Sequential Ubiquitination of Ribosomal Protein uS3 Triggers the Degradation of Non-functional 18S rRNA

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Glutamate synthesis via photoreduction of NADP+ by photostable chlorophyllide coupled with polyethylene-glycol

Chlorophyllide a was coupled with alpha-(3-aminopropyl)-omega-methoxypoly(oxyethylene) (PEG-NH2) to form a PEG-chlorophyllide conjugate through an acid-amide bond. The conjugate catalyzed the reduction of methylviologen in the presence of 2-mercaptoethanol. It also catalyzed the photoreduction of NADP+ or NAD+ in the presence of ascorbate as an electron donor and ferredoxin-NADP+ reductase as the coupling enzyme. Utilizing the reducing power of NADPH generated by PEG-chlorophyllide conjugate under illumination, glutamate was synthesized from 2-oxoglutarate and NH4+ in the presence of glutamate dehydrogenase. PEG-chlorophyllide conjugate was quite stable toward light illumination compared with chlorophyll a. The increase in the molecular weight of PEG in the PEG-chlorophyllide conjugates was accompanied by the enhancement of photostability of the conjugate and also by the increased solubility in the aqueous solution.     

An exact test for the association between the disease and alleles at highly polymorphic loci with particular interest in the haplotype analysis

The association analysis between the disease and genetic alleles is one of the simple methods for localizing the susceptibility locus in the genes. For revealing the association, several statistical tests have been proposed without discussing explicitly the alternative hypotheses. We therefore specify two types of alternative hypotheses (i.e., there is only one susceptibility allele in the locus, and there is an extension or shortening of alleles associated with the disease) and derive exact tests for the respective hypotheses. We also propose to combine these two tests when the prior knowledge is not sufficient enough to specify one of these two hypotheses. In particular, these ideas are extended to the haplotype analysis of three-way association between the disease and bivariate allele frequencies at two closely linked loci. As a by-product, a factorization of the probability distribution of the three-way cell frequencies under the null hypothesis of no three-way interaction is obtained.     

Antimicrobial alkaloids from Zanthoxylum tetraspermum and caudatum

Two benzophenanthrene alkaloids, 8-acetonyldihydronitidine and 8-acetonyldihydroavicine were isolated from Zanthoxylum tetraspermum stem bark along with liriodenine, sesamin, lichexanthone and (+)-piperitol-gamma,gamma-dimethylallylether. The species endemic to Sri Lanka, Z. caudatum, contained sesamin, savinin, liriodenine, decarine and 8-O-desmethyl-N-nornitidine. 8-Acetonyldihydronitidine and 8-acetonyldihydroavicine showed significant antibacterial activity while the former along with liriodenine was strongly antifungal. Savinin exhibited potent spermicidal activity. Both savinin and sesamin exhibited significant insecticidal activity.     

Involvement of cortical microtubules in plastic extension regulated by gibberellin in Lemna minor root

We aimed to analyze the rheological characteristics during elongation of the root segments in Lemna minor. The elastic component of segment elongation (EC) increased for the first 6 h, and then almost stopped. However, the plastic component of the segment elongation (PC) began to rapidly increase from 6 h onwards. Uniconazole-P, a gibberellin biosynthesis inhibitor, inhibited the total elongation of root segments (TE), and this inhibition was mainly caused by suppression of the rapid increase in the PC after 6 h. Concomitant with this inhibition, the cortical microtubule (CMT) array within root epidermal cells became disorganized in the presence of uniconazole-P from 6 h onwards. Adding GA3 abolished the inhibition of TE by uniconazole-P treatment, and this recovery was caused not by the increase in the EC but by an increase in the PC. Furthermore, the CMT arrays also recovered their characteristic organization in the presence of GA3. These findings suggest that endogenous gibberellin accelerates TE by activating the PC via control of CMT arrays. This conclusion is also supported by rheological analysis where propyzamide was used to disrupt microtubules. We suggest that endogenous gibberellin controls the PC via its influence over the transverse arrangement of CMTs.     

