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Biomedical subjects

H Hashizume

Publications and source records attributed to H Hashizume.

At least 109 records · Page 6Linked to original sources
PubMed1997

Percutaneous release for trigger finger in idiopathic and hemodialysis patients.

Sixty-seven trigger fingers of 58 idiopathic and hemodialysis patients were treated by percutaneous A1-pulley release technique. Severity of triggering was classified into five grades for treatment selection and prediction of possible results. Results were excellent in 41 fingers, good in 9, fair in 7, and poor in 10, requiring additional treatment. The results of the lower grades were better, and those of the higher grades were poor. Excellent or good results appeared to depend on the proper selection of the patients according to the grading system and confirmation of triggering disappearance just after the release. There were neither infections nor neuro-vascular deficits after treatment. Compared to conventional open release, this treatment was found to be more useful from the standpoints of ease and safety of the technique, and the patients' quick return to normal life.

Adult↗
PubMed1997

Antithrombotic effects of the novel inhibitor of thrombin-induced offtelet aggregation and thrombus formation, 3-[2-[1,1':2',1"]-terphenyl-4'-yl)ethyl]phenoxyacetic acid.

The new compound 3-[2-([1,1':2,1"]-terphenyl-4'yl)ethyl]phenoxyacetic acid (F1070) was synthesized and its effects on platelet aggregation induced by thrombin, thrombin receptor agonist peptide (TRAP), ADP and collagen were evaluated in humans, guinea pigs and rats, and were compared with the effects of he thrombin antagonists argipidine and (D)Phe-Pro-Arg-CH2Cl (FPR). F1070 inhibited the platelet aggregation induced by these agonists and was highly selective in its inhibition of thrombin. F1070 inhibited fibrin formation induced by thrombin, but far less effectively than argipidine. In a guinea pig model of extracorporeal circulation thrombosis, F1070 (10 mg/kg p.o.) significantly inhibited the development of a thrombus. F1070 is thus a key compound that should facilitate the development of new orally active antithrombotic drugs that are specific for thrombin.

Animals↗
PubMed1997

Antithrombotic effects of 3-([1:1',2':1"]-3'-terphenyl)propanol in animals.

3-([1:1',2':1"]-3'-Terphenyl)propanol (CAS 186835-06-3, F050) and acetylsalicylic acid (ASA) inhibited platelet aggregation induced by CaCl2, arachidonic acid, collagen, adenosine diphosphate (ADP) and thrombin in guinea pigs, rabbits and rats in vitro. However, F050 had a wider spectrum of actions than ASA. Orally administered F050 inhibited platelet aggregation ex vivo. F050 significantly reduced the thrombus formation in the extracorporeal circulation thrombosis model in guinea pigs. It inhibited erythrocyte hemolysis induced by hypotonic NaCl, while ASA did not. F050, but not ASA, inhibited increases in platelet [CA2+]i caused by thrombin in guinea pigs. F050 is a parent compound that will facilitate the development of an orally active drug for the treatment of thrombotic diseases.

Animals↗
PubMed1996

Pathomechanism of pain-related behavior produced by allografts of intervertebral disc in the rat.

