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Biomedical subjects

S Kusunoki

Publications and source records attributed to S Kusunoki.

At least 37 records · Page 2Linked to original sources
PubMed2001

A prospective multicenter trial to determine the incidence of transient neurologic symptoms after spinal anesthesia with phenylephrine added to 0.5% tetracaine.

The addition of vasoconstrictors for spinal anesthesia is controversial, since an increase in the incidence of transient neurologic symptoms (TNS) has been reported. A multicenter, randomized, double-blind study was conducted to assess the effectiveness of spinal anesthesia with phenylephrine in addition to tetracaine as well as the incidence of neurological complications. We studied 64 patients with comparable demographic characteristics who were scheduled for elective surgery for a lower limb, or a gynecological or urological procedure. The patients were allocated randomly into 2 groups. Group P (n = 34) received 0.5% tetracaine in 10% glucose with 0.025% phenylephrine, while group C (n = 30) received 0.5% tetracaine in 10% glucose. Our results showed that only 2 patients (6.7%) in group C experienced TNS, and their symptoms disappeared within 72 hr after anesthesia, while none of the patients (0%) in group P complained of symptoms. The incidence of TNS was thus not significantly different between the two groups. Six hours after the sensory block, group P patients demonstrated sensory disturbance, with the median spinal dermatome corresponding to the L1 segment. Moreover, systolic blood pressure in group P was significantly higher than that in group C, 5 min, 15 min, and 20 min after injection. The incidence of TNS in the present study does not seem to be greater after surgery with spinal anesthesia using 0.5% hyperbaric tetracaine and 0.5 mg phenylephrine than without phenylephrine. Randomized, double-blind, cross-over trials with a larger sample size would be required in the future to obtain more reliable results.

Anesthesia, Spinal↗
PubMed2001

[Guillain-barré syndrome associated Campylobacter jejuni serotype Penner 2: a case report].

We described a 15-year-old male who had Guillain-Barré syndrome(GBS). Nine days after watery diarrhea, the patient developed pain and weakness of foot muscles. On admission, the nerve conduction studies revealed peripheral neuropathy with axonal degeneration and demyelination. Campylobacter jejuni(C. jejuni) with serotype of Lior 4, Penner 2 was isolated from his stool culture. IgM anti-GM 1 antibody and other various anti-ganglioside antibodies were detected in his serum. After receiving plasma exchange and intravenous immunoglobulin therapy, he was able to walk without assistance. In general, C. jejuni with the serotype Penner 19 has been isolated from many GBS patients. In this patient, C. jejuni with the serotype of Penner 2 was isolated. The serotype is detected commonly in Miller Fisher syndrome.

Adolescent↗
PubMed2001

[A case of Guillain-Barré syndrome after Campylobacter jejuni enterocolitis: anti-ganglioside antibody levels with or without Guillain-Barré syndrome].

A 38-year old man developed enterocolitis one day after he had ingested raw chicken. Nine days later, his grip strength weakened. Eleven days later, he was admitted to our hospital with weakness of four limbs, dysphagia and dysarthria. Serum anti-Campylobacter jejuni antibody and anti-ganglioside antibodies (GM1, GD1a, GD1b, GalNAc-GD1a) were positive, and motor action potentials were not evoked at all extremities. He was diagnosed as having Guillain-Barré syndrome. After receiving immune absorption therapy and plasma exchange therapy, the patient improved. Another person who had also consumed the same raw chicken developed colitis only. Five weeks later, the anti-GalNAc-GD1a-IgG antibody titers (O.D. 490 nm) of the patient and the other man who developed colitis were 0.324 and 0.118, respectively. It was suggested that the pathogenesis of Guillain-Barré syndrome after Campylobacter jejuni enterocolitis may be related to the type and titer of anti-ganglioside antibodies and also to the sensitivity of the individual.

Adult↗
PubMed2001

[Pathogenetic mechanisms of autoimmune neuropathies caused by antiglycolipid antibodies].

