Biomedical subjects

H Hashizume

Publications and source records attributed to H Hashizume.

At least 91 records · Page 5Linked to original sources

PubMed1997

X-ray reflectivity at the L edges of Gd.

Preparations are underway for the experimental investigation of the roughness of magnetic interfaces in rare-earth multilayers by combining the grazing-angle X-ray scattering technique with the resonant magnetic scattering of hard X-rays. Theoretical considerations show that for small scattering angles, 2theta, the asymmetry ratio, A = [I(+) - I(-)]/[I(+) + I(-)], depends on 2theta and varies as 1/cos theta. The first step towards the goal of determining the magnetic roughness has been taken by measuring the chemical roughness (via specular reflectivity) of a Gd thin-film sample at five photon energies close to the L(3) absorption edge, which yielded the dispersion corrections, f' and f'', to the Gd atomic form factor in good agreement with the calculation of Cromer & Liberman [J. Chem. Phys. (1970), 53, 1891-1898].

Journal Article↗

PubMed1997

Palmitoyl-L-carnitine modifies the myocardial levels of high-energy phosphates and free fatty acids.

Long-chain acylcarnitines, such as palmitoyl-L-carnitine (PALCAR), are known to accumulate in the myocardium during ischemia. We examined whether exogenous PALCAR modifies the myocardial levels of high-energy phosphates (HEP) and free fatty acids (FFA) in the heart, and whether d-cis-diltiazem and l-cis-diltiazem, an optical isomer having less potent Ca2+ channel blocking action than d-cis-diltiazem, attenuate the PALCAR-induced myocardial changes. Rat hearts were perfused aerobically at a constant flow according to the Langendorff's technique, while being paced electrically. PALCAR (5 microM) decreased the tissue levels of adenosine triphosphate and creatine phosphate and increased the tissue level of adenosine monophosphate, and produced mechanical dysfunction. In addition, PALCAR (5 microM) increased markedly the tissue levels of FFA, especially those of arachidonic and palmitoleic acids, and the release of creatine kinase (CK) from the myocardium. These alterations in the myocardial levels of HEP and FFA induced by PALCAR were significantly attenuated by d-cis-diltiazem (15 microM) or l-cis-diltiazem (15 microM). Both drugs also attenuated the PALCAR-induced CK release. The present study demonstrates that PALCAR modifies the tissue levels of HEP and FFA in the heart and that both d-cis- and l-cis-diltiazem protect the myocardium against the PALCAR-induced changes through mechanisms other than Ca2+ channel blocking action.

Adenine Nucleotides↗

PubMed1997

Lysophosphatidylcholine induces Ca2+-independent cellular injury attenuated by d-propranolol in rat cardiomyocytes.

In isolated rat cardiomyocytes, exogenous lysophosphatidylcholine (LPC) (15 microM) increased the intracellular Ca2+ concentration (Ca2+]i) from 72 +/- 5 to 3042 +/- 431 nM accompanied by cell injury as indicated by the hypercontracture of the cells and the increase in creatine phosphokinase (CPK) release. In order to understand whether the cell injury induced by LPC was a consequence of the elevation of [Ca2+]i, the effect of LPC was examined in the Ca2+-free solution containing EGTA. Under the Ca2+ -free conditions, LPC did not increase [Ca2+]i, whereas it still inflicted injury on the cells in terms of cell-shape change and CPK release to the same degree as that under the Ca2+-present condition. Addition of ryanodine (10 microM) failed to prevent the changes in cell-shape and CPK release induced by LPC under both Ca2+-free and Ca2+-present conditions. Preincubation of the myocytes with d-propranolol (50 microM) inhibited the LPC-induced changes in cell-shape and CPK release under both Ca2+ -free and Ca2+ -present conditions (p < 0.05). Our study provides clear evidence that the cellular injury induced by LPC could be independent of the increase in [Ca2+]i, and the Ca2+-independent cellular injury induced by LPC could be attenuated by d-propranolol, although the mechanism remains unknown.

