ESTIMATION OF CHANGES IN THE AVAILABILITY OF EACH INDIVIDUAL ESSENTIAL AMINO ACID IN FOOD PROTEINS

A technique has been developed for determining decreases in the availability of individual essential amino acids in a food as a result of processing, cooking or other treatments. Diets containing casein and free L-amino acids were used to establish critical dietary amino acid levels. These critical levels were such that reductions of 20% in the level of any of nine essential amino acids significantly reduced protein utilization as estimated by rat bioassays. When these critical levels were used in evaluating amino acid availability in unheated and heated lactalbumin, each of the nine essential amino acids was found to be affected by the heat treatment.     

NUTRITIVE VALUE OF BREAKFAST CEREAL-MILK COMBINATIONS

The protein quality of 11 breakfast cereal-milk mixtures combined as normally eaten (1 oz cereal and 4 oz fluid milk) was determined by using a modified slope-ratio assay. Slope ratios (milk = 100) of three of the mixtures (oatmeal-milk, cream of rice-milk and shredded wheat-milk) were higher than that of milk alone. Using protein content and slope ratios it was calculated that 1 oz of the various cereals could increase potential protein value over that of milk alone by 26 to 117%, and that some of the mixtures could supply as much as 22% of the recommended daily allowance for an 8–10-yr-old child. It is suggested that information of this sort combining the protein quality of food mixtures as eaten with the protein content of a serving would be welcomed by consumers.     

Treatment of donor mice with an alpha beta T-cell receptor monoclonal antibody induces prolonged T-cell nonresponsiveness and effectively prevents lethal graft-versus-host disease in murine recipients of major histocompatibility complex (MHC)-matched and MHC-mismatched donor marrow grafts

The purpose of this study was to determine whether the administration of high doses of an anti-T-cell receptor (TCR) monoclonal antibody (H57-597) to donor animals could induce a state of T-cell nonresponsiveness and prevent the development of graft-versus-host disease (GVHD) in murine recipients of major histocompatibility complex (MHC)-matched (B10.BR[H-2k] --> AKR/J[H-2k]) and mismatched (B10.BR[H-2k] --> DBA/2[H-2d]) marrow grafts. Transplantation of H57-597-treated B10.BR T cells into irradiated AKR or DBA mice resulted in protection from GVHD, which was otherwise lethal in transplanted recipients receiving untreated T cells. The administration of H57-597-treated T cells did not compromise alloengraftment in either strain combination and was found to accelerate donor T-cell reconstitution in recipients of MHC-matched marrow grafts. Optimal protection for GVHD was dependent on the duration of antibody exposure in donor mice. T cells from donor exposed to antibody for only 1 day caused lethal GVHD, whereas exposure for at least 4 days was necessary to abrogate graft-versus-host reactivity. The ability of antibody treatment to protect against the development of GVHD could not be ascribed to the antibody-induced production of Th2 cytokines, the induction of a T- or non-T-suppressor cell population, or the preferential depletion of CD4+ T cells by H57-597. Donor T cells exposed to H57-597 antibody were detectable in recipients for up to 5 weeks after transplantation, indicating that these cells were not eliminated in the host immediately after bone marrow transplantation and contributed to enhanced donor T-cell reconstitution. Moreover, in B10.BR --> DBA chimeras that did not have any clinical evidence of GVHD, potentially MIs-reactive donor-derived Vbeta6+ T cells were present in the spleens of recipients at comparable numbers to normal mice but appeared functionally nonresponsive in vivo. These data strongly suggested that protection from GVHD was due to the fact that antibody treatment resulted in a state of prolonged T-cell anergy that persisted despite the presence of potential costimulatory signals in the recipient. This observation is of potential clinical significance in that it shows that the prevention of GVHD can be accomplished without posttransplantation immunosuppression or the need for in vitro or in vivo T-cell depletion.     

The Academy of Psychosomatic Medicine practice guidelines for psychiatric consultation in the general medical setting. The Academy of Psychosomatic Medicine

This practice guideline seeks to provide guidance to psychiatrists who regularly evaluate and manage patients with medical illnesses. The guideline is intended to delineate the knowledge base, professional expertise, and integrated clinical approach necessary to effectively manage this complex and diverse patient population. This guideline was drafted by a work group consisting of psychiatrists with clinical and research expertise in the field, who undertook a comprehensive review of the literature. The guideline was reviewed by the executive council of the Academy of Psychosomatic Medicine and revised prior to final approval. Some of the topics discussed include qualifications of C-L consultants, patient assessment, psychiatric interventions (e.g., psychotherapy, pharmacotherapy), medicolegal issues, and child and adolescent consultations.     

Persistent membrane translocation of protein kinase C alpha during 12-0-tetradecanoylphorbol-13-acetate-induced apoptosis of LNCaP human prostate cancer cells

Others have reported that the phorbol ester 12-0-tetradecanoylphorbol-13-acetate (TPA), an activator and down-regulator of most protein kinase C (PKC) isozymes, can induce apoptotic cell death of androgen-sensitive LNCaP but not androgen-insensitive PC-3 or DU 145 human prostate cancer cells. As a first step toward uncovering the mechanism by which TPA induces apoptosis of LNCaP cells, we quantified expression of PKC isozyme mRNAs in unmodified and TPA-resistant LNCaP cells and in naturally TPA-resistant PC-3, PC-3M, and DU 145 cells. All of the cell lines and normal prostate expressed RNAs for PKC alpha, delta, epsilon, eta, and mu; only DU 145 cells and normal prostate expressed PKC beta and theta RNAs, and none expressed PKC gamma. The amount of PKC alpha RNA and protein was 6- to 38-fold lower, and PKC mu RNA was 4.5- to 16.5-fold higher in unmodified and TPA-resistant LNCaP cells than in the androgen-independent cells. We examined the effects of TPA on PKC alpha and mu mRNA levels and on membrane translocation of PKC alpha. Incubation with TPA for 6 h or more induced 95% inhibition of cell growth, a transient 12-fold increase and 5-fold decrease in PKC alpha and mu mRNA levels, respectively, and prolonged translocation of PKC alpha to non-nuclear membranes in unmodified LNCaP cells and in TPA-resistant LNCaP cells from which TPA had been removed for 10 days. TPA-resistant LNCaP cells in the continuous presence of TPA, or 24 h after removal of TPA, had down-regulated PKC alpha and remained resistant to re-addition of TPA. These data demonstrate a strong correlation of the presence and absence of membrane PKC alpha with apoptosis and resistance to apoptosis, respectively.