Intractable hiccup and nausea in neuromyelitis optica with anti-aquaporin-4 antibody: a herald of acute exacerbations.

BACKGROUND: Intractable hiccup and nausea (IHN) are unique symptoms in neuromyelitis optica (NMO). Recent studies have strongly suggested that the pathogenesis of NMO is closely associated with anti-aquaporin-4 (AQP4) antibody. However, clinical implications of IHN and the relationship with anti-AQP4 antibody remain unknown. METHODS: The past medical records of 35 patients with seropositivity for anti-AQP4 antibody were reviewed. We also followed the titres of anti-AQP4 antibody in a patient with NMO, who had newly developed IHN. RESULTS: Of the 35 patients, 15 patients (43%) had episodes of IHN. There was a total of 35 episodes of IHN in these 15 patients and, of the 35 episodes, hiccup was seen in 23 episodes (66%) and nausea was seen in 28 episodes (80%). The IHN frequently preceded (54%) or accompanied (29%) myelitis or optic neuritis. The IHN was often preceded by an episode of viral infection. The titres of anti-AQP4 antibody were remarkably increased when the intractable hiccup appeared in a case. CONCLUSIONS: IHN could be a clinical marker for the early phase of an exacerbation. Careful observation may be needed when INH is seen in patients with NMO, and the early initiation of the treatment could prevent subsequent neurological damage.

Amino acid sequence of dimeric myoglobin from Cerithidea rhizophorarum.

The complete amino acid sequence of the dimeric myoglobin from Cerithidea rhizophorarum, a common gastropodic mollusc on the Japanese coast having an elongated many-whorled shell, has been determined. The monomer is composed of 151 amino acid residues, is acetylated at the amino terminus, and 75 residues out of 151 are homologous with the monomer of myoglobin from the whelk Busycon canaliculatum. Unlike Aplysia myoglobin, which lacks the distal histidine, Cerithidea myoglobin contains three histidines in its monomer, His-66 being assigned to the distal position, and in its oxymyoglobin form its stability properties show a very strong pH dependence.

Correlations between proton nuclear magnetic resonance imaging and retrospective histochemical images in experimental cerebral infarction.

Evaluation of ischemic brain injury in experimental cerebral infarction in gerbils and rats was performed by means of both proton nuclear magnetic resonance imaging ([1H]NMR-CT) and various histochemical analyses. In vivo nuclear magnetic resonance (NMR) imaging was carried out employing saturation recovery, inversion recovery, and spin echo pulse sequences. Spatial resolution of the images was excellent. The ischemic lesions were detected with a remarkable contrast in inversion recovery and spin echo images within a few hours after insult. Those changes in NMR images consistently corresponded with the various retrospective histochemical observations, especially with methods related to brain edema (K+ staining) rather than structural (enzymatic) studies. Calculated T1 and T2 relaxation times indicated the evolution of the edema state in the brain in situ. They correlated excellently with the retrospective water content measurement. As a result, detailed characterization of the edema state induced by cerebral ischemia was possible in vivo using [1H]NMR imaging.

Characterization of experimental ischemic brain edema utilizing proton nuclear magnetic resonance imaging.

Correlations between T1 and T2 relaxation times and water and electrolyte content in the normal and ischemic rat and gerbil brains were studied by means of both nuclear magnetic resonance (NMR) spectroscopic and imaging methods. In the spectroscopic experiment on excised rat brains, T1 was linearly dependent on tissue water content and T2 was prolonged in edematous tissue to a greater extent than expected by an increase in water content, showing that T2 possesses a greater sensitivity for edema identification and localization. Changes in Na+ and K+ content of the tissue mattered little in the prolongation of relaxation times. Serial NMR imaging of gerbil brains insulted with permanent hemispheric ischemia offered early lesion detection in T1- and especially T2-weighted images (detection as soon as 30 min after insult). The progressive nature of lesions was also imaged. Calculated T1 and T2 relaxation times in regions of interest correlated excellently with tissue water content (r = 0.892 and 0.744 for T1 and T2, respectively). As a result, detection of cerebral ischemia utilizing NMR imaging was strongly dependent on a change in tissue water content. The different nature of T1 and T2 relaxation times was also observed.