Adrenergic beta-Antagonists↗

PubMed1997

Guyon's canal syndrome. A different clinical presentation caused by an atypical fibrous band.

An atypical case of Guyon's canal syndrome is reported. A 40-year-old woman with hypoaesthesia and claw-finger deformity of the little finger, hypothenar muscle atrophy but no first dorsal interosseous muscle atrophy, underwent release of a fibrous band to decompress the ulnar nerve at the deep branch just proximal to the branch to the abductor digiti minimi muscle. The claw-finger deformity recovered 1 week after surgery.

Adult↗

PubMed1997

The central slip attachment fracture.

Eight displaced central slip attachment fractures were treated by open reduction and internal fixation to avoid boutonniere deformity, to reduce the fracture anatomically and to allow early mobilization of the joint. This injury should be recognized as a disruption of the dynamic extensor mechanism associated with an intraarticular fracture, fracture-dislocation or soft tissue injury of the PIP joint. We have grouped central slip attachment fractures into three types according to the mechanism of injury, with suggested methods of treatment.

Adolescent↗

PubMed1997

Hair cycle-dependent expression of heat shock proteins in hair follicle epithelium.

BACKGROUND: Heat shock proteins (HSPs) have a physiologic function in unstressed cells, which is believed to include a role as a "molecular chaperone." The hair cycle is characterized by rhythmic tissue remodelling processes, and is an intriguing model for studying the relation between keratinocyte differentiation and HSP expression under physiologic circumstances. We have therefore studied, by immunofluorescence, the expression of selected HSPs during the murine hair cycle. METHODS: The association between hair follicle cycling and the expression of three selected HSPs (HSPs 27, 60, and 72) was examined by immunofluorescence, using the depilation-induced hair cycle of C57BL/6 mice. RESULTS: HSP expression was absent from telogen follicles, and was restricted predominantly to keratinocytes in the bulge and the cycling epithelial portion of the hair follicle during anagen and catagen. Immunoreactivity for HSPs 27, 60, and 72 in the hair bulb increased significantly during anagen VI and the catagen transformation of the follicle, and decreased again abruptly with completion of the catagen-telogen transformation. The expression pattern of HSPs 60 and 72 in situ was cytoplasmic, whereas that of HSP 27 was both cytoplasmic and nuclear. CONCLUSIONS: These observations suggest that the synthesis of HSPs by hair bulb keratinocytes is related to the anagen-catagen transformation of the follicle, possibly reflecting keratinocyte apoptosis and/or terminal differentiation in the regressing, cycling portion of the follicle. In addition, the rather proximal localization of HSP expression makes it unlikely that the HSPs examined interact with the more distally located intrafollicular gamma/delta T-cell receptor-positive lymphocytes.

Animals↗

PubMed1997

Protective effects of dilazep and its derivative K-7259 on the haemolysis induced by amphiphiles in rat erythrocytes.

The effects of dilazep and K-7259, a dilazep derivative, on the haemolysis (as evidenced by release of haemoglobin) induced by palmitoyl-L-carnitine (PAL-CAR) or palmitoyl 1-alpha-lysophosphatidylcholine (PAL-LPC) have been determined in rat erythrocytes. At concentrations above the critical micelle concentration both PAL-CAR and PAL-LPC induced haemolysis; the concentrations of PAL-CAR and PAL-LPC producing 50% haemolysis were approximately 13 and 14 microM, respectively. The 50% haemolysis induced by PAL-CAR or PAL-LPC was attenuated by dilazep (1, 10 or 100 microM) but not at the highest concentration used (1 mM). K-7259 attenuated the 50% haemolysis induced by PAL-CAR or PAL-LPC at concentrations ranging from 1 microM to 1 mM. Similarly, dilazep (1 to 100 microM) and K-7259 (1 microM to 1 mM) significantly or insignificantly attenuated the 25% and 75% haemolysis induced by PAL-CAR or PAL-LPC. Neither dilazep nor K-7259 affected micelle formation by PAL-CAR or PAL-LPC, nor, at concentrations of 1 and 10 microM, did they attenuate the haemolysis induced by osmotic imbalance (hypotonic haemolysis). These results suggest that both dilazep and K-7259 protect the erythrocyte membrane from the damage induced by PAL-CAR or PAL-LPC. The protective effects of dilazep and K-7259 are mediated by some mechanism other than prevention of micelle formation or protection of the erythrocyte membrane against osmotic imbalance.

