12 research outputs found

    Breast cancer incidence highest in the range of one species of house mouse, Mus domesticus

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    Incidence of human breast cancer (HBC) varies geographically, but to date no environmental factor has explained this variation. Previously, we reported a 44% reduction in the incidence of breast cancer in women fully immunosuppressed following organ transplantation (Stewart et al (1995) Lancet346: 796–798). In mice infected with the mouse mammary tumour virus (MMTV), immunosuppression also reduces the incidence of mammary tumours. DNA with 95% identity to MMTV is detected in 40% of human breast tumours (Wang et al (1995) Cancer Res55: 5173–5179). These findings led us to ask whether the incidence of HBC could be correlated with the natural ranges of different species of wild mice. We found that the highest incidence of HBC worldwide occurs in lands where Mus domesticus is thse resident native or introduced species of house mouse. Given the similar responses of humans and mice to immunosuppression, the near identity between human and mouse MTV DNA sequences, and the close association between HBC incidence and mouse ranges, we propose that humans acquire MMTV from mice. This zoonotic theory for a mouse-viral cause of HBC allows testable predictions and has potential importance in prevention. © 2000 Cancer Research Campaig

    Methenamine Silver Stain Impregnates Amyloid-related Components of Senile Plaques in the Alzheimer Brains as Clearly as βprotein Immunostaining

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    We developed a new type of methenamine silver (MS) stain for senile plaques (SP) on paraffin-embedded tissue sections. This method is a modification of both Gomori's methenamine silver nitrate, and Jone's periodic acid-methenamine silver (PAM) stains. We omitted chemical preoxidation by either periodic acid in the PAM stain or chromic acid in Gomori's stain, and determined the best condition of silver solution for SP. This resulted in selective staining of SP and amyloid angiopathy, because capillary basement membranes, corpora amylacea, macrophage granules, and nerve cell pigments remained unstained. The argyrophilia of SP was not affected by pretreatment with aldehyde blocking reagents. In comparison with βprotein immunostain, our MS stain showed almost the same staining pattern as that of the βprotein immunostain. Moreover, the argyrophilia of SP was selectively abolished by formic acid pretreatment, which has been shown to destroy β-pleated sheet structure of amyloid, suggesting that our MS stain impregnates amyloid-related components of SP. Our MS stain is a new, rapid, easy, and reliable method, and sensitive enough for routine or screening studies of the SP

    Comparison of total MU and segment areas in VMAT and step-and-shoot IMRT plans

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    We compared treatment plans for volumetric intensity-modulated arc therapy (VMAT) and step-and-shoot intensity-modulated radiation therapy (IMRT) in terms of their monitor unit (MU) and segment area at each control point to investigate the difference between the two methods. We investigated three sites: prostate (three cases), head and neck (three cases), and pleura (two cases). We used the total MU and the MU weighted average of segment area (MWSA) in each plan to compare VMAT and IMRT plans. VMAT plans tended to have a larger MWSA and a lower total MU than did IMRT plans in all sites, although there was little difference between dose indices in either irradiation technique. We conclude that VMAT is a better treatment technique due to its higher MU efficiency caused by the larger segment area

    両側下オリーブ核肥大変性を呈した脳幹梗塞 : 特に星状細胞機能と神経可塑性について

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    要旨:症候性軟口蓋振戦(SPT)を伴い両側下オリーブ核(IO)肥大変性(IOHD)を認めた脳幹梗塞例を報告し, IOHDの病態についてIOの機能的特性と星状細胞の神経保護作用の面から考察した。IOHDは歯状核オリーブ路(DOP)の障害による経シナプス変性であり,神経細胞の変性•脱落と共に慢性的な肥胖星状細胞増多を特徴とする。IOの機能的特性は, DOPを介する小脳からのGABA作動性抑制性入力と中脳•間脳結合域などからの興奮性入力(グルタミン酸作動性と谁測されている)を同時に受け, 小脳プルキンユ細胞に登上線維を出力し, 発振器として運動学習や運動誤差修正に働くことである。一方,星状細胞の様々な機能の中で,グルタミン酸依存性のシナプス伝達調節作用が, 神経保護の面から注目されている。DOPの障害により抑制性入力が途絶し, 過剰な興奮性入力(恐らくグルタミン酸作動性)にさらされたIOのシナプスでは, その可塑性に向けてIO神経細胞と星状細胞との間に, 懸命なかつ絶望的とも言える相互作業が続く。その中で,次第に神経細胞変性と星状細胞の肥大が進打し, やがて徐々に神経細胞は脱落に向かう。しかし, IOはなお長期間活動的であり, 抑制を失った発振器としてのIOは, 臨床的にはSPTを発現し続ける。 IOHDは単なる変性ではなく, 抑制性入力が途絶したIO神経細胞と星状細胞の両者により織りなされる, 神経可塑性に向けてのmodulation過程と考えられる。IOHDの病態には, IO神経細胞の機能的特性と共に星状細胞の神経保護作用が重要である。Abstract: Inferior olivary hypertrophic degeneration (IOHD), the distinguishing features of which are neuronal degeneration and chronic gemistocytosis, is thought as being a transsynaptic degeneration resulting from the interruption of the dentato-olivary pathway (DOP). Bilateral IOHD associated with brainstem infarction with symptomatic palatal tremor (SPT) was reported here. In addition, the pathology of IOHD was discussed on the basis of the structural and functional properties of the olive and astrocytes. In the neural network called the three-element loop, olivary dendritic spines receive both inhibitory GABAergic inputs via the DOP and excitatory inputs (which are presumed to be glutamatergic) from the mesodiencephalic junction. By sending climbing fibers to the cerebellar Purkinje cells, the olive is considered to work as an oscillator for motor learning and motor-error correction. Among the various functions of astrocytes, the glutamate dependent synaptic regulation by these cells is an emerging concept In the presence of interruption of inhibitory inputs, both olivary neurons and astrocytes make serious, but rather desperate, efforts toward neuroprotection from excessive excitatory (probably glutamatergic) inputs, followed by gradual progression of neural degeneration and astrocytic hypertrophy. In IOHD, the olive may remain hyperactive for a long time after the onset of the causative disease; thus, the SPT may continue throughout tifo as an expression of the dysfunction of the olivary oscillator. IOHD is not only a degenerative, but also a modulating process for neuroplasticity that occurs in the neuron astrocyte interaction after the loss of inhibitory inputs to the olive. In addition to the unique properties of olivary neurons, the potential role of astrocytes in neuroprotection is crucial for the development of IOHD.17KJ0000871059
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