Free dorsoulnar perforator flap transfers for the reconstruction of severely injured digits

The aim of this study was to investigate the feasibility of transferring the free dorsoulnar perforator flap nourished by the cutaneous perforator branched dorsoulnar artery to reconstruct severely injured fingers under upper arm anesthesia. Between April of 2001 and April of 2002, 13 free dorsoulnar perforator flaps were used in 13 patients. There were 11 men and two women ranging in age from 18 to 64 years, with an average age of 38 years. The affected fingers were one thumb, four index fingers, five middle fingers, two ring fingers, and one little finger. All cases were performed under upper arm anesthesia combined with intravenous local anesthesia. The operative time ranged from 103 to 140 minutes, with an average time of 120 minutes. The flap size ranged from 1 x 3 to 3 x 4 cm, and was transferred from the same forearm of the injured finger. All donor sites were closed primarily without a skin graft. The aim of reconstruction for fingers was to repair a traumatic defect (five cases), partial necrosis following replantation (two cases), and soft-tissue defects resulting from resection of a scar (three cases) and to revascularize ischemic fingers (three cases). All flaps survived completely. After repair of the flow-through circulation of the common digital artery and ischemic finger, a postoperative angiogram showed the vascular patency and hypervascularity of the reconstructed fingers, and the patients' complaints were reduced. The free dorsoulnar perforator flap under regional anesthesia is first reported; it may become one valuable option as a very small flap for the treatment of repairing intercalated or segmental defects as a flow-through flap for soft-tissue defects and ischemic fingers.     

The yeast nuclear cap binding complex can interact with translation factor eIF4G and mediate translation initiation

The mRNA cap structure is bound by either the nuclear (CBC) or the cytoplasmic (eIF4F) cap binding complex. Following mRNA export, CBC must be exchanged for eIF4F in the cytoplasm. It is not known how this exchange occurs or how this RNP remodeling event is integrated with mRNA function. Here we report genetic and biochemical evidence that the yeast translation initiation factor eIF4G associates with CBC, and that eIF4E, the eIF4F component that binds both the cap and eIF4G, antagonizes this interaction. Furthermore, we find that CBC can stimulate translation in extracts containing an eIF4G protein deficient for eIF4E binding. These data suggest that eIF4E binding to the eIF4G-CBC complex on newly exported mRNA displaces CBC, and that the first round of translation on mRNA may occur via a different mechanism than subsequent rounds.     

Sustained enhancement of Ca(2+) influx by glibenclamide induces apoptosis in RINm5F cells

Cytosolic Ca(2+) elevations are known to be involved in triggering apoptosis in many tissues, but the effect of sustained enhancement of Ca(2+) influx on apoptosis in beta cells remains unknown. We have found that the viability of RINm5F cells is decreased dose-dependently by continuous exposure to glibenclamide at concentrations from 10(-7) to 10(-4) M, and that this effect is partially ameliorated by pretreatment with cycloheximide. Electrophoresis of the cells exposed to glibenclamide revealed ladder-like fragmentation characteristic of apoptosis, and which also is suppressed by cycloheximide pretreatment. By using terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) staining, we detected increased DNA fragmentation in the nuclei of the cells exposed to glibenclamide, and staining with Hoechst 33342 and propidium iodide showed a dose-dependent increase in the number of cells with the chromatin condensation and fragmentation in their nuclei that is characteristic of apoptosis. The effects of glibenclamide on cell viability and apoptotic cell death were partially inhibited by treatment with Ca(2+) channel blocker, and by reducing the extracellular Ca(2+) concentration during glibenclamide exposure, suggesting that they may be derived from increased Ca(2+) influx. Furthermore, only the percentage of apoptotic cells, and not that of necrotic cells, increased with the increasing intracellular Ca(2+) concentration during glibenclamide exposure. In conclusion, we have demonstrated that the sustained enhancement of Ca(2+) influx caused by glibenclamide exposure can induce apoptotic cell death in a pure beta cell line.