Pheophytin a, a low molecular weight compound found in the marine brown alga Sargassum fulvellum, promotes the differentiation of PC12 cells

We identified and characterized a neurodifferentiation compound from the marine brown alga Sargassum fulvellum collected from the Japanese coastline. Several instrumental analyses revealed the compound to be pheophytin a. Pheophytin a did not itself promote neurite outgrowth of PC12 cells. However, when PC12 cells were treated with a low concentration of pheophytin a (3.9 microg/ml) in the presence of a low level of nerve growth factor (10 ng/ml), the compound produced neurite outgrowth similar to that produced by a high level of nerve growth factor (50 ng/ml). Pheophytin a also enhanced signal transduction in the mitogen-activated protein kinase signaling pathway, which is also induced by nerve growth factor. The effect of pheophytin a on neurite outgrowth of PC12 cells was completely blocked by U0126, a representative mitogen-activated protein kinase kinase inhibitor. These results suggest that pheophytin a enhances the neurodifferentiation of PC12 cells in the presence of a low level of nerve growth factor and that this effect is mediated by activation of a mitogen-activated protein kinase signaling pathway.     

Protein kinase C activity in human thyroid carcinoma and adenoma.

Protein kinase C (PKC) activity was examined in the cytosolic and particulate fractions of homogenates obtained from 12 papillary thyroid carcinomas, 12 follicular thyroid adenomas, and the adjacent normal thyroid tissue. Particulate PKC activity was elevated significantly in thyroid carcinomas compared with normal thyroid tissue (P < 0.01) and adenomas (P < 0.05). By contrast, cytosolic PKC activity of carcinomas and adenomas was lower significantly than that of normal thyroid tissue (P < 0.01). The percentage of particulate PKC activity in carcinoma and adenoma was higher than in normal thyroid tissue (carcinoma, P < 0.001; adenoma, P < 0.01). The average particulate PKC activity of carcinomas more than 3 cm in diameter was significantly lower than that of carcinomas less than or equal to 3 cm in diameter (P < 0.05). The average cytosolic PKC activity of carcinomas more than 3 cm also was lower significantly than that of smaller carcinomas (P < 0.05). These results suggest that alterations in PKC activity may be important in the development of papillary thyroid cancer.     

Biological activities of Bacteroides forsythus lipoproteins and their possible pathological roles in periodontal disease

Bacteroides forsythus is a gram-negative, anaerobic, fusiform bacterium and is considered to be an etiological agent in periodontal disease. A lipoprotein fraction prepared from B. forsythus cells by Triton X-114 phase separation (BfLP) activated human gingival fibroblasts and a human monocytic cell line, THP-1, to induce interleukin-6 production and tumor necrosis factor alpha production. BfLP was found to be capable of inducing nuclear factor-kappaB translocation in human gingival fibroblasts and THP-1 cells. By using Chinese hamster ovary K1 cells transfected with Toll-like receptor genes together with a nuclear factor-kappaB-dependent CD25 reporter plasmid, it was found that signaling by BfLP was mediated by Toll-like receptor 2 but not by CD14 or Toll-like receptor 4. BfLP induced apoptotic cell death in human gingival fibroblasts, KB cells (an oral epithelial cell line), HL-60 cells (a human myeloid leukemia cell line), and THP-1 cells but not in MOLT4 cells (a T-cell leukemia cell line). Caspase-8, an initiator caspase in apoptosis, was found to be activated in these cells in response to BfLP stimulation. Thus, this study suggested that BfLP plays some etiological roles in oral infections, especially periodontal disease, by induction of cell activation or apoptosis.     

The molecular structures of 1,1-diphenylethyl methacrylate and triphenylmethyl methacrylate

The molecular structures of 1,1-diphenylethyl methacrylate (1,1-DPEMA) and triphenylmethyl methacrylate (TrMA) were determined by means of X-ray diffraction. 1,1-DPEMA: monoclinic, space group P2₁/a,a = 9,666(6), b = 19,94(2), c = 8,132(6) Å, β = 104,49(7)°, and Z = 4; TrMA: monoclinic, space group P2₁/n, a = 17,349(3), b = 9,487(2), c = 11,254(2) Å, β = 102,30(2)°, and Z = 4. Both structures were solved by the direct method and refined by the block-diagonal least-squares procedure to R = 0,175 and 0,056 for non-zero reflections, respectively. In both molecules, conformations about the C(1)? C(2) and C(1)? O(1) bonds are all synperiplanar and one of the two or three phenyl groups attached to the C(5) atom is in trans to the O(2).     

