Effects of collagen hydrolysate on the tibialis anterior muscle and femur in senescence-accelerated mouse prone 6.

OBJECTIVES: Effects of collagen hydrolysate (CHD) on the oxidative capacity of the tibialis anterior muscle and the cortical and trabecular density of the femur were investigated in senescence-accelerated mouse prone 6 (SAMP6). METHODS: Sixteen-week-old male SAMP6 mice were divided into control (CON) and CHD groups. The CON group was given normal water, while the CHD group was given water containing CHD. Fibre cross-sectional areas (CSAs), fibre succinate dehydrogenase (SDH) staining intensity, and SDH activity of the tibialis anterior muscle were determined at 42 and 60 weeks of age. The cortical and trabecular density of the femur and serum osteocalcin levels were also determined. RESULTS: The fibre SDH staining intensity and muscle SDH activity were higher in the CHD group at 60 weeks of age than in the age-matched CON group. The cortical and trabecular density and serum osteocalcin levels were greater in the CHD group at 60 weeks of age than in the age-matched CON group. CONCLUSION: CHD inhibited th age-induced decrease in muscle oxidative capacity and bone density of SAMP6 mice. There is a possibility that CHD is effective for inhibition of age-induced degeneration in the musculoskeletal system.

Quenching electron runaway in positive high-voltage-impulse discharges in air by laser filaments.

Strong hard (ε>100 keV) x rays being observed from impulse atmospheric discharges with maximal voltages from U=0.5 to 0.9 MV just before the breakdown were completely stopped with the use of femtosecond-laser-filament plasma. Runaway electrons generating such x rays and being estimated to achieve their maximal energy, ε~U, near the positive electrode disappear if a laser filament plasma is ignited perpendicularly to the runaway near the positive electrode. A preheating mechanism for formation of the electron runaway in air is proposed.

Excellent performance of aromatic polyguanamines induced by multiple hydrogen bondable tetraazacalix[2]arene[2]-triazine ring in their main chain.

A series of poly(guanamine) (c-PG)s containing tetraazacalix[2]arene[2]-triazine (mPDA2CyC2) were successfully prepared by solution polycondensation of mPDA2CyC2 with various aromatic diamines in an aprotic organic solvent with a lithium chloride additive (5 wt%) at 150 °C for 6 hours. The number-average molecular weights (M n)s of these c-PG polymers reached up to 31 500, with a relatively broad molecular weight distribution (M w/M n) of 5.3. They showed good solubility in aprotic organic solvents, such as N-methylpyrrolidone and N,N-dimethylacetamide at a concentration of 2 mg mL-1. The glass transition temperatures (T g) of the c-PG polymers were in the range 359 °C-392 °C, approximately 160 °C higher than those of counterpart polymers (i.e., with no aza-calixarene-based PG (l-PG)). The coefficients of thermal expansion (CTEs) of the c-PG polymers were 29.7-48.1 ppm K-1 (at 100 °C-150 °C), much lower than those of l-PG samples, i.e., 59.1-85.1 ppm K-1. Transparent and almost colorless c-PG films were successfully prepared by a solution casting method, showing maximum tensile strength (σ S), modulus (E γ), and elongation at break (E b) values of 151 MPa, 6.3 GPa, and 4.4%, respectively, for the c-PG polymer from mPDA2CyC2 and 4,4'-oxydianiline monomers. The corresponding l-PG film exhibited σ S, E γ, and E b values of just 76 MPa, 5.4 GPa, and 1.6%, respectively. These outstanding thermal and mechanical properties of the c-PG polymers can be attributed to their multiple hydrogen bonding interaction between mPDA2CyC2 residues in the polymer backbone. This interaction was identified by infrared spectroscopy measurements at the broad absorption band around 3000-3400 cm-1.

Transcatheter arterial embolisation in four dogs with hepatocellular carcinoma.

