Influence of the Crystallization Firing Process on Marginal and Internal Adaptation of Silicate-based Glass-ceramic Inlays Fabricated With a CAD/CAM Chairside System.

OBJECTIVE: Computer-aided design/computer-aided manufacturing (CAD/CAM) systems are widely used in dental treatment. Clinicians can use chairside CAD/CAM technology, which has the advantage of being able to fabricate inlays on the same day. We aimed to evaluate the effects of crystallization firing processes, fabrication methods (one-step and two-step), and materials on marginal and internal adaptations of silicate-based glass-ceramic all-ceramic inlays fabricated with CAD/CAM chairside systems. METHODS: Ten artificial mandibular left first molars were prepared with standardized ceramic class II mesialocclusal (MO) inlay cavities. Optical impressions were obtained using CEREC Omnicam Ban. IPS e-max CAD (IE), (Ivoclar Vivadent, Schaan, Liechtenstein), Initial LiSi Block (LS) (Hongo, Bunkyoku, Tokyo, Japan), VITA Suprinity (SP), (Vita Zahnfabrick, Bad Säckingen, Germany), and Celtra Duo (CD) (Ivoclar Vivadent, Schaan, Liechtenstein) (n=10) were milled using CEREC MC XL (Bensheim, Germany). IE and SP were crystallization-fired using CEREC Speed Fire. The silicone replica technique was used for the measurement of internal (axial and pulpal walls) and marginal (cervical and occlusal edge) adaptations. The adaptations were measured using a thin layer of light-body polyvinyl siloxane impression material placed between the master tooth inlay preparation and restoration. Marginal and internal adaptations of IE, LS, SP, and CD were measured using a stereomicroscope (500×). For IE and SP, marginal and internal adaptations were measured before and after the crystallization firing process. Data analyses were conducted using one-way ANOVA and the Tukey test. For IE and SP, marginal and internal adaptations before and after the crystallization firing process were analyzed using the t-test. The significance level was set at α=0.05. RESULTS: One-way ANOVA revealed statistically significant differences in occlusal and cervical edge marginal adaptations among the material groups (p<0.001). The Tukey HSD test revealed a significant difference in marginal occlusal and cervical edge adaptations between LS and CD groups and IE and SP groups (p≤0.05). For IE and SP inlays, the t-test revealed a significant difference between occlusal and cervical edge adaptations before the crystallization firing process and those after the crystallization firing process, with the latter group showing a more significant discrepancy in adaptation than the former group (p≤0.05). CONCLUSIONS: Fabrication methods (one- and two-step) affected the marginal adaptation compatibility but not internal compatibility of MO inlays. The crystallization firing process affected the marginal adaptation of inlays using lithium silicate or lithium disilicate glass-ceramics. However, adaptation to the cavity was considered clinically acceptable for all materials.

Overexpression of yccL (gnsA) and ydfY (gnsB) increases levels of unsaturated fatty acids and suppresses both the temperature-sensitive fabA6 mutation and cold-sensitive secG null mutation of Escherichia coli.

A multicopy suppressor of the cold-sensitive secG null mutation was isolated. The suppressor contained sfa and yccL, the former of which has been reported to be a multicopy suppressor of the fabA6 mutation carried by a temperature-sensitive unsaturated fatty acid auxotroph. Subcloning of the suppressor gene revealed that yccL, renamed gnsA (secG null mutant suppressor), was responsible for the suppression of both the secG null mutation and the fabA6 mutation. In contrast, the sfa gene did not suppress the fabA6 mutation. The ydfY (gnsB) gene, encoding a protein which is highly similar to GnsA, also suppressed both the secG null mutation and the fabA6 mutation. Although both gnsA and gnsB are linked to cold shock genes, the levels of GnsA and GnsB did not exhibit a cold shock response. A gnsA-gnsB double null mutant grew normally under all conditions examined; thus, the in vivo functions of gnsA and gnsB remain unresolved. However, overexpression of gnsA and gnsB stimulated proOmpA translocation of the secG null mutant at low temperature and caused a significant increase in the unsaturated fatty acid content of phospholipids. Taken together, these results suggest that an increase in membrane fluidity due to the increase in unsaturated fatty acids compensates for the absence of the SecG function, especially at low temperature.

Outbreak of severe infection due to adenovirus type 7 in a paediatric ward in Japan.

Between November 1996 and January 1997, 14 patients were diagnosed as having infection caused by adenovirus type 7 in a paediatric ward of Asahikawa Kosei Hospital. The age range of the patients was from two months to five years. Their diseases and abnormal laboratory findings were pneumonia in all 14, leukocytopenia in 10, myositis in nine, gastroenteritis in eight, encephalitis in five, liver dysfunction in three, pleuritis in two, inappropriate secretion of antidiuretic hormone syndrome in two, and thrombocytopenia in two. The infected patients, except for the first had been hospitalized in the paediatric ward for treatment of another disease and re-admitted because of high fever and coughing a few days after improvement or discharge. It is thought that the cause of the outbreak was hospital-acquired infection.

Molecular cloning of a novel protein containing the association domain of calmodulin-dependent protein kinase II.

