Lactate concentration, body weight and meat quality in nelore cattle feedlot finished

The objective of this study was to determine blood lactate concentration during the finishing period and after slaughter and to verify its influence on body weight and meat quality traits of Nellore bulls feedlot finished. Ninety Nellore males were used, with a mean initial body weight of 390 ± 37 kg and age of 24 months. Lactate concentration in the blood was measured by spectrophotometry on days 1 (Lac01), 14 (Lac14), 27 (Lac27) and 69 (Lac69) of the feedlot period and immediately after slaughter (Lac96). Fresh meat samples were collected from the Longissimus thoracis muscle for determination of luminosity (L *), red (a *) and yellow (b *) intensity, shear force and pH of unaged meat and aged for seven days. Lactate concentrations were analyzed by the PROC MIXED of the SAS program, considering in the model the effects of pen and day of blood samples collection. Simple correlations between the studied variables were estimated using the procedure CORR of the program SAS. The lactate was stable during the confinement period, with mean values equal to 4.83 ± 0.30 mMol/L; 5.68 ± 0.29 mMol/L; 5.03 ± 0.29 mMol/L and 4.15 ± 0.31 mMol/L for Lac01, Lac14, Lac21 and Lac69, respectively. The highest mean lactate concentration was obtained on the day of slaughter (Lac96: 10.77 ± 0.27 mMol/L). Significant association was detected between a * and b * color parameters of the unaged meat and the lactate concentration at the day of slaughter (Lac96). There is no association between blood lactate concentration at the day of slaughter and body weight of Nellore animals feedlot finished. Blood lactate concentration on the day of slaughter is associated with the coloring of the meat and is independent of other measures of meat quality in Nellore animals feedlot finished

Ontogeny of kainate receptor gene expression in the developing rat midbrain and striatum

Kainate (KA) receptors are a family of ionotropic glutamate receptors, which mediate the excitatory synaptic transmission in various areas of the mammalian CNS. We have studied the expression pattern of the genes encoding for KA receptor subunits (Glur5-1, Glur5-2, Glur6, Glur7, KA1 and KA2) in rat prenatal (E), postnatal and adult ventral mesencephalon (MES) and striatum (STR) and in fetal midbrain primary cultures. Each receptor subunit shows a unique area- and temporal-expression pattern. In MES the onset of both Glur5 subunits is delayed when compared to the other subunits. In addition, most of the transcripts for KA subunits gradually increase during embryonic development and show a slight decrease during the first postnatal week. Differently, Glur6 and KA2 mRNAs show a sharp increase at E14.5 and decrease thereafter, reaching the lowest levels during late embryonic and postnatal development. In the STR, the gene expression of all KA subunit mRNAs is higher during embryonic development than after birth, except KA1 transcripts, that show a peak at P5. In embryonic MES primary cultures, Glur5-2, Glur6 and KA2 mRNAs are higher at the beginning of the culture when compared to older cultures, while the other subunit mRNAs do not show significant variation throughout the days in vitro. Thus, all the KA receptor subunit transcripts appear independently regulated during MES and STR development, probably contributing to the establishment of the fine tuning of the excitatory circuits reciprocally established between these CNS areas. © 2002 Elsevier Science B.V. All rights reserved

Expanding the clinical and neuroradiologic phenotype of primary microcephaly due to ASPM mutations

OBJECTIVE: To determine the spectrum of clinical, neuropsychological, and neuroradiologic features in patients with autosomal recessive primary microcephaly (MCPH) due to ASPM gene mutations. METHODS: ASPM was sequenced in 52 unrelated MCPH probands. In patients with ASPM mutations, we evaluated the clinical phenotype, cognition, behavior, brain MRI, and family. RESULTS: We found homozygous or compound heterozygous ASPM loss-of-function mutations in 11 (22%) probands and 5 siblings. The probands harbored 18 different mutations, of which 16 were new. Microcephaly was severe after 1 year of age in all 16 patients, although in 4 patients the occipital-frontal circumference (OFC) at birth was decreased by only 2 SD. The OFC Z score consistently decreased after birth. Late-onset seizures occurred in 3 patients and significant pyramidal tract involvement in 1 patient. Intellectual quotients ranged from borderline-normal to severe mental retardation. Mild motor delay was noted in 7/16 patients. Language development was delayed in all patients older than 3 years. Brain MRI (n = 12) showed a simplified gyral pattern in 9 patients and several malformations including ventricle enlargement (n = 7), partial corpus callosum agenesis (n = 3), mild cerebellar hypoplasia (n = 1), focal cortical dysplasia (n = 1), and unilateral polymicrogyria (n = 1). Non-neurologic abnormalities consisted of short stature (n = 1), idiopathic premature puberty (n = 1), and renal dysplasia (n = 1). CONCLUSIONS: We provide a detailed description of features associated with ASPM mutations. Borderline microcephaly at birth, borderline-normal intellectual efficiency, and brain malformations can occur in ASPM-related primary hereditary microcephal