Geographic body size variation in the periodical cicadas Magicicada: implications for life cycle divergence and local adaptation.

Seven species in three species groups (Decim, Cassini and Decula) of periodical cicadas (Magicicada) occupy a wide latitudinal range in the eastern United States. To clarify how adult body size, a key trait affecting fitness, varies geographically with climate conditions and life cycle, we analysed the relationships of population mean head width to geographic variables (latitude, longitude, altitude), habitat annual mean temperature (AMT), life cycle and species differences. Within species, body size was larger in females than males and decreased with increasing latitude (and decreasing habitat AMT), following the converse Bergmann's rule. For the pair of recently diverged 13- and 17-year species in each group, 13-year cicadas were equal in size or slightly smaller on average than their 17-year counterparts despite their shorter developmental time. This fact suggests that, under the same climatic conditions, 17-year cicadas have lowered growth rates compared to their 13-years counterparts, allowing 13-year cicadas with faster growth rates to achieve body sizes equivalent to those of their 17-year counterparts at the same locations. However, in the Decim group, which includes two 13-year species, the more southerly, anciently diverged 13-year species (Magicicada tredecim) was characterized by a larger body size than the other, more northerly 13- and 17-year species, suggesting that local adaptation in warmer habitats may ultimately lead to evolution of larger body sizes. Our results demonstrate how geographic clines in body size may be maintained in sister species possessing different life cycles.

Regional and cellular distribution of protein kinase C in rat cerebellar Purkinje cells.

Protein kinase C (PCK) is a family of isoforms that are implicated in subcellular signal transduction. The authors investigated the distribution of several PKC isoforms (PKC-alpha, PKC-beta, PKC-gamma, PKC-delta, and PKC-epsilon) within major cerebellar cell types as well as cerebellar projection target neurons, including Purkinje neurons, cerebellar nuclear neurons, and secondary vestibular neurons. PKC-alpha, PKC-beta, PKC-gamma, PKC-delta, and PKC-epsilon are found within the cerebellum. Of these isoforms, PKC-gamma and PKC-delta are highly expressed in Purkinje cells. PKC-gamma is expressed in all Purkinje cells, whereas the expression of PKC-delta is restricted to sagittal bands of Purkinje cells in the posterior cerebellar cortex. In the lower folia of the uvula and nodulus, Purkinje cell expression of PKC-delta is uniformly high, and the sagittal banding for PKC-delta expression is absent. Within the cerebellar nuclei, PKC-delta-immunolabeled axons terminate within the medial aspect of the caudal half of the ipsilateral interpositus nucleus. PKC delta-immunolabeled axons also terminated within the caudal medial and descending vestibular nuclei (MVN and DVN, respectively), the parasolitary nucleus (Psol), and the nucleus prepositus hypoglossi (NPH). PKC-gamma-immunolabeled axons terminated in all of the cerebellar nuclei as well as in the lateral and superior vestibular nuclei and the MVN, DVN, Psol, and NPH. The projection patterns of PKC-immunolabeled Purkinje cells were confirmed by lesion-depletion studies in which unilateral uvula-nodular lesions caused depletion of PKC-immunolabeled terminals ipsilateral to the lesion in the vestibular complex. These data identify circuitry that is unique to cerebellar-vestibular interactions.

Involvement of dopamine D(2) receptors in complex maze learning and acetylcholine release in ventral hippocampus of rats.

In the current study we focus on the involvement of dopamine D(2) receptors in the ventral hippocampus in memory performance and acetylcholine release. Using the aversively motivated 14-unit T-maze (Stone maze) the injection of raclopride, a D(2) receptor antagonist, into the ventral hippocampus (8 microg/kg) was found to impair memory performance. Co-injection of quinpirole, a D(2) receptor agonist (8 microg/kg), overcame the impairment in performance. Microdialysis study revealed that quinpirole infusion (10-500 microM) into the ventral hippocampus stimulated acetylcholine release in a dose-dependent manner, and systemic injection of quinpirole (0.5 mg/kg, i.p.) also stimulated acetylcholine release in the ventral hippocampus. Infusion of eticlopride, another D(2) receptor antagonist, into the ventral hippocampus suppressed acetylcholine release in the hippocampus induced by systemic injection of quinpirole. Taken together, we suggest that D(2) receptors in the ventral hippocampus are involved in memory performance, possibly through the regulation of acetylcholine.

The elevation of plasma adrenocorticotrophic hormone and expression of c-Fos in hypothalamic paraventricular nucleus by microinjection of neostigmine into the hippocampus in rats: comparison with acute stress responses.