STUDY DESIGN: This study was designed to evaluate whether allografts of intervertebral disc materials produce hyperalgesia in the rat and whether an immune response, pH, or chemicals correlate with the induced hyperalgesia. OBJECTIVE: To elucidate the pathomechanisms of radicular pain secondary to lumbar disc herniation. SUMMARY OF BACKGROUND DATA: It has been reported that a low pH, an autoimmune reaction, or chemical radiculitis is likely responsible for radicular pain associated with lumbar disc herniation. In animal studies, it has been shown that hyperalgesia (an increased sensitivity to painful stimuli) involves activation of phospholipase A2 and nitric oxide synthase. METHODS: Fat, nucleus pulposus, and anulus fibrosus were allografted into the epidural space at L6 in the rat. Withdrawal response thresholds to mechanical stimuli and withdrawal response latencies to thermal stimuli on the tail and pH in the applied tissues were measured after surgery. Interleukin-1, phospholipase A2, and nitric oxide synthase were examined in the applied tissues using immunohistochemistry, nicotineamide adenine dinucleotide phosphate-diaphorase histochemistry, and in situ hybridization. RESULTS: Allografted fat did not produce hyperalgesia. Allografts of nucleus pulposus and nucleus pulposus plus anulus fibrosis showed evidence of mechanical and thermal hyperalgesia, respectively. There were no observed changes in pH over time. Although interleukin-1 was demonstrated in all applied tissues, phospholipase A2 was only observed around the applied nucleus A2 was only observed around the applied nucleus pulposus and nucleus pulposus plus anulus fibrosus. Nitric oxide synthase was only markedly increased around the applied tissues. CONCLUSION: The nucleus pulposus and anulus fibrosus produce different forms of hyperalgesia (mechanical vs. thermal) associated with different and distinct immunohistochemical changes. It is possible that radicular pain of a lumbar disc herniation results from chemicals, such as phospholipase A2 and nitric oxide.

Adipose Tissue↗
PubMed1996

Histopathology of Kienböck's disease. Correlation with magnetic resonance and other imaging techniques.

Histopathological studies of extracted whole lunate bones obtained from 10 patients with Stage 3 Kienböck's disease at surgery for tendon-ball replacement were correlated with magnetic resonance imaging (MRI), computed tomography (CT) and tomography images made prior to surgery. A reforming zone, or a reactive interface between the reactive new bone and granulation tissue formation, and new vascularization were observed surrounding the bone necrosis area showing empty lacunae, fatty necrosis, and disappearance of osteoid. Findings of CT, tomography and microradiography of slices of extracted lunate bone confirmed that fractures of the articular cartilage and the subchondral bone occurred secondarily by overloading, and showed the extent of the collapsed area of the lunate. MRI showed complete loss of signal intensity in T1 images of the lesion of the lunate in advanced Stage 3 Kienböck's disease. MRI is at present unable to distinguish bone necrosis, the histological reactive interface or surrounding hyperaemia in detail. However, the low-intensity arc, or the reactive interface present on MRI in early Stage 3, sometimes correlates with the histological findings of osteoid and granulation zones.

Adult↗
PubMed1996

Dorsally displaced epiphyseal fracture of the phalangeal base.

A dorsally displaced epiphyseal fracture of the middle phalanx (Salter-Harris Type I) is described. The epiphyseal fragments were attached to the central slip of the extensor tendon and collateral ligaments. The articular surface of the PIP joint was intact and smooth. The epiphysis was reduced and fixed without cutting the central slip or the collateral ligaments 8 months after injury. This kind of fracture can occur in the PIP and DIP joints, and presents special diagnostic difficulties. Open reduction is evidently necessary to correct the displacement.

Child↗
PubMed1996

The Galeazzi-equivalent lesion in children revisited.

A fracture at the medial end of the distal third of the radius with an epiphyseal separation of the distal ulna in a 16-year-old boy is described. This injury, known as the Galeazzi-equivalent lesion in children, is characterized by complete distal ulnar epiphyseal separation without rupture of the distal ligamentous stabilizing system between the radius and ulna, which includes the triangular fibrocartilage complex, interosseous ligaments and periosteal tube of the ulnar. The Galeazzi fracture-dislocation and the Galeazzi-equivalent lesion appear to be completely dissimilar in their pathological anatomy. We suggest calling the latter a "pseudo-Galeazzi injury".

Adolescent↗
PubMed1996

Vascular reconstruction in limb salvage operations for soft tissue tumors of the extremities.

