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Biomedical subjects

L Baca

Publications and source records attributed to L Baca.

10 recordsLinked to original sources

Cage size and flight speed of the tobacco hawkmoth Manduca sexta

Flight speeds and behaviors of the sphinx moth Manduca sexta were recorded in chambers of four different sizes (0.57, 8.5, 44 and 447 m3). Mean horizontal speed increased linearly with the cube root of chamber volume from 0.57 m s-1 in the smallest chamber to 3.4 m s-1 in the largest. The maximum horizontal speed observed was 5.3 m s-1 in the largest chamber. Speeds decreased linearly with the logarithm of hawkmoth proximity to the wall. In a tunnel chamber (the third largest), moths often flew in a scalloped-shaped path. At the top of the scallop, they glided for 1­5 wing beats. In the largest chamber, moths could be recorded flying at angles other than horizontal (0 °). At flight angles greater or less than 0 °, mean speed decreased linearly with angle until ±40 °. At greater angles, speeds remained between 1 and 2 m s-1. Moths also flew closer to the wall at flight angles deviating from the horizontal. An allometric analysis of the flight speeds of insects and birds suggests that M. sexta may be able to fly at 7­10 m s-1. We conclude that chamber size limits the flight speed and modifies the flight behavior of the tobacco hawkmoth.

Journal Article↗

Linking empirically based theory and evaluation: the Family Bereavement Program.

Evaluated the effects of a theoretically derived program to prevent mental health problems in children who had experienced the death of a parent. The program was designed to improve variables in the family environment which were specified as mediators of the effects of parental death on child mental health. The evaluation design involved the random assignment of families to either an intervention or control group. The program led to parental ratings of increased warmth in their relationships with their children, increased satisfaction with their social support, and the maintenance of family discussion of grief-related issues. The program also led to parent ratings of decreased conduct disorder and depression problems and overall problems in older children. Significant correlations between the family environment variables and child mental health problems provided further empirical support for the theory underlying the program. Implications for program redesign were derived by reconsidering the adequacy of the program components to change theoretically mediating variables.

Adaptation, Psychological↗

The use of structural equation modeling in generative research: toward the design of a preventive intervention for bereaved children.

Describes a generative study of processes which may lead to symptomatology in children who have experienced the death of a parent. Based on existing literature, four putative mediating variables were identified: parental demoralization, family warmth, negative family events, and positive stable family events. Structural equation modeling techniques were used to compare several potential causal models involving these variables. The results were most consistent with a model in which bereavement was not directly related to the child symptomatology, but rather its effects were transmitted through these four mediational mechanisms. The implications of the results of the structural modeling for the design and evaluation of preventive interventions are discussed briefly.

Adaptation, Psychological↗

Regulation of cytokine and viral gene expression in monocytes infected with the human immunodeficiency virus.

Monocytes treated with interferon-alpha (IFN-alpha) at virus challenge show no evidence of human immunodeficiency virus (HIV) infection: no p24 antigen or reverse transcriptase (RT) activity, no viral mRNA and no proviral DNA. Levels of p24 antigen and RT activity in monocytes infected with HIV 1-3 weeks before IFN-alpha treatment gradually decrease to baseline. HIV-induced cytopathic changes are markedly reduced, as are levels of HIV mRNA: the frequency of productively infected cells is less than or equal to 1%. But, levels of proviral DNA in the IFN-alpha-treated and control HIV-infected cells are indistinguishable, and remain so through 3 weeks. Large quantities of proviral DNA in IFN-alpha-treated cells with little active transcription suggest true microbiological latency. The major potential source for IFN-alpha in HIV-infected patients is the macrophage. With any of 15 virus isolates, tumor necrosis factor-alpha, interleukin-1 beta, interleukin-6, IFN-omega or IFN-beta are not detected nor the mRNA expressed in HIV-infected or uninfected monocytes. Both uninfected and HIV-infected monocytes produce high levels of these cytokines after treatment with synthetic double-stranded RNA (poly-I:C). Uninfected monocytes also produce high levels of IFN-alpha after treatment with Poly-I:C, Newcastle disease virus or herpes simplex virus. In marked contrast, HIV-infected monocytes express no IFN-alpha activity or mRNA before or after treatment with any of these agents. The markedly diminished capacity of HIV-infected monocyte to produce IFN-alpha reflects a specific transcriptional block and may be an adaptive mechanism of virus to alter basic microbicidal functions of this cell.(ABSTRACT TRUNCATED AT 250 WORDS)

Cytokines↗

Restriction of HIV replication in infected T cells and monocytes by interferon-alpha.

Human recombinant interferon-alpha (IFN alpha) restricted viral replication in human immunodeficiency virus- (HIV) infected T cells and monocytes. With T cells, reverse transcriptase (RT) activity in culture fluids was reduced threefold from that of control infected cells by IFN treatment, but HIV p24 antigen levels were unchanged. In contrast, levels of p24 antigen and RT activity in lysates of IFN-treated infected cells were threefold greater than those of controls. These differences suggest that the mechanism for IFN-induced antiviral effects in HIV-infected T cells resides in the terminal events (assembly and release) of the virus replication cycle. Monocytes treated with IFN at the time of virus challenge showed no p24 antigen or RT activity, no HIV-specific mRNA, and no proviral DNA in cells for up to 3 weeks after infection. IFN treatment of chronically infected monocytes also decreased virus replication, as assessed by p24 antigen, mRNA and RT detection assays. However, levels of proviral DNA in the IFN-treated and control HIV-infected cells were indistinguishable. The presence of large quantities of proviral DNA in cells with little or no evidence for active transcription documents a situation approaching true microbiological latency.

DNA, Viral↗