Effects of different levels of zinc on the performance and immunocompetence of broilers under heat stress.

Male broilers were used to evaluate the effect of zinc on performance and immune competence during heat stress (HS). Broilers raised in either a thermoneutral (TN, 23.9 degrees C constant) or HS (23.9 to 35 degrees C cycling) environment were fed a low zinc diet (LZ; 34 mg/kg), an adequate zinc diet (AZ; 68 mg/kg), or a supplemental zinc diet (HZ; 181 mg/kg). Humoral immunity was assessed by intravenous injection of 7% SRBC followed by evaluation of serum for antibody titers in primary and secondary responses. Cell-mediated immunity was assessed using a Sephadex stimulation method to recruit abdominal exudate cells (AEC) to evaluate macrophage phagocytic ability. The HS birds consumed 12.5% less feed, gained 24.6% less weight, and had lower feed efficiency when compared to TN birds. Dietary zinc levels did not impact growth performance or plasma zinc concentration. Numbers of AEC, macrophages in AEC, phagocytic macrophages, and internalized opsonized and unopsonized SRBC were increased by HZ. Total, IgM, and IgG antibody titers for primary and secondary responses were significantly increased in birds receiving HZ under TN conditions. Tibia zinc concentration increased with increasing zinc levels but did not change with temperature. Lymphoid organ weights, primary and secondary antibody responses, incidences of macrophages in AEC, phagocytic ability of macrophages, and plasma zinc concentration were all significantly reduced by HS. These results indicate that the immune response of broilers can be influenced by the level of zinc in the diet and by environmental conditions.

Brain amino acid concentrations and Ca2+-dependent release in intractable depression assessed antemortem.

The concentrations of 3 putative neurotransmitters (glutamate, aspartate and gamma-aminobutyrate), 4 related amino acids and 5 non-transmitter-related amino acids have been measured in neurosurgical samples (frontal cortex) from patients with intractable depression and controls. In addition, the glutamate receptor agonist 2-amino-4-sulpho-butanoic acid (homocysteic acid) has been identified in human brain and measured in these samples. There were no changes in the concentrations of amino acids in depressed patients compared to control with the exception of aspartic and homocysteic acids which were elevated in a sub-group of patients with depression compared to control. The Ca2+-dependent release (K+-stimulated) of putative neurotransmitters has been demonstrated for the first time from brain tissue of depressed patients. Glutamate release was unaltered from the control value. Aspartate values showed unexplained variability but it's release and that of gamma-aminobutyrate were elevated in some depressed subjects. These results do not support the hypothesis of reduced amino acid function in depressive illness.

Amino acid levels in depression: a preliminary investigation.

Plasma, cerebrospinal fluid and brain tissue amino acid levels were measured in 14 patients with affective illness and generally confirm previous findings. There was no correlation between these values and age, sex, family history and levels of anxiety. GABA levels measured in cortex tissue were negatively correlated with depressive mood (P less than 0.05), supporting a possible involvement of GABA in depressive illness.