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Biomedical subjects

T Ohira

Publications and source records attributed to T Ohira.

At least 73 records · Page 4Linked to original sources

Computed tomographic analysis of hemifacial spasm: narrowing of the posterior fossa as a possible facilitating factor for neurovascular compression.

Hemifacial spasm can be caused by vascular compression of the facial nerve at the root exit zone from the brainstem. Several case reports suggest that narrowing of the cerebellopontine angle cistern caused by Paget's disease, abnormal elevation of the petrous bone caused by hyperplasia, or contralateral acoustic neurinoma may increase the chance of vascular compression of the facial nerve. Therefore, posterior fossa narrowness has been evaluated in 34 patients with hemifacial spasm by measuring the petrous angle and pons diameter index to elucidate whether narrowing of the posterior fossa can act as a facilitating factor for neurovascular compression. The petrous angle in the hemifacial spasm group was significantly smaller than that in the control group, which consisted of 33 patients with an unruptured supratentorial aneurysm, and the pons diameter index in the hemifacial spasm group was significantly greater than that in the control group. These results indicate that the cerebellopontine angle cistern of patients with hemifacial spasm is narrower resulting in more crowded cranial nerves and vascular structures compared with patients without hemifacial spasm. The narrowness of the cerebellopontine angle cistern may be a possible factor in facilitating neurovascular compression in hemifacial spasm.

Adult↗

Molecular cloning of a molt-inhibiting hormone cDNA from the kuruma prawn Penaeus japonicus.

The crustacean molt-inhibiting hormone (MIH) is released from the X-organ sinus gland complex and suppresses ecdysteroid synthesis by the Y-organ. In the present study, we have isolated a cDNA which encodes a MIH (Pej-SGP-IV) of the kuruma prawn Penaeus japonicus in order to study its expression and characterize the structure of its precursor. A cDNA fragment was isolated using RT-PCR with two degenerate oligonucleotide primers that were designed based on the peptide sequence of Pej-SGP-IV, and this fragment was used as a probe to screen an eyestalk cDNA library. In a positive cDNA clone (814 base pairs (bp)), an open reading frame of 315 bp was found; the conceptually translated protein consists of a putative signal peptide (28 residues) and Pej-SGP-IV (77 residues). In Northern blot analysis using a cDNA probe, specific hybridization to a transcript of 0.95 kb was seen in RNA extracted from the eyestalk but not from hepatopancreas, abdominal muscle, brain, thoracic ganglia or abdominal ganglia. The level of the Pej-SGP-IV mRNA in the eyestalk did not change significantly during the molt cycle.

Animals↗

Electrophysiological investigation of hemifacial spasm after microvascular decompression: F waves of the facial muscles, blink reflexes, and abnormal muscle responses.

In patients with hemifacial spasm, it has been said that the spasm is due to cross compression of the facial nerve by a blood vessel and that microvascular decompression (MVD) of the facial nerve is an effective treatment. The F waves, which result from backfiring of antidromically activated motor neurons of the facial motor nucleus, are indices of the excitability of the facial motor nucleus and are enhanced in patients with hemifacial spasm. Measuring blink reflexes and abnormal muscle responses (lateral spread), a characteristic sign of hemifacial spasm, has been used to investigate the mechanism of hemifacial spasm pathophysiologically. Thus the authors measured F waves of the facial muscle, blink reflexes, and abnormal muscle responses before and after MVD in patients suffering from hemifacial spasm to investigate the excitability of the facial motor nucleus and the course of the cure of hemifacial spasm after MVD. The authors obtained facial nerve-evoked electromyograms in 20 patients with hemifacial spasm before and after the MVD procedure. On the spasm side, the F waves and blink reflexes were enhanced preoperatively compared to those on the normal side and abnormal muscle responses were recorded in all patients. In 12 patients whose hemifacial spasm had not disappeared completely for 5.1 +/- 1.7 (mean +/- standard error) months following the MVD procedure, F waves were still enhanced significantly and abnormal muscle responses were still recordable, albeit at lower amplitude. Within 1 month after the hemifacial spasm had disappeared completely. F waves were still significantly enhanced in 17 patients and abnormal muscle responses were recorded in seven of 15 patients. Subsequently, the enhanced F waves and abnormal muscle responses disappeared completely. The authors' study supports the hypothesis that the cause of hemifacial spasm is hyperexcitability of the facial motor nucleus and suggests that additional surgery should not be performed for at least 2 years after MVD, because that period is necessary for the disappearance of the hyperexcitability of the facial motor nucleus.