Antiglycolipid antibody titers are frequently elevated in the serum of patients with autoimmune neuropathies. Some antibodies may be involved in the pathogenesis because glycolipids are surface antigens in the nervous system. Sensory ataxic neuropathy was induced in rabbits sensitized with GD1b ganglioside, which is localized in the rabbit primary sensory neurons of the larger cytoplasms. Systemic infusion of high-titer anti-GD1b antiserum to rabbits pre-inoculated with adjuvant caused vacuolar degeneration with macrophage infiltration in a few axons in the dorsal column of the spinal cord. Anti-GD1b antibody therefore may cause degeneration in rabbit sensory neurons with central axons extending to the dorsal column. Investigations on the clinical features of GBS patients with monospecific anti-GD1b IgG antibodies showed that the antibodies are associated with sensory disturbance, especially disturbance in the deep sensation, and with primary demyelinating form. GD1b is localized in primary sensory neurons and paranodal myelin in the human peripheral nervous system. Monospecific anti-GD1b IgG antibodies may bind to those regions and be involved in the pathogenesis of sensory disturbance and demyelination. Thus, some antiglycolipid antibodies may determine the clinical features of GBS by binding to the regions where the antigens are localized.

Animals↗
PubMed2000

Chronic motor axonal neuropathy associated with antibodies monospecific for N-acetylgalactosaminyl GD1a.

We report on three patients with chronic motor neuropathy who had elevated titers of immunoglobulin (Ig)G antibodies against N-acetylgalactosaminyl GD1a (GalNAc-GD1a) and normal titers of antibodies against other gangliosides. Presenting with progressive muscular atrophy, fasciculations, and no sensory deficits, the patients had been diagnosed to have motor neuron disease. Electrodiagnostic features were predominantly axonal. Two patients clinically improved after intravenous Ig infusion and cyclophosphamide therapy. Increased titers of IgM antibodies to GalNAc-GD1a were also found in two of 15 patients with multifocal motor neuropathy with conduction block but were associated with concomitant rise of anti-GM1 antibodies. These three cases represent a chronic motor axonal neuropathy in which antibody testing for a minor ganglioside was helpful for instituting therapy.

Action Potentials↗
PubMed2000

Expression of major bone extracellular matrix proteins during embryonic osteogenesis in rat mandibles.

It is not known how bone proteins appear in the matrix before and after calcification during embryonic osteogenesis. The present study was designed to investigate expressions of the five major bone extracellular matrix proteins--i.e. type I collagen, osteonectin, osteopontin, bone sialoprotein and osteocalcin--during osteogenesis in rat embryonic mandibles immunohistochemically, and their involvement in calcification demonstrated by von Kossa staining. Wistar rat embryos 14 to 18 days post coitum were used. Osteogenesis was not seen in 14-day rat embryonic mandibles. Type I collagen was localized in the uncalcifed bone matrix in 15-day mandibles, where no other bone proteins showed immunoreactivity. Osteonectin, osteopontin, bone sialoprotein and osteocalcin appeared almost simultaneously in the calcified bone matrix of 16-day mandibles and accumulated continuously in 18-day mandibles. The present study suggested that type I collagen constitutes the basic framework of the bone matrix upon which the noncollagenous proteins are oriented to lead to calcification, whereas the noncollagenous proteins are deposited simultaneously by osteoblasts and are involved in calcification cooperatively.

Animals↗
PubMed2000

Ataxic form of chronic inflammatory demyelinating polyradiculoneuropathy (CIDP).

We reported a 64-year-old male with an eight-month history of gait disturbance and sensory impairment. The patient initially noticed unsteadiness of gait and numbness in his feet, and these symptoms progressed until he was unable to walk without assistance five months later. Vibratory sensation and position sense were markedly diminished, and deep tendon reflexes were absent in all extremities. Motor conduction velocities were slow with prolonged distal latencies, and sensory nerve action potentials (SNAP) were not elicited. Sural nerve biopsy revealed a mild loss of myelinated fibres and segmental demyelination. Cerebrospinal fluid showed normal cell count with protein 526 mg/dL. Anti-GM1, anti-GM2 and anti-GA1 antibodies in serum were positive. We diagnosed chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) presenting ataxia. Steroid therapy provided immediate improvement of symptoms and signs. This case suggests that CIDP should be considered as one of the potential causes of ataxic neuropathy.

Ataxia↗
PubMed2000

Guillain-Barré syndrome with antibody to a ganglioside, N-acetylgalactosaminyl GD1a.

