Blister formation on tungsten damaged by high energy particle irradiation

In order to investigate the effect of radiation damage on hydrogen behavior in tungsten, tungsten samples with radiation damage of up to 3.5 dpa were irradiated by a mixed hydrogen-carbon ion beam. The radiation damage was produced with 700 keV negative hydrogen ion beam irradiation. The number density of blisters produced by the mixed ion beam irradiation decreased with increasing radiation damage. This was especially observed for blisters with diameters of 20 μm or less. This result showed that radiation damage produced by high-energy particle irradiation suppresses blister formation on tungsten surfaces.     

Sorption characteristics of fluoride on to magnesium oxide-rich phases calcined at different temperatures

The effect of calcination temperature during production of magnesium oxide-rich phases from MgCO(3) on the sorption of F(-) ions in the aqueous phase has been investigated. Magnesium oxide-rich phases were formed by calcination at over 873 K for 1h. Higher calcination temperatures produced more crystalline MgO with smaller specific surface area and provided larger values of the total basicity per unit surface area. The higher calcination temperatures lead to slower F(-) removal rate, and lower equilibrium F(-) concentrations, when the equilibrium F(-) concentrations are less than 1 mmol dm(-3). Larger total basicity per unit surface area made the reactivity with F(-) ions in aqueous phase more feasible, resulting in a greater degree of F(-) sorption. For equilibrium F(-) concentrations more than 1 mmol dm(-3), lower calcination temperatures favored the co-precipitation of F(-) with Mg(OH)(2), probably leading to the formation of Mg(OH)(2-x)F(x), and the achievement of larger sorption density. This is the first paper which describes the relationship between the solid base characteristics obtained by CO(2)-TPD for MgO with different calcination temperatures as a function of the reactivity of F(-) sorption in the aqueous phase.     

Electron emission characteristics of needle type semiconductor diamond electron emitters by pulsed bias operation and X-ray generation

Electron emission characteristics of needle-type semiconductor diamond electron emitters with pulsed bias operation were evaluated. An X-ray generation experiment was performed. Fowler–Nordheim plotting confirmed that field emission completely governed the electron emission. Maximum emission current of 4.2 mA was achieved using an n-type diamond needle. The needle tip, with area smaller than 1 μm², had estimated electron emission density greater than 4.2 × 10⁵ A/cm². The effective emission area obtained from the Fowler–Nordheim plot was several 10^? 13 cm². For adopting and emission area of 1 × 10^? 12 cm², the estimated electron emission density was higher than 4.2 × 10⁹ A/cm². Furthermore, the average emission current was 0.5–0.6 mA. This large electron emission was continued for several seconds and repeatable. A threshold electric field existed for electron emission higher than 50 kV/mm; pulsed electron emissions of less than 30 ms were created by slow triangular waveform shaped bias voltage supplied at frequencies of 5–10 Hz. An improved vacuum level and pulsed bias operation prevented damage to diamond electron emitters and steady electron emission better than with thermoelectronic emission and high bias voltage supply in DC mode; continuous X-ray generation of 1 h was achieved.     

Rapid and progressive CD4+ decline in a monkey infected with an SIV+HIV-1 chimeric virus

We previously constructed a simian immunodeficiency virus+human immunodeficiency virus type 1 (HIV-1) chimeric virus, NM-3rN to generate a pathogenic HIV-1 in macaque monkeys. During the in vivo passage of this virus in several monkeys, a viral strain, R43-56 was obtained which acquired a better replication ability in vivo. MM121, one of the three monkeys inoculated with the R43-56, showed weight loss, diarrhea and a rapid and continuous decrease in CD4+ lymphocytes at the moribund stage. An autopsy revealed generalized lymphadenopathy, dehydration, and ileocecal intussusception. In situ hybridization showed that the virus infection was in systemic lymphoid organs. We are presently monitoring the survivors to obtain candidates for a more virulent virus. R43-56 may be a better challenge virus and useful tool for human acquired immunodeficiency syndrome research.     

Interferon-gamma-inducing factor gene transfection into Lewis lung carcinoma cells reduces tumorigenicity in vivo