Animals↗

PubMed1997

Protective effect of amiloride against reperfusion damage as evidenced by inhibition of accumulation of free fatty acids in working rat hearts.

To examine whether amiloride protects against ischemia-induced or reperfusion-induced damage to the heart, mechanical and metabolic studies were performed in the isolated, working rat heart. Ischemia decreased both mechanical function and the tissue levels of high-energy phosphates and increased the tissue levels of free fatty acids (FFAs). Reperfusion restored the levels of high-energy phosphates but further increased FFA accumulation. For this reason, accumulation of FFAs was used as an indicator of both ischemia-induced and reperfusion-induced damage. Drugs were added to the perfusion solution 5 min before ischemia until the end of ischemia (pre) or until 10 min after reperfusion (pre + post). Diltiazem (1 or 5 mumol/L pre) decreased the mechanical function of the non-ischemic heart and attenuated both ischemia-induced and reperfusion-induced accumulation of FFAs. Amiloride (50 mumol/L pre) did not affect the mechanical function of the non-ischemic heart or attenuate ischemia-induced or reperfusion-induced FFA accumulation effectively. However, amiloride (50 mumol/L pre + post) did markedly attenuate the reperfusion-induced accumulation of FFAs. In conclusion, diltiazem attenuates both ischemia-induced and reperfusion-induced myocardial damage, probably through its energy-sparing effect as a result of a decrease in mechanical function before ischemia. In contrast, amiloride attenuates only the reperfusion-induced myocardial damage through mechanisms other than the energy-sparing effect.

Amiloride↗

PubMed1997

Cardioprotective effect of K-7259, a novel dilazep derivative, against ischemia-reperfusion damage in isolated, working rat hearts.

Global ischemia (15 min) followed by reperfusion (10, 20 or 30 min) was performed in isolated, working rat hearts. Ischemia depressed mechanical function, which was not restored by reperfusion of 20 min. Preischemic administration of K-7259 (N,N'-bis[4-(3,4,5-trimethoxyphenyl)butyl]homopiperazine dihydrochloride) (1, 5 or 10 microM) decreased the function before ischemia, but it attenuated the ischemia-induced dysfunction during reperfusion (20 min). Postischemic administration of K-7259 (10 microM) or dilazep (20 microM) also attenuated the ischemia-induced dysfunction during reperfusion (30 min). Ischemia-reperfusion (10 min) increased the tissue malondialdehyde level, and postischemic administration of K-7259 (10 microM) or dilazep (20 microM) attenuated the malondialdehyde accumulation. K-7259 has a cardioprotective effect when given either before or after ischemia.

Animals↗

PubMed1997

Beneficial effects of dilazep on the palmitoyl-L-carnitine-induced derangements in isolated, perfused rat heart: comparison with tetrodotoxin.

The present study was carried out to determine the effect of dilazep, having an inhibitory effect on the Na+ channel, on the mechanical dysfunction and metabolic derangements induced by palmitoyl-L-carnitine in isolated rat heart and to compare the effect of dilazep with that of tetrodotoxin, a specific inhibitor of the Na+ channel. Rat hearts were perfused aerobically at a constant flow according to Langendorff's technique and paced electrically. Palmitoyl-L-carnitine (5 microM) decreased the left ventricular developed pressure and increased the left ventricular end diastolic pressure (i.e., it produced mechanical dysfunction), decreased the tissue level of adenosine triphosphate and increased the tissue level of adenosine monophosphate (i.e., it produced metabolic derangements). These mechanical and metabolic alterations induced by palmitoyl-L-carnitine were attenuated by either dilazep (1 microM) or tetrodotoxin (3 microM). On the other hand, neither dilazep nor tetrodotoxin modified the mechanical function and energy metabolism of the normal (palmitoyl-L-carnitine-untreated) heart. These results suggest that inhibition of the Na+ channel with dilazep or tetrodotoxin is responsible, at least in part, for attenuating the palmitoyl-L-carnitine-induced mechanical dysfunction and metabolic derangements in the heart.