A retrospective case study of 33 Guillain-Barré syndrome (GBS) patients with the antibody to the ganglioside N-acetylgalactosaminyl GD1a (GalNAc-GD1a) was made to investigate the clinical features of GBS with this antibody. Patients were classified into three groups: (i) 25 with IgG antibody (group G, titre >/= 1 : 40); (ii) 16 with high-titre IgG antibody (group G-high, titre >/=1:320; selected from group G patients), and (iii) eight with IgM antibody but without elevation of IgG (group M, normal range <1:40 for both IgM and IgG). The control group consisted of 72 GBS patients without anti-GalNAc-GD1a antibody. Compared with the control group, the G-high and G group patients were characterized as having had antecedent gastrointestinal infection (87% and 72% versus 31%, both P < 0.001), uncommon cranial nerve involvement (19% and 36% versus 54%, P = 0.02 and 0.2, respectively), distal-dominant weakness (94% and 68% versus 36%, P < 0.001 and P = 0.01, respectively) and no sensory signs (81% and 60% versus 25%, P < 0.001 and P = 0.003, respectively). Electrophysiological findings indicative of axonal dysfunction were significantly more common in the G-high and G group patients (63% and 52% versus 14%, both P < 0.001). The pure motor variant that showed neither sensory signs nor abnormalities in sensory conduction studies was also more frequent in these groups (44% and 32% versus 9%, both P < 0.001). IgG anti-GalNAc-GD1a antibody may be a marker of the pure motor and the axonal variants of GBS, and therefore it, as well as anti-GM1 antibody, must be investigated in these forms in order to diagnose and understand the variants. By contrast, mild weakness, frequent facial palsy (75%) and a high incidence of IgM anti-GM2 antibody reactivity (88%) were characteristic of group M, indicating that the GBS in that group resulted from a different immune mechanism from that in the G group.

Adult↗
PubMed2000

[Pain management for patients with cancer--current problems in a pain clinic].

One hundred and twenty-three patients with early or advanced cancer who had been referred to our pain clinic were studied retrospectively to investigate current problems with pain management for cancer patients. Pain due to advanced cancer and prolonged post-thoracotomy pain were two major reasons for referral. It was found that 51.7% of the patients with advanced cancer had not been treated appropriately with the WHO protocol for cancer pain relief before referral; however, increased administration of morphine did not necessarily relieve cancer pain, and in fact decreased the QOL of some patients; and 47.7% of patients with cancer pain were effectively treated with nerve block therapy. The present investigation also indicates that many patients who had undergone thoracotomy suffered prolonged post thoracotomy pain. Although post-thoracotomy pain was refractory to NSAIDs, trigger point injections with or without intercostal nerve block were effective in 65.4% of such patients. We conclude that further propagation of the WHO protocol for cancer pain relief, appropriate use of nerve block and establishment of practical guidelines for multidisciplinary management of pain are mandatory for improving the QOL of patients with cancer.

Aged↗
PubMed2000

[Immunoadsorption therapy with TR-350 (tryptophan column) for Guillain-Barré syndrome: investigation including serum antiganglioside antibody assay].

Immunoadsorption therapy (IAT) using TR-350 was performed for 14 patients with Guillain-Barré syndrome (GBS). Presence of serum antiganglioside antibodies (AGA) was investigated in all the patients in the acute phase. In 14 patients studied, 6 men and 8 women, ages from 24 to 74 years(mean, 42.5 years), 7 patients had suffered from common cold and 3 from diarrhea before neurological onset. Ophthalmoplegia was seen in 6 patients, facial palsy in 6, bulbar palsy in 3 and cerebellar sign in 2. Functional grade scores (FGS) by Hughes et al. of the patients were from 5 to 1 (mean, 3.3). In 4 patients, whose FGS were 1 or 2, IAT were performed, because of worsting of bulbar palsy, bilateral facial palsy and limb weakness. Relapse occurred in one patient. IAT was started from 2 to 18 days (mean, 8.4) after neurological onset and performed 3 to 14 times (mean, 7.5) for each patient. Mean FGS improved from 3.3 to 2.1 after IAT. The mean time to improve 1 grade was 10.3 days and mean time to improve 2 grades was 39.0 days. The mean FGS after 1 month was 1.4 and that after 3 months was 0.4. Some of 14 patients had elevated titers of AGA in sera in the acute phase. Four patients had anti-GQ1b IgG antibody and showed external ophthalmoplegia. One patient with anti-GD1b IgG antibody had cerebellar signs as well as peripheral neuropathy. Those AGAs decreased after IAT in parallel with improvement. IAT is an effective treatment in acute phase of GBS.

Acute-Phase Reaction↗
PubMed1999

Serum antibody against a peripheral nerve myelin ganglioside, LM1, in Guillain-Barré syndrome.

