An infection of cow with Mortierella wolfii

A Japanese black cow from a farm in Gunma prefecture showed pyrexia, anorexia and depression. An autopsy revealed hepatic lesions consisting of numerous approximately spherical pale lesions scattered about on the surface and cut parts. The inflammatory lesions were observed in the right lobe of the lung. A part of the trachea was whitish and thickened. Histologically, necrotic foci were observed throughout most of the liver with fungal proliferation about the blood vessels. The lesions of the lung were seriously exudative and the fungus was also present in some of the bronchiole and on bloodvessel walls. Mortierella wolfii was isolated from the liver. The hyphae in the liver were identical in appearance with those seen in the tissues of rabbits experimentally inoculated with M. wolfii.This report is the first case of M. wolfii infection in Japan     

TaqI polymorphism in the LDL receptor gene and a TaqI 1.5-kb band associated with familial hypercholesterolemia

Summary The low density lipoprotein (LDL) receptor gene was analyzed in 67 unrelated healthy Japanese and 38 members of six consecutive families with familial hypercholesterolemia (FH) by Southern blot hybridization with TaqI, an LDL receptor cDNA fragment containing exons 1 to 8 being used as a probe. A new TaqI RFLP at the LDL receptor locus was detected with allele frequencies of 0.67 and 0.33. The data obtained with smaller cDNA subfragment probes revealed that the TaqI RFLP site is located within 1.1 kb of the 5 side of the EcoRI site of exon 5. The TaqI RFLP was in linkage disequilibrium with the PstI RFLP but showed no significant linkage disequilibrium with the RFLPs for AvaII, ApaLI/I15, PvuII, NcoI, and ApaLI/3. Among the seven RFLPs at the LDL receptor locus, the TaqI RFLP was the only useful genetic marker in one of the six families with FH. Furthermore, the association of an additional TaqI 1.5-kb band with a mutant LDL receptor gene was observed in another family with FH in which the proband was homozygous for all of the seven RFLPs. The data obtained with various restriction enzymes and smaller cDNA subfragments probes suggested that a minor change in nucleotide sequences in the region including exons 5 to 8 is present in the mutant gene. These data suggest that the TaqI RFLP is a useful genetic marker at the LDL receptor locus and that TaqI serves for the analysis of some mutant LDL receptor genes, when used with small LDL receptor cDNA probes.     

Efficient Synthesis of 2′-Bromo-2′-Deoxy-3′,5′-O-TPDS-pyrimidine Nucleosides by Boron Trifluoride Catalyzed Reaction of O2,2′-Anhydro-(1-β-D-Arabinofuran0Syl)pyrimidine Nucleosides with Lithium Bromide

Abstract

Efficient syntheses of 2′-bromo-2′-deoxy-3′,5′-O-TPDS-uridine (5a) and 1-(2-bromo-3,5-O-TPDS-β-D-ribofuranosyl)thymine (5b) from uridine and 1-(β-D-ribofuranosyl)thymine are described, respectively. The key step is a treatment of 3′,5′-O-TPDS-O²,2′-anhydro-1-(β-D-ardbinofuranosyl)uracil (4a) and -thymine (4b) with LiBr in the presence of BF₃-OEt₂ in 1,4-dioxane at 60°C to give 5a and 5b in 98%, and 96% yield, respectively.

     

Protective Effect of Sclerin on a Lead-acetate Injury Affecting the Growth and Porphyrin Metabolism in Rat

While a continuous ingestion of lead acetate added in drinking water suppressed the rat growth, depressing in some degree the level of hepatic δ-aminolevulinate (ALA) dehydratase, a very small amount of sclerin (SCL) added simultaneously in the water restored the growth and dehydratase level. Moreover, subcutaneous injection of SCL to the rat not only maintained the ALA dehydratase level, but prevented a marked depression of the level of mitochondrial ALA synthetase in liver caused by intraperitoneal injection of lead acetate. Injection of SCL alone increased tolerably (about 1.8 times) the mitochondrial ALA synthetase, but little the extramitochondrial synthetase. The treatment by SCL was attended by a initial decrease, then a gradual increase in the activity of microsomal drug metabolizing enzyme.     

Deterioration of Antarctic Krill Muscle during Freeze Storage

The effects of freezing on the heat-induced gelation, Ca²⁺-ATPase activity and myofibril structure of Antarctic krill muscle were investigated. Muscle from freshly caught krill was immediately stored at-20°C in the presence (to prevent freezing) (glycerol krill) and absence (frozen krill) of glycerol. Several protease inhibitors, monosodium glutamate and Ca²⁺ were individually added to glycerol krill to inhibit endogenous proteolysis. The examinations described above were carried out after about 3-month storage at-20°C. In glycerol krill (unfrozen state), viscoelastic parameters of the heat-induced gels and Ca²⁺-ATPase activities of all the krill samples were similar to those of “surimi” (raw fish meat paste) of Alaska pollack which gave gel of good quality, although the micro structure (Z-lines) of myofibrils was different among the glycerol krill samples. In frozen krill, however, the parameters of the gel were different from those of “surimi”, the ATPase activity was completely lost and disruption of the myofibril structure occurred. Refreezing (-20°C) of glycerol krill after removal of glycerol resulted in a marked decrease in the gelation ability. These results suggest that freezing of krill muscle causes deterioration of the gelation ability.     