The cDNA of a novel protein, which contains the association domain of alpha isoform of calmodulin-dependent protein kinase II (CaM-kinase II alpha), was cloned from rat skeletal muscle. This protein, called alpha KAP, consisted of 200 amino acid residues with a molecular weight of 22,583. alpha KAP has a highly hydrophobic amino-terminal stretch of 25 amino acids which is absent from CaM-kinase II alpha, suggesting that this protein is either a secretory protein or an integral membrane protein. Northern blot analysis with a probe specific for alpha KAP detected three distinct mRNA species of 4.0, 2.4, and 1.5 kb in rat skeletal muscle. The 4.0- and 2.4-kb RNAs were also detected in heart, and at much lower levels in lung, kidney, and testis. Western blot analysis, using antibody raised against a synthetic peptide corresponding to the carboxyl-terminal 15 amino acids, revealed a single band corresponding in mobility to a molecular weight of 21,000 in crude extracts of both rat skeletal muscle and bacteria transformed with the cDNA, suggesting that no significant post-translational modification, such as excision of the amino-terminal hydrophobic segment, occurred. This, together with the fact that alpha KAP was recovered in the high-speed pellet in skeletal muscle, indicated that this protein may be an integral membrane protein.

[Combined effect of sulbactam/cefoperazone and other antibiotics against clinical isolates of multi-resistant strains. II. In vitro combined effects of sulbactam/cefoperazone with imipenem/cilastatin, cefuzonam, flomoxef, amikacin or tobramycin].

We evaluated combined effects of sulbactam/cefoperazone (SBT/CPZ) with each of imipenem/cilastatin (IPM), cefuzonam, flomoxef, amikacin (AMK) and tobramycin (TOB) against 324 clinical strains. Through this study, we obtained the following results. 1. Against Serratia marcescens and Enterobacter cloacae, good synergism was obtained by combining SBT/CPZ with IPM, AMK, or TOB. 2. Against Pseudomonas aeruginosa, good synergism was obtained by combining SBT/CPZ with AMK or TOB. 3. When SBT/CPZ was used in combination with IPM, antagonism was observed among about 45% of strains of P. aeruginosa.

[Estimate of aztreonam (AZT) hydrolyzing enzymes from clinically isolated AZT-resistant gram-negative bacilli].

The MICs of Aztreonam (AZT) against 590 clinical isolates of Gram-negative bacilli were determined. About 13.4% (79 strains) of the isolates were AZT-resistant (MIC; 12.5 micrograms/ml less than or equal to). The resistance pattern against various beta-lactams and the effects on MICs of combination of Clavulanic acid (CVA) and AZT against AZT resistant strains suggested that AZT was inactivated by either type of IV (K1), Va (OXA1), or PSE2 beta-lactamases.

[Combined effect of sulbactam/cefoperazone and other antibiotics against clinical isolates of multi-resistant strains. I. Effect of sulbactam against beta-lactams resistant strains and in vitro combined effect of sulbactam/cefoperazone with each of piperacillin, latamoxef, ceftazidime, fosfomycin and doxycycline].

We evaluated relationships between production of beta-lactamase and their resistances to beta-lactams, effect of sulbactam (SBT), a beta-lactamase inhibitor, against beta-lactam resistant strains, and combined effect of sulbactam/cefoperazone (SBT/CPZ) with other antibiotics against multi-resistant strains. Through these studies, we obtained the following results. 1. Most of the strains resistant to beta-lactams were beta-lactamase producers. 2. Relationships between the production of beta-lactamase and their resistances to beta-lactams indicate that their resistances generally were the highest in producers of both penicillinase (PCase) and cephalosporinase (CEPase), moderate in producers of either PCase or CEPase, and the lowest in beta-lactamase non-producers. Most of highly-resistant strains of MRSA appeared to be beta-lactamase non-producers though some exceptions were observed among methicillin-resistant Staphylococcus aureus (MRSA), Serratia marcescens and Pseudomonas aeruginosa. 3. SBT showed good effect against PCase producers, moderate effect against producers of both PCase and CEPase, little effect against CEPase producers, and no effect against beta-lactamase non-producers. 4. Results of combined effect of SBT/CPZ with other antibiotics indicated that good synergism was obtained by combining SBT/CPZ with fosfomycin (FOM) or piperacillin against multi-resistant strains of Proteus spp., Enterobacter cloacae, and S. marcescens, by combining SBT/CPZ with ceftazidime (CAZ) or FOM in methicillin-sensitive S. aureus and by combining SBT/CPZ with CAZ in P. aeruginosa. 5. Better synergism was obtained with the higher concentrations of antibiotics.

Antihypertensive effect of tryptic hydrolysate of milk casein in spontaneously hypertensive rats.

1. Repeated oral administrations of tryptic hydrolysate of bovine milk casein (CEI) showed antihypertensive effect in spontaneously hypertensive rats. 2. Single oral administration of CEI antagonized the pressor response to angiotensin I. 3. Bovine milk casein hydrolysate inhibited the angiotensin I-converting enzyme (ACE) activity. Three peptides with ACE-inhibiting activity were isolated from CEI. 4. It is suggested that ACE-inhibiting peptides in the tryptic hydrolysate milk casein are absorbed from the intestinal tract and produce an antihypertensive effect.