55 research outputs found
Respostas reprodutivas e metabólicas de ovelhas alimentadas com bagaço de caju desidratado, durante o pós-parto
Effect of mating management and PMSG dose on lambing outcome in ewes bred in late anoestrus
Causes of declining fertility in dairy cows during the warm season
In the Northern Hemisphere, from June to September and in the Southern Hemisphere from December to March, there are periods of reduced fertility (sub-fertility) in dairy cows that are described as summer infertility. Several factors contribute to sub-fertility during this time, such as ambient temperature, humidity and photoperiod. During the warm season there is a reduction in feed intake that may compromise the energy balance of the cow and/or induce an imbalance in the activity of the hypothalamo-hypophyseal-ovarian axis. These factors reduce the reproductive performance of the cow and compromise the quality of oocytes, embryos and corpora lutea. This paper reviews current knowledge on the metabolic and endocrine mechanisms that induce summer infertility and describe their effects on follicle, oocyte and embryo development in dairy cows
Untersuchungen über das Auftreten der Guignardia-Blatträune der Roßkastanie (Aesculus hippocastanum) in Westdeutschland und ihren Erreger
Follicular helper T-cells and virus-specific antibody response in primary and reactivated human cytomegalovirus infections of the immunocompetent and immunocompromised transplant patients
Analysis of human cytomegalovirus (HCMV) primary infection in immunocompetent (n=40) and immunocompromised transplant patients (n=20) revealed that the median peak antibody titre neutralizing infection of epithelial cells was 16-fold higher in immunocompromised patients. The mechanism of this finding was investigated by measuring: (i) HCMV DNAemia; (ii) HCMV neutralizing antibodies; (iii) ELISA IgG antibody titre to HCMV glycoprotein complexes gHgLpUL128L, gHgLgO and gB; and (iv) HCMV-specific (IFN-gamma(+)) CD4(+) and CD8(+) T-cells. Circulating CXCR5(+) CD4+ (memory T follicular helper - T-FH-cells) were identified as activated TFH (ICOS+PD-1(++)CCR7(lo)) and quiescent cells. In the early stages of primary infection, activated TFH cells increased in number. Concomitantly, both neutralizing and IgG antibodies to HCMV glycoproteins reached a peak, followed by a plateau. A stop in antibody rise occurred upon appearance of HCMV-specific CD4(+) T-cells, HCMV clearance and progressive reduction in activated TFH cells. The main differences between healthy and transplant patients were that the latter had a delayed DNA peak, a much higher DNA load and delayed activated TFH cells and antibody peaks. Similar events were observed in clinically severe HCMV reactivations of transplant patients. A preliminary analysis of the specificity of the activated TFH cell response to viral proteins showed a major response to the pentamer gHgLpUL128L and gB. In conclusion, in the absence of T-cell immunity, one of the first lines of defence, during primary infection, is conferred by antibodies produced through the interaction of TFH cells and B-cells of germinal centres, resulting in differentiation of B-cells into antibody producing plasma cells
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