Gene structure of calcium-dependent protease retains the ancestral organization of the calcium-binding protein gene.

The gene structure of calcium-dependent protease (Ca2+-protease) was determined. It comprises at least 21 exons, and these were assigned to the 4 functional domains of the protease. The protease domain does not show clear correlation between exons and functional units, but the calmodulin-like calcium-binding domain shows strong correlation. Each of the 4 consecutive calcium-binding regions in the C-terminal part of Ca2+-protease is encoded by one exon. This gene structure supports the idea that the 4 calcium-binding regions of calcium-binding proteins such as calmodulin arose by 2 steps of gene duplication.

Analysis of spinocerebellar ataxia type 1 (SCA1)-related CAG trinucleotide expansion in Japan.

Spinocerebellar ataxia type 1 (SCA1) is a neurodegenerative disorder caused by expansion of a CAG trinucleotide repeat. We analyzed CAG repeat expansion in 25 families in the northeast of Japan with hereditary ataxia of Menzel type. Twenty of 38 patients in 12 families had expanded allele for SCA1. The number of CAG repeats correlated with the age at onset. Although the relationship between anticipation and the number of CAG repeats in successive generations was not ascertainable, there was a tendency to paternal bias for the accelerated age at onset. Study of the number of CAG repeats in various tissues showed no differences in the repeat length in lymphocytes, muscle, or brain; sperm, however, showed an obvious expansion. This may be a clue to a possible mechanism for the molecular basis of paternal anticipation of the disease. The SCA1 gene was transcribed from both wild and mutated alleles in muscles of affected individuals, but the repeat length was the same for both the muscle cDNA and the lymphocyte genomic DNA. These results suggest that, in the area of Japan where SCA1 is prevalent, 48% of families with spinocerebellar degeneration have SCA1 mutation.

Elemental diet modulates the growth of Clostridium difficile in the gut flora.

BACKGROUND AND AIMS: Tube feeding is regarded as a risk factor for Clostridium difficile-associated diarrhoea. Recently, we reported that C. difficile toxin was frequently found in patients receiving an elemental diet. The present study was conducted to clarify whether elemental diets are associated with the growth of C. difficile in the gut flora. METHODS: C. difficile was cultured for 72 h in various concentrations of elemental diet containing 3% thioglycollate, and the growth rate or activity of C. difficile was evaluated by Gram stain or by measuring optical density at 560 nm. Faecal samples from 10 healthy adults were cultured in elemental diet + 3% thioglycollate. RNA was extracted from faeces with glass powder, which can eliminate PCR inhibitors, and mRNA of C. difficile toxin B was measured by reverse transcription PCR. RESULTS: Maximum OD560 value during culture in thioglycollate-containing elemental diet was 2.4 times higher than that in thioglycollate alone (P = 0.0163). Viability of C. difficile was decreased in thioglycollate but not in thioglycollate-containing elemental diet. Toxin B mRNA was detected in five faecal samples (50%) before culture and in all samples after culture. CONCLUSIONS: Our results suggest that an elemental diet can modulate the growth of C. difficile in the gut flora.

The effect of transient ischemia on 2-[14C]deoxyglucose metabolism in the rat hippocampus pretreated with kainic acid.

CA1 pyramidal neurons are selectively vulnerable to ischemia. 2-[14C]Deoxyglucose (2-DG) autoradiography was employed to measure local glucose utilization in the rat hippocampus after transient ischemia, under the condition of unilateral prevention of ischemic CA1 pyramidal cell necrosis by unilateral lesioning of Schaffer collaterals (left side). Columnar 2-DG uptake patterns in the CA1 region with intact Schaffer collaterals (right side) was observed 19-22 h after recirculation, though no laterality was noted 3 and 8 h after recirculation. In the right subiculum, higher 2-DG uptake was observed 19-22 h after recirculation in 5 out of 8 animals. These results suggest that Schaffer collaterals play a role in modulating glucose metabolism in the CA1 and subiculum during recirculation.