Four dogs with hepatocellular carcinoma were treated by transcatheter arterial embolisation. In all dogs, the tumour-supplying arteries were selectively embolised with gelatine sponge particles. Post-embolisation tumour volumes decreased relative to pre-embolisation volumes in all dogs. No adverse reactions were observed in three dogs after treatment but one dog showed pancreatitis. These results suggest that transcatheter arterial embolisation is a feasible treatment for dogs with hepatocellular carcinoma.

Laser ion acceleration via control of the near-critical density target.

Duration-controlled amplified spontaneous emission with an intensity of 10(13) W/cm(2) is used to convert a 7.5-microm -thick polyimide foil into a near-critical plasma, in which the p -polarized, 45-fs , 10(19) -Wcm (2) laser pulse generates 3.8-MeV protons, emitted at some angle between the target normal and the laser propagation direction of 45 degrees . Particle-in-cell simulations reveal that the efficient proton acceleration is due to the generation of a quasistatic magnetic field on the target rear side with magnetic pressure inducing and sustaining a charge separation electrostatic field.

[Surgical management of acute aortic dissection complicated with cerebral malperfusion].

Although type A acute aortic dissection is considered a surgical emergency, the optimal treatment of patients with preoperative cerebral malperfusion remains controversial. From September 1994 to December 2005, 68 consecutive patients with type A aortic dissection underwent emergent surgical treatment. Eight patients showed preoperative newly-developed neurological deficits. The hospital mortality rate was 25% (2 of the 8 patients). Of the 8 patients, 1 with preoperative coma died due to severe brain injury. Another with acute myocardial infarction and left hemiparesis died due to low output syndrome in the immediate postoperative period. Three of the others had persistent left hemiplegia. One of these patients showed new paraplegia early postoperatively. The preoperative neurological deficit of the remaining 3 patients had improved in some degree. The optimal strategy should be taken individually under the accurate and prompt evaluations of hemodynamic and neurological state in such patients.

Foregut cyst of the oesophageal wall in a cynomolgus monkey (Macaca fascicularis).

Congenital oesophageal cysts of foregut origin are rare in animals and human beings. This report describes a case in a 4-year-old cynomolgus monkey with no clinical symptoms. The cyst, which was located within the oesophageal submucosal tissue near the mid-point of the oesophagus, was lined with pseudostratified ciliated epithelium and had a thin layer of submucosal tissue. The cyst was surrounded by a smooth muscle layer which was partly intermingled with the circular muscle layer of the oesophagus. The muscularis mucosae of the oesophagus was not shared with the cyst wall. Simple tubular glands were present, opening into the cyst lumen. No communication between the cyst lumen and the oesophagus was observed. Cartilaginous tissue, which is a diagnostic feature of bronchogenic cysts, was not identified in the cyst wall. On the basis of the histopathological features, a foregut cyst of the oesophagus was diagnosed.

Inhibition of proliferation of MCF-7 breast cancer cells by a blocker of Ca(2+)-permeable channel.

In MCF-7 breast cancer cells, insulin-like growth factor-1 (IGF-1) increased the calcium-permeability of the cells by activating a voltage-independent calcium-permeable channel. IGF-1 also induced oscillatory elevation of cytoplasmic free calcium concentration in these cells. An anti-allergic compound, tranilast, reduced the calcium-permeability augmented by IGF-1 in a dose-dependent manner and blocked the oscillatory elevation of cytoplasmic free calcium concentration. Tranilast did not affect early intracellular signals activated by IGF-1, including receptor autophosphorylation, activations of Ras, mitogen-activated protein kinase and phosphatidylinositol 3-kinase. Tranilast inhibited increases in [3H]-thymidine incorporation, DNA content and cell number induced by IGF-1. The ID50 for [3H]-thymidine incorporation and DNA content were about 10 microM. The inhibitory effect of tranilast was reversible, and cell viability was not affected. Treatment with tranilast increased the number of cells in the G1 phase suggesting that this compound induced G1 arrest. Tranilast also reduced the phosphorylation of the retinoblastoma protein. These results indicate that tranilast inhibits the IGF-1-induced cell growth in MCF-7 cells by blocking calcium entry.

