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Masao Kinoshita

Publications and source records attributed to Masao Kinoshita.

14 recordsLinked to original sources
PubMed2004

[A case of gastric cancer with a synchronous hepatic metastasis responding to postoperative oral administration of UFT and intermittent intrahepatic arterial chemotherapy of 5-FU].

A 65-year-old male was admitted to our hospital because of sudden onset of upper abdominal pain due to the perforation of gastric cancer with synchronous hepatic metastasis. He underwent total gastrectomy with lymphatic dissection of D1 + alpha. Pathological diagnosis of the surgical specimen was moderately differentiated tubular adenocarcinoma. The cancer progression was fStage IV (T1, N0, H1, P0). Since 50 days after surgery, he had received oral administration of UFT (300-600 mg/day) and intermittent intrahepatic arterial infusion of 5-FU (one injection, 500 mg/2 weeks). Seven months after the start of chemotherapy, the size of hepatic lesion was reduced. Thirteen months later, the tumor became necrotic with cystic change. Furthermore, 22 months later, abdominal CT scan showed complete response. He has been well without recurrence for 38 months following the start of chemotherapy.

Adenocarcinoma↗
PubMed2004

[A case of eosinophilic pneumonia possibly associated with 5-aminosalicylic acid (5-ASA)].

A 30-year-old man was diagnosed as having ulcerative colitis and was treated with 2,250 mg/day of 5-aminosalicylic acid (5-ASA). After 4 weeks of the administration, the patient complained of cough and fever and was admitted to our hospital. His chest radiograph showed infiltrative shadows bilaterally in the lung fields. Peripheral blood analysis indicated eosinophilia. We confirmed eosinophilic pneumonia by bronchoalveolar lavage and transbronchial lung biopsy. Improvement in clinical symptoms and radiological findings was obtained after the cessation of 5-ASA and initiation of prednisolone. Finally, mesalazine-induced eosinophilic pneumonia was diagnosed on the basis of his clinical course. The literature contains a few reports on patients with mesalazine-induced eosinophilic pneumonia.

Adult↗
PubMed2003

Influence of temocapril on cultured ventral spinal cord neurons.

Temocapril, a angiotensin-converting enzyme (ACE) inhibitor, was tested for neurotrophic activity in primary explant cultures of ventral spinal cord of fetal rats (VSCC). Temocapril had a remarkable effect on neurite outgrowth with a 4.2- to 5.1-fold increased over that of control VSCC at their effective concentrations. In temocapril-treated VSCC, choline acetyltransferase (ChAT) activity was also increased 2.4-3.2 times over that of control at 10(-9) and 10(-8) M, respectively. Our data suggest that temocapril is a candidate for neurotrophic factors on spinal motor neurons in vitro. A possible therapeutic role for temocapril in damaged motor neurons, such as in motor neuropathy and amyotrophic lateral sclerosis, remains to be defined.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2003

Temocapril prevents motor neuron damage and upregulation of cyclooxygenase-II in glutamate-induced neurotoxicity.

To examine the possible neuroprotective effect of temocapril, one kind of angiotensin-converting enzyme inhibitor, against glutamate-induced neurotoxicity, we analyzed the pharmacologic utility of temocapril in a post-natal organotypic culture model of motor neuron degeneration. Treatment with 10(-5) M of glutamate resulted in a motor neuron loss and decreased activity of choline acetyltransferase (ChAT). Cotreatment of 10(-5) M of glutamate and temocapril revealed protective effect on motor neuron death and decreased activity of ChAT. Next we performed reverse transcription-PCR analysis for cyclooxygenase-II (COX-II). COD-II mRNA was upregulated in glutamate-treated culture. Cotreatment with temocapril and glutamate inhibited upregulation of COX-II. Taken together, temocapril may have therapeutic potential for diseases which associate with upregulation of COX-II, in addition to its role in glutamate excitotoxicity.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2003

Oral administration of a neuroprotective compound T-588 prevents motoneuron degeneration after facial nerve avulsion in adult rats.

