An attempt to hybridize Drosophila species using pole cell transplantation

We have made hybrid embryos in Drosophila by pole cell transplants, by transferring pole cells from two species, D. rajasekari and D. eugracilis, into sterile D. melanogaster hosts. These females were then mated to melanogaster males and the older these females were, the further their hybrid offspring developed. In the case of the rajasekari/melanogaster hybrids, the embryos form cuticle but had defective heads, while the eugracilis/melanogaster hatched as larvae that grew but did not moult to the second instar. Hybrid pole cells could be transferred to melanogaster hosts but they failed to make eggs.     

An attempt to reverse performance deficits associated with depression and experimentally induced helplessness.

The learned helplessness model of depression predicts that any effective treatment for reactive depression should also reverse performance deficits associated with experimentally induced helplessness, and vice versa. A study was conducted to test this prediction. Ss were 62 college students who were exposed to experimental manipulations designed to induce helplessness or who scored above a group mean on the Beck Depression Inventory. Depressed and helpless Ss were randomly assigned to 4 groups. The 2 treatment groups received either E. Velten's (1968) mood statements for the induction of elation or a set of simple anagrams to solve. The 2 remaining groups were exposed to no-treatment conditions. All Ss were tested for helplessness on a series of concept formation problems. Results fail to confirm the predictions of the learned helplessness model of depression. Although treatment was effective with helpless Ss, the performance of treated depressed Ss was not enhanced. Also, depressed Ss given anagrams performed more poorly than depressed Ss given mood statements. Several possible explanations for the findings are considered. (27 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Successful islet autotransplantation in humans: functional insulin secretory reserve as an estimate of surviving islet cell mass

Bafilomycin A1, a specific inhibitor of vacuolar type H(+)-ATPase, can inhibit the growth of a variety of cultured cells in a dose-dependent manner, but its mechanism is unclear. The aim of this study was to examine whether bafilomycin A1 inhibits the growth of Capan-1 human pancreatic cancer cells through apoptosis. The effect of bafilomycin A1 on tumour growth in vitro and in vivo was examined using an MTT assay and an in vivo tumour model. The presence or absence of apoptosis was determined by morphology and DNA analysis of tumour cells. The concentration of bafilomycin A1 for 50 per cent inhibition of cell viability during 72 h by the MTT assay was 5 nm. In DNA analysis, a ladder of fragmented DNA was detected in Capan-1 cells treated with bafilomycin A1 at concentrations greater than 10 nm for 24 h. Nude mice bearing a xenografted Capan-1 cell line tumour received 4 weeks of bafilomycin A1 (1.0 mg/kg per day). This treatment significantly inhibited tumour growth compared with controls after 21 days (P < 0.05). Histopathological examination of tumour cells in the treated group demonstrated signs of apoptosis with chromatin condensation and cell shrinkage. These observations suggest that bafilomycin A1 inhibits the growth of Capan-1 human pancreatic cancer cells through apoptosis.     

Initiation of autoimmune diabetes by developmentally regulated presentation of islet cell antigens in the pancreatic lymph nodes

Little is known about the events triggering lymphocyte invasion of the pancreatic islets in prelude to autoimmune diabetes. For example, where islet-reactive T cells first encounter antigen has not been identified. We addressed this issue using BDC2.5 T cell receptor transgenic mice, which express a receptor recognizing a natural islet beta cell antigen. In BDC2.5 animals, activated T cells were found only in the islets and the lymph nodes draining them, and there was a close temporal correlation between lymph node T cell activation and islet infiltration. When naive BDC2.5 T cells were transferred into nontransgenic recipients, proliferating cells were observed only in pancreatic lymph nodes, and this occurred significantly before insulitis was detectable. Surprisingly, proliferation was not seen in 10-day-old recipients. This age-dependent dichotomy was reproduced in a second transfer system based on an unrelated antigen artificially expressed on beta cells. We conclude that beta cell antigens are transported specifically to pancreatic lymph nodes, where they trigger reactive T cells to invade the islets. Systemic or extrapancreatic T cell priming, indicative of activation via molecular mimicry or superantigens, was not seen. Compromised presentation of beta cell antigens in the pancreatic lymph nodes of juvenile animals may be the root of a first "checkpoint" in diabetes progression.     

