VX2 carcinoma, pulmonary metastases, and neutrophilic leukocytosis. Possible animal model of tumor-associated granulocytosis.

In New Zealand white rabbits bearing the transplantable VX2 carcinoma intramuscularly in the hind limbs uniformly a granulocytosis syndrome developed, characterized by peripheral blood neutrophilia and marked granulocytic bone marrow hyperplasia, whereas the syndrome did not always develop in animals bearing the tumor intraabdominally. The relationship between the extent of pulmonary metastases and granulocytosis/bone marrow hyperplasia was significant (P less than 0.005). This positive correlation (correlation coefficient = 0.85) existed for both animals bearing intraabdominal tumors and animals bearing intramuscular tumors. The granulocytic syndrome occasionally occurred in rabbits with mild degrees of pulmonary metastatic involvement, but never with total absence of pulmonary metastases. Hypercalcemia occurred prior to the appearance of pulmonary metastases and was not essential to the development of granulocytosis. These data suggest that granulocytosis in VX2 carcinoma-bearing rabbits is dependent on the presence of tumor in the lungs and is not directly related to implantation site. This tumor-bearing animal model may be suitable for studies of tumor-associated granulocytosis in vivo.     

Mode of delivery and risk of developing allergic disease

The aim of this study was to quantify the relationship between mode of delivery and subsequent incidence of allergic disease. The analysis is based on data derived from a birth cohort of 24,690 children who contributed data to the West Midlands General Practice Research Database. We found no convincing evidence to suggest that babies born by caesarean, forceps, or breech delivery had an increased risk of developing allergic disease.     

An investigation of the post-tetanic potentiation of end-plate potentials at a mammalian neuromuscular junction

1. End-plate potentials (e.p.p.s) were recorded intracellularly from neuromuscular junctions in curarized or Mg-paralysed rat diaphragm-phrenic nerve preparations in vitro. In Mg-paralysed preparations after 1000 impulses at 100/sec the amplitude of e.p.p.s elicited at 1/sec before and after the tetanus was on average greater than the control amplitude for 120 +/- 30 sec.2. The post-tetanic potentiation (P.T.P.) of e.p.p. amplitudes was not thought to be dependent upon post-tetanic hyperpolarization (P.T.H.) of nerve terminals as it lasted longer than the hyperpolarization generated by an identical tetanus; was unaffected by hyperpolarizing currents which reduced P.T.H. or depolarizing currents which prolonged P.T.H.; and was diminished in solutions containing 30% of the normal NaCl concentration or 1% ethyl alcohol, both of which procedures prolong P.T.H. The magnitude and duration of P.T.P. were influenced by the pH of the bathing solution in the range 7-7.5 although there was no change in P.T.H. under these conditions. The inability of polarizing currents to influence P.T.P. was also thought inconsistent with the hypothesis that P.T.P. is due to an increase in available transmitter.3. P.T.P. was not thought to be due to sodium accumulation in nerve terminals, for P.T.P. was reduced or abolished by procedures which would be expected to increase the intraterminal sodium ion concentration. These procedures were: exhibition of metabolic inhibitors (1.8 x 10(-6)M antimycin A, 3-5 mM sodium azide or 1 mM sodium iodoacetate), exhibition of cardiac glycosides (7.7 x 10(-6)M digoxin or 0.42 mM ouabain), and omission of glucose or potassium ions from the bathing solution. Abolition of P.T.P. by potassium-free solutions was also thought to be inconsistent with the hypothesis that P.T.P. is due to a reduction in the potassium concentration in nerve terminals.4. P.T.P. was not thought to be due to terminal volume changes, for no consistent effect upon the quantal content of e.p.p.s could be detected in hypo- or hyperosmotic solutions.5. It was concluded that the only hypothesis for P.T.P. not excluded by our experiments was that P.T.P. is due to some change in ionized calcium at a membrane site important in transmitter release.     

Failure to produce conditioning with low-dose trimethylthiazoline or cat feces as unconditioned stimuli

Trimethylthiazoline (TMT), a derivative of fox feces, has been reported to fail to produce aversive conditioning as an unconditioned stimulus (UCS) when presented in large amounts (I. S. McGregor, L. Schrama, P. Ambermoon, & R. A. Dielenberg, 2002). Experiment I evaluated very low TMT levels that nonetheless produced defensive behaviors in rats during exposure. Although each level (0.01, 0.05, and 0.10 microl TMT) produced significant change in defensiveness, none resulted in significant changes the following day in the absence of TMT. Experiment 2 evaluated cat urine, cat feces, and cat fur/skin odor against a no-odor control. Urine produced no significant changes, but feces and fur/skin odors elicited virtually identical changes in defensive behaviors during exposure. When tested the next day in the absence of odor, the fur/skin odor-exposed group showed significant differences on the same behaviors as during exposure, but the feces-exposed group showed no differences on any measure. Results suggest that lack of conditioning to TMT may relate to the type of predator odor rather than the amount, predator species, or possible lack of odor components in TMT that are present in natural feces. Predator feces may also be less effective as a UCS because they are poorly predictive of the actual presence of the predator, suggesting the need for a reevaluation of UCS functions in aversive conditioning.     

LH-RH in picomole concentrations evokes excitation and inhibition of rat arcuate neurones in vitro

A medial sagittal brain slice was developed, which enabled electrophysiological recording from spontaneously active neurones adjacent to the infundibular recess of the rat arcuate nucleus. Luteinizing hormone-releasing hormone (LH-RH) (10 nM-10 pM) significantly altered the frequency of 21 out of 31 units tested, exciting 14 and inhibiting 7 others. The excitatory responses were often not maintained during the exposure to LH-RH but either returned to pre-exposure frequency or displayed an inhibition of discharge. A neural model incorporating recurrent inhibition of LH-RH-excited neurones is proposed to explain these responses, thought to be endogenously evoked by collateral innervation of the arcuate nucleus by medial preoptic neurones projecting to the median eminence.     

Cytology and lineage of NG2-positive glia

We present evidence that NG2+ glia are an integral part of an oligodendrocyte/synantocyte (OS) lineage stream the progenitors of which begin to produce both glial phenotypes at about birth. The NG2 CSPG is differentially distributed within the OS lineage, being expressed in progenitors and synantocytes but not in oligodendrocytes. All cells in the OS lineage, except the primordial stem cells, express O4. The oligodendrocyte line reacts with CD9, but synantocytes are CD9–. Nonetheless, synantocytes are morphologically complex and specialised glia which contact axolemma in myelinated fibres at nodes of Ranvier and synaptic terminals, and form >99% of all NG2+ glia in the adult CNS. Thus, the other NG2+ phenotype, the adult oligodendrocyte progenitor cell (AOPC), constitutes a small population of <1% of all NG2+ glia in the mature CNS. AOPC are a heterogeneous set of cells probably originating from multiple sources which, by definition, produce oligodendrocytes in the adult to replace loss after trauma, demyelination and normal wear and tear. The definitive functions of synantocytes remain undefined.     

Quality of life profiles and their association with clinical and demographic characteristics and physical activity in people with a stoma: a latent profile analysis

Quality of Life Research - Quality of life can be negatively impacted by the formation of a stoma and is influenced by a number of factors. Research to date treats people with a stoma as a...