Serum IgG antibody against LM1, the predominant ganglioside in the human peripheral nerve myelin, was found in 7 out of 140 patients with Guillain-Barré syndrome (GBS) in the acute phase, 1 out of 33 patients with chronic inflammatory demyelinating polyneuropathy (CIDP), and 2 out of 47 patients with Miller Fisher syndrome (MFS). Anti-LM1 IgM antibody was detected only in 2 patients, each with GBS and MFS. The clinical and electrophysiological features of the seven GBS patients with anti-LM1 IgG antibody in the serum were investigated. Six patients recovered to grade 1 within one month of the onset of neuropathy. Electrophysiological studies revealed demyelination in five patients, of which one had axonal damage in addition, whereas sufficient evidence of demyelination or axonal degeneration was not observed in the remaining two. Five had a respiratory tract infection before the onset of neuropathy, and also had serum anti-GQ1b IgG antibody. IgG antibody against LM1 might be involved in the pathogenetic mechanisms of GBS, as a possible demyelinating factor. Presence of both anti-GQ1b and anti-LM1 antibodies may be associated with some infectious agent(s) affecting the respiratory tract.

Antibodies, Bacterial↗
PubMed1999

Degeneration of rabbit sensory neurons induced by passive transfer of anti-GD1b antiserum.

Systemic infusion of high-titer anti-GD1b antiserum to two rabbits pre-inoculated with keyhole limpet hemocyanin and Freund's complete adjuvant was performed. The two rabbits had low-titer anti-GD1b antibody in sera. Although no apparent clinical signs were observed, pathological examinations showed vacuolar degeneration with macrophage infiltration in a few axons in the dorsal columns of the spinal cords from the two rabbits. No such pathological changes were observed in the other two pre-inoculated rabbits infused with normal rabbit sera. Anti-GD1b antibody therefore may cause degeneration in rabbit sensory neurons with central axons extending to the dorsal column.

Animals↗
PubMed1999

Rabbit experimental sensory ataxic neuropathy: anti-GD1b antibody-mediated trkC downregulation of dorsal root ganglia neurons.

We previously reported experimental sensory neuropathy in rabbit induced by the immunization of ganglioside GD1b. The major pathological change in diseased rabbits was degeneration of primary sensory neurons with central axons extending to the dorsal column of the spinal cord. The loss of primary sensory neurons that mediate proprioceptive sensation prompted us to investigate the expression of trkC in dorsal root ganglia (DRG) because this type of neuron is thought depend mainly on neurotrophin-3-mediated trkC signaling. Northern blotting analysis revealed markedly reduced expression of trkC in DRG of diseased rabbits in acute phase. This result together with the absence of lymphocytic infiltration in DRG of diseased rabbits at any stage suggests the anti-GD1b antibody-mediated downregulation of trkC expression could be one of the pathogenesis of this experimental sensory ataxic neuropathy.

Animals↗
PubMed1999

Dorsal root ganglia neuron-specific promoter activity of the rabbit beta-galactoside alpha1,2-fucosyltransferase gene.

The rabbit H-blood type alpha1,2-fucosyltransferase (RFT-I), gene and its biosynthetic products, H antigens (Fucalpha1,2Galbeta), are abundantly expressed in a subset of dorsal root ganglia (DRG) neurons. To investigate the regulatory mechanisms for the RFT-I gene expression, we determined the genomic structure and promoter activity of this gene. PCR amplification of the 5' cDNA end analysis revealed two transcriptional start sites, 498 and 82 nucleotides upstream of the translational initiation codon, the latter site yielding a major 3.1-kb transcript specifically expressed in DRG, as revealed by Northern blotting. Promoter analysis of the 5'-flanking region of the RFT-I gene using a luciferase gene reporter system demonstrated strong promoter activity in PC12 cells, which express the rat H-type alpha1,2-fucosyltransferase gene, and Neuro2a mouse neuroblastoma cells. Deletion analysis revealed the 704-base pair minimal promoter region flanking the translational initiation codon, for which two distinct promoter activities were detected and differentially used in PC12 and Neuro2a cells. The minimal promoter region contained a GC-rich domain (GC content 80%), in which a Sp1 binding sequence and a GSG-like nerve growth factor-responsive element were found, but lacked TATA- and CAAT-boxes. Promoter analysis with a primary culture of DRG neurons demonstrated that the minimal promoter region of the RFT-I gene was sufficient for the expression of a reporter gene in DRG neurons. We conclude that the TATA-less GC-rich minimal promoter region of the RFT-I gene controls DRG small neuron-specific expression of the RFT-I gene.

Animals↗