Strategies for graft immunomodulation in islet transplantation

BACKGROUND: The cortex of patients with schizophrenia exhibits a deficit in neuropil, but the nature and extent of cellular abnormalities remain unclear. To gain further insight into this abnormality, neuronal and glial somal size were analyzed in postmortem brains from 9 patients with schizophrenia, 10 normal (control) patients, and 7 patients with Huntington disease, the latter representing a known neurodegenerative disorder. METHODS: A 3-dimensional image analyzer was used to measure the perimeters of 10722 neuronal and 19913 glial profiles in Brodmann areas 9 and 17. Neurons and glia were classified by size and layer to assess specific vulnerabilities with respect to cortical architecture and circuitry. RESULTS: The schizophrenic prefrontal cortex was characterized by a downward shift in neuronal sizes accompanied by 70% to 140% per layer increases in the density of small neurons. In layer III only, a significant reduction in mean neuronal size was associated with a significant decrease in the density of very large neurons in sublayer Illc. Neither neuronal size in occipital area 17 nor glial size in prefrontal or occipital cortexes were reduced. In cortex with Huntington disease, neuronal degeneration was evidenced by concurrence of reduced neuronal size, decreased density of large neurons, and dramatic elevation in density of large glia. CONCLUSIONS: Distinct cytometric abnormalities support the hypothesis that neuronal degeneration in the prefrontal cortex is not a prominent feature of the neuropathological changes in schizophrenia, although an ongoing process in Huntington disease. Rather, schizophrenia appears to involve more subtle abnormalities, with the largest corticocortical projection neurons of layer IIIc expressing the greatest somal reduction.     

High prevalence of antibodies to glutamic acid decarboxylase in comparison to islet cell antibodies in patients with long-standing insulin-dependent diabetes mellitus

To elucidate the clinical significance of antibodies to glutamic acid decarboxylase (GAD Ab) compared to islet cell antibodies (ICA) in recent-onset and long-standing insulin-dependent diabetes mellitus (IDDM). We examined GAD Ab and ICA in 29 recent-onset and 85 long-standing patients with IDDM. GAD Ab was detected by a radioimmunoassay kit using purified pig brain GAD as an antigen. The prevalence of GAD Ab in the recent-onset diabetic patients was 55.2%, slightly lower than that of ICA (65.5%). In contrast, the prevalence of GAD Ab in long-standing diabetic patients was 42.4%, which was significantly higher than that of ICA (23.5%) (p < 0.01). GAD Ab were consistently detected in approximately 40% of patients with long-standing disease, while ICA decreased according to duration of disease. The GAD Ab titer in ICA-positive patients (mean +/- SD, 1588.2 +/- 6755.1; range, 6-38574) was significantly higher than that in ICA-negative patients (mean +/- SD, 13.4 +/- 17.9; and range, 5-72 units) (p < 0.001). These findings suggest that GAD Ab are more useful than ICA to know participation of immune disorders in long-standing patients with IDDM.     

Resumption of morphine self-administration by ex-addict rats: An attempt to modify tendencies to relapse.

Studied relapse tendencies in 69 morphine-dependent male hooded rats which had learned to drink bitter solutions of the drug in preference to water. Prolonged enforced abstinence (110 days) did not prevent Ss from resuming self-administration of morphine. Since the bitter taste of morphine may have become a secondary reinforcer, an attempt was made to extinguish responding for this source of reward. Abstinence was shortened to 12 days, during which Ss were given solutions of quinine to drink. On subsequent relapse tests these Ss consistently took less morphine than controls. Ss injected with methadone during the 1st 8 days of abstinence initially consumed slightly more morphine on relapse tests than did controls, but this difference was not maintained. (22 ref.) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

无底柱分层推进留矿采矿法的尝试

介绍了文峪金矿无底柱分层推进留矿采矿法的试验研究。结果表明,采场结构合理生产能力大,解决了厚矿体回采及下中段生产安全问题。     

Use of islet cells in cell therapy

The results of our previous work [Hibino et al., Biochim. Biophys. Acta 1174 (1993) 162-170] suggested that a highly repetitive DNA component facilitates bending of the helix axis to be recognized by the nuclear scaffold proteins from rat liver, P123 and P130. In the present experiment, it was shown that binding of these proteins to such a repetitive DNA component from rat liver nuclei (370-bp XmnI fragment) is based on a cooperative mode of interaction, although the binding activity of P130 is much higher than that of P123. The immunoblot analysis with anti-phosphoamino acid antibodies suggested that phosphorylation of serine and threonine residues occurs on P123 and P130, but also of tyrosine residue(s) on P130. The phosphatase assay showed that phosphoryl groups on these proteins may be involved in altering the DNA binding activities of the proteins. Thus, the results in the present study imply that phosphorylation of a nuclear scaffold protein in addition to the degree of bending of the DNA helix axis plays an important role in anchoring chromatin to the nuclear scaffold and in construction of a higher-order chromatin structure.