The objective of this field trial was to evaluate effects of a single administration of 2.2 mg/kg of body weight (BW) of flunixin meglumine (FM) in addition to a systemic antibiotic treatment in cows with acute puerperal metritis (APM). Outcome variables tested were proportion of cows with a fever, prevalence of chronic endometritis 18 to 22 and 32 to 35 d in milk (DIM), and reproductive performance measures in the current lactation. In addition, serum concentrations of haptoglobin and fibrinogen were analyzed. Daily milk yield within 6 d after the first treatment was recorded. Cows were examined 4 to 5 DIM by rectal palpation and vaginoscopy, and rectal temperature was measured. Fetid vulvar discharge and a body temperature > or = 39.5 degrees C were signs of APM. Cows with APM were treated in the reference group with 1.0 mg/kg of BW of ceftiofur on 3 to 5 consecutive days (CEF, n = 119). In the study group, cows received the same antibiotic treatment as in CEF and 2.2 mg/kg of BW of FM on treatment d 1 (CEF + FM, n = 119). Blood samples were collected 4, 6, and 10 DIM and analyzed for concentrations of haptoglobin and fibrinogen. A group of cows without APM remained untreated and served as controls (n = 9). There were no significant differences between CEF and CEF + FM in the proportion of cows with fever 1 d after the first treatment (33.6 vs. 46.2%), milk yield per milking 10 DIM (7.5 +/- 0.3 vs. 7.6 +/- 0.3 kg in primiparous, 9.6 +/- 0.4 vs. 10.6 +/- 0.4 kg in multiparous cows), prevalence of chronic endometritis 32 to 35 DIM (64.3 vs. 52.2%), and in reproductive performance (31.5 vs. 34.3% conception to first AI, 58.0 vs. 54.6% pregnancy rate, 107.8 +/- 36.9 vs. 101.6 +/- 41.4 d open). Compared with the control, CEF and CEF + FM had significantly greater concentrations of haptoglobin (1.1 +/- 0.28 vs. 1.9 +/- 0.06 and 1.8 +/- 0.07 mg/mL at 4 DIM; 0.3 +/- 0.15 vs. 1.1 +/- 0.06 and 1.2 +/- 0.07 mg/mL at 10 DIM) and fibrinogen (2.2 +/- 0.17 vs. 3.9 +/- 0.14 and 3.7 +/- 0.13 g/L at 4 DIM; 1.9 +/- 0.1 vs. 2.6 +/- 0.1 and 3.0 +/- 0.13 g/L, respectively, at 10 DIM) on all test days. The additional treatment with FM had no effect on these acute phase proteins. In conclusion, the single administration of 2.2 mg/kg of BW of FM in addition to a systemic antibiotic treatment of cows having APM did not result in beneficial effects on clinical cure, milk yield within 6 d after the first treatment, or reproductive performance.

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By the year 2050, the world’s elderly population may increase exponentially, raising the rate of disease characteristic of this group, such as prostate cancer (PCa) and benign prostatic hyperplasia (BPH). Prostate disorders have a multifactorial etiology, especially age and genetic factors. Currently, PCa is the second most frequent neoplasm in the male population worldwide. The fibromodulin gene encodes a small leucine-rich proteoglycan (SLRP) which acts in the collagen fibrillogenesis pathway, cell adhesion, and modulation of TGF-β signaling pathways, which has been recently associated with PCa. The present study sequenced the coding region of the FMOD in a sample of 44 PCa, 90 BPH, and 82 controls from a Brazilian population, and the results identified 6 variants: 2 missenses (p.(Tyr42Ser) and p.(Pro24Ala)); 3 synonymous (p.(His253=), p.(Asn353=), and p.(Glu79=)); and 1 intronic (c.980-114A>G). Of these, p.(Tyr42Ser), p.(Pro24Ala), and p.(Asn353=) are rare variants, and p.(Tyr42Ser) was predicted as potential pathogenic by the algorithms used here, in addition to not being observed in controls, suggesting that may be a potential biomarker for development of PCa and BPH. In conclusion, we identified for the first time, in Brazilian individuals with PCa and BPH, a potentially pathogenic variant in the analysis of FMOD gene. Further studies are needed to investigate the deleterious effect of this variant on the structure and/or function of the FMOD protein.

Background: Regular physical activity has an important role in energy expenditure and combats the development of obesity. During exercise, PPARGC1A is overexpressed, stimulating an increase of the expression of FNDC5. This protein is cleaved to release the hormone irisin, which activates a browning process in white adipose tissue through an increase in UCP1 expression. As a result, irisin leads to mitochondrial heat production and energy expenditure. Objectives: The aim of this study was to investigate whether genetic variants in genes related to browning are associated with severe obesity and obesity-related features. This case-control study comprised 210 individuals with severe obesity (median body mass index [BMI] 45.6 [range 40.5-52.2]) and 191 normal-weight subjects ). Methods: Genomic DNA was extracted from peripheral blood and the genotypes of the PPARGC1A (rs8192678, rs3736265, rs2970847, and rs3755863) and UCP1 (rs6536991 and rs12502572) genes were obtained using Taqman ® assay. For the FNDC5 gene, screening of exons 3-5 as well as their intron-exon boundaries was performed using automatic sequencing. Results: Our results demonstrated that PPARGC1A rs2970847 and UCP1 rs12502572 are associated with severe obesity. Furthermore, these polymorphisms influence anthropometric traits, such as BMI, body weight, and body adiposity index. Our findings also showed a dose-effect relationship between PPARGC1A rs8192678 and fasting plasma glucose. Finally, 5 rare mutations were identified in FNDC5, and 1 of these is a novel missense mutation. Conclusion: This study shows that genetic variants in the activation of brown-like adipocyte pathway play an important role in the susceptibility to severe obesity.

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