OBJECTIVE: R(-)-1-(benzo[b]thiophen-5-yl)-2-[2-(N,N-diethylamino) ethoxylethanol hydrochloride (T-588), a synthetic compound, has been shown to have neuroprotective potentials for neuronal cells. We investigated whether orally administered T-588 can rescue injured motoneurons after facial nerve avulsion in adult rats. METHODS: The right facial nerves of adult Fischer 344 male rats were avulsed and the animals were freely administered solution of 0.05% (w/v) T-588 or received T-588 (3-30 mg/kg/day) through an oral tube for 1-4 weeks. Facial motoneurons on both sides of the facial nuclei were counted in Nissl-stained sections, and choline acetyltransferase (ChAT) immunoreactivity in injured motoneurons and ChAT enzyme activities in the ventral brain stem tissue containing the facial nuclei were examined. RESULTS: Both free oral administration of 0.05% T-588 solution and oral tube administration of T-588 (30mg/kg/day) improved the survival of facial motoneurons at 3 or 4 weeks after avulsion. These treatments ameliorated ChAT immunoreactivity in injured motoneurons and the tissue ChAT enzyme activities at 1-week postoperation examined. CONCLUSION: These results indicate that oral administration of T-588 ameliorates the survival of injured motoneurons and supports their neuronal function after facial nerve avulsion in adult rats. T-588 may have therapeutic potential in motoneuron injury or motor neuron diseases in humans.

Administration, Oral↗
PubMed2002

The diagnostic interval in amyotrophic lateral sclerosis.

We studied whether there are any parameters that influence the period between onset of symptoms and confirmation of diagnosis in 117 patients with ALS (65 male, 52 female). The mean age of diagnosis was 57 years for men and 59 years for women. Bulbar-onset patients were older at diagnosis than limb-onset patients both men and women. Patients with bulbar-onset appeared to be more frequent in women (33:19). Contrariwise, limb-onset patients were more frequently male (43:22). The time to confirmation was much shorter with symptoms of bulbar-onset (10.5 months in male, 9.8 months in female) than for those with limb-onset (13.7 months in male, 14.8 months in female) in male, respectively, female ALS patients. The diagnosis of ALS was established in all cases by neurologists in our study.

Adult↗
PubMed2002

T-588 enhances neurite outgrowth and choline acetyltransferase in cultured rat spinal ventral horn neurons.

T-588(R(-)-1-(benzo(b)thiophen-5yl)-2-[2(N,N-diethylamino)ethoxy]ethanol hydrochloride) is a novel compound which has been shown to exhibit a wide range of neurotrophic effects both in vivo and in vitro. This compound can slow the motor deterioration of wobbler mouse motor neuron disease. However, it is not known whether this compound has a trophic effect on spinal motor neurons. We have studied the effect of T-588 on neurite outgrowth and choline acetyltransferase(ChAT) activity in primary explant cultures of ventral spinal cord of fetal rats(VSCC). Cultures were treated with T-588 from day 1 to 1 week. T-588 treated VSCC, compared with control VSCC, had a significant neurite promoting effect at ranged between 10(-8) molar(M) and 10(-5) M, with 2.3 to 5.3 fold increased over that of control VSCC. In T-588 treated VSCC, ChAT activity was increased 1.5 times over that of control at 10(-6), and 10(-5) M respectively. Our data showing T-588 has neurotrophic action on VSCC and suggests a potential use of T-588 in treating diseases that involve degeneration and death of spinal motor neurons, such as motor neuropathy and motor neuron disease.

Animals↗
PubMed2002

Polymyositis and dermatomyositis associated with malignancy: a 30-year retrospective study.

BACKGROUND: Polymyositis and dermatomyositis in association with malignancy are paraneoplastic syndromes, but the incidence, treatment and factors that predict associated cancer and its prognosis all remain unclear. PATIENTS AND METHOD: During the 30-year period 1969-99, we treated 64 patients who had polymyositis (including two with cancer) and 28 patients who had dermatomyositis (including 10 with cancer). We compared the clinical findings of the patients who had cancer with the findings of those who did not have cancer. RESULTS: The risk of cancer is significantly higher in dermatomyositis and somewhat higher in polymyositis. An increased cancer risk was found in male patients with dermatomyositis who were older than 50 years. Cancer was diagnosed within 4 years before or after the diagnosis of polymyositis or dermatomyositis, and usually within 1 year. An operation was not possible in many of the patients with cancer because of the advanced stage of the disease. CONCLUSION: Our findings suggest that early discovery of malignancy is critical in cases of polymyositis and dermatomyositis.

Adult↗
PubMed2002

Trophic effect of olmesartan, a novel AT1R antagonist, on spinal motor neurons in vitro and in vivo.