Adenosine Diphosphate↗

PubMed1997

Fractures of the base of the middle phalanx of the finger. Classification, management and long-term results.

We classified fractures of the base of the middle phalanx into five types: 1) single palmar fragment; 2) single dorsal fragment; 3) two main fragments; 4) not involving the articular surface, including epiphyseal separation in children; and 5) all others. Types 1 and 2 were subclassified into avulsion, split and split-depression. Surgery is recommended for unstable type-1 avulsion fractures, type-2 avulsions which may develop buttonhole deformities, and all fractures which displace articular cartilage surfaces. Long-term follow-up showed that surgical treatment which produced good stability and congruity gave good results. These should be the primary aims of treatment.

Adolescent↗

PubMed1997

A new approach to the development of anti-ischemic drugs. Substances that counteract the deleterious effect of lysophosphatidylcholine on the heart.

Lysophosphatidylcholine (LPC) is an amphiphilic metabolite that can be produced from membrane-phospholipids by activation of phospholipase A2 (PLA2), and it accumulates in the heart during ischemia and reperfusion. It is known that LPC is an arrhythmogenic substance. Recent studies have revealed that LPC produces mechanical and metabolic derangements in perfused working rat hearts, and Ca(2+)-overload in isolated cardiac myocytes. Thus, LPC possesses an ischemia-like effect on the heart. LPC accumulated in the myocardium activates phospholipase A2, establishing a vicious circle; i.e. LPC itself has an ability to produce another LPC. Therefore, a drug that has an anti-LPC effect would protect or improve ischemia/reperfusion damage. This article will review the effect of LPC in relation to ischemia, and consider a possibility of developing new anti-ischemic drugs on the basis of the anti-LPC action.

Adrenergic beta-Antagonists↗

PubMed1997

Detection of mineral density on the surface of mouse parietal bones: backscattered electron imaging of low accelerating voltage scanning electron microscopy.

Backscattered electron (BSE) imaging of scanning electron microscopy (SEM) was applied to a study on the mineral density of the bone surface. The neonatal and adult mouse parietal bones freed of the periosteum and covering cells were examined in a field emission scanning electron microscope equipped with a high sensitivity BSE detector at 1-30 kV accelerating voltages. The mineral density of the bone surface was observable in BSE images at 5 kV accelerating voltage while only the topographic structures of the surface were obtained under an accelerating voltage less than 5 kV. As the accelerating voltages increased from 5 kV, the bright areas were extended, probably due to the imaging of the calcified bone matrix under the uncalcified osteoid. The bone surface is usually divided into smooth and rough areas according to its irregularities. BSE images at 5 kV clearly showed that the smooth areas were further divided into dark and bright areas which apparently corresponded to the uncalcified osteoid and calcified bone matrix, respectively. Bright granules, about 1.0-3.0 microns in diameter, were sometimes observed at the border between the osteoid and calcified bone matrix; these granular calcified areas were regarded as the calcifying front forming the calcified bone matrix from the osteoid. The present study demonstrated that the distribution of the osteoid on the mouse parietal bone surface changes depending on age: the osteoid occupied a large area in the parietal bone surface in neonatal mice, but was small in adult mice. Thus, low accelerating voltage SEM using BSE provides new information on the distribution of the osteoid and the bone matrix calcification under both normal and pathological conditions.

Aging↗

PubMed1997

Carpal tunnel syndrome induced by two types of calcium deposition.

Two rare cases of carpal tunnel syndrome caused by calcification in the carpal tunnel are reported. One case involved a tumorous calcification consisting of basic calcium phosphate, and the other involved a diffuse calcification consisting of a mixture of calcium pyrophosphate dihydrate and basic calcium phosphate. These cases suggest that the shape of carpal tunnel calcifications is influenced by the nature of calcifying substance itself, i.e., whether it is heterogenous or homogenous.