Adult↗

[Practical localization of the central sulcus using a video display during surgery by cortical somatosensory evoked potentials and how to discern precentral P20 and central P25].

In patients with lesions around the central sulcus, cortical surface somatosensory evoked potentials (SEPs) have been applied for the purpose of localization of the central sulcus based on the polarity inversion of postcentral N20 to precentral P20 across the central sulcus. We have intraoperatively monitored SEPs to infer the location of the central sulcus in 16 cases since December 1988. Intraoperative localization of the central sulcus has been most useful in patients with frontal lobe gliomas in which the localization of the central sulcus enables the surgeon to extensively resect tumor without postoperative motor weakness. The localization of the central sulcus, however, might be misjudged by using the polarity inversion criterion alone, because central P25 following N20 and P20 complicates SEP waveforms. It is significant that P25, which is recorded also posterior to the central sulcus, is discerned from the precentral P20. In order to solve this matter, we regarded only the positivity in SEP waveforms having the identical peak latency to that of N20 as the precentral P20. Positive potentials having a later peak latency than that of N20 are the superposition of P20 and P25, and might also be recorded posterior to the central sulcus. For the observation of the polarity inversion of N20 to P20 across the central sulcus, a multi-channel SEP should be recorded using a sheet of silicone rubber embedded in a 16-electrode array consisting of a 4 by 4 grid. We projected the exposed cortical surface on the video display through the microscope apparatus and marked the locations of the recording electrodes on the video display. This enabled the location of the recording electrodes to correspond easily and precisely to the cortical surface. Our reliable and simple method of intraoperative localization of the central sulcus by cortical SEPs monitoring is presented in a practical case.

Adolescent↗

[Gene diagnosis with an affinity sensor, BIACORE--principle and applications].

We are developing new techniques for detecting point mutations by DNA-DNA hybridization and DNA-protein interaction analysis with an affinity sensor, BIACORE. To detect point mutations by the hybridization method using synthetic oligonucleotides, we already found that the length of the probe and the location of mismatches were important. The PCR products of the N-ras gene derived from Hep G2 cells, which have heterozygous point mutations at codon 61 in the gene, were analyzed and the point mutations were detected with 13-mer probes. We suggest that the detection method using DNA-DNA hybridization is useful for detecting known point mutations. However, detect unknown mutations, E. coli mismatch recognition protein, MutS, was employed. All mismatches in immobilized 20 base pairs of double-strand DNA could be detected by MutS binding. We have started to apply of the MutS to the detection of point mutations in PCR products.

Bacterial Proteins↗

Cloning and sequence analysis of a cDNA encoding a crustacean hyperglycemic hormone from the Kuruma prawn Penaeus japonicus.

The crustacean hyperglycemic hormones (CHHs) are released from the X-organ sinus gland complex and regulate the glucose level in the hemolymph. In the present study, we have isolated a complementary DNA that encodes a CHH (Pej-SGP-III) of the Kuruma prawn Penaeus japonicus to study its expression and the structure of its precursor. In a cDNA clone of 774 base pairs (bp), an open reading frame of 345 bp was found. The conceptually translated protein consists of a signal peptide (24 residues), a CHH-precursor-related peptide (CPRP, 17 residues), and Pej-SGP-III (72 residues). This CPRP in P.japonicus was homologous to, but significantly shorter than, those in other crustacean species. In a Northern blot analysis, the cDNA specifically hybridized to a seemingly single mRNA species (approximately 0.8 kb) in the eyestalk. This mRNA was not detected in the hepatopancreas or abdominal muscle.

Amino Acid Sequence↗

[Cooperative multicentre study on posttraumatic epilepsy].

