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Biomedical subjects

Shingo Konno

Publications and source records attributed to Shingo Konno.

12 recordsLinked to original sources
PubMed2006

Histological and immunohistological changes of the skeletal muscles in older SJL/J mice.

SJL/J mice have been studied as the model animals for autoimmunological diseases. Recently it was clarified that SJL/J mice have a defect of dysferlin. Human limb girdle muscular dystrophy 2B and Miyoshi myopathy also have a defect of dysferlin. In this study we present the histological and immunohistological changes in the natural course. Histological study revealed that SJL/J mice had inflammatory, degenerative changes, and neurogenic changes in later ages. As for interstitial inflammatory cells, the macrophages were dominant in any age, and in the T cell subset, the CD4+ T cells were more abundant than the CD8+ T cells, and few B cells were seen. The laboratory data showed a high level of creatine kinase in all ages. It is suspected that the inflammatory changes were induced by the primary immunological abnormality or by the defect of dysferlin in SJL/J mice.

Aging↗
PubMed2006

Subacute combined degeneration of the spinal cord concomitant with gastric cancer.

We report a rare case of subacute combined degeneration of the spinal cord concomitant with gastric cancer. A 67-year-old man was admitted because of posterior column symptoms, pyramidal tract sign and peripheral neuropathy with severe hyperchromic anemia. He was treated with mecobalamin 1 mg IM, after which his anemia and neurological signs recovered. He was diagnosed as having subacute combined degeneration with pernicious anemia. Subsequent stomach biopsy revealed gastric cancer, and the patient underwent gastrectomy. It is a well known association that chronic atrophic gastritis is associated with gastric cancer or subacute combined degeneration. Our findings suggest that in this case subacute combined degeneration and gastric cancer are independent of each other; rather, both resulted from chronic atrophic gastritis.

Aged↗
PubMed2006

[A case of primary HIV infection presenting as mononeuritis multiplex].

A 34-year-old man presented with gait disturbance. He had a low grade fever and diarrhea for a few days prior to admission. Two weeks after he started to have diarrhea, he developed gait disturbance with a left foot drop. The cerebrospinal fluid obtained on admission showed pleocytosis (30/microl) and increased protein. The motor nerve conduction velocities (MCV) of the left peroneal nerve and the tibial nerve were slow, but the right peroneal and tibial MCVs were within normal limits. A test for human immunodeficiency virus (HIV) antibody was positive. The Western blot was positive with bands of gp160 and p24, confirming HIV infection. Seroconversion-related neuropathy of HIV was diagnosed. Acute HIV infection should be included in the differential diagnosis of mononeuritis multiplex. Before full-fledged AIDS development, it is important to find early stage of HIV infection in patients, so that we can treat them more effectively by means of anti-HIV drugs.

Adult↗
PubMed2005

Hydroxyl radical formation in skeletal muscle of rats with glucocorticoid-induced myopathy.

Steroid myopathy is a well-known adverse effect of glucocorticoids that causes muscle weakness and atrophy; however, its pathogenic mechanism is still unclear. Recently, oxidative stress was reported to contribute to steroid myopathy, but there is no report that actually attempts to measure hydroxyl radical. I developed an animal model of steroid myopathy in rat with dexamethasone (9-Fluoro-11beta,17, 21-trihydroxy-16alpha-methylpregna-1,4-diene-3,20-dione), and measured hydroxyl radical using the salicylate trapping method. There was significant dose-dependent relation between both 2,5- and 2,3-dihydroxybenzoic acids and dexamethasone in the treated group, compared to the control group. These results suggest that hydroxyl radical plays a role in the pathogenesis of steroid myopathy.

Animals↗
PubMed2005

[A case of Brown-Vialetto-van Laere (BVVL) syndrome in Japan].