Decreased collagenase expression in cultured systemic sclerosis fibroblasts.

One cause of the excessive deposition of collagen in systemic sclerosis is thought to be abnormal functioning of fibroblasts. The purpose of this study is to determine whether there is decreased expression of collagenase in systemic sclerosis fibroblasts. In this study, we analyzed collagen and collagenase expression in dermal fibroblasts derived from eight patients with systemic sclerosis and compared the findings with those from nine sex- and age-matched healthy subjects. Increased collagen synthesis accompanying enhanced mRNA levels was observed in two of eight strains, whereas all eight strains showed remarkable decreases in collagenase activity and production. There were no differences in the levels of collagenase mRNA between the systemic sclerosis strains and the normal strains. Results suggest that decreased collagenase expression is a characteristic of systemic sclerosis fibroblasts, and both increased collagen expression and decreased collagenase expression in systemic sclerosis fibroblasts may result in the excessive accumulation of collagen in patients with systemic sclerosis. It is also suggested that decreased collagenase expression is altered at translational and/or post-translational levels.

Up-regulation of upstream stimulatory factors by protein malnutrition and its possible role in regulation of the IGF-binding protein-1 gene.

Protein malnutrition drastically induces the expression of the IGF-binding protein-1 (IGFBP-1) gene. We have previously shown that the region between -77 and -112 bp upstream of the rat IGFBP-1 gene contributes to the response of this gene to amino acid limitation. In an attempt to elucidate the basis of the responsiveness of this putative amino acid response unit (AARU), we searched the nucleus of the rat liver for a trans-acting factor whose binding to AARU was dependent on protein nutrition. Liver nuclear extracts of rats fed a protein-free diet and of those fed a control diet were compared by EMSA using the AARU as probe. One of the protein-probe complexes underwent a drastic increase after dietary protein deprivation. Assays using specific antibodies and several competitor oligonucleotides led to identification of the protein composing the complex as upstream stimulatory factor-1 (USF) and USF-2. The binding site of the USF proteins in the AARU turned out to be a CACGGG sequence that was homologous to the consensus USF-binding sequence (E box; CANNTG). Further, Western blot analyses showed that a protein-free diet caused significant increases in USF-1 and USF-2 levels. Thus, elevated expression of the IGFBP-1 gene under protein malnutrition can be attributable to increased binding of USF to its promoter, which results from increased USF levels. The data suggest that the changes in these ubiquitously distributed transcription factors play an important role in the nutritional regulation of expression of mammalian genes.

Lack of association between lumbar disc degeneration and osteophyte formation in elderly japanese women with back pain.

Our study was designed to assess the contributions of the physical and constitutional factors to osteophyte formation, disc degeneration, and bone mineral density (BMD) in lumbar vertebrae of elderly postmenopausal women. A total of 126 Japanese women with back pain, aged over 60 years, were invited to participate in the study. Then 80 subjects with a full set of data for physical examinations, radiographs, MRI, and DXA were examined. TaqI polymorphism of vitamin D receptor (VDR) gene was examined in 60 subjects. Prevalence rates of osteophytes (on radiographs) and disc degeneration (on MRI) were 61 and 68%, respectively. Body weight and BMI correlated significantly with anteroposterior (AP) and lateral (LAT) BMD (r = 0.354 for weight, r = 0.347 for BMI) and mean osteophyte area (r = 0.557 for weight, r = 0.486 for BMI), and body weight also correlated with number of discs with osteophytes. However, these did not correlate with the disc area or the number of degenerated discs. Stepwise regression analysis revealed that body weight and LAT-BMD values independently related to the osteophyte area. Disc area (r = 0.386 for AP view) and osteophyte area (r = 0.384 for AP view) significantly correlated with BMD. However, disc area and osteophyte area did not correlate with each other (r = 0.056). The proportion of degenerated discs was higher in the lower lumbar discs, but not the proportion of discs with osteophytes. Frequencies of T and t alleles of VDR did not correlate with disc degeneration, osteophyte formation, or osteoporosis. Our data showed that increases in osteophyte formation and BMD in the lumbar vertebrae are influenced by body weight and BMI, but did not correlate with disc area, which correlated inversely with BMD. Disc degeneration and osteophyte formation seem to represent two different factors that affect lumbar spine in elderly women.