A multicentre cooperative prospective study have been conducted to investigate the factors influencing posttraumatic epilepsy (PTE) and to evaluate the prophylactic effect of anticonvulsants. Since April 1994, patients with head injury have been observed following our protocol as follows; anticonvulsants are administered only to the patients with brain parenchymal injury for one month just after head trauma and no anticonvulsants are administered after one month after trauma to any patients except those with posttraumatic epilepsy (PTE). Brain parenchymal injury included traumatic subarachnoid hemorrhage, acute subdural hematoma, contusion, intracerebral hematoma, and diffuse axonal injury. To April 1996, 635 patients with head injury have been registered and analyzed. During the follow-up period, 14 patients (2.2%) developed PTEs, which had only been observed in patients with brain parenchymal injury. Multiple regression analysis revealed that two factors, early epilepsy and brain parenchymal injury, could contribute to the prediction of PTE. The frequency of PTE in this study was compared with that in our previous retrospective study (Nakamura, 1995), in which anticonvulsants were administered to the patients with head injury. There was no significant difference in the percentage of patients having PTE between the group treated without anticonvulsants in this study and the untreated group in previous retrospective study. Anticonvulsants treatment after head injury was not likely to have a prophylactic effect against the development of PTE.

Adolescent↗

Hypersensitivity of NIH3T3 cells transformed by H-ras gene to DNA-topoisomerase-I inhibitors.

We examined the effects of the introduction of H-ras oncogene into murine cell line NIH3T3 on growth inhibition by topoisomerase-I (topo-I) inhibitors. The H-ras-transformed cells (pT22-3) showed approximately 12-fold increased sensitivity to a novel topo-I inhibitor, NB-506 [6-N-formylamino-12,13-dihydro-1,11-dihydroxy-13-(beta-D-glucopyranosyl) -5H-indolo(2,3-a)pyrrolo(3,4-c) carbazole-5,7(6H)-dione], compared with the parental NIH3T3 cells. pT22-3 also showed increased sensitivity to other topo-I inhibitors such as camptothecin (approx. 3.0-fold) and CPT-11 (irinotecan, approx. 3.0-fold). Transformation of NIH3T3 by another oncogene (erbB2) did not affect their sensitivity to these topo-I inhibitors. pT22-3 had approximately 32-fold higher topo-I activity than NIH3T3, but the same topo-I content. In a cell-free system, topo-I activity was increased 2-fold by addition of the H-ras protein precipitated from pT22-3 cells. Topo I in the nuclear extract of pT22-3 was eluted easily by low concentrations of NaCl compared with that of NIH3T3, suggesting a qualitative change in pT22-3 topo 1. Increased phosphorylation of topo I was observed in pT22-3. Furthermore, NB-506 decreased the amount of the GTP-bound form of the H-ras product in pT22-3 cells. These results suggest that the high growth-inhibitory effect of a topo-I inhibitor, NB-506, on H-ras-transformed NIH3T3 cells is due to the H-ras-mediated signal-transduction pathway.

3T3 Cells↗

Effects of beta- and gamma-carboline derivatives of DNA topoisomerase activities.

beta-Carbolines, harman (1-methyl-9H-pyrido[3,4-b]indole) and norharman (9H-pyrido[3,4-b]indole) and gamma-carbolines, 3-amino-1,4-dimethyl-5H-pyrido[4,3-b]indole (Trp-P-1) and 3-amino-4-methyl-5H-pyrido[4,3-b]indole (Trp-P-2), are present in cooked foods and cigarette smoke. We studied the effects of these heterocyclic amines on the activity of DNA topoisomerases. Trp-P-1 and Trp-P-2 inhibited topoisomerase I (topo I) activity with ED50 values of 1.48 and 1.55 micrograms/ml, respectively, in a relaxation assay. Harman and norharman inhibited topo I activity but with much higher ED50 values, 23.8 and 34.4 micrograms/ml, respectively. Trp-P-1 and Trp-P-2 also inhibited topoisomerase II (topo II) activity at about 50 micrograms/ml, in a decatenation assay. Harman and norharman showed a much lower inhibitory effect on topo II activity. None of these compounds stabilized the cleavable complex mediated by topo II. Trp-P-1 and Trp-P-2 intercalated into DNA at concentrations inhibitory to topoisomerases. We considered that the intercalation with DNA and the inhibition of DNA topoisomerases by heterocyclic amines might be partly related to their inhibition of DNA excision repair and their enhancing effect on UV- or chemically induced mutagenic activity.

