Urbanization is a major cause of loss of coastal wetlands. Urbanization also exerts significant influences on the structure and function of coastal wetlands, mainly through modifying the hydrological and sedimentation regimes, and the dynamics of nutrients and chemical pollutants. Natural coastal wetlands are characterized by a hydrological regime comprising concentrated flow to estuarine and coastal areas during flood events, and diffused discharge into groundwater and waterways during the non-flood periods. Urbanization, through increasing the amount of impervious areas in the catchment, results in a replacement of this regime by concentrating rain runoff. Quality of run-off is also modified in urban areas, as loadings of sediment, nutrients and pollutants are increased in urban areas. While the effects of such modifications on the biota and the physical environment have been relatively well studied, there is to date little information on their impact at the ecosystem level. Methodological issues, such as a lack of sufficient replication at the whole-habitat level, the lack of suitable indices of urbanization and tools for assessing hydrological connectivity, have to be overcome to allow the effects of urbanization to be assessed at the ecosystem level. A functional model is presented to demonstrate the impact of urbanization on coastal wetland structure and function.

Cellular and immunoglobulin components of bronchoalveolar fluid recovered by bronchoscopic lavage were evaluated in 32 control patients, 10 normal volunteers, and 60 patients with the following interstitial lung diseases: idiopathic pulmonary fibrosis, pulmonary fibrosis associated with collagen-vascular disease, eosinophilic granuloma, sarcoidosis, and hypersensitivity pneumonitis. The percentage of lymphocytes distinguished two general disease categories: those with increased lymphocytes (sarcoidosis and hypersensitivity pneumonitis); and those with normal lymphocytes (idiopathic pulmonary fibrosis, pulmonary fibrosis associated with collagen-vascular disease, and eosinophilic granuloma). Patients in all five disease categories had elevated IgG levels and percentages of neutrophils compared with control patients, with the highest proportion of neutrophils found in idiopathic pulmonary fibrosis. Immunoglobulin levels also helped distinguish among patient groups, in that patients with hypersensitivity pneumonitis had lavage IgG/albumin ratios greater than 1, whereas patients with sarcoidosis had ratios less than 1; and with infrequent exceptions, the finding of IgM in lavage fluid was limited to patients with hypersensitivity pneumonitis.

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Pulmonary granulomata of sarcoidosis are composed primarily of mononuclear phagocytic cells that are probably derived from blood monocytes. To evaluate the concept that recruitment of blood monocytes to the sarcoid lung is mediated by chemoattractants produced by immune effector cells within the lung, we obtained mononuclear cells from lung and blood of six patients with active pulmonary sarcoidosis, six normal subjects, and six patients with active idiopathic pulmonary fibrosis and studied their ability to secrete a chemotactic factor for monocytes. Lung T lymphocytes from all sarcoidosis patients, but not from normal subjects or patients with idiopathic pulmonary fibrosis, spontaneously secreted such a mediator. Lung T lymphocytes from patients with sarcoidosis secreted more monocyte chemotactic factor than did blood T lymphocytes from the same patients. The accumulation of monocytes in the lung in patients with pulmonary sarcoidosis may be mediated by local production of monocyte chemotactic factor by lung T lymphocytes.

Experiments were conducted to study the effects of a low protein-high carbohydrate diet on growth and thyroid function in obese and lean male and female Zucker rats. The nine feeding regimens included animals ad libitum fed either a 22% casein and 59% carbohydrate diet (control) or an 8% casein and 73% carbohydrate diet (low protein) and appropriate pair-fed groups to control for the lean rats eating less than the obese rats and the rats fed the low-protein diet eating less than those fed the control diet. The rats were 4 weeks old at the start of the experiment which lasted 7 weeks. Final body size, tibia length and nonfat dry mass of the lean rats were dependent primarily on the amount of protein consumed, whereas growth of the obese rats was related to total energy intake rather than to protein intake. The relative hyperphagia, decreased efficiency of energy utilization and increased oxygen consumption and serum T3 concentrations in the lean rats fed the low-protein diet were consistent with the development of an adaptive thermogenesis, allowing the excess non-protein energy to be dissipated through excess heat production. There was no evidence for such an adaptive thermogenesis in the obese rats. The suggestion that the obese rats were already overeating for protein and storing the excess energy as fat and that the decreased thyroid response might be part of a protective mechanism against overheating was discussed.

Among 80 Black patients with sarcoidosis, 11 families were identified as containing multiple cases. Monogenic modes of inheritance were reasonably excluded by informal inspection of pedigree patterns and by poor fit of corrected ratios within sibships to the expected ratio for all sibships at risk. The observed familial distribution conforms in several respects to properties that are descriptive of multigenic traits. Additionally, heritability based only on female probands was estimated to be between 60% and 70%. A larger sample size should permit analysis of additional multigenic properties.

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