New records of subcutaneous mites (Acari:Hypoderatidae) in birds, with examples of potential host colonization events.

New host, geographic records, or both are established for 14 species of hypoderatid deutonymphs from 14 species of birds in North America. Ten of these records are regarded as examples of a potential host colonization event where these hypopi have become established in hosts other than those with which they are normally associated. Herein, potential host colonization events by hypoderatid deutonymphs are regarded as more of an ecologically determined than physiologically specific phenomenon, often specifically related to sharing of nesting sites in the same rookeries by different host taxa. Neottialges ibisicola Young & Pence is placed as a junior synonym of Neottialges plegadicola Fain. The taxonomic status of Hypodectes propus from columbid versus ardeid hosts needs further study.

Redescription of Alcedinectes alcyon (Acari:Hypoderatidae) from the belted kingfisher (Aves:Coraciiformes; Alcedinidae).

Alcedinectes alcyon (Boyd) is redescribed based on specimens collected from its belted kingfisher, Megaceryle alcyon (L.), type host in Florida. This species differs from A. cerylei Fain by the chaetotaxy of tarsus III. A. alcyon has a long stout apical seta that tapers to a curved tip resembling that seen on tarsus III of the genus Tytodectes (Ispidectes) Fain. The equivalent seta in A. cerylei is a stout spine. There are other minor differences between these species in the pattern of idiosomal sclerotization and leg chaetotaxy. The chaetotaxy and solenidiotaxy of legs I and II in Alcedinectes closely resemble that of Amazonectes psittaci Fain & Vercammen-Grandjean from parrots (Psittaciformes), whereas the morphology and chaetotaxy of the idiosoma resemble that of Tytonectes (Ispidectes) spp. which also occurs in kingfishers (Coraciiformes). The long stout seta that tapers to a curved tip on tarsus III in A. alcyon also links the genus Alcedinectes with Tytodectes (Ispidectes).

L-Homocysteic acid as an alternative cytotoxin for studying glutamate-induced cellular degeneration of Huntington's disease and normal skin fibroblasts.

Huntington's Disease (HD) and normal skin fibroblasts in culture were exposed to several acidic amino acids structurally related to L-glutamate which have excitotoxic properties in the nervous system. L-Homocysteic acid, a sulfonic acid analogue of glutamate, was the only other acidic amino acid causing fibroblast degeneration similar to that induced by glutamate. None of the other compounds tested, including the D isomer of homocysteic acid, were as toxic as 30 mM glutamate. As previously noted with glutamate treatment, HD fibroblasts demonstrated an increased sensitivity to L-homocysteic acid compared to controls. In contrast to glutamate, no cellular metabolism of L-homocysteic acid could be detected; a property which may account for the increased cytotoxicity of L-homocysteic acid compared to glutamate. The identification of L-homocysteic acid, a glutamate analogue which undergoes limited metabolism, should enable the elucidation of the toxic mechanism of glutamate and facilitate the determination of the site conferring increased sensitivity of cultured HD fibroblasts to glutamate.

The mechanism of glutamate-induced degeneration of cultured Huntington's disease and control fibroblasts.

Human cultured skin fibroblasts undergo rapid cellular degeneration and cell death when exposed to moderate levels of glutamate (10-30 mM). Huntington's disease (HD) skin fibroblast cultures are more sensitive to the toxic effects of glutamate (Gray et al. 1980) and elucidation of the toxic mechanism may bear on degenerative processes occurring in the HD brain. Glutamate toxicity was found to be inversely related to cystine content in the culture medium. Supplementing culture media with cystine effectively suppressed toxicity of L-Glu and that of a closely related but more potent analogue, L-homocysteic acid (L-HCA). Glutamate and L-HCA treatment provoked a rapid and marked decrease in cellular glutathione levels prior to cell death. Depletion of cellular glutathione with buthionine sulfoximine potentiated the toxicity of glutamate and L-HCA. Glutamate- or L-HCA-induced cell death also could be reduced or inhibited by co-treatment with antioxidants, thereby suggesting that free radical-induced peroxidative damage may ultimately be responsible for the loss of cell viability. While no site for the differential sensitivity of HD and normal fibroblasts to glutamate was clearly discerned, our results suggest that HD fibroblasts are more susceptible to peroxidative damage. The increased deposition of lipofuscin (Tellez-Nagel et al. 1974) and abnormal neuronal membrane ultrastructure seen in HD (Roizin et al. 1979) suggest similar degenerative processes may occur in HD brain.

Alteration of human breast tumor cell membrane functions by chromosome-mediated gene transfer.

BOT-2 cells (human breast tumor origin) have an impaired ability to utilize exogenous thymidine. Previous studies revealed this deficiency to be the permeation event rather than phosphorylation, since the cells have active thymidine kinase. Chromosome-mediated gene transfer was used to transfer genetic information in the form of metaphase chromosomes, from HeLa-65 cells to the BOT-2 cells, correcting the permease deficiency. Poly-L-ornithine or lipochromes were used for facilitation of chromosome uptake. After selection on HAT medium, transferant clones were isolated at a frequency of 4 x 10(-5) and 1 x 10(-5), respectively. Transferants MGP-1 and MGL-1 are stable after 18 months and have been characterized on the bases of purine and pyrimidine nucleoside uptake, relative thymidine kinase activities, alkaline phosphatase activities, and hydrocortisone-induced alkaline phosphatase activity. MGP-1 demonstrates positive thymidine uptake and incorporates radiolabeled thymidine into DNA. MGL-1 remains thymidine transport-deficient and surveys on HAT by increasing endogenous dihydrofolate reductase activity. Alkaline phosphatase activity in MGL-1 is similar to HeLa-65, 2% of that in BOT-2, and in addition, is inducible 25-30-fold by 3 micro M hydrocortisone. We have separated, genetically, a thymidine permease function from phosphorylation in cells of human origin and have transferred genetic information for the regulation of alkaline phosphatase.

Population density and regulation of cell division in 3T3 cells. I. Inorganic phosphate levels, uptake and release.

Triggering mechanisms for initiating density dependent inhibition of cell division in 3T3 cell monolayers are activated approximately two to three population doublings prior to cessation of cell division at monolayer confluency. This activation occurs at a critical contact cell density of approximately 8 X 10(3) cells/cm2. During this period there are selective controls on transport and storage of required low molecular weight nutrients. A possible correlation between orthophosphate and rates of cell division has been investigated. We have demonstrated a relationship between cellular concentrations of orthophosphate and initiation of density dependent inhibition of cell division. Prior to critical intercellular contact, the [Pi] in 3T3 is 10 mM. During critical contact, this concentration is quickly reduced to approximately 2 mM and remains at this concentration to confluency. Similar alterations do not occur in Py 3T3 cells, which maintain a concentration of approximately 2 mM Pi regardless of cell density. After confluent 3T3 cells are released from inhibition of cell division the [Pi] must increase several-fold before DNA synthesis commences. These are physiological changes in 3T3 cellular [Pi] as a function of cell density, and cannot be attributed to nutrient depletion, altered transport of Pi into the cell, increased [ATP], or increased [PPi] levels. The controlled modulation of [Pi] may regulate glycolysis and coordinate counter-ion changes (Ca++) may regulate mitochondrial activity.