We have reported that the microinjection of neostigmine into the hippocampus of rats induced responses similar to stress responses in terms of catecholamines and glucose in plasma. In order to test the hypothesis that hippocampal neostigmine injection is a possible animal model of acute stress responses, we investigated c-Fos expression in the hypothalamic paraventricular nucleus (PVN) and plasma levels of adrenocorticotrophic hormone (ACTH) after hippocampal neostigmine injection and compared these levels with those resulting from stressful conditions such as immobilization and insulin-induced hypoglycemia. The patterns of expression of Fos-ir in the PVN after microinjection of neostigmine into the hippocampus were not different from those seen in the two stressful situations. After microinjection of neostigmine, plasma ACTH levels significantly increased. Taken together, the results of this study indicate that microinjection of neostigmine into the hippocampus is a potential experimental model for acute stress responses.

Low plasma epinephrine in elderly female subjects of dementia of Alzheimer type.

One of the robust features of brain pathologies of dementia of Alzheimer type (DAT) is the impairment of the hippocampus, especially the cholinergic system. Several animal studies have suggested that the cholinergic system in the hippocampus is involved in the control of the plasma level of catecholamines and glucose. The stimulation of the hippocampal cholinergic system has resulted in the elevation of plasma catecholamines and glucose in rats. In the present study, we measured the plasma level of epinephrine, norepinephrine, dopamine, glucose, and insulin during a fasting state in the morning in hospitalized DAT (n=66), vascular dementia (VD) (n=28), or non-demented (ND) (n=21) females (mean age DAT=82. 49+/-4.98, VD=82.86+/-5.86, ND=82.95+/-7.77, respectively). Statistical analysis showed that the plasma level of epinephrine during a fasting state in DAT subjects was significantly lower than that of ND subjects; however, in VD subjects the level of epinephrine was not different from that of ND subjects. Other values did not differ significantly among the groups.

Inhibition of inducible nitric oxide synthase gene expression by indomethacin or ibuprofen in beta-amyloid protein-stimulated J774 cells.

Recent studies show that a mononuclear phagocyte lineage, including microglia, plays a possible role in the pathogenesis of Alzheimer's disease through nitric oxide (NO)-mediated neurotoxicity. Epidemiological studies show that nonsteroidal anti-inflammatory drugs (NSAIDs) have a protective effect against Alzheimer's disease. Based on these observations, it has been hypothesized that an anti-Alzheimer's disease effect of NSAIDs could result from the inhibition of NO synthesis. We report here that indomethacin or ibuprofen dose-dependently reduce beta-amyloid protein and interferon-gamma-induced NO production, accompanied by an inhibition of inducible nitric oxide synthase mRNA expression in J774 cells, a murine macrophage cell line. Aspirin, however, does not produce such an effect, suggesting that the cyclooxygenases pathway is not involved in the inhibitory effects of NSAIDs on beta-amyloid protein and interferon-gamma-induced NO production in J774 cells.

Characterization of lattice defects in strontium titanate single crystals by X-ray topography and transmission electron microscopy

Lattice defects in SrTiO3 single crystals were characterized by X-ray topography and transmission electron microscopy. We examined two groups of crystals whose lapped faces were (001) and (011), respectively. After taking X-ray topographs, crystals which included relatively many defects were chosen for detailed investigation by transmission electron microscopy, which gave the following results: (i) some subgrain boundaries observed by X-ray topography were small-angle tilt boundaries; and (ii) many dislocations were found in the region where thick line contrast was observed in X-ray topographs. Most of them had <100> type Burgers vectors.

Factors of glass-ionomer cements influencing the bond strength to resin composites.

The bond strength between composites and various particle sizes of glass-ionomer cements was investigated. The best bond strength was obtained after use of a small-particle cement and with the highest powder-to-liquid ratio employed for mixing the cement. In addition, use of a small-particle cement and the highest powder:liquid ratio produced cements with significantly stronger tensile strengths. Failure usually occurred within the cement. Consequently, the recorded bond strength actually reflected the tensile strength of the relevant cement.

[Neuro-Behcet disease mimicking a thalamic tumor].