A spatial light modulator based on fused-silica plates for adaptive feedback control of intense femtosecond laser pulses.

A novel spatial light modulator (SLM) made of an array of fused-silica plates was developed for the purpose of feedback control for intense femtosecond laser pulses over a wide spectral range. Dispersion compensation for 20-fs pulses from a Ti:sapphire oscillator was successfully demonstrated using the SLM with an adaptive feedback control system. The SLM was also applied to the output pulses from a Ti:sapphire amplifier for compensation of material.

Transmural compression-induced proliferation and DNA synthesis through activation of a tyrosine kinase pathway in rat astrocytoma RCR-1 cells.

Gliosis results from abnormal proliferation of glial cells and often occurs in response to brain or spinal cord injury. There are many factors that trigger gliosis associated with such injuries, including ischemia, humoral factors produced by the injured tissue, and possibly mechanical compression itself. In the present study, the effects of mechanical compression on cell proliferation and DNA synthesis were examined in vitro with the rat astrocyte cell line RCR-1. Pressure was applied to cells by instilling compressed helium into sealed plates or flasks in which the partial pressure of oxygen were maintained constant. Compression resulted in time- and intensity-dependent increases in cell number and [3H]thymidine incorporation, with maximum effects apparent at 10 min and 120 mmHg. Compression-induced cell proliferation and DNA synthesis were not inhibited by gadolinium (Gd3+), a blocker of stretch-activated ion channels, or by inhibitors of protein kinase A, protein kinase C, or Ca2+/calmodulin-dependent protein kinases. However, the tyrosine kinase inhibitor genistein inhibited these effects of compression in a concentration-dependent manner. Conditioned medium from compressed cells also induced cell proliferation and DNA synthesis at atmospheric pressure in a genistein-sensitive manner. These results suggest that transmural compression triggers the release of a factor (or factors) that induces cell proliferation and DNA synthesis through a tyrosine kinase pathway in RCR-1 cells.

Adrenomedullin increases intracellular Ca2+ and inositol 1,4,5-trisphosphate in human oligodendroglial cell line KG-1C.

The effects of adrenomedullin (AM), a hypotensive peptide, were investigated in cultured human oligodendroglial cell line KG-1C. Human AM increased the intracellular Ca2+ concentration ([Ca2+]i) at concentrations greater than 10(-7) M. Human calcitonin gene-related peptide (CGRP), a peptide structurally related to AM, also increased [Ca2+]i with a potency similar to that of AM. AM increased [Ca2+]i in the absence of extracellular Ca2+. Further, AM increased inositol 1,4,5-trisphosphate (Ins(1,4,5)P3) level in a concentration-dependent manner similar to that of AM-induced [Ca2+]i, suggesting that AM-induced elevation of [Ca2+]i is due to Ca2+ release from Ins(1,4,5)P3-sensitive stores. AM (10(-9) to 10(-6) M) increased cAMP in a concentration-dependent manner. Forskolin also increased cAMP, but did not mimic the [Ca2+]i-raising effect of AM. These findings suggest that functional AM receptors are present in oligodendroglial KG-1C cells and that AM increases [Ca2+]i through a mechanism independent of cAMP.

Lower number and thinner myelin of large myelinated fibers in human cervical compression radiculopathy.

