Evaluation of quantum confinement effect in nanocrystal Si dot layer by Raman spectroscopy.

Quantum confinement effect in the nanocrystal-Si (nc-Si) was evaluated by Raman spectroscopy. The nc-Si dot layers were fabricated by the H2 plasma treatment for the nucleation site formation followed by the SiH4 irradiation for the nc-Si growth. Post-oxidation annealing was also performed to improve the crystalline quality. After post-oxidation annealing for 5 or 10 min, the asymmetric broadening on the lower frequency sides in Raman spectra were obtained, which can be attributed to the phonon confinement effect in nc-Si. Furthermore we confirmed that hydrostatic stress of approximately 500 MPa was induced in nc-Si after post-oxidation annealing.

Morphologic and hemodynamic changes after stent placement for experimental carotid aneurysm.

SUMMARY: Stent assisted coil embolization is useful in treating broad neck aneurysms, and there are many kinds of stents that can be applied in the cerebral artery, however their characteristics are not well known. We investigated and compared morphologic and hemodynamic changes before and after stent placement when several different kinds of stents were applied to experimental aneurysms. Experimental aneurysms in eight pig carotid arteries were used. Stents were placed covering the aneurysm orifice. Five Cordis stents (coil stent), two GFXs (multilink stent), and one Multilink (tube stent) were used in this study. After coil placement, the arteries were perfused with 70% ethanol, the specimens were embedded in polyester plastic resin and thin slices were stained with hematoxylin-eosin. Blood flow in the aneurysm was measured using digital subtraction angiography. The parent artery was stretched in multilink stent (GFX) cases, and was most markedly stretched by use of the tube stent (Multilink). Stent placement with any type of stent decreased intra-aneurysmal blood flow.

[A study on the effects of physical load placed on high school baseball managers during midsummer games].

We examined the influence of physical load placed on high school baseball managers during midsummer games under extremely hot and humid conditions. The factors used to determine physical load were the following: body weight, oral temperature, amount of walking, pedometer count, heart rate, and serum biochemical elements. These factors were measured before and after the games. Twenty-two managers participated in this study. All games were played under high temperatures of 32.4 +/- 3.5 (mean +/- S.D) degrees Celsius dry-bulb, 27.1 +/- 3.0 degrees Celsius wet-bulb, 33.8 +/- 3.6 degrees Celsius black-glove, 29.1 +/- 3.3 degrees WBGT, which are likely to cause heart-related illness. The results were as follows. 1. After the games, significant body weight loss and oral temperature rise were found. Those findings were thought to be caused by the rise in oral temperature in a hot environment which was accompanied by hyperhidrosis. 2. The average hemoconcentration ratio based on the changes in total protein during the games was 105 percent, suggesting that hemoconcentration and dehydration were caused by sweating in a hot environment. 3. A significant increase in total protein, albumin, LDH, high density lipoprotein cholesterol, calcium, hemoglobin, and a decrease in triglyceride were observed after the games, which were thought to be influenced by sweating and by increased metabolism in a hot environment. 4. The values of triglyceride, Fe, uric nitrogen, calcium and hemoglobin after the games which were adjusted by the hemoconcentration ratio were significantly lower than those before the games. 5. A prolonged game time caused a significant increase in total protein value during the games and a decrease in hemoglobin between the level before the games and the adjusted level after the games compared with those values in the short game time group. From the above, even though high school baseball managers join in practices in a hot environment and become accustomed to it, we found that they had a great physical load on their bodies during the games in midsummer.

[A study on the effects of physical load on high school baseball players during midsummer games].

This study attempted to measure the physical load on high school baseball players during games played under extremely hot and humid conditions in the summer. The factors used to determine physical load were the following: body weight, oral temperature, blood pressure, heart rate, and serum biochemical elements. These were measured before and after the game. One hundred twenty-six baseball players from 7 high schools participated in this study. All the games were played under conditions of high temperature 34 degrees Celsius dry-bulb, 26 degrees Celsius wet-bulb, 41 degrees Celsius black-globe, 30 degrees WBGT, which are likely to cause heat-related illnesses. The results were as follows. 1) The physical load of baseball players during the game showed a 1.8 percent decrease in average body weight due to perspiration, a 0.35 degrees C increase in oral temperature and an increase in the heart rate. Examination of the serum biochemical elements showed that muscle deviation ferment changed due to muscular activity and blood condensed due to perspiration. The physical load levels of baseball players were influenced more by extreme heat than by exercise during the game. 2) The group of starting players showed higher body weight loss, oral temperature, heart rate, blood condensation and muscle deviation ferment levels than the group of players on the bench due to the difference in the length of exposure to summer heat and the amount of physical exertion. The changes in physical load levels during the game for the group of starting players were greater than those for the group for players on the bench. 3) Considering the changes in body weight, blood condensation and muscle deviation ferment, we can say that physical loads of players differed according to their positions, the pitcher having the greatest load, followed in descending order by the catcher, infielders, and outfielders. It has been recommended that high school baseball players should take different kinds of rest depending on their positions in order to recover from fatigue as soon as possible after a game.