Breast Neoplasms↗

The neural origin generating early cortical components of SEP: topographical analysis using temporal-second-order-differentiation of cortical SEPs.

In order to identify dipole generators of the N20/P20 and P25, we employed second-order-differentiation in the temporal dimension (temporal-second-order-differentiation; TSOD) with delta t = 2 msec. The rate of variation in the voltage of cortical SEPs calculated by TSOD identified responses of each dipole, reflecting the density of neuronal firing. On topographic analysis, the distributions of N20/P20 and P25 conformed to the shape of gyrus better in the TSOD maps than in the isovoltage maps. The TSOD maps indicated that N20 and P25 were post-central components and that P20 was a pre-central one. Therefore, we concluded that the two dipoles generating N20/P20 and P25 were located in the posterior wall of the central sulcus (area 3b) and the crown (areas 1 and 2) of the post-central gyrus, respectively.

Brain Mapping↗

Improvement by eicosanoids in cancer cachexia induced by LLC-IL6 transplantation.

Cachexia frequently occurs in the late stages of cancer, and is difficult to manage. We previously reported that interleukin-6 (IL-6) cDNA transfection into Lewis lung carcinoma (LLC-IL6) induced cachexia-like symptoms in C57BL/6 mice. This was thought to be a useful experimental model of cancer cachexia. We have examined the effects of two eicosanoids, docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA), in order to evaluate whether they could relieve cachexia. LLC-IL6-bearing animals were divided into three treatment groups receiving DHA, EPA or water as the control; 80-microliter samples of these compounds (purity > 95%) were administered orally by catheter daily starting 7 days after tumor transplantation. Tumor growth curves were similar in the three groups. There were no differences in water or food intake in the three groups. However, body weight, a marker of cachexia, was significantly higher in treated mice than in the control group. Sixteen days after tumor transplantation, the mean body weight was 17.45 g (P < 0.05), 17.2 g and 16.41 g in the groups receiving DHA, EPA and water respectively. The eicosanoids did not affect serum levels of IL-6. Ubiquitination of muscle protein, a marker of proteolysis coupled to cachexia, was compared in LLC-IL6- and LLC-transplanted mice. The eicosanoids prevented the ubiquitination of approximately 180 kDa protein. These results suggest that eicosanoids may prevent the cachexia mediated by IL-6.

Animals↗

Electrophysiological investigation of hemifacial spasm: F-waves of the facial muscles.

In patients with hemifacial spasm (HFS), the spasm is due to cross-compression of the facial nerve by a blood vessel. There are currently two hypotheses for the mechanism of HFS: 1) the spasm is caused by ephaptic transmission and an increase in excitability at the site of compression; and 2) the spasm is caused by hyperexcitability in the facial nerve nucleus. In peripheral nerves, F-waves, which result from the backfiring of antidromically activated anterior horn cells, have been proposed as indices of proximal motoneuron conduction and anterior horn cell excitability. Enhancement of the F-waves indicates increased anterior horn cell excitability. We have therefore measured F-waves in the facial muscle of HFS patients in order to investigate the excitability of the facial nerve nucleus. The authors obtained facial nerve evoked responses from 20 HFS patients before microvascular decompression (MVD), 10 HFS patients after MVD and 10 healthy controls. The F-waves, obtained with surface electrodes from the mentalis muscle, were the second response after the M-wave. On the patient's spasm side, the F-wave duration, F/M amplitude ratio and frequency of F-wave appearance significantly increased compared with those of the normal side or healthy controls; minimum latency and chronodispersion did not significantly differ between these groups. In patients whose spasm disappeared completely following MVD, the abnormal muscle response (lateral spread), which is a characteristic sign of HFS, and the enhancement of the F-wave eventually also disappeared. Because of the correlation between HFS and F-waves, the authors' study supports the hypothesis that the cause of HFS is hyperexcitability of the facial motonucleus.