The authors conducted a morphometric investigation of the histopathological alterations in myelinated fibers (MFs) of the nerve roots of C-6, which showed macroscopic indentation, presumably due to cervical spondylotic radiculopathy. In six cadavers, designated as the radiculopathy group, in which the nerve roots of C-6 showed indentation due to compression on one side (indented side) and the remaining nerve roots (normal side) showed a normal appearance macroscopically, morphometric findings of the nerve roots and the MFs on both the indented and normal sides were evaluated and subjected to blind comparison. Seven cadavers with normal-appearing C-6 nerve roots served as controls. In the control group, there were no differences in the morphometric parameters: that is, total transverse fascicular area, total number of small and large MFs, and relationship between myelin thickness and the radius of the axon between the right and left sides in either the ventral or dorsal roots. There was no evidence found of axonal degeneration, ongoing demyelination, or loss of MFs in either the ventral or dorsal roots in the radiculopathy group on the indented side. However, there were significantly lower numbers of large MFs per root and significantly thinner myelin sheaths relative to axon size on the indented side compared with those on the normal side in both the ventral and dorsal roots. These findings are characteristic alterations of the MFs produced by chronic low-grade compression.

Leukocyte counts and concentrations of soluble adhesion molecules as predictors of coronary atherosclerosis.

BACKGROUND: Authors of recent studies have reported that there is a relationship between level of adhesion molecules and atherosclerosis. In an animal study it was demonstrated that there is an interaction between adhesion molecules and leukocytes in atherosclerotic tissue. OBJECTIVE: To study the relationships between coronary-artery atherosclerosis and both differential blood-leukocyte count and concentrations of soluble adhesion molecules in patients with and without coronary artery disease (CAD). METHODS: Our subjects were 168 patients who underwent diagnostic coronary angiography. Forty-eight patients had normal coronary angiograms (control group), and 120 patients had significant coronary-artery stenoses (diameter stenosis > 70%) in at least one major coronary-artery branch (CAD group). Total and differential blood-leukocyte counts, and concentrations of soluble intercellular adhesion molecule-1 (sICAM-1) and vascular cell adhesion molecule-1 (sVCAM-1) were assayed prior to angiography. RESULTS: Monocyte counts for patients in the CAD group were significantly greater than those for patients in the control group (366 +/- 99 versus 258 +/- 44/microl, P < 0.0001), as were the sICAM-1 concentrations (272 +/- 52 versus 203 +/- 24 ng/ml, P < 0.0001). The mean concentrations of sVCAM-1 in members of the two groups were the same (671 +/- 138 versus 668 +/- 97 ng/ml, P=0.4). There was a higher incidence of significant coronary-artery stenosis among patients with both a high monocyte count and a high concentration of sICAM-1 (> or = mean + SD) than there was among patients with a low monocyte count and a low concentration of sICAM-1 (> or = mean - SD; 100 versus 25%, P < 0.0001). CONCLUSIONS: Higher levels both of monocyte counts and of serum concentrations of ICAM-1 may serve as markers for coronary atherosclerosis.

Circulating adhesion molecules and severity of coronary atherosclerosis.

BACKGROUND: Circulating leukocytes are recruited at atherosclerotic sites through a family of adhesion molecules. Circulating forms of adhesion molecules in peripheral blood can be quantified now. OBJECTIVE: To evaluate the relationship between circulating adhesion molecules and severity of coronary atherosclerosis. METHODS: Subjects included 81 patients undergoing diagnostic coronary angiography, 12 of whom had normal coronary arteries (control group). The remaining 69 patients with demonstrable coronary atherosclerosis were divided into two groups by use of Gensini scores, namely mild atherosclerosis (n = 36, Gensini score 1-20) and severe atherosclerosis (n = 33, Gensini score > 20). Serum levels of circulating intercellular adhesion molecule-1 (ICAM-1), vascular cellular adhesion molecule-1 (VCAM-1), and E-selectin of groups measured before angiography were compared. RESULTS: Circulating levels of ICAM-1 in members of mild and severe atherosclerosis groups were significantly higher than those in members of the control group, whereas there was no significant difference among circulating levels of VCAM-1 in members of the three groups. Circulating levels of E-selectin in members of the mild atherosclerosis group were significantly higher than those in members of the severe atherosclerosis and control groups. CONCLUSIONS: These findings suggest that E-selectin is related to the early stage, and ICAM-1 is related to the advanced stage, of coronary atherosclerosis. With progression of atherosclerosis, one-step adhesion by ICAM-1 could become more important than multistep adhesion involving E-selectin, ICAM-1, and VCAM-1. These molecules may serve as markers for severity of coronary atherosclerosis.