Aged↗

PubMed1997

Histopathology and clinical results of carpal tunnel syndrome in idiopathic cases and hemodialysis patients.

The results of the histological examinations of specimens of the tenosynovium of the flexor tendon, the epineurium and the transverse carpal ligament from two groups of Japanese patients with carpal tunnel syndrome (idiopathic and hemodialysis) were compared. Amyloid deposits, positively identified as beta 2-microglobulin, appeared in all patients in the long-term hemodialysis group, but in no patients in the idiopathic group. Although the pathogenesis differed between the two groups, both resulted in nerve compression in the carpal tunnel. Therefore, surgical release is considered beneficial for both groups.

Aged↗

PubMed1997

Endoscopic carpal tunnel pressure measurement: a reliable technique for complete release.

Carpal tunnel syndrome is diagnosed by clinical symptoms, Tinel's sign, Phalen's test and electromyography. Carpal tunnel pressure measurement can also aid in the precise identification of excessive pressure sites that indicate locations for release. In this study, pressure measurements made during endoscopic carpal tunnel release at 5 points were significantly higher anywhere in the carpal tunnel than outside the tunnel and decreased markedly after release. We concluded that our measurement technique can improve the reliability of endoscopic carpal tunnel release by decreasing the likelihood of missing any nerve entrapment sites.

Adult↗

PubMed1997

Osteoporosis due to testicular atrophy in male leprosy patients.

A study was conducted to examine the relationship of testicular atrophy to bone metabolism in male leprosy patients. The study consisted of 31 leprosy patients (mean age: 62.0 years) and 31 healthy control men (mean age: 60.0 years). Measurements were made of their serum levels of free testosterone (FT), estradiol (E2), luteinizing hormone (LH) and 25-hydroxyvitamin D (25 OHD). Bone mineral density (BMD) was measured at radial sites and the lumbar vertebral bodies (L2-L4) by dual-energy X-ray absorptiometry using a Hologic QDR-2000 densitometer. FT and E2 levels were significantly lower and LH levels higher in leprosy patients than in controls. This represents a primary hypogonadal pattern. A value of 7.20 pg/ml of FT ( = Mean - 1 SD of control) was used as a cut off value, and the subjects were subdivided into a hypogonadal group (HG) and a non hypogonadal group (non-HG). When the subjects were compared for differences in age, age at onset of disease, duration of disease, body mass index and BMD, only the duration of disease and BMD were significantly different between the two groups. Furthermore, BMD of the forearm significantly correlated with FT levels (r = 0.689, P < 0.0001). Low BMD may be due to orchitis and testicular atrophy.

Aged↗

PubMed1997

Muscle strength in rheumatoid elbow: quantitative measurement and comparison to Larsen's X-ray grade.

Accurate assessment of elbow function is important to determine the total ability of the arm. The purpose of this study was to clarify the relationship between isometric muscle strength of the elbows of patients with rheumatoid arthritis (RA) and Larsen's X-ray evaluation. Fifty-six elbows of 45 RA patients aged 47 to 77 years (mean age, 63 years) were tested. Muscle strength was measured with an isometric torque-cell dynamometer. Test-retest reliability of the dynamometer was proven by measuring 12 elbows of 6 healthy young men. In RA patients, elbow flexion and extension strength decreased in proportion to increases in the severity of Larsen's grades from Grade 1 to 4. However, Grade 5 elbows had greater muscle strength than those in Grade 4. Forearm pronation and supination strength also decreased in proportion to increases in the severity of Larsen's grades from Grade 1 to 5. This quantitative study made it clear that the muscle strength of RA patients' elbows almost completely correlates to X-ray finding according to the grade of Larsen's evaluation based on X-rays. With regard to muscle strength of postoperative elbows, both flexion strength and supination strength after total elbow replacement (TER) were about two times greater than before TER, and after synovectomy it was as great as those in non-operative RA patients of Grade 2.

Adult↗