Adult↗

Abnormal muscle response (lateral spread) and F-wave in patients with hemifacial spasm.

In patients with hemifacial spasm (HFS) the spasm is due to cross compression of the facial nerve by a blood vessel and microvascular decompression (MVD) has proved to be a successful treatment. Abnormal muscle response (AMR), which can be elicited by one facial nerve branch stimulation in muscles innervated by other branches of the facial nerve, is specific for patients with HFS, and the AMR consists of a constant response occurring about 10 ms after stimulus and an afterdischarge with long duration (variable response, autoexcitation). The F-wave in facial muscles is a small recurrent discharge that antidromically propagates to the facial motonucleus and returns orthodromically down the same axon. We measured the AMRs and F-waves of facial muscles in HFS patients in order to investigate the relationship of both potentials and the origin of the AMRs. We obtained facial nerve evoked electromyograms from 10 HFS patients. The afterdischarges of the AMRs and the enhanced F-waves were always elicited at the same time by marginal mandibular branch stimulation of the facial nerve. There was a linear correlation between the duration of these two potentials in each case. Between the duration of the afterdischarge of the AMRs elicited in the mentalis muscles by the zygomatic branch stimulation of the facial nerve and that of the F-waves in the mentalis muscles, there was also a linear correlation in 10 cases. These results suggest that the F-wave and the afterdischarge have the same origin and that the AMR is an exaggerated F-wave.

Adult↗

Effect of repetitive stimulation on lateral spreads and F-waves in hemifacial spasm.

The lateral spread (LS) response, which can be elicited in muscles innervated by other branches of the facial nerve, is electromyographycally specific for patients with hemifacial spasm (HFS), occurring about 10 ms after stimulus. The F-wave in facial muscles, which is a late response that antidromicaly propagates to the facial motonucleus and returns orthodromicaly down the same axon, revealed a trend toward enhancement in patients with HFS. The LSs were facilitated by repetitive stimulation during the microvascular decompression (MVD) operation, which has proved to be a successful treatment, and the F-waves were also facilitated by repetitive stimulation on the spasm side more than on the normal side. Greater facilitation of these responses was in direct proportion to higher stimulation rates and greater numbers of stimulations. The repetitive stimulation of the facial nerve may result in activation of the motoneuron pool and in the lowering of the threshold of somatic membranes. These results support the hypothesis that hemifacial spasm is caused by hyperexcitability of the facial motonucleus, which is increased by antidromic repetitive stimulation.

Electric Stimulation↗

Strength-duration curve of conductive spinal cord evoked potentials in cats.

Strength-duration curves of the ascending and descending conductive spinal cord potentials (SCEPs) in cats were obtained using constant current stimuli. For the formulation of numeric indices of excitability, the rheobase is defined as the minimal current strength below which response cannot occur even if the current continues, and the chronaxie is defined as the minimal duration of a current required to evoke the potential at twice the rheobase strength. The chronaxies and rheobases were calculated from the constructed strength-duration curves. The purpose of this study is to produce strength-duration curves and to evaluate the utility of chronaxies and rheobases for SCEPs. This study showed the following results: (1) there was a hyperbolic relationship between stimulus strength and stimulus duration at threshold values, similar to that seen in peripheral nerves; (2) the ascending and descending tracts of SCEP were mediated through the same pathway (based on the similar chronaxies and rheobases); (3) following spinal cord compression the chronaxie and rheobase increased significantly (P < 0.05), which is similar to peripheral nerve disturbance. However, the rheobase decreased significantly following slight spinal cord compression (P < 0.05) and systemic cooling (P < 0.01), and the strength-duration curve shifted showing a tendency towards decrease of the galvanic threshold, therefore, amplitude augmentation with slight compression and with decrease in temperature seems to contribute to the reduction of the threshold. The strength-duration curve, the chronaxie and the rheobase may be useful in assessing spinal cord function.

Animals↗

F-wave in patients with hemifacial spasm: observations during microvascular decompression operations.

