Effects of ortho-substituents on the living polymerization of phenylacetylenes by MoOCl4-based catalysts

Polymerization of phenylacetylenes (PAs) having various ortho-substituents were examined by using MoOCl₄—n-Bu₄Sn—EtOH (mole ratio 1:1:1) as catalyst. Phenylacetylenes with no or sterically small ortho-substituents did not polymerize in a living fashion. On the other hand, in the polymerization of phenylacetylenes having medium-sized substituents (e.g., CH₃, Cl, Br, and iPr), the number-average molecular weights M_n of polymers increased in direct proportion to monomer consumption, while the polydispersity ratios were 1,2– 1,3, which is in favor of living polymerization. Further, monomers having bulky ortho-groups (CF₃ and Me₃Ge) exhibited excellent living nature with small polydispersity ratios of ≈ 1,1. Thus, it is concluded that not the electronic but the steric effect of the ortho-substituent is important to achieve living polymerization.     

Immunohistochemical analysis of MCT1, MCT2 and MCT4 expression in rat plantaris muscle

All three forms of recombinant low voltage-activated T-type Ca²⁺ channels (Ca_v3.1, Ca_v3.2 and Ca_v3.3) exhibit a small, though clearly evident, window T-type Ca²⁺ current ( I _Twindow) which is also present in native channels from different neuronal types. In thalamocortical (TC) and nucleus reticularis thalami (NRT) neurones, and possibly in neocortical cells, an I _Twindow-mediated bistability is the key cellular mechanism underlying the expression of the slow (< 1 Hz) sleep oscillation, one of the fundamental EEG rhythms of non-REM sleep. As the I _Twindow-mediated bistability may also represent one of the cellular mechanisms underlying the expression of high frequency burst firing in awake conditions, I _Twindow is of critical importance in neuronal population dynamics associated with different behavioural states.     

Kupffer cell-mediated cytotoxicity against hepatoma cells occurs through production of nitric oxide and adhesion via ICAM-1/CD18

Rat Kupffer cell (KC)-mediated cytotoxicity against both thesyngeneic hepatoma cell line AH70 and hepatocytes was evaluatedby changes in mitochondrial function, and the possible roleof ICAM-1/CD18 in the interaction between the cells was studied.Rhodamine 123 fluorescence, a marker of the mitochondrial membranepotential, decreased in AH70 cells after co-culture with KC,while that in hepatocytes was unchanged by co-culture. Thisdecrease was blocked by anti-ICAM-1, anti-CD18 and the Inhibitionof nitric oxide synthesis. Cytometric studies demonstrated thatICAM-1 expression on AH70 cells increased after addition ofIFN-, IL-1ß, tumor necrosis factor (TNF)- or KC, whilein hepatocytes ICAM-1 was not increased. Anti-ICAM-1 pretreatmentinhibited the increase in ICAM-1 expression and the decreasein rhodamine 123 fluorescence on AH70 cells after co-culturewith KC. CD18 on KC was increased only after co-culture withAH70. TNF- but not IFN- was detected in the supernatant of co-culturebetween KC and AH70 cells, and this production was partiallyinhibited by anti-ICAM-1 and anti-CD18. The activity of Induciblenitric oxide synthase in Kupffer cells and the levels of nitritesand nitrates in the co-culture supernatant increased over time,and this increase was attenuated either by addition of NO synthesisinhibitors, anti-ICAM-1 or anti-CD18. These results indicatethat the rat KC causes mitochondrial dysfunction in cancer cellsvia the production of NO and cell-to-cell adhesion via ICAM-1/CD18has an Important role in this cytotoxic process.     

De novo interstitial deletion of 4q[46,XX,del(4)(q27q28.2)] with intact blood group-MN locus,confining its locus to 4q28.2–4q31.1

We report a malformed female infant withde novo interstitial deletion of 4q[46,XX,del(4)(q27q28.2)]. The MN blood type analysis of the family members showed that the patient had an intact blood group-MN locus. The locus of the gene responsible for the MN antigen activity is confined to a 4q28.2–4q31.1 segment on the basis of the result of this patient and the previous mapping data.     

The effects in the excess administration of prostaglandin E1 on the indicator enzymes of organella membrane in gastric mucosa

Administration of excess vitamin A to rats causes gastric ulceration. In this study the effects on the gastric mucosa of excess vitamin A and excess prostaglandin E1, alone and in combination, were studied. Prostaglandin E1 protected against ulceration by vitamin A. Vitamin A labilized marker enzymes from four different membrane systems, namely those of the lysosomes, mitochondria, endoplasmic reticulum and plasma membrane, whereas only the effect on lysosomes was prevented by prostaglandin E1. Indeed, the prostaglandin alone labilized the enzymes from plasma membrane and endoplasmic reticulum and also damaged mitochondrial membranes. Both vitamin A and prostaglandin E1 caused a reduction in the total number and an increase in irregularly-shaped mitochondria in the parietal cells and produced dilation of the endoplasmic reticulum in both parietal and chief cells. It is noteworthy that prostaglandin E1 effectively prevents ulceration by vitamin A despite the extent to which it damages these membrane systems. These findings lend support to the hypothesis that vitamin A ulceration of the gastric mucosa is mediated via release of lysosomal enzymes, following damage to the lysosomal membranes.     