A case of neuro-Behcet disease presenting as a thalamo-lenticular expanding lesion is reported. A 41-year-old female was admitted with mental deterioration and right hemiparesis. She had been suffering from recurrent oral and genital ulcers and erythema nodosum for several years before admission. Neurological examination on admission revealed poor mental activity, dysarthria and right hemiparesis. Lumbar puncture showed CSF pleocytosis. CT and MRI revealed a thalamo-lenticular expanding lesion. CT showed a homogeneous hypodense lesion of the left lenticulothalamic region, which was enhanced in the central part, exerting a mild mass effect. MRI also revealed the lesion better. The T2 weighted images showed a high intensity signal in the left thalamo-lenticular region and the left peduncle. The T1 weighted images showed a low signal in the corresponding areas with a central enhancement with Gd-DTPA. EEG, SPECT and angiography indicated normal findings. Histologic study of the brain biopsy tissue ruled out a tumor but did not show any specific diagnosis. The patient improved with steroid therapy. In conclusion, the clinical and radiological presentation of neuro-Behcet disease can mimic a cerebral tumor. In such cases, stereotactic biopsy is useful to exclude suspicion of a cerebral tumor.

Non-projectiveness of X-ray Pendellösung-fringed diffraction images.

It has been experimentally found that X-ray moiré fringes are not exactly given as a projected figure from the specimen crystal as predicted by the standard theory of X-ray dynamical diffraction, but show a kind of spatial oscillation along the beam path out of the crystal. This paper reports that a similar spatial oscillation has been found for Pendellösung fringes in a similar experiment recording plane-wave X-ray topographs of a silicon wedge crystal onto a set of multi-stacked films. The oscillation of the Pendellösung fringes was easily found among the simultaneous topographs on the multi-stacked films by examining the fringe profiles, and was also found in topographic images by somewhat careful inspection. It is noteworthy that a simple reciprocal correspondence was observed between the amplitude of fringe oscillation and the fringe contrast. This finding of non-projectiveness, i.e. the fringe oscillation noted above, in Pendellösung fringes as well as in moiré fringes suggests that the non-projectiveness occurs as a very basic property of X-ray interference fringes produced by crystal diffraction.

Population dynamics of sexual and resource competition.

Interspecific competition is usually thought of in terms of resource competition. Closely related species, however, may often compete also for a "sexual niche," a sexual resource. Both sexual and resource competition are likely to affect the dynamics of closely related sympatric species. Here, a combined model of sexual and resource competition is developed and analyzed in terms of phase planes. Population dynamics involving sexual competition alone are characterized by competitive exclusion and dependence on relative initial population size of the competing species. This dependence on initial population size is due to the nonlinear equilibrium isoclines of sexual competition, which contrast with the linear isoclines of the Lotka-Volterra competition equations. Dependence on initial population size is stronger when sexual competition is severe and/or when growth rates of the two species are low. Additional dynamic possibilities arise under combined sexual and resource competition. If the sexual competition is strong, competitive exclusion is the only outcome. But if sexual competition is weak, and if stable coexistence would occur without sexual competition, then both stable coexistence and competitive exclusion may occur simultaneously. A species that is relatively rare initially may be excluded, but when both species are initially of comparable abundance both will persist. Adding sexual competition to resource competition thus introduces additional uncertainty concerning the outcome of competition between two sympatric species.

Populations can persist in an environment consisting of sink habitats only.

Populations that live in environments with different habitats have to distribute their offspring over these habitats. When population densities go to equilibrium, the evolutionary optimum is an ideal free distribution. Under an ideal free distribution, no offspring should be put into sink habitats. However, when the environmental conditions in a habitat are not constant but fluctuate, allocating offspring to sink habitats can increase the long term growth rate of a population. We demonstrate this principle in a simple model for offspring allocation. As a consequence, it is possible that populations persist in environments that only consist of sink habitats.

Expression of telomerase RNA, telomerase activity, and telomere length in human gliomas.

To understand the mechanisms of telomere maintenance in human gliomas, telomerase activity, telomerase RNA expression and telomere length of surgically excised glioma samples were analyzed. Sixty-five percent of gliomas exhibited telomerase activity, the occurrence of which was not related to their histological malignancy scale. Not only the telomerase-positive gliomas, but also the telomerase-negative gliomas and normal brain expressed telomerase RNA, suggesting that the presence of telomerase RNA component does not indicate the presence of telomerase activity. Compared with telomerase-positive gliomas, telomerase-negative gliomas had long heterogeneous telomeric terminal restriction fragments. These data suggest that in addition to the telomerase-dependent mechanism, a telomerase-independent mechanism for telomere maintenance may be present in human gliomas.

Activity-dependent distribution of protein kinase C-delta within rat cerebellar Purkinje cells following unilateral labyrinthectomy.