In patients with hemifacial spasm (HFS), the spasm is due to cross compression of the facial nerve by a blood vessel. There are currently two hypotheses how the cross compression can cause HFS: 1. the spasm is caused by ephaptic transmission and hyperexcitability at the site of compression; and 2. the spasm is caused by hyperexcitability in the facial motonucleus. In peripheral nerves, F-waves, which result from the backfiring of antidromically activated anterior horn cells, have been proposed as indices of anterior horn cell excitability. Enhancement of the F-waves in facial muscles also indicates increased excitability of the facial motonucleus. On the other hand, abnormal muscle response (AMR), which can be elicited by stimulating one branch of the facial nerve and recording electromyographically from muscles innervated by other branches of the facial nerve, is specific for patients with HFS. We have therefore measured the AMRs and the F-waves in the facial muscle of HFS patients under anesthesia in order to investigate the excitability of the facial motonucleus. We obtained facial nerve evoked electromyograms from 14 HFS patients during microvascular decompression (MVD) operation. The F-waves, obtained with surface electrodes from the mentalis muscle, were defined as the second response after the M-wave. The F-waves in facial muscles cannot usually be elicited during surgical anesthesia using inhalation anesthetics. However, the F-waves were elicited on the spasm side in 10 out of 14 patients with HFS and the F-waves disappeared after MVD under anesthesia, as the early responses (R1) of the blink reflex were elicited on the spasm side before MVD under anesthesia. The F-waves elicited during anesthesia were suppressed significantly, compared with those before MVD. These results suggest that excitability in facial motonucleus increased on the spasm side.

Electric Stimulation↗

Developmental patterns and characteristic symptoms of petroclival meningiomas.

Thirty-six cases of petroclival meningiomas with clearly defined anatomical features were selected to analyze the site of tumor attachment and the displacement of the trigeminal nerve. The tumors were classified into four categories according to the origin and extension of the tumor: clival origin medial to the trigeminal nerve (upper clivus type), clival origin with dumbbell extension to the cavernous sinus (cavernous sinus type), tentorial origin over the trigeminal nerve (tentorium type), and petrous apex origin lateral to the trigeminal nerve (petrous apex type). Patients with tumors in each category had characteristic neurological symptoms. Patients with the upper clivus type had oculomotor nerve paresis as a single symptom, if suprasellar tumor extension was present. Patients with the cavernous sinus type commonly presented with abducens nerve paresis caused by epidural tumor invasion around Dorello's canal. Dumbbell tumor extension along the venous drainage of the cavernous sinus was a significant problem for surgical removal in this type. Half of the patients with the tentorium type had a characteristic symptom of trigeminal neuralgia caused by retrograde tumor invasion into Meckel's cave from its orifice, but the cavernous sinus was not involved. The main complaint of patients with the petrous apex type was hearing disturbance, but no epidural or parasellar extension was present. Clinical symptoms and magnetic resonance imaging provide important information about the origin and extension patterns of these tumors, especially the presence or absence of tumor extension into the cavernous sinus. Abducens nerve paresis or trigeminal neuralgia suggests tumor invasion into the cavernous sinus or Meckel's cave, respectively.

Adult↗

[A case of renal transplantation from an ABO-incompatible donor successfully pretreated with double filtration plasmapheresis].

A 40-year-old female, whose blood type was A, Rh+, was admitted to our hospital for kidney transplantation from her younger brother whose blood type was B, Rh+. Before the transplantation, we performed 4 sessions of double filtration plasmapheresis (DFPP) to remove the anti-B antibodies. The serum anti-B antibody titer lowered from X32 to X4. The kidney transplantation was carried out following the splenectomy. The warm ischemic time was 8 minutes and the cold ischemic time was 47 minutes. Five immuno-suppressive agents including cyclospolin, azathioprine, prednisolone, anti-lymphocyte globulin (ALG), and deoxyspergualin were administered in the initial period. Nine days after the transplantation, an acute rejection occurred, and 15 sessions of hemodialysis were needed. However, Methylprednisolone and OKT3 treatment resulted in recovery of the graft function. Seventy-four days after the transplantation, she was discharged with the serum creatinine concentration of 1.3 mg/dl. The DFPP before transplantation was useful to remove the anti-RBC antibody from the patient receiving an ABO incompatible kidney allograft.

ABO Blood-Group System↗