DNA single-strand breaks in postischemic gerbil brain detected by in situ nick translation procedure.

Using an in situ nick translation procedure, DNA single-strand breaks (SSB) in postischemic gerbil hippocampus were investigated after 15-min forebrain ischemia followed by 0-4h of recirculation. In the control group, increased SSB were noticed in the ependymal cell layer and the dentate gyrus. After 15-min ischemia without recirculation, no remarkable changes in SSB were observed. However, after 1 h of recirculation, a marked increase in SSB was recognized throughout the hippocampus, especially in the cells in CA1 subfield and the dentate gyrus. After 4 h of recirculation, SSB decreased to a level near that of the control group. The results of the present study indicate that ischemic insults may injure intranuclear DNA during postischemic recirculation periods. Although many factors may be involved, activated endonuclease due to an intracellular Ca2+ rise, free radicals, and postischemic hyperthermia appear to be involved in this phenomenon.

A case of superficial peroneal nerve injury during ankle arthroscopy.

We report a case of superficial peroneal nerve (SPN) injury caused by ankle arthroscopy. A 20-year-old woman underwent arthroscopy on her right ankle because of chronic ankle pain after a sprain. After arthroscopy, the patient complained of pain on the dorsum of her right foot and felt a radiating pain from the anterolateral portal to the dorsomedial aspect of her foot. Eight months after arthroscopy, we found that a neuroma had developed on the intermediate dorsal cutaneous nerve, and performed neurolysis of the SPN. Her symptoms gradually decreased after surgery, and had disappeared by 45 months. To avoid such an injury of the SPN, the safest placement of the anterolateral portal is necessary and is, according to our previous anatomic study, 2 mm lateral to the peroneus tertius tendon.

Arthroscopic diagnosis of tibiofibular syndesmosis disruption.

PURPOSE: We have been able to diagnose tibiofibular syndesmosis injury by ankle arthroscopy, and in the present study we compare these results with the results from plain radiographs. TYPE OF STUDY: Case series. METHODS: Thirty-eight type-B (Weber system) distal fibular fractures in 38 patients were diagnosed to determine whether tibiofibular syndesmosis disruption was present. According to the Lauge-Hansen system, 16 patients had supination-external rotation fractures and 22 had pronation-abduction fractures. Standard non-weight-bearing anteroposterior radiographs and mortise radiographs were evaluated. Furthermore, ankle arthroscopy was performed on all patients. RESULTS: Tibiofibular syndesmosis disruptions were diagnosed in 16 of the 38 patients (42%) by anteroposterior radiography, 21 of 38 patients (55%) by mortise radiography, and 33 of 38 patients (87%) by ankle arthroscopy. All of the patients who were diagnosed with tibiofibular syndesmosis disruption by anteroposterior radiography and mortise radiography were also confirmed by ankle arthroscopy to have injured their tibiofibular syndesmosis. In 12 patients, ankle arthroscopy was the only method used to diagnose the tibiofibular syndesmosis disruption. CONCLUSIONS: Ankle arthroscopy excels in term of the diagnosis ratio for tibiofibular syndesmosis disruption compared with both anteroposterior and mortise radiography. Therefore, we conclude that ankle arthroscopy is necessary for the correct diagnosis of tibiofibular syndesmosis disruption.

MR imaging of multiple sclerosis simulating brain tumor.

Multiple sclerosis may sometimes present as a mass lesion that is indistinguishable from brain tumor both clinically and radiologically. We describe two cases of multiple sclerosis simulating brain tumor on computed tomography (CT) scans and magnetic resonance (MR) images, one of which was proved and another was suggestive to be demyelinating disease by biopsy. Steroid therapy produced regression of the lesions of MR images and CT scans. Our cases and others in the literature suggest strategies for detecting multiple sclerosis presenting as a mass lesion.

Bandage distraction technique for ankle arthroscopy.

