabetes mellitus (IDDM) is a polygenic disease caused by autoimmune destruction of insulin-producing beta cells in the islets of Langerhans. Its onset is preceded by a long and variable period in which lymphoid cells infiltrate the pancreas but first remain outside the islets (peri-insulitis) before invading them (insulitis). Among susceptibility loci, only the major histocompatibility complex (MHC) has been clearly assigned. Genetic study of the nonobese diabetic (NOD) mouse model for insulin-dependent diabetes mellitus has revealed genetic linkage of insulitis and of early onset diabetes with two non-MHC loci mapping to chromosome 3 and 11 respectively. Here we report a close association of periinsulitis with a third non-MHC locus mapping to chromosome 1. Successive stages in the progression of diabetic disease thus appear to be controlled by distinct genes or sets of genes.

[Identification and localization on chromosome 1 of a gene controlling the occurrence of periinsulitis in NOD diabetic mice]. / Identification et localisation sur le chromosome 1 d'un gène contrôlant la survenue de la périinsulite chez la souris diabétique NOD.

Diabetic NOD (Non Obese Diabetic) mice show early pancreatic infiltration of mononuclear cells around Langerhans islets (periinsulitis). Study of (NOD x C57BL/6) F1 and F2 mice reveals that periinsulitis is constantly associated with a similar infiltration of salivary glands (sialitis) and is controlled by a dominant susceptibility locus. Segregation analysis of periinsulitis and microsatellite DNA markers indicates that the gene controlling periinsulitis maps to chromosome 1, close to the Bcl-2 locus.

Glucocorticoids modulate vascular reactivity in the rat.

To clarify the role of endogenous glucocorticoids in the regulation of blood pressure, the cardiovascular effects of RU 486, a steroid derivative with antiglucocorticoid properties, were investigated in Wistar rats. Pressor responses to angiotensin II (Ang II), norepinephrine, and vasopressin were studied in normal conscious rats before and after administration of RU 486. At 20 mg/kg/day, RU 486 significantly blunted pressor responses to Ang II and norepinephrine, whereas those to vasopressin were not greatly affected. At a lower dose, RU 486 did not alter pressor responses; at a higher dose, it augmented them, probably through its agonistic glucocorticoid effect. At 20 mg/kg/day, RU 486 antagonized the enhancing effect of a glucocorticoid agonist on pressor responses to Ang II, norepinephrine, and vasopressin. Cardiac output and renal blood flow were measured in anesthetized rats by the microsphere method. RU 486 at 20 mg/kg/day did not alter basal cardiac output and renal blood flow. RU 486 pretreatment attenuated pressor responses to Ang II and norepinephrine but did not alter cardiac output. It significantly blunted the decrease in renal blood flow and the increase in renal vascular resistance induced by Ang II. In rats fed a low sodium diet (where the pressor systems are stimulated), administration of RU 486 (20 mg/kg/day for 5 days) decreased total peripheral vascular resistance by 29% and mean blood pressure by 20 mm Hg. This effect was unrelated to any antimineralocorticoid activity of the compound, as shown by unchanged urinary sodium excretion, sodium balance, and plasma renin concentration. In contrast, it was due to the antiglucocorticoid activity, as shown by restoration of mean blood pressure by corticosterone, the major glucocorticoid in rats. Renal vascular resistance decreased during RU 486 administration in anesthetized (-25%) and unanesthetized (-19%) rats. Glomerular filtration rate, estimated from inulin clearance in conscious rats, did not change significantly. In conclusion, the present results suggest that endogenous glucocorticoids increase vascular reactivity and therefore contribute to blood pressure regulation. They also participate in the control of renal hemodynamics. This effect is most apparent in salt-restricted rats. The vascular action of glucocorticoids was unmasked by the administration of the antiglucocorticoid compound RU 486.

[Role of glucocorticoids in the regulation of blood pressure]. / Rôle des glucocorticoïdes dans la régulation de la pression artérielle.

Glucocorticoids contribute to the regulation of blood pressure: glucocorticoid excess produces hypertension, and glucocorticoid deficiency is accompanied by low blood pressure. The role of endogenous glucocorticoids has been assessed in animals by using an antiglucocorticoid derivative, RU 486. It has been shown that glucocorticoids enhance vascular reactivity to angiotensin II and norepinephrine. They participate in the maintenance of blood pressure, most particularly in animals on low sodium intake where pressor systems are stimulated and vascular sensitivity has to be preserved. The exact mode of action of glucocorticoids is still debated.

[The role of glucocorticoids in the cardiovascular adaptation to sodium restriction in the rat]. / Rôle des glucocorticoïdes dans l'adaptation cardiovasculaire à la restriction sodée chez le rat.

The role of glucocorticoids (Gs) in the regulation of blood pressure has been examined using an antiglucocorticoid, RU 486, at a dose of 20 mg.kg-1 day-1 X 5 days, in male Wistar rats on a low sodium diet. In unanesthetized and chronically catheterized rats, RU 486 administration decreases mean blood pressure (MBP) by approximately 14 mmHg, without altering growth rate or urinary sodium excretion. Corticosterone administration (1 mg.kg-1 day-1) restores MBP nearly to basal level. Glomerular filtration rate evaluated from inulin clearance is unchanged whereas PAH clearance increases and filtration fraction decreases slightly. In anesthetized rats, RU 486 pretreatment decreases MBP, increases cardiac output (radiolabelled microsphere method), and depresses total and renal vascular resistance. In conclusion, endogenous Gs contribute to blood pressure control in salt-restricted rats, possibly by increasing vascular reactivity to catecholamines and angiotensin.

Effects of gluco- and antiglucocorticoids on renal and aortic prostaglandin synthesis.

The effects of glucocorticoid agonists RU 26988 (G) and dexamethasone (D) and antagonist RU 486 (AG) on aortic and renal prostaglandin (PG) production were studied in Wistar rats. Blood pressure increased in rats administered G (20 mg X kg-1 X day-1) during 1 or 3 days; such increase was prevented by AG (100 mg X kg-1 X day-1). Renal papillary PGE2 release was increased after a 3-day administration of G, and this was prevented by AG. Neither G nor AG altered basal 6-keto-PGF1 alpha aortic production. However, G inhibited and AG magnified the stimulatory effect of ionophore A 23187, added in vitro, on 6-keto-PGF1 alpha production; AG reversed G inhibition. In addition, AG alone (20 mg X kg-1 X day-1 X 3 days) enhanced the stimulatory effect of angiotensin II (10(-8) M), added in vitro, on 6-keto-PGF1 alpha release. In vitro studies were performed on renomedullary interstitial cells grown in culture; G and D depressed PGE2 production in a dose-dependent manner; AG at equimolar 10(-8) M concentration inhibited this effect. In conclusion, AG inhibits the effects of G on blood pressure and PG synthesis. G exerts strong depressor activity on in vitro PGE2 renal production, whereas in vivo effects are more complex. Endogenous G inhibits aortic prostacyclin production, an action unmasked by AG administration. Diminished stimulation of vascular prostacyclin synthesis may contribute to vascular hyperreactivity in G-induced hypertension.