Here we report a sixty-year-old woman of Brown-Vialetto-van Laere (BVVL) syndrome in Japan. She had sensorineural deafness, weakness and atrophy of her extremities from 15 years of age. Her neurological symptoms slowly progressed. She first visited our hospital in 1993 when she was 49 years old. At that time, she had distal muscle weakness and atrophy of the four extremities and bulbar palsy. Deep tendon reflexes were absent and the plantar toe reflex was flexor. EMG revealed neurogenic changes and the nerve conduction studied were normal. The vital capacity was marked decreased. On August 10, 2003, she was admitted to our hospital because of CO2 narcosis. She had III, VII, X, XI, XII cranial nerve palsy, distal muscle weakness and atrophy of the four extremities. From her neurological symptoms and signs, we made a diagnosis of BVVL syndrome. MRI revealed no high signal in pyramidal tract by FLAIR image. ABR showed no response, and VEP demonstrated delay of the P100. She was intubated, and was attached to a respirator to improve her CO2 narcosis. After treatment she improved and did not need to be assisted by a respirator during daytime. During night time, she had apnea, and her blood gas showed the retention of CO2, and she still required the respiratory assistance during her sleep. This is the first report of BVVL syndrome in Japanese literature.

Bulbar Palsy, Progressive↗
PubMed2005

[Infected and calcified chronic subdural hematoma presenting an attitude of acute hematoma on MRI: case report].

We report a case of calcified chronic subdural hematoma with unusual magnetic resonance imaging (MRI) findings. A 50-year-old male with no marked medical history presented with fever for two weeks. Computed tomography (CT) revealed a thick, calcified subdural hematoma of low-iso mixed density. MRI showed characteristic signals of hematoma in the acute stage. Total removal of the hematoma by craniotomy was performed after rapid deterioration of consciousness. At surgery, a muddy hematoma and a small amount of pus were seen within the calcified capsule. Diagnosis of infected and calcified chronic subdural hematoma was established. His symptoms were resolved completely within the following few months. As the mechanisms of delayed signal sequence of hematoma on MRI, we speculate existence of tissue hypoxia associated with infection and paramagnetic effects of free radicals and ions associated with inflammation, necrosis and calcification.

Calcinosis↗
PubMed2004

Bone density in myasthenia gravis patients receiving long-term prednisolone therapy.

Osteoporosis is an adverse effect of prednisolone therapy, although no study has been conducted on myasthenia gravis patients receiving high-dose prednisolone. We measured bone density in 36 patients (26 females and 10 males) who had undergone long-term prednisolone administration, and found a decrease in bone density in 31% of female patients and osteoporosis in only 11.5% (three cases). This frequency is lower than the presumptive rate of the general population in Japan (22.6%). No osteoporosis was detected in male patients. In conclusion, prednisolone-treated patients with myasthenia gravis have an acceptable risk of bone loss if prophylactic medication is administered.

Absorptiometry, Photon↗
PubMed2004

T-588 protects motor neuron death following axotomy.

R(-)-1-(benzo [b] thiophen-5-yl)-2-[2-(N,N-diethylamino)ethoxy] ethanol hydrochloride) (T-588) enhances acetylcholine release. This compound slows the motor deterioration of wobbler mouse motor neuron disease and enhances neurite outgrowth and choline acetyltransferase activity in cultured rat spinal motor neurons. We examined the ability of T-588 on axotomized spinal motor neuron death in the rat spinal cord. After the postnatal 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 T-588 for 14 consecutive days rescued spinal motor neuron death. Our results showing in vivo neurotrophic activity of T-588 for motor neurons support the applicability of T-588 for the treatment of motor neuron diseases, such as amyotrophic lateral sclerosis and motor neuropathies.

Animals↗
PubMed2003

T-588 protects motor neuron death against glutamate-induced neurotoxicity.

To examine the possible neuroprotective effect of T-588 against glutamate-induced neurotoxicity, we analyzed the pharmacological utility of T-588 in a postnatal organotypic culture model of motor neuron degeneration. Treatment with 10(-5) M of glutamate resulted a motor neuron loss and decreased activity of choline acetyltransferase (ChAT). Cotreatment of 10(-5) M of glutamate and T-588 revealed a protective effect against motor neuron death and decreased ChAT activity. We concluded that T-588 may play important roles in the survival and maintenance of spinal motor neurons in its neuroprotection against glutamate-induced neurotoxicity. Our data may provide a rationale for designing a therapeutic strategy for protection against pathologically induced motor neuron damage or cell death such as amyotrophic lateral sclerosis and motor neuropathy.

Animals↗
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↗