Synthesis of optically active polymers by asymmetric catalysts. IV. Dialkylzinc – alcohol system as catalyst for asymmetric-selective polymerization of propylene oxide

The system diethylzinc/optically active alcohol was examined as catalyst for asymmetric-selective polymerization of propylene oxide. Optically active alcohols with rigid structure are effective for the asymmetric selection. D (–)-1-Methoxypropanol-2 as well as poly(D -propylene oxide) of low molecular weight with hydroxyl end groups select L (–)-propylene oxide. ?Catalyst control”? mechanism of the stereoselection in the polymerization is suggested on this and other bases.     

Modulation during sleep of the cat trigeminal neurons responding to tooth pulp stimulation

Sleep-induced changes in the trigeminal neuron responses to electrical stimulation of the cat tooth pulp were studied. Two parameters were adopted: One was the evoked spike number at two times the threshold intensity (2 X T response magnitude), which would reveal the level shifting of the neuronal response by the sleep-regulatory system. Another was the rate of change in the response intensity when the stimulus was raised to a level of 0.7 time the arousal threshold during light slow wave sleep (sensitivity gradient), which would reflect the influences of the pain-modulatory system driven by strong noxious inputs. It was found that during sleep the two indexes tended to show a correlated change; the neurons which came to have a greater 2 X T response magnitude tended to have a smaller sensitivity gradient than during wakefulness, and vice versa. It was suggested that two contrasting populations of tooth pulp neurons might be differentiated, and that the sleep-regulatory system and the pain-modulatory system would have differential but correlated controls over these two kinds of neurons.     

PRIMARY LEIOMYOSARCOMA OF BONE

A 62-year-old female with primary leiomyosarcoma of the left femur is reported with a review of 21 cases reported in the literature. The resected specimen showed that the tumor extended from the femoral head to the diaphysis for 13cm in length. The tumor showed mainly intramedullary proliferation, but extraosseous growth was also noted at the great trochanter. Microscopic examination revealed well differentiated leiomyosarcoma characterized by interlacing bundles of fusiform cells with eosinophilic cytoplasm and rod-shaped hyperchromatic nuclei. PAP stain of actin on the tumor cells was positive. On electron microscopy, microfilament of 6–8 nm in diameter, dense bodies, plnocytotic vesicles, marginal attachment plate, and basal lamina were noted. The patient died with pulmonary metastasis, 1 year and 7 months after the operation. An autopsy showed metastases in the right pelvic cavity and bilateral lungs, and confirmed the primary site to be the left femur.     

Pathological analysis of hypertrophic cardiomyopathy simulating dilated cardiomyopathy

The pathomorphologic features of hypertrophic cardiomyopathy simulating dilated cardiomyopathy in the late stage (HCM-DCM) were compared with those of ordinary hypertrophic cardiomyopathy (HCM). Seven autopsied hearts with HCM-DCM and 11 with HCM were assessed quantitatively using an image analyzer. Unlike HCM, significant left ventricular enlargement and wall thinning were observed in HCM-DCM, and the percentage areas of massive fibrosis and disarray were significantly greater. In HCM-DCM, the disarray was distributed diffusely, whereas massive fibrosis was distributed more intensively in the ventricular septum and anterior wall than in the lateral and posterior wall. Narrowing of intramyocardial small arteries was observed more frequently in HCM-DCM, especially in the ventricular septum and anterior wall, than in HCM. These results suggest that the enlargement and wall thinning of the left ventricle in HCM-DCM are attributable to non-uniform progression of massive fibrosis, which is closely related to small-arterial lesions.     

Unique properties of fetal lymphoid progenitors identified according to RAG1 gene expression

RAG1/GFP knockin mice were exploited to isolate and characterize fetal lymphoid progenitors. CD11b and IL-7Ralpha are expressed in a developmental stage-dependent fashion, revealing how substantial numbers of early lymphoid progenitors were discarded or neglected in previous studies. The myeloerythroid potential of fetal progenitors in clonal assays declined in synchrony with activation of the RAG1 locus but was not completely extinguished. Lymphoid differentiation corresponded to patterns of gene expression previously found for adult marrow, but no fraction of fetal liver was enriched with respect to B + T progenitors. Also, unlike adults, fetal lymphoid progenitors transiently expressed endothelial cell markers. These findings help to reconcile discrepancies in previous reports and suggest that the fetal immune system arises via unique mechanisms.     