Light Actions in the Germination of Cocklebur Seeds II. Possible Origin of the Diversity of Light Responses in Seed Germination

In negatively photoblastic, lower seeds of cocklebur (Xanthiumpennsylvanicum Wallr.), the respective germination-inhibitingeffects of red (R) and far-red (FR) lights were found in theproximal and near-tip zones of the axial tissues. In contrast,the germination-stimulating effect of R in positively photoblastic,upper cocklebur seeds was manifested in the near-tip zone ofthe axes, the R effect being reversed when FR was given to thezone. The R-sensitive zone in the upper seeds, however, shiftedtowards the more proximal zone as the period of pre-soakingat low temperatures increased. This shift was accompanied bythe ability to germinate in the dark in the upper seeds. In the lower seeds, R inhibited axial growth in the near-tipzone, whereas FR inhibited it in the proximal zone. In contrast,axial growth in the near-tip zone of the upper seeds was promotedby R. In both seeds, light had little effect on the growth ofthe radicle tip. Pre-soaking at low temperatures induced dark-germinationby hastening the axial growth of the upper seeds, thus allowingthe upper seed to resemble the lower one. We therefore proposea hypothesis that explains the diversification of photoresponsesin seed germination. (Received August 7, 1984; Accepted December 24, 1984)     

Effect of High Temperature on the Development of Cyanide-Sensitive Respiration in the Germination Process of Spinach Seeds

Germination of spinach (Spinacia oleracea L. var. grabra cv.Nobel) seeds was inhibited at a high temperature (35?C). Effectsof KCN on the respiration of seeds incubated at 20 and 35?Cwere compared in order to investigate the mechanism of inhibitionof seed germination by high temperature. Respiration of germinatingseeds incubated at 20?C was inhibited about 50% by 5 mM. KCNsolution, whereas it hardly inhibited the weak respiration ofthe seeds at 35?C. Germination of seeds was delayed by exogenousKCN. When the KCN solution was renewed daily, germination wascompletely inhibited. Pericarp removal promoted germinationat 35?C, but atypical germination (cotyledons emerging earlierthan a radicle) took up more than half of the total germination.The inhibitory action of KCN on the respiration of seeds wasnot altered by pericarp removal. A KCN addition, even at 20?C,elicited atypical germination in the pericarp-less seeds. Theseresults show that cyanide-sensitive respiration is needed toinduce typical spinach seed germination (root emergence), butis rendered inoperative by high temperatures thus bringing aboutpoor germination and atypical germination. (Received December 1, 1984; Accepted February 8, 1985)     

ATP production by sorbitol-treated cells of a methanol yeast, Candida boidinii (Kloeckera sp.) No. 2201

The phosphorylation system of AMP by sorbitol-treated cells of a methanolutilizing yeast, Candida boidinii (Kloeckera sp.) No. 2201, was investigated for the production of ATP. Firstly, reaction conditions for the ATP production were optimized. Under the optimal conditions, 20–30 g 1^?1 of ATP were produced in the conversion rate of 60–70% from AMP. Activities of reactions involved in the ATP-producing system were compared with cells from different cultures to prepare the cells having the higher activity and to know the essential reaction limiting the rate of the system. The energy efficiency of this system was also discussed.     

Early-Stage Induction of SWI/SNF Mutations during Esophageal Squamous Cell Carcinogenesis

The SWI/SNF chromatin remodeling complex is frequently inactivated by somatic mutations of its various components in various types of cancers, and also by aberrant DNA methylation. However, its somatic mutations and aberrant methylation in esophageal squamous cell carcinomas (ESCCs) have not been fully analyzed. In this study, we aimed to clarify in ESCC, what components of the SWI/SNF complex have somatic mutations and aberrant methylation, and when somatic mutations of the SWI/SNF complex occur. Deep sequencing of components of the SWI/SNF complex using a bench-top next generation sequencer revealed that eight of 92 ESCCs (8.7%) had 11 somatic mutations of 7 genes, ARID1A, ARID2, ATRX, PBRM1, SMARCA4, SMARCAL1, and SMARCC1. The SMARCA4 mutations were located in the Forkhead (85Ser>Leu) and SNF2 family N-terminal (882Glu>Lys) domains. The PBRM1 mutations were located in a bromodomain (80Asn>Ser) and an HMG-box domain (1,377Glu>Lys). For most mutations, their mutant allele frequency was 31–77% (mean 61%) of the fraction of cancer cells in the same samples, indicating that most of the cancer cells in individual ESCC samples had the SWI/SNF mutations on one allele, when present. In addition, a BeadChip array analysis revealed that a component of the SWI/SNF complex, ACTL6B, had aberrant methylation at its promoter CpG island in 18 of 52 ESCCs (34.6%). These results showed that genetic and epigenetic alterations of the SWI/SNF complex are present in ESCCs, and suggested that genetic alterations are induced at an early stage of esophageal squamous cell carcinogenesis.