Eight patients with vascular threatening soft tissue tumors underwent wide excision of the tumors followed by vascular reconstruction. Superficial femoral vessels were resected in 6 patients and popliteal vessels in 2 patients. Arterial reconstruction was performed with a synthetic graft in 4 and a reversed saphenous vein graft in 4. Venous reconstruction was performed with a synthetic graft in 5 and a saphenous vein graft in 2. Adjuvant multimodality treatment was used in 6 patients. After an average of 30 months, the revascularized vessels were found to be patent in 5 patients with arterial reconstruction and in 1 patient with venous reconstruction. Six patients maintained functional extremities. Two other patients had to have amputations, 1 because of a deep infection that involved the grafts and the other because of an acute occlusion of the reconstructed artery. Edema of the leg, which was treated successfully with an elastic support and elevation of the leg, has been observed in all patients after operation. No local recurrence has been observed with an average followup period of 42.5 months. Pulmonary metastasis developed in 2 patients, and 1 of them underwent a pulmonary metastasectomy. Limb salvage in vascular threatening soft tissue tumors using vascular reconstruction techniques is useful and preferable in some patients.

Adult↗
PubMed1996

Effects of beta-adrenoceptor antagonists on Ca(2+)-overload induced by lysophosphatidylcholine in rat isolated cardiomyocytes.

1. The effects of beta-adrenoceptor antagonists including (-)- and (+)-propranolol, (-)- and (+)-penbutolol, timolol, pindolol, atenolol, acebutolol and practolol on the Ca(2+)-overload induced by lysophosphatidylcholine (LPC) were examined in isolated cardiomyocytes of the rat. 2. Fura-2 was used for measurement of the intracellular calcium concentration ([Ca2+]i). LPC (15 microM) produced a rapid increase in [Ca2+]i from 72 +/- 5 to 3042 +/- 431 nM which coincided with a decrease in the percentage of rod-shaped cells from 69 +/- 2 to 5 +/- 2%. 3. Preincubation with (-)-propranolol (20 microM), (+)-propranolol (50 microM), or (-)- or (+)-penbutolol (20 microM), the lipophilicity of which is higher than other beta-adrenoceptor antagonists, significantly inhibited both the increase in [Ca2+]i and the cell-shape change induced by 15 microM LPC. The inhibitory effects of the four drugs on the LPC-induced increase in [Ca2+]i and cell-shape change were concentration-dependent. The IC50S of (-)-propranolol, (+)-propranolol, (-)- and (+)-penbutolol for the increase in [Ca2+]i were 1.28, 10.50, 0.67 and 0.76 microM, respectively. 4. Pretreatment with pindolol, timolol, acebutolol, practolol, atenolol or lignocaine did not inhibit the increase in [Ca2+]i and the morphological change induced by LPC. 5. LPC markedly increased the release of creatine phosphokinase from 9 +/- 1 to 45 +/- 2% which could be significantly reduced by (-)- or (+)-propranolol but not by acebutolol or timolol. 6. The protective effects of (-)- and (+)-propranolol, (-)- and (+)-penbutolol against the Ca(2+)-overload induced by LPC were not associated with the beta-adrenoceptor antagonistic action, but probably with an unknown action which is related to the preservation of membrane integrity. Further studies are necessary to clarify the exact mechanisms of the protective action of these beta-adrenoceptor antagonists against the Ca(2+)-overload induced by LPC.

Adrenergic beta-Antagonists↗
PubMed1996

[A new approach to the understanding of the mechanism of ischemia/reperfusion damage in the heart and the effects of anti-ischemic drugs].

The classical understanding of the mechanism of anti-anginal or anti-ischemic drugs is an increase in blood supply to the heart and/or a decrease in oxygen consumption of the heart, maintaining energy balance in the heart between supply and demand and hence maintaining the tissue levels of high-energy phosphates. This scheme is reasonable. During reperfusion following ischemia, however, there is more serious damage to the heart, although the tissue levels of high-energy phosphates increase. This is probably because toxic substances are generated in the heart during ischemia/reperfusion. We propose that both lysophosphatidylcholine and palmitoyl-L-carnitine that accumulate in the myocardium during ischemia/reperfusion are candidates for the toxic substances that accelerate ischemia/reperfusion damage to the heart. Therefore, drugs that have anti-lysophosphatidylcholine and/or anti-palmitoyl-L-carnitine effects are promising for the treatment of ischemic heart diseases. We found that K-7259, a novel derivative of dilazep having a minimal effect on the normal heart, is a drug that attenuates the deleterious effects of both lysophosphatidylcholine and palmitoyl-L-carnitine on the heart, and therefore attenuates the ischemia/reperfusion damage.