Protein kinase C isoforms PKC-delta and PKC-gamma are expressed in Purkinje cells in the uvula-nodulus of the cerebellum. We examined the effect of Purkinje cell activity on the transcription, expression and intracellular distribution of PKC-delta and PKC-gamma. Relative changes in activity were induced by unilateral labyrinthectomy (UL), decreasing the activity of Purkinje cells on the side of the labyrinthectomy relative to the contralateral side with intact vestibular input. After a UL, there was decreased immunolabeling of Purkinje cell axon terminals in the ipsilateral caudal vestibular complex by antisera to PKC-delta, but not PKC-gamma. Western blots prepared from the uvula-nodulus and caudal vestibular complex showed an increase in the cytosolic PKC-delta and a decrease in membrane-associated PKC-delta in the ipsilateral uvula-nodulus 12-48 h after the UL. Hybridization histochemistry and semiquantitative reverse transcription polymerase chain reaction (RT-PCR) demonstrated no change in transcription of PKC-delta mRNA in the uvula-nodulus 1-240 h after unilateral labyrinthectomy. We conclude that both PKC-delta and PKC-gamma are constitutively expressed in Purkinje cells. The targeting of PKC-delta, but not PKC-gamma, to Purkinje neuron synaptic terminals is influenced by activity.

MRA demonstration of "periarteritis" in Tolosa-Hunt syndrome.

BACKGROUND: Modern magnetic resonance imaging (MRI) diagnosis of Tolosa-Hunt syndrome rests upon demonstration of cavernous sinus abnormalities. We present a case of Tolosa-Hunt syndrome who has no abnormal mass lesion in the cavernous sinuses on MRI but with a diagnostic lesion on magnetic resonance angiography (MRA). CLINICAL PRESENTATION: A 48-year-old woman developed acute periorbital pain and abducens palsy of the right side at the first episode, and subacute peri-orbital pain and rapidly deteriorating visual acuity on the left side at the second episode with a four months interval. MRI showed no soft-tissue abnormality in the cavernous sinuses. FINDINGS: MRA demonstrated a narrowing of the right cavernous carotid artery at the first episode, and narrowings of the left clinoid carotid and ophthalmic arteries at the second episode. Based on these findings, the patient underwent urgent steroid therapy and the symptoms resolved dramatically in each episode. Follow-up MRA confirmed resolution of arterial narrowings. INTERPRETATION: MRA may help prompt the noninvasive diagnosis in certain cases of Tolosa-Hunt syndrome with little inflammatory reaction in the cavernous sinus but with predominant intra- and juxta-cavernous periarteritis.

Establishment of two glioma cell lines from two surgical specimens obtained at different times from the same individual.

We established two glioma cell lines from two surgical specimens obtained at different times from the same patient. One (No. 9R), which was derived from the recurrent tumor (glioblastoma, grade IV), proliferated more rapidly in vitro than the other (No. 9) from the primary tumor (slightly anaplastic astrocytoma, grade II-III). No. 9R showed heterotransplantability in nude mice, whereas No. 9 did not. These findings indicate that No. 9R has a more aggressive or malignant nature than No. 9. Both cell lines showed homozygous deletion of the representative tumor suppressor p16 and p15 genes, but no p53 gene alteration. However, examination of the overall mRNA expression profile using a commercially available cDNA-spotted membrane revealed much higher expression levels of several mRNAs, at least, in No. 9R than in No. 9, although the relationship between these mRNAs and the growth potentials remained unknown. These two cell lines, derived from the same individual, with different proliferating potentials may be useful for studies on the molecular bases of glioma malignancy and progression.

Rare-type mutations of MMAC1 tumor suppressor gene in human glioma cell lines and their tumors of origin.

A total of 10 glioma cell lines were examined to evaluate the status of the MMAC1 gene, a candidate tumor suppressor gene. Six cell lines showed mutations with presumed loss of heterozygosity and 1 cell line showed no mRNA expression. The 6 mutations consisted of 3 3-bp deletions (codons 17, 101 or 199), 1 missense mutation (codon 252) and 2 truncation mutations (1 nonsense mutation at codon 233 and 12-bp insertion at codon 241). Among them, the 3-bp deletions, which are a rare type of mutation in MMAC1 gene, were located in the N-terminal half (codons 1-212) of the coding region, which is considered important in MMAC1 function. The missense mutation was located unusually in the C-terminal half (codons 212-403), but it was in a small region in which some other reported missense mutations are clustered. Thus, these 4 mutations were suggested to have functional effects on the MMAC1 activity, like the other 2 mutations with predicted protein truncations. By sequence analysis of cDNA clones, we confirmed that all the mutations including these 4 rare ones were in the MMAC1 gene, not in the PTH2 pseudogene. In 2 cases, we also examined the primary glioma tissues from which the cell lines had been derived and found the same mutations as in the cell lines in both cases. This suggested that the mutations in these cell lines were derived from the primary glioma tissues, but not from artifacts arising during long-term in vitro cultivation.