Specific versus placebo effects in biofeedback: Some brief back-to-basics considerations

Following the semantic complexities raised in earlier papers, this paper seeks to return to some of the more basic considerations arising from the preceding discussion. A critical part of the context of that discussion is the increasingly important issue of accountability. In this context, the citing of supportive studies is not enough, one must also be able to justify the logical relevance of those studies. The discussion therefore turns of the logic of treatment evaluation, which must be treated as objectively as possible. Also critical is the distinction between the question of whether an effect is present and the question of what the source of that question might be. In the quest for treatment evaluation, only the former question is important. However, this quest is one that is in the interest of researchers, clinicians, and consumers, for all of whom only the facts will do.The preparation of this paper was supported by grants from the National Science and Engineering Research Council of Canada to both authors. We are indebted to Hal Scher for comments on an earlier draft.     

Releases of Norepinephrine and Dopamine in Ventriculocisternal Perfusions in Hepatectomized and Laparotomized Rats

Abstract: The completely hepatectomized rat has frequently been used as a model to study changes in the economy of norepinephrine (NE) and dopamine (DA) in hepatic coma. Hypothermia characteristically develops in hepatectomized rats and also occurs in patients in hepatic coma and is associated with improved survival in both. The aims of the present study were to measure both release and uptake of NE and release of DA in brain in warm (37°C) and cool (30–32°C) rats at 3–5 h after laparotomy or hepatectomy. Ventriculocisternal perfusions of the brain were performed on rats under basal conditions and during releases evoked by 40 m M K⁺. Basal releases of NE and DA and evoked release of DA were greater in the warm hepatectomized rats than in all other groups. In some studies, 10⁻⁵ M amitriptyline was added to the perfusates to assess whether neuronal uptake was changed after hepatectomy. Uptake of released NE was equally robust in cool hepatectomized as in cool laparotomized rats but could not be measured in warm hepatectomized rats because of amitriptyline toxicity in these rats. Decreases in NE and increases in DA content were found in most areas of the brain after perfusion. Increased releases of NE and DA may contribute to the pathogenesis of hepatic encephalopathy.     

Insecticidal effectiveness ofMammea Americana (Guttiferae) extracts on larvae ofDlabrotica Virgifera Virgifera (Coleoptera:Chrysomelidae) andTrichoplusia Ni (Lepidoptera:Noctuidae)

Seed and leaf extracts ofMammea americana (mamey apple) have a historical use as a biopesticide with the active components previously characterized. We reexamined the utility of this natural bioinsecticide in light of existing sources of material as a by-product of the fruit processing industry. Our results addDiabrotica virgifera virgifera andTrichoplusia ni to the list of insects which are susceptible to the insecticidal ingredients ofM. americana and confirms earlier reports of activity againstBlatella germanica, Periplaneta americana, andPlutella xylostella. We report LD5Os for crude hexane extracts ofM. americana leaves and seeds againstT. ni. These materials represent renewable sources of bioinsecticides for agriculture, and should regenerate interest in coumarin-type compounds for novel pesticidal action.     

Gastric evacuation rates of white perch,Morone americana,determined from laboratory and field data

Synopsis Gastric evacuation rates (R) of white perch,Morone americana, were determined in laboratory experiments and by using field data. The resulting relationship ofR and temperature (T) for white perch wasR = 0.028e^0.106T (r² = 0.98). The high r² of the regression indicates good agreement of the combined laboratory and field data. Our rate compares well with those available for other species; and especially for Eurasian perch, which has a similar thermal existence to white perch in Lake Erie.     

Functional specialization and differential regulation of short‐chain carboxylic acid transporters in the pathogen Candida albicans

The major fungal pathogen Candida albicans has the metabolic flexibility to assimilate a wide range of nutrients in its human host. Previous studies have suggested that C. albicans can encounter glucose‐poor microenvironments during infection and that the ability to use alternative non‐fermentable carbon sources contributes to its virulence. JEN1 encodes a monocarboxylate transporter in C. albicans and we show that its paralogue, JEN2, encodes a novel dicarboxylate plasma membrane transporter, subjected to glucose repression. A strain deleted in both genes lost the ability to transport lactic, malic and succinic acids by a mediated mechanism and it displayed a growth defect on these substrates. Although no significant morphogenetic or virulence defects were found in the double mutant strain, both JEN1 and JEN2 were strongly induced during infection. Jen1‐GFP (green fluorescent protein) and Jen2‐GFP were upregulated following the phagocytosis of C. albicans cells by neutrophils and macrophages, displaying similar behaviour to an Icl1‐GFP fusion. In the murine model of systemic candidiasis approximately 20–25% of C. albicans cells infecting the kidney expressed Jen1‐GFP and Jen2‐GFP. Our data suggest that Jen1 and Jen2 are expressed in glucose‐poor niches within the host, and that these short‐chain carboxylic acid transporters may be important in the early stages of infection.     

Ethanol and prostaglandin E1: Biochemical and behavioral interactions

Low concentrations of ethanol enhanced prostaglandin (PG) E₁-stimulated adenosine-3′, 5′-cyclic monophosphate (cAMP) accumulation in human platelets and in rat brain slices. Ethanol also potentiated platelet synthesis of PGE₁ from dihomo-gamma-linolenic acid. These interactions may derive from the fluidizing effects of ethanol on lipid-containing cell membranes, and suggest a possible role for PGE₁ as a mediator of certain acute effects of ethanol. The derivative possibility that “down regulation” of PGE₁ systems is involved in the development of ethanol dependence is supported by data showing that PGE₁ administered to mice following chronic exposure to ethanol reduced withdrawal syndrome intensity.