Food, health, and the urban environment.

Both the production and the consumption of food should help reduce the risk of food-borne and non-communicable disease and prevent micro-nutrient deficiency. That a safe healthy diet can also be environmentally sound is a bonus. Growing foods that promote health in an environment near to consumers can contribute to reduced fuel consumption, pollution, transport and packaging costs, and can promote biodiversity. This approach can also help create local jobs, improve access to food, and promote a sustainable environment. The World Health Organization recommends an intake of more than 400 grams of vegetables (in addition to potatoes) and fruit every day because this helps prevent non-communicable diseases and micro-nutrient deficiency. Therefore, urban food and nutrition policies are needed to promote health through an integrated approach to food, health, and the environment within local communities. The benefits of developing urban food and nutrition policies to help increase local food production include environmental, social, direct, and indirect economic benefits, in addition to the health benefits. These issues are discussed in this paper.

A method for cloning T-lymphocytic precursors in agar.

A new technique for the culture of T-lymphocytic colonies is reported. The method may be regarded as a human lymphocyte precursor cell assay, as is the myeloid colony culture for granulocyte-macrophage progenitors. The colonies arise under the simultaneous stimulation of phytohemagglutin and a leukocyte feeder. A linear relationship is found between colony numbers and cell numbers plated. The colonies represent aggregates of lymphoblast-like cells, the majority of which are capable of E-rosette formation, are responsive in mixed lymphocyte cultures, and do not exhibit surface immunoglobulins. Their density distribution profile is very similar to that of myeloid colony-forming cells. The finding that most of these colony-forming cells are recovered in the so-called lymphocyte-free stem cell fraction following density fractionation suggests that they originate from a lymphocytic precursor.

Nature of the delayed graft-versus-host reactivity of fetal liver cell transplants in mice.

Experiments were designed to determine which actual differences in the cellular composition between fetal liver and bone marrow account for the distinct types of graft-versus-host (GvH) disease. The assay of reactive lymphocytes (by in vitro mitogenic stimulation) in fetal liver transplants in mice, the purification of hemopoietic stem cells (HSC) of the transplants, and the quantitation of HSC numbers in the grafts traced the basis for the distinctly weak type of GvH disease after fetal liver cell grafts. It was found that transplantation of purified HSC concentrates did not modify the severity of GvH mortality. The moderate character of the delayed GvH disease was shown to depend on the presence of an HSC population in fetal liver with different qualities and not on numerical differences between the HSC in fetal liver and bone marrow. Data collected also demonstrated that when GvH disease occurred in the recipients of transplants of fetal liver, it shared the characteristic histologic features of the bone marrow GvH syndrome. The recovery of mitogen responsiveness of spleen cells may have been delayed in fetal liver allotransplantation as compared to syngeneic grafting. By supportive infusion of lymphoid cells, it was suggested that the immunodeficiency coinciding with GvH disease represented a secondary manifestation of the disease rather than a primary impairment in lymphoid differentiation.