Alterations in the INK4a/ARF locus and their effects on the growth of human osteosarcoma cell lines

Two different proteins, p16(INK4a) and p14(ARF), encoded by the INK4a/ARF locus play important roles in the RB and p53 pathways, respectively. This study was performed to determine genetic and epigenetic alterations in the INK4a/ARF locus and their effects on the growth of osteosarcoma. Among six cell lines examined, both p16(INK4a) and p14(ARF) exons were homozygously deleted in two cell lines, MG63 and HOS, and both p16(INK4a) and p14(ARF) promoters were methylated in one cell line, U2OS. Wild-type mRNA and proteins for p16(INK4a) and p14(ARF) were expressed in three other cell lines, SaOS2, HuO9, and G292. Transfection studies were performed using two cell lines, U2OS and MG63. Both the RB and p53 genes were wild types in U2OS, whereas p53 but not RB was mutated in MG63. Both p16(INK4a) and p14(ARF) suppressed the growth of U2OS, whereas p16(INK4a) but not p14(ARF) suppressed the growth of MG63. p53 only did not suppress the growth of MG63 either; however, coexpression of p14(ARF) with p53 increased the fraction of the G0/G1 phase in MG63 cells. The data presented here demonstrate the importance of genetic and epigenetic alterations in the INK4a/ARF locus for the growth of osteosarcoma and thus will be useful to further understand the biologic behavior of osteosarcoma in association with the defects in the p53 and RB pathways.     

A segment of the Mecp2 promoter is sufficient to drive expression in neurons

Rett syndrome (RTT) is caused by mutations in the gene encoding methyl CpG-binding protein 2 (MeCP2). Although MeCP2 shows widespread expression in both neuronal and non-neuronal tissues, the symptoms of RTT are largely neurological. Herein, we have identified the regulatory region of the mouse Mecp2 gene that is sufficient for its restricted expression in neurons. A segment of the Mecp2 gene (-677/+56) exhibited strong promoter activity in neuronal cell lines and cortical neurons, but was inactive in non-neuronal cells and glia. The region necessary for neuronal-specific promoter activity was located within a 19 bp region (-63/-45). Several nuclear factors were found to bind to this region and some of these factors were enriched in nuclear extracts prepared from the brain. To examine the activity of the Mecp2 promoter in vivo, we generated transgenic mice expressing the LacZ reporter driven by the -677/+56 region of the Mecp2 gene. The transgene was expressed in the mesencephalon as early as embryonic day 10 and in the hindbrain and spinal cord by E12. Interestingly, a marked induction of transgene expression was observed postnatally throughout the brain, similar to that of endogenous MeCP2. However, expression of the transgene was absent in non-neuronal tissues that are known to express Mecp2. Taken together, these data indicate that the -677/+56 region of the Mecp2 promoter partially recapitulates the native expression pattern of the Mecp2 gene, which possesses restricted expression in neurons of the central nervous system.     

Iodine-poly(vinyl alcohol) interactions, 4. Stoichiometry of iodine/iodide in the polyiodide ion bound in the cage of poly(vinyl alcohol)

Aqueous poly(vinyl alcohol) (PVA)-iodine-boric acid solution was treated with anion exchange resin and the system involving only the cage complex was isolated. The system was then extracted with carbon tetrachloride, and I₂ and I^?, which were released from the complex, were separated and pooled in the carbon tetrachloride and the aqueous layers, respectively. From the absorption spectra of the layers the amounts of I₂ and I^? were determined. The ratio I₂/I^? was found to be approximately 2,0, which corresponds to the I₂/I^? stoichiometry in the complex. This result suggested that the major species bound in the PVA cage are pentaiodide ions, i.e., I with linear configuration and/or I₂· I with distorted chain structure. Judging from the resonance Raman spectrum of the PVA-iodine solution that had been revealed before, it was concluded that the two absorption bands of the complex at λ_max = 650 and 355 nm are ascribed to the I and I₂ · I ions, respectively.     

A complex composed of USF1 and USF2 activates the human FcepsilonRI alpha chain expression via a CAGCTG element in the first intron

The high-affinity IgE receptor, FcepsilonRI, is a key regulatory molecule in the allergic reaction. During the course of studies to find cis-acting elements for FcepsilonRI alpha chain gene expression, a CAGCTG sequence located in the first intron was revealed to serve as a crucial enhancer element. Electromobility shift assays using antibodies and in vitro translation products showed that the CAGCTG element was recognized by the USF1/USF2 complex. As was the case for other intronic cis-elements, the CAGCTG element regulated the promoter in an orientation- and position-dependent manner. Overexpression of USF2 antisense repressed the FcepsilonRI alpha chain gene promoter and decreased the amount of alpha chain mRNA in mast cell lines. All these results indicated that the USF1/USF2 complex activates the human FcepsilonRI alpha chain gene expression via the CAGCTG element in the first intron.