1H and 13C NMR spectra of poly(propyl α-bromoacrylate) and poly(methyl α-bromoacrylate)

The ¹³C NMR spectra measured at 25 MHz of the methyl and propyl esters of isotactic and syndiotactic poly(α-bromoacrylate) were sufficiently resolved to be analysed for pentad tacticity sequences. The pentad tacticity of the syndiotactic polymers prepared with free radical initiators at ?40°C agreed with those calculated for Bernoullian sequence distributions based on P_r values of 0,83–0,87. The tacticities of the isotactic polymers prepared with heterogeneous catalysts were determined on the basis of these assignments. Good internal consistency was obtained between the calculated and observed pentad proportions from the quaternary and carbonyl carbon peaks in the spectra of these polymers. The order of chemical shifts for the meso and racemic dyads and tetrads in these polymers were opposite to those found in the equivalent methacrylate polymers, but as with the latter, the ¹³C-T₁ values were longer in the isotactic than in the syndiotactic polymers.     

Early detection of the no-reflow phenomenon in reperfused acute myocardial infarction using technetium-99m tetrofosmin imaging

Evaluation of myocardial perfusion in the early stage of acute myocardial infarction (MI) is clinically important for adjunctive therapies to minimize infarct size. To determine the role of early scintigraphic detection of impaired myocardial reperfusion after primary coronary angioplasty (PTCA) in patients with acute MI, semiquantitative technetium-99m tetrofosmin single-photon emission tomographic (SPET) imaging was performed before primary PTCA (before; area at risk), 60 min after PTCA (after) and at 1 month (1 M; final infarct) in 35 patients with acute MI. The left ventricle was divided into 13 segments and the defect score was calculated as the sum of the perfusion defect of each segment, from 3 (complete defect) to 0 (normal perfusion). A significant myocardial perfusion change after PTCA was defined as a change in the defect score (before minus after PTCA) of >/=4. The echocardiographic asynergic score was defined as the number of asynergic (severe hypokinetic or akinetic) segments corresponding to the analogous segments on SPET images, and recovery of wall motion was calculated as absolute change in the asynergic score (before PTCA minus 1 M). Among the 35 patients, 15 (43%) had a change in the defect score of <4 (no reflow: group 1) while 20 had a change in the defect score of >/=4 (reflow: group 2). There were no significant differences between the two groups with respect to the time between admission to PTCA, revascularization time, collateral grade or Thrombolysis in Myocardial Infarction (TIMI) flow grade before PTCA. Despite the lack of a difference in area at risk between the two groups (group 1 = 12.8+/-4.3 and group 2 = 15.1+/-4.7), final infarct size in group 1 was significantly larger compared with that in group 2 (8.1+/-4.3 vs 4.9+/-3.0, P<0.001). Recovery of wall motion was significantly smaller in group 1 than in group 2 (4.3+/-1.7 to 3.5+/-1.5 vs 4. 1+/-2.1 to 1.6+/-1.6, P<0.001). In conclusion, a small change (<4) in defect score (scintigraphic no-reflow phenomenon) after primary PTCA indicates persisting impaired myocardial perfusion or irreversible cellular damage just after PTCA which is associated with poor recovery of wall motion, as compared with that observed in cases of reflow (>/=4 in defect score).     

Multi-step hydration/dehydration mechanisms of rhombohedral Y2(SO4)3: a candidate material for low-temperature thermochemical heat storage

To evaluate rhombohedral Y₂(SO₄)₃ as a new potential material for low-temperature thermochemical energy storage, its thermal behavior, phase changes, and hydration/dehydration reaction mechanisms are investigated. Rhombohedral Y₂(SO₄)₃ exhibits reversible hydration/dehydration below 130 °C with relatively small thermal hysteresis (less than 50 °C). The reactions proceed via two reaction steps in approximately 0.02 atm of water vapor pressure, i.e. “high-temperature reaction” at 80–130 °C and “low-temperature reaction” at 30–100 °C. The high-temperature reaction proceeds by water insertion into the rhombohedral Y₂(SO₄)₃ host structure to form rhombohedral Y₂(SO₄)₃·xH₂O (x = ∼1). For the low-temperature reaction, rhombohedral Y₂(SO₄)₃·xH₂O accommodates additional water molecules (x > 1) and is eventually hydrated to Y₂(SO₄)₃·8H₂O (monoclinic) with changes in the host structure. At a water vapor pressure above 0.08 atm, intermediate Y₂(SO₄)₃·3H₂O appears. A phase stability diagram of the hydrates is constructed and the potential usage of Y₂(SO₄)₃ for thermal energy upgrades is assessed. The high-temperature reaction may act similarly to an existing candidate, CaSO₄·0.5H₂O, in terms of reaction temperature and water vapor pressure. Additionally, the hydration of rhombohedral Y₂(SO₄)₃·xH₂O to Y₂(SO₄)₃·3H₂O should exhibit a larger heat storage capacity. With respect to the reaction kinetics, the initial dehydration of Y₂(SO₄)₃·8H₂O to rhombohedral Y₂(SO₄)₃ introduces a microstructure with pores on the micron order, which might enhance the reaction rate.

To evaluate rhombohedral Y₂(SO₄)₃ as a new potential material for low-temperature thermochemical energy storage, its thermal behavior, phase changes, and hydration/dehydration reaction mechanisms are investigated.