Adrenergic beta-Antagonists↗
PubMed1996

Capillary architecture in the skeletal muscles in the rat hind limb.

We observed differences in the capillary architecture of the skeletal muscles that have different fiber metabolism. The soleus, the vastus intermedius and the tibialis anterior muscles of adult Wistar rats were prepared using two different techniques. Samples for adenosine triphosphatase (ATPase) staining were prepared following Dubovitz's method, and the distributions of fiber type, Types 1, 2A and 2B, were analyzed. Then, corrosion casts of capillary architecture of these muscles prepared following Murakami's method were observed with a scanning electron microscope (SEM) and compared with the fiber distribution. The fiber type composition of the soleus muscle showed Type 1 (slow-twitch) dominance and that of the vastus intermedius and the tibialis anterior muscle showed Type 2 (fast-twitch) dominance. The capillaries of the soleus muscle were tortuous, and this was thought to be advantageous for blood supply. In contrast, the capillaries of the vastus intermedius and tibialis anterior muscles had a relatively parallel pattern. Additionally, two different patterns of capillary architecture that appeared to correspond to certain metabolic characteristic of different muscle fiber types were preserved with corrosion casting. In conclusion, comparative studies on capillary architecture of the skeletal muscles are useful for analyses of its function.

Adenosine Triphosphatases↗
PubMed1996

K-7259, a novel dilazep derivative, and d-propranolol attenuate H2O2-induced cell damage.

We studied the effects of dilazep, K-7259 (a novel derivative of dilazep) and d-propranolol on the change in cell shape and accumulation of nonesterified fatty acids (NEFA) induced by hydrogen peroxide (H2O2) in isolated rat cardiac myocytes. Myocytes were incubated in a Krebs-Ringer bicarbonate buffer containing 2 mM diethyltriamine pentaacetic acid (DETAPAC) and 2mM FeSO4 for 10 min, and then treated with 2mM H2O2 for 50 min. Before the treatment with H2O2, the percentage of the number of rod-shaped cells to that of total cells was 66 +/- 2%, and decreased to 35 +/- 3%, 25 +/- 4% and 14 +/- 2%, after 30, 40 and 50 min of the H2O2 treatment, respectively. The levels of NEFA (lauric, myristic, palmitoleic, arachidonic, linoleic, palmitic, oleic and stearic acids) increased after the treatment with H2O2. In the absence of FeSO4 and DETAPAC, however, H2O2 did not have these effects, and therefore all the experiments with drugs were performed in the presence of Fe2SO4 and DETAPAC. K-7259 (30 microM) and d-propranolol (50 microM) attenuated both the changes in cell shape and accumulation of NEFA induced by H2O2, whereas dilazep (30 or 50 microM) did not. N-(2-mercaptopropionyl)glycine (2 mM), an .OH scavenger, inhibited the H2O2-induced changes completely. These results suggest that K-7259 and d-propranolol attenuate the H2O2-induced changes in cell shape and accumulation of NEFA, probably because of their .OH-scavenging effect.

Animals↗
PubMed1996

Shoulder pain in long-term haemodialysis patients. A clinical study of 166 patients.