In ankle arthroscopy, the joint space of the talocrural joint is often too narrow for insertion of the scope and instruments. Various distraction devices for this procedure have been used to widen the joint space. Bandage distraction is effective and noninvasive, but it is difficult to extend the posterior joint space sufficiently for insertion of the scope. Here we describe a new bandage distraction method that can extend the posterior joint space adequately. Using our method, the anterior and posterior joint spaces on direct lateral radiographs were measured after adding the distraction force in nine healthy volunteers (18 ankles; three men and 6 women). This was compared to a previously reported method. The posterior joint space was widened a greater amount when our new bandage distraction technique was used.

[Restriction fragment length polymorphism of coagulase gene of methicillin-resistant Staphylococcus aureus can be used as an epidemiological marker].

In order to see the restriction fragment length polymorphism (RFLP) of coagulase gene of Methicillin-resistant Staphylococcus aureus (MRSA) and the type of coagulase, a total of 118 strains of MRSA from 1986 to 1994 was collected from the Akita University Hospital, six hospitals in Akita Prefecture and a hospital in Aomori Prefecture. The RFLP analysis using the Alu I restriction enzyme brought us four kinds of electrophoretic patterns (A, B, C, D). Patterns A (87%) and B (13%) were detected in our hospital and only pattern A was detected in other hospitals in Akita. On the other hand, Patterns A (68%), B (26%), C (3%) and D (3%) were detected in Aomori. In coagulase type analysis, all strains in Akita showed type II, and the strains in Aomori also showed type II except for one strain (type IV). From the above results, the polymorphism of coagulase gene of MRSA can be useful as an epidemiological marker to examine the extent of MRSA infection in a prefecture unit or in a larger area.

[Microbiological characterization of clinical isolates of Staphylococcus epidermidis].

As a result of recent development in medical practice including use of new antimicrobial agents, coagulase-negative Staphylococci (CNS) that were once considered nonpathogenic contaminants have captured attention as causes of disease. The 43 clinical isolates of Staphylococcus epidermidis sensu stricto and 7 isolates of S. epidermidis from the medical staffs were characterized with regard to (1) their biochemical profiles, (2) slime productivity, (3) beta-lactamase productivity and (4) plasmid patterns. Most of the isolates have an identical biochemical profile code. The slime production was observed in the 9 strains isolated from pleural effusions or the tubes used for pleural drainage. These strains had a similar antimicrobial susceptibility profile that are commonly seen in multi-resistant strains of methicillin-resistant Staphylococcus aureus (MRSA). In addition, most of these strains produced beta-lactamase. For the plasmid profiling, we selected 12 isolates that possessed 5 distinct antimicrobial susceptibility profiles. Upon agarose gel electrophoresis, 8 isolates were shown to possess a 1.9 kb plasmid. These 8 isolates had resistance against tobramycin (TOB) and erythromycin (EM). Emergence of S. epidermidis as causes of disease will increasingly necessitate the detailed microbiological characterization of the clinical isolates.

[Cytomegalovirus ascending myelitis in an immunocompetent adult].

A 32-year-old man was hospitalized because of tetraparesis, sensory loss below cervical line, and urinary bladder dysfunction. Two months prior to this admission, he had suffered from cytomegalovirus (CMV) mononucleosis characterized by fever, presence of atypical lymphocytes and high serum titers of CMV-IgG/IgM antibodies. A lumbar puncture yielded clear fluid with 104 leukocytes (predominantly mononuclear cells)/mm3; protein, 102 mg/dl; and CMV-IgG antibodies (EIA), 1210. CMV antibody serum/CSF ratio was decreased to 2.08 (normal range > or = 20), indicating intrathecal production of CMV antibodies. T2-weighted images of spinal MRI showed diffuse high signal intensity lesions throughout the cord below C3 vertebral body level. A diagnosis of ascending myelitis secondary to CMV infection was made. Methylprednisolone pulse therapy led to some improvement in his neurologic dysfunctions. This is the first case report of CMV ascending myelitis in a previously healthy adult.

[Autotopagnosia ameliorated by looking at the image reflected in a mirror].

