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M Raabe

Publications and source records attributed to M Raabe.

28 records · Page 2Linked to original sources
PubMed1982

[Neuroendocrine control of reproduction in insects].

The major reproductive processes in insects are regulated by neurohormones. Neurohormones act according to two distinct modes, either directly upon the target organs or by controlling the activity of the endocrine glands which, in turn, influence the different reproductive steps. The majority of identified neurohormones are produced in the brain; their origin in particular neurosecretory cells, while established in a few cases, is often unknown. Neurohormones are also produced, outside the brain, in the ventral nerve cord ganglia. They intervene namely in the regulation of egg-laying. The best known release sites of neurohormones are the cephalic and metameric neurohemal organs. Moreover, the neurohormones are also released in close contact with or within the target organs.

Animals↗
PubMed1976

[Autogenesis and cerebral neurosecretion in Aedes detritus (Haliday, 1833) (Diptera - Culicidae].

In anautogenous females of the Dipteran Culicidae Aedes detritus (Haliday, 1833), the neurosecretory products synthesized by the A cells of the pars intercerebralis are stored in the pericarya in absence of blood meal; on the contrary, in the autogenous females they are steadily released from emergency till the stages 3-4 of vitellogenesis; a slight storage occurs by the end of vitellogenesis. These facts suggest the important meaning of these cells in the regulation processes of vitellogenesis in Mosquitoes.

Aedes↗
PubMedDate not supplied

Using genetically engineered mice to understand apolipoprotein-B deficiency syndromes in humans.

Several human diseases are characterized by defects in the synthesis and secretion of the apolipoprotein (apo) B-containing lipoproteins. Familial hypobetalipoproteinemia is caused by mutations in the apo-B gene and is characterized by abnormally low plasma concentrations of apo-B and low-density lipoprotein (LDL) cholesterol. Another apo-B deficiency syndrome, abetalipoproteinemia, is caused by mutations in the gene for microsomal triglyceride transfer protein (MTP). MTP is a microsomal protein that is thought to transfer lipids to the apo-B protein as it is translated, allowing it to attain the proper conformation for lipoprotein assembly. A third apo-B deficiency syndrome, Anderson's disease (or chylomicron retention disease), is characterized by the inability to secrete apo-B-containing chylomicrons from the intestine but an apparently normal capacity to secrete lipoproteins from the liver. To more fully understand these human apo-B deficiency syndromes, our laboratory has generated and characterized gene-targeted mouse models. This review summarizes what has been learned from these animal models.

Abetalipoproteinemia↗