Sequential acquisition of norfloxacin and ofloxacin resistance by methicillin-resistant and -susceptible Staphylococcus aureus.

The acquisition of ofloxacin resistance by a susceptible clinical Staphylococcus aureus strain was found to be achieved in two sequential steps: the first step was accompanied by 4-fold increases in the ofloxacin MIC and 8- to 16-fold increases in the norfloxacin MIC. The second step was accompanied by further increases in both the ofloxacin and the norfloxacin MICs. A mutation of the gyrA gene resulting in an amino acid substitution was found in the second-step but not in the first-step resistant subclone. On the other hand, there was no difference in the accumulation of norfloxacin in the parent strain and the resistant subclones of each step. The rates of mutation to resistance in the steps were (1.58 to 6.81) x 10(-9) and (0.71 to 2.59) x 10(-9), respectively, and did not depend on whether the parent strain was resistant to methicillin. Some implications of these observations for clinical as well as mechanistic aspects of the prevalence of methicillin- and ofloxacin-resistant S. aureus are discussed.

Mutations in the rfbT gene are responsible for the Ogawa to inaba serotype conversion in Vibrio cholerae O1.

In cultures of Vibrio cholerae strains of Ogawa serotype, variant strains which had undergone serotype conversion from Ogawa to Inaba were identified. The rfbT genes cloned from the parent strains were found to produce a 31-kDa protein in the maxicell system, and to cause serotype conversion when introduced into E. coli cells expressing Inaba serotype specificity. On the other hand, rfbT genes cloned from the variant strains neither produced the 31-kDa protein nor caused serotype conversion. Nucleotide sequence of these rfbT genes as well as those of two clinical Vibrio cholerae strains of Inaba serotype revealed that mutations causing premature termination of their rfbT genes were invariably present in strains expressing Inaba serotype specificity. The results strongly suggested that genetic alteration of the rfbT gene is responsible for serotype conversion of Vibrio cholerae O1.

Identification and nucleotide sequence determination of the gene responsible for Ogawa serotype specificity of V. cholerae 01.

The gene encoding a protein of 27 kDa, which is specifically expressed in Vibrio cholerae of serotype Ogawa, was identified and its nucleotide sequence determined. The plasmid carrying this gene was found to convert serotype specificity from Inaba to Ogawa when introduced into the Escherichia coli DH5(pVCI112) cell which harbors a cloned 20-kilobase genomic DNA fragment of V. cholerae NIH35A3 and expresses the 01 antigen of Inaba serotype.

Identification of the genomic region determining serotype specificity of Vibrio cholerae 01.

A 2.1-kb genomic region responsible for Ogawa serotype specificity of Vibrio cholerae 01 was identified by cosmid cloning and recombinant plasmid experiments. The plasmid carrying this region derived from Ogawa type Vibrio cholerae NIH 41 coded for a specific protein of 27 kD, and was found to convert serotype specificity from Inaba to Ogawa when co-introduced into the Escherichia coli cells harboring a cloned 20-kilobase genomic DNA fragment of Inaba type Vibrio cholerae 35A3.

A point mutation in norA gene is responsible for quinolone resistance in Staphylococcus aureus.

Two norA genes associated with hydrophilic quinolone resistance in Staphylococcus aureus were identified on the two recombinant plasmids pMR8736 and pSA209; the former was derived from a quinolone-resistant strain MR8736, and the latter was derived from a fluoroquinolone-susceptible strain 209P. We compared functions of these two genes, norA8736 and norA209 respectively, by introducing them into E. coli MC1061. Both genes expressed a novel protein of 52 kilodalton (kD) in size in MC1061. However, only norA8736 could confer hydrophilic quinolone resistance to the host cell, which was accompanied by a significant decrease in the uptake of a hydrophilic quinolone, norfloxacin, by the cell. Subcloning and recombinant plasmid analyses localized the hydrophilic quinolone-resistance marker to the 0.5 kilobase (kb)-long HpaI-HinfI DNA fragment of pMR8736. Nucleotide sequencing of this region and the corresponding region of pSA209 revealed that the hydrophilic quinolone resistance conferred by norA8736 was caused by a single nucleotide substitution from A (adenosine) in norA209 to C (cytosine), which corresponded to a single amino acid substitution from Asp to Ala.