A 52-year-old right-handed man presented progressive dystonia and apraxia of his right hand of five years' duration. He also suffered from parkinsonian features such as rigidity or impaired postural reflexes. Serial investigation of brain MRI revealed progressive cerebral atrophy, which started in the left parietal lobe, and subsequently extended to both hemispheres. He was clinically diagnosed as corticobasal degeneration. He could not point at any part of his own body in response to verbal or visual commands. On the other hand, he could point at every part of the examiner's body or of the illustrated body image. Deep sensations and linguistic functions were not involved. This cognitive impairment was regarded as autotopagnosia. In contrast with inability to recognize any part of the own body in response to the commands, he could name every part of his body as soon as the examiner touched there. Moreover, his symptoms of autotopagnosia were ameliorated by looking at himself in a mirror; he could point at any part of his own body. Disconnection between primary proprioceptive sensory area and the center of body schema was thought to be the mechanism of autotopagnosia in this patient, because the impairment improved with the aid of visual or tactile informations. We speculated the lesion was the left parietal lobe.

[Molecular epidemiological analysis of Pseudomonas aeruginosa by pulsed-field gel electrophoresis].

In order to see the nosocomial infection by Pseudomonas aeruginosa (P. aeruginosa) in the Akita University Hospital, we analyzed the serotype and genotype for 150 strains isolated from various clinical specimens from 1994 to 1996. One hundred strains chosen at random were divided into 11 serotypes by serotyping and into 50 genotypes by pulsed-field gel electrophoresis of Spe I-digested P. aeruginosa genomic DNAs. Serotype E strains, most common, gave 17 genome patterns. Fifty strains separated periodically in certain wards had further 7 genome patterns. The strains isolated from one patient with different times or with different serotypes showed the same stable genotype. Genome patterns were inconsistent with susceptibility to antimicrobial agents. Both drug-susceptible and -resistant strains were found in strains with the same genome pattern. The genome pattern was identical, even though the susceptibility was different due to isolation time or storage. This suggested that the multidrug-resistant strains of P. aeruginosa expanded in the hospital were not derived from one original strain.

[Nosocomial infections and clinical microbiology].

Hospital-acquired infection with strains of methicillin-resistant Staphylococcus aureus (MRSA) have considerably increased in recent years. In addition to being resistant to methicillin, these strains are resistant to practically all forms beta-lactams, aminoglycosides and many other antibiotics. There appears no cost-effective control and preventive measures for this common but also potentially life-threatening disease. Although not clearly presented, the overall cost for the treatment of patients infected with MRSA should be enormous. Can laboratory medicine (or clinical microbiology) contribute to this global medical problem? Multiple strains of MRSA circulate within a hospital and some strains are even localized within specific wards. These facts suggest yet undisclosed routes of transmission and/or foci of infection. Triumph over these versatile organisms may have to await the development of new antibiotics effective for MRSA.

[Methicillin-resistant Staphylococcus aureus infection in the Akita University Hospital: surveillance and microbiology data].

In order to control the nosocomial infections by methicillin-resistant Staphylococcus aureus (MRSA) in the Akita University Hospital, the systematic surveillance for MRSA-infection has been done since October in 1991. We reviewed MRSA-isolation numbers, MRSA-detected patient numbers, risk factors of nosocomial infection and patient's basic diseases with the data of a total 336 cases, and then examined the microbiological characteristics of MRSA strains which had been isolated in our hospital in 1986 approximately 1994. The results obtained are as follows; 1) MRSAs were isolated at 13 per month on the average and the detection rate was 0.81 to 1,000 inpatients per day. 2) MRSAs were isolated more in the surgical ward. 3) Patients with 0 year old and more than 60 years old were more infected. 4) MRSA was isolated more from the immunocompromised patients with underlying diseases such as malignant tumors but half of the diseases were not affected by MRSA. 5) Seventy percent of patients had the risk factors of MRSA-transmission such as surgical operation and IVH-cathetering. 6) All isolates of MRSA strains in our hospital showed type II in coagulase type analysis and resistance to minocycline and ofloxacin. 7) It was suggested that one strain expanded throughout the hospital by several DNA analysis with the mecA gene in MRSA. These surveillance and microbiology data will be useful for our nosocomial mecA gene in MRSA. These surveillance and microbiology data will be useful for our nosocomial infection control.