Olmesartan is a novel compound which has been shown to exhibit various neuropharmacological effects. For the purpose of clarifying the effect of Olmesartan on spinal motor neurons, we studied the following tests. We studied the effect in vitro of Olmesartan on neurite outgrowth and choline acetyltransferase (ChAT) activity in primary explant cultures of ventral spinal cord (VSCC) of fetal rats. Olmesartan-treated VSCC, compared with control VSCC, had a significant neurite outgrowth and increased activity of ChAT. The effect was dose-related in neurite outgrowth. However, there was no relationship between activity of ChAT andgiven doses of Olmesartan. We examined in vivo the effect of Olmesartan on axotomized spinal motor neuron death in the rat spinal cord. After post-natal unilateral section of sciatic nerve, there was approximately a 50% survival of motor neurons in the fourth lumbar segment. In comparison with vehicle, intraperitoneal injection of Olmesartan for consecutive 14 days reduced spinal motor neuron death. There was no relationship between number of surviving neurons and doses of Olmesartan. These in vitro and in vivo studies showed that Olmesartan has a neurotrophic effect on spinal motor neurons. Our data suggest a potential therapeutic use of Olmesartan in treating diseases that involve degeneration and death of motor neurons, such as motor neuropathy and amyotrophic lateral sclerosis.

Amyotrophic Lateral Sclerosis↗
PubMed2002

Protective effect of interleukin-3 and erythropoietin on motor neuron death after neonatal axotomy.

Several members of hematopoietic factors are known to have neuroprotective effects against axotomized motor neuron death. We carried out a study to determine whether interleukin-3 (IL-3) and erythropoietin (EPO) rescue spinal motor neuron death following axotomy. Unilateral sciatic nerve was transected in neonatal rats. Different doses of IL-3, EPO, or vehicle were administered daily for two weeks by intraperitoneal injection. After treatment, the number of spinal motor neurons was determined at the level of L4 segment In comparison with vehicle, both IL-3 (10 microg kg(-1)) and EPO (5.0 mg kg(-1)) significantly prevented the loss of motor neurons. Protective potentials is the same between them. These results suggest that IL-3 and EPO play a role for motor neuron survival in vivo and suggest the potential use of these hematopoietic factors in treating diseases that involve degeneration and death of motor neurons, such as motor neuropathy and amyotrophic lateral sclerosis.

Animals↗
PubMed2002

Unusual fatty infiltration of the soleus muscle in a patient with congenital nemaline myopathy: fat-suppression muscle MRI.

A 27-year-old man developed gait disturbance over a three-year period. Histochemical analysis suggested nemaline bodies, type I fiber atrophy and type II fiber hypertrophy. Conventional magnetic resonance imaging (MRI) showed a severe degree of homogenous hyperintensity in the soleus muscle. Fat-suppression MRI exhibited marked diffuse hypointensity in the soleus muscle. MRIs demonstrated unusual fatty proliferation of the soleus muscle. Fat-suppression MRI of skeletal muscles is beneficial in evaluating the accurate topography and degree of fatty infiltration. Radiological patterns of muscle damage are variable in patients with congenital nemaline myopathy, similar to the heterogeneous clinical aspects.

Adipose Tissue↗
PubMed2002

Acetazolamide-induced muscle weakness in hypokalemic periodic paralysis.

A 46-year-old man with hypokalemic periodic paralysis (HypoPP) and diabetes mellitus (DM) had worsened muscle weakness after acetazolamide (ACZ) treatment. During the paralytic episode, serum potassium levels were reduced, and serum chloride and insulin levels were increased. The data suggested proximal renal tubular acidosis due to ACZ. We determined arterial-venous concentrations of potassium, insulin and glucose across the forearm. Venous potassium levels were markedly reduced. ACZ is thought to potentiate potassium uptake into muscles. Hyperinsulinemia and DM could contribute to ACZ-induced exacerbation in our patient. We should pay more attention to ACZ-treated HypoPP patients with hyperinsulinemia and DM.

Acetazolamide↗
PubMed2002

Molecular and cellular mechanism of glutamate receptors in relation to amyotrophic lateral sclerosis.

Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disorder of the central nervous system (CNS) with an unknown etiology. This disorder is characterized clinically by muscular weakness and wasting, and pathologically by selective degeneration of the corticospinal tracts and motor neurons of the brain stem and spinal cord. Median survival following onset is 3 to 5 years. Riluzole, an antiglutamatergic agent has been shown to have modest beneficial effects on survival. Glutamate is the main excitatory neurotransmitter in the CNS and excessive activation of glutamate receptors is excitotoxic to neurons. Glutamate receptor-mediated excitotoxicity has been proposed to explain the pattern of selective neuronal cell death and clinical manifestation of ALS. Activation of glutamate receptors leading to elevation of intracellular calcium may play a major role. This review will focus on the current understanding of the molecular and cellular mechanisms of glutamate receptors in relation to ALS.

Amyotrophic Lateral Sclerosis↗