We reviewed 166 adult patients on long-term haemodialysis, dividing them into three groups according to the presence and type of shoulder pain. The 24 patients in group A, with spontaneous pain related to a supine posture, had been under haemodialysis for significantly longer than the others, and had a much higher incidence of carpal tunnel syndrome. Open or arthroscopic resection of the coracoacromial ligament in 21 shoulders relieved pain during haemodialysis and night pain, and histological examination showed amyloid deposits and inflammatory-cell infiltration in the subacromial bursa in almost all cases, and in the tenosynovium of the bicipital groove in some. We conclude that one type of shoulder pain experienced by patients on long-term haemodialysis is caused by the subacromial impingement of amyloid deposits. This should be distinguished from other types of shoulder pain, because it can be relieved by resection of the coracoacromial ligament.

Adult↗
PubMed1996

Eosinophilic pustular folliculitis effectively treated with recombinant interferon-gamma: suppression of mRNA expression of interleukin 5 in peripheral blood mononuclear cells.

Eosinophilic pustular folliculitis (EPF) is characterized clinically by pruritic grouped follicular papules and pustules on the trunk, limbs, and face, and, histologically, by follicular infiltration with eosinophils. The blood eosinophil count is elevated in most patients. Oral minocycline, nonsteroidal anti-inflammatory drugs, diaminodiphenylsulphone, and corticosteroids may induce remission. We report two Japanese men with EPF who responded poorly to the usual therapy. Intravenous injections of recombinant interferon-gamma (rIFN-gamma), 5 x 10(5) to 2 x 10(6) Japan Reference Unit (JRU) (1 JRU roughly corresponds to 4 NIH units) daily for 7 days, cleared the skin lesions and returned the peripheral eosinophil counts to normal in both patients. However, the lesions recurred 2-3 days after rIFN-gamma was stopped. Both patients have received intravenous rIFN-gamma once or twice a week for nearly 1 year without systemic side-effects. Reverse transcriptase-polymerase chain reaction revealed a decreased expression of interleukin 5 (IL-5) mRNA in peripheral mononuclear cells after the rIFN-gamma therapy. rIFN-gamma may become the treatment of choice in recalcitrant EPF, although further studies are needed. It may work by interfering with the immunological function of type 2 T-helper cells, including IL-5 production responsible for the growth and differentiation of eosinophils.

Adult↗
PubMed1996

Non-traumatic paralysis of the posterior interosseous nerve.

We treated 31 patients with non-traumatic paralysis of the posterior interosseous nerve over 15 years. There were 10 men and 21 women of mean age 40.3 years (17 to 71). Six were managed conservatively, and 25 by operation. In 14 patients entrapment occurred at the supinator, including three who had double compression at both the entrance and exit from the muscle. In four it was caused by a ganglion, in one by a lipoma, in one by a dislocated radial head and in two by a marked constriction in the nerve of unknown cause. The remaining three patients were retrospectively diagnosed as having neuralgic amyotrophy, the only observable change at operation being slight oedema of the nerve. Paralysis recovered in 24 out of the 25 patients at between 2 to 18 months (mean 5.6) after operation, and the one failure was treated later by tendon transfer.

Adolescent↗
PubMed1996

In vitro antiplatelet activity of the carbinol analogue of ketoprofen, 3-(1-methyl-2-hydroxyethyl)-benzophenone.

3-(1-Methyl-2-hydroxyethyl)-benzophenone (F025) is a close structural analogue of ketoprofen, in which the carboxylic acid of ketoprofen is reduced to a carbinol moiety. The in vitro effects of F025 on platelet aggregation, cyclooxygenase and hypotonic NaCl-induced erythrocyte hemolysis were examined in comparison with those of ketoprofen. Although the inhibitory activity of F025 on collagen, arachidonic acid and ADP-induced platelet aggregation was between 2 and 20 times that of ketoprofen in healthy volunteers, guinea pigs, rabbits and rats, F025 had only one-tenth of the inhibitory action of ketoprofen on sheep seminal vesicle cyclooxygenase F025, but not ketoprofen, inhibited hypotonic NaCl-induced erythrocyte hemolysis in guinea pigs. The substantial antiplatelet activity of F025 may be due to membrane stabilization as well as to cyclooxygenase inhibition.

Animals↗