Epitope analysis of HLA-DR-restricted helper T-cell responses to Der p II, a major allergen molecule of Dermatophagoides pteronyssinus

T-cell epitopes of Der p II, a major allergen of Dermatophagoides pteronyssinus , were analyzed by using human T-cell clones. We tested 38 cloned T cells from two Japanese patients with allergic rhinitis, and identified at least two peptides (K33-T47 and 158-C73) as helper T-cell epitopes. The former epitope was shown to be restricted by HLA-DRB1* 1502, and the latter by HLA-DRB1* 0405, both of which are typical Japanese HLA-DR alleles, suggesting that those T-cell epitopes might be important for the onset of house-dust mite allergy in the Japanese population. We prepared 15 analog peptides of the HLA-DRB1* 1502-restricted 15-mer peptide. Of those 15 residues, five (F35, L37, A39, F41, and E42) were critical for the epitope activity, and three residues (F35, A39, and E42) seemed to be included in anchor motifs for HLA-DRB1* 1502. The epitope peptide was also recognized by HLA-DRB1* 1502-positive healthy donors; however, only allergic T cells showed Th2 functions. Antigen-presenting cells of nonallergic donors were able to activate allergic T cells to express Th2 function. This seemed to suggest that antigen recognition of T cells, as well as additional unknown factors which promote Th2, rather than Th1, responses, might be important for the onset of house-dust mite allergy.     

Rice protein 16KD--a major allergen in rice grain extract.

The allergenic activity of Rice protein 16 KD (RP16KD) isolated from water soluble rice proteins was examined by radioallergosorbent test (RAST), RAST inhibition and histamine release assay. All of the 31 sera which showed positive RAST values for rice grain extract were positive for RP16KD RAST. Furthermore, there was a significant correlation (r = 0.56, p less than 0.01) between these RAST values. PR16KD effectively inhibited IgE binding to the rice grain extract disc in RAST inhibition assays using 4 sera with positive RAST values for both antigens. In 17 subjects with positive RAST values for rice grain extract, a significant positive correlation (r = 0.53, p less than 0.05) was found between the maximum percent histamine releases from their leukocytes by rice grain extract and RP16KD. These data strongly suggest that RP16KD is one of the major allergens of rice grain.     

Different corticostriatal projections from two parts of the cortical masticatory area in the rabbit

The cortical masticatory area (CMA) elicits rhythmic jaw movements in response to repetitive stimulation and is involved in the control of mastication. Based on jaw movement patterns, the CMA is divided into two parts. One is the part of the CMA in which a T-pattern similar to jaw movements during food transport in natural mastication is evoked by electrical stimulation. The other is more dorsomedially located, and during chewing a C-pattern similar to jaw movements can be induced. However, it is still not known which region of the putamen receives projections from the CMA and whether projections originate from both parts of the CMA. In this study, electrophysiological and histological experiments were undertaken in rabbits to investigate projections from the CMA to the putamen. Both experiments showed that the ventral region of the putamen received projections from the CMA. The density of the projections from the CMA area inducing the T-pattern seemed to be higher than that from the area inducing the C-pattern. Furthermore, the peak latency of the evoked potentials from stimulation of the CMA area inducing the T-pattern was shorter than that from stimulation of the area inducing the C-pattern. The data obtained from the present study indicate the functional role of the ventral region of the putamen in the regulation of mastication, and further suggest that the corticostriatal pathway is involved in the transition between behavioral jaw movement patterns.     

Intensified IgA mesangial deposits after administration of sheep anti-type IV collagen serum in mice

Sheep anti-type IV collagen serum was intravenously administered to male mice of the BALB/c, C3H and ddY strains, and their kidneys were morphologically studied monthly for 10 months thereafter. By immunofluorescence, the sheep IgG was seen to have immediately become conjugated to the glomeruli, mainly in a mesangial pattern. Successively, autologous mouse C3 and IgG appeared with the same type of distribution. Within 3 to 4 months after the start of the experiment, mouse IgA also appeared in the mesangium, especially in ddY mice. The intensity and frequency of mesangial IgA deposition and the serum IgA level increased with time in this strain. BALB/c and C3H mice also showed the same tendency of mesangial IgA deposition, although to a lesser degree. In summary, it was concluded that mesangial IgA deposition was due to non-immunological local trapping, on the basis of the results obtained by ELISA analysis of the sera and renal eluate. Although the ddY mouse is known to show spontaneous mesangial IgA deposition associated with a high serum IgA level with aging, these characteristics were much accelerated and intensified by this antiserum treatment. The relation of this observation to the pathogenesis of human IgA nephritis is discussed.