Coronary flow velocity patterns immediately after reperfusion reflect the pathologic characteristics of reperfused myocardium in canine models of acute myocardial infarction.

BACKGROUND: It is difficult to evaluate the extent of myocardial injury after successful reperfusion following acute myocardial infarction (AMI). We investigated the relationship between the coronary flow velocity pattern immediately after reperfusion and pathologic characteristics after myocardial reperfusion injury in dogs. METHODS: We measured distal coronary flow velocity variables in the left circumflex coronary artery in a canine model of AMI (n = 12) 10 min after the release of a clamp (3-10 h clamp procedure) using a 0.35 mm Doppler guide-wire. Dogs were divided into two groups according to presence or absence of early systolic retrograde coronary flow. Hearts were excised 2 h after reperfusion and examined histopathologically. RESULTS: The clamping time tended to be longer in dogs with early systolic retrograde coronary flow. Neutrophil infiltration was observed in the myocardium of dogs without systolic retrograde flow (n = 9); hemorrhage was rarely detectable and the myocardium maintained a bundle form. However, the bundle form of the myocardium became rough, and the severity of the incidence of hemorrhage tended to increase as the ratio of the diastolic coronary flow velocity to systolic velocity (DSVR) decreased. Vacuolar degeneration of the myocardium was also observed in hearts with a relatively low DSVR. In the group with systolic retrograde flow (n = 3), hearts were characterized by coagulation necrosis, marked vacuolar degeneration of the myocardium and diffusely distributed red cells in the intermyocytes. Systolic antegrade flow velocity was much reduced in this group, resulting in a markedly increased DSVR. These findings appeared to be related to severe myocardial damage. CONCLUSIONS: Coronary flow velocity patterns immediately after successful reperfusion appear to reflect the pathologic characteristics of the reperfused myocardium in dogs with AMI.

Hepatopulmonary syndrome-discussion of cardiopulmonary parameters.

We report a 70-year-old man with hepatopulmonary syndrome (HPS) in C liver cirrhosis. Hypoxemia worsened markedly, especially on exertion, while the hepatic function was clinically stable. Contrast echocardiography, 99mTc macroaggregated albumin (99mTcMAA) lung scan, and pulmonary angiography were performed. The findings suggested the presence of both intrapulmonary vascular dilatation and substantial right-to-left shunt. The contribution of intrapulmonary vascular abnormalities in patients with severe liver cirrhosis without abnormal chest radiography and spirometry tests when marked hypoxemia is present should be investigated.

Muscle function in 164 men and women aged 20--84 yr.

PURPOSE: The purpose of the present study was to investigate the effect of aging in men and women on muscle functional properties, i.e., muscle force and force per unit of cross-sectional area (force/CSA). METHODS: A total of 164 volunteers participated in this study and were divided into five groups according to their chronological age as follows: 20s (20--39 yr old), 40s, 50s, 60s, and 70s (70--84 yr old). Isokinetic (0, 60, 180, and 300 degrees.s(-1)) knee extensor and flexor peak torque, and CSA of the quadriceps femoris (QF) muscle of the mid-thigh were measured. RESULTS: Peak torque during knee extension and flexion was inversely related to age in both men and women. This was the case irrespective of the speed of contraction in both genders (men: r = -0.797 to -0.756, all P < 0.001, women: r = -0.639 to -0.530, all P < 0.001). A significant correlation was observed between CSA of QF and peak torque during isometric knee extension in men (r = 0.827, P < 0.001) and women (r = 0.657, P < 0.001). During isometric contraction, the force/CSA exhibited a significant decrease with increasing age in men (r = -0.518, P < 0.001) but not in women (r = -0.207, NS). CONCLUSION: These results thus suggest that muscle strength losses would be mainly due to a decline in muscle mass in both genders, whereas age-related decline in muscle function in men may also be the result of neural factors, such as muscle recruitment and/or specific tension.