The operative mortality and morbidity in patients with severe left ventricular dysfunction who undergo coronary artery bypass grafting (CABG) remain high. The low ejection fraction is the major risk factor for operative mortality. However, ejection fraction (EF) alone may not necessarily be an accurate predictor of operative mortality. We studied the correlation between indices of left ventricular volume and operative mortality. One thousand patients undergoing isolated coronary bypass operations were divided into three groups according to their preoperative ejection fraction. Fifty patients (group I) had severe left ventricular dysfunction (EF < or = 0.3), 56 patients (group II) had moderately left ventricular dysfunction (0.3 < EF < or = 0.4) and 894 patients (group III) had good left ventricular function (EF > 0.4). We analyzed the relationship between hospital mortality and left ventricular volume in 106 patients with an EF < or = 0.4. RESULTS: Cardiac index was not significantly different among the three groups. The left ventricular end-diastolic pressure (LVEDP) and mean pulmonary artery pressure in groups I an II were higher than those in group III. The left ventricular end-diastolic volume (LVEDV) was 146 +/- 44 ml/m2 in Group I, 112 +/- 31 ml/m2 in Group II and 82 + 30 ml/m2 in Group III, respectively (Group I versus II, p < 0.05, Group I and II versus III, p < 0.01). The left ventricular end-systolic volume (LVESV) was 111 +/- 38 ml/m2 in Group I, 72 +/- 21 ml/m2 in Group II and 30 +/- 14 ml/m2 in Group III, respectively (Group I versus II, p < 0.05, Group I and II versus III, p < 0.01). The LVEDV and LVESV were higher in Group I than in Group II and both in Groups I and II were higher than in Group III. The hospital mortality of any cause before discharge was 8.0% (4/50) in Group I, 3.6% (2/56) in Group II, and 2.0% (18/894) in Group III. The mortality in Group I was higher than that in Group III, but the mortality between Groups I and II was not different. We assessed correlations between large left ventricle with left ventricular dysfunction and operative mortality in 106 patients with ejection fractions of < or = 0.4. The hospital mortality in patients with both under fraction 0.4 and an LVESV > or = 140 ml/m2 was 50% (4/8). This rate was higher than in patients with an LVESV between 80 and 140 ml/m2 (1.8%, 1/55) (p = 0.0006) and an LVESV less than 80 ml/m2 (2.3%, 1/43), (p = 0.0013). The hospital mortality in patients with an LVEDV > or = 200 ml/m2 was 67% (4/6). It was also higher than that in patients with an LVEDV between 200 and 120 ml/m2 (1.7%, 1/58), (p = 0.0001), and an LVEDV less than 120 ml/m2 (2.4%, 1/42), (p = 0.0004). We conclude that patients with a low ejection fraction and an elevated LVESV or LVEDV are at increased risk for hospital death following CABG.     

Complex gangliosides are essential in spermatogenesis of mice: possible roles in the transport of testosterone

Mice, homozygous for disrupted ganglioside GM2/GD2 synthase (EC 2.4. 1.94) gene and lacking all complex gangliosides, do not display any major neurologic abnormalities. Further examination of these mutant mice, however, revealed that the males were sterile and aspermatogenic. In the seminiferous tubules of the mutant mice, a number of multinuclear giant cells and vacuolated Sertoli cells were observed. The levels of testosterone in the serum of these mice were very low, although testosterone production equaled that produced in wild-type mice. Testosterone was found to be accumulated in interstitial Leydig cells, and intratesticularly injected testosterone was poorly drained in seminiferous fluid in the mutant mice. These results suggested that complex gangliosides are essential in the transport of testosterone to the seminiferous tubules and bloodstream from Leydig cells. Our results provide insights into roles of gangliosides in vivo.     

High cancer susceptibility and embryonic lethality associated with mutation of the PTEN tumor suppressor gene in mice

BACKGROUND: Germ-line and sporadic mutations in the tumor suppressor gene PTEN (also known as MMAC or TEP1), which encodes a dual-specificity phosphatase, cause a variety of cancers such as Cowden disease, glioblastoma, endometrial carcinoma and prostatic cancer. PTEN is widely expressed, and Cowden disease consistently affects various organ systems, suggesting that the PTEN protein must have an important, although as yet poorly understood, function in cellular physiology. RESULTS: Homozygous mutant mice lacking exons 3-5 of the PTEN gene (mPTEN3-5) had severely expanded and abnormally patterned cephalic and caudal regions at day 8.5 of gestation. Embryonic death occurred by day 9.5 and was associated with defective chorio-allantoic development. Heterozygous mPTEN3-5 mice had an increased incidence of tumors, especially T-cell lymphomas; gamma-irradiation reduced the time lapse of tumor formation. DNA analysis of these tumors revealed the deletion of the mPTEN gene due to loss of heterozygosity of the wild-type allele. Tumors associated with loss of heterozygosity in mPTEN showed elevated phosphorylation of protein kinase B (PKB, also known as Akt kinase), thus providing a functional connection between mPTEN and a murine proto-oncogene (c-Akt) involved in the development of lymphomas. CONCLUSIONS: The mPTEN gene is fundamental for embryonic development in mice, as mPTEN3-5 mutant embryos died by day 9.5 of gestation, with patterning defects in cephalic and caudal regions and defective placentation. Heterozygous mice developed lymphomas associated with loss of heterozygosity of the wild-type mPTEN allele, and tumor appearance was accelerated by gamma-irradiation. These lymphomas had high levels of activated Akt/PKB, the protein product of a murine proto-oncogene with anti-apoptotic function, associated with thymic lymphomas. This suggests that tumors associated with mPTEN loss of heterozygosity may arise as a consequence of an acquired survival advantage. We provide direct evidence of the role of mPTEN as a tumor suppressor gene in mice, and establish the mPTEN mutant mouse as an experimental model for investigating the role of PTEN in cancer progression.