Synovitis of the wrist caused by Mycobacterium florentinum.

Mycobacterium florentinum is a newly identified, rare, slow-growing species of nontuberculous mycobacteria (NTM). Here, we report a case of M. florentinum-induced synovitis of the wrist in an immunocompromised Japanese patient. M. florentinum was identified by sequence analysis of the rpoB, hsp65, and 16S rRNA genes. The M. florentinum strain in this study could not be differentiated from certain M. triplex strains by the hsp65 or 16S rRNA sequences alone, because they occasionally shared more than 99 % sequence identity. The isolated M. florentinum strain was only susceptible to clarithromycin and amikacin. Initially, the patient was treated with clarithromycin, levofloxacin, and ethambutol, and then with clarithromycin, levofloxacin, and rifampicin. To our knowledge, M. florentinum-induced synovitis has not been previously reported. Our results suggest that, in addition to other well-known pathogenic NTM, the recently identified M. florentinum strain should be considered as a possible cause of synovitis. Moreover, we should be cautious when identifying M. florentinum because this strain closely resembles M. triplex in genotype.

Diagnostic usefulness of diffusion-weighted magnetic resonance imaging in influenza-associated acute encephalopathy or encephalitis.

A magnetic resonance imaging (MRI) study was performed for a 20-month-old girl with an influenza type A infection who presented acute encephalopathy. Conventional MRI performed 8 days after the onset of encephalopathy, including T1-weighted, T2-weighted, and fluid-attenuated inversion recovery imaging, revealed only vague lesions in the right frontal, temporal, and parietal lobes. In contrast, diffusion-weighted imaging (DWI) then demonstrated the lesions much more intensively. On the 26th day, the lesions previously observed on DWI had become less discernible. The hyperintensity observed on DWI might reflect cytotoxic edema. Thus, DWI may be useful for evaluation of acute influenzal encephalopathy/encephalitis.

Malignant fibrous histiocytoma of soft tissue producing granulocyte colony-stimulating factor.

We treated a rare case of malignant fibrous histiocytoma (MFH) of soft tissue that produced granulocyte colony-stimulating factor (G-CSF). The patient, an 80-year-old woman, was admitted because of a feeling of abdominal fullness and leg edema. An elastic, hard, tender tumor was palpated in the right thigh. Histopathological examinations of the tumor revealed atypical and prominent pleomorphic spindle-shaped cells with funicular arrangement, which were compatible with the diagnosis of MFH. Prominent leukocytosis (up to 84,300/microl), a high serum G-CSF concentration (82 pg/ml) and positive immunohistochemical staining of the tumor tissue for G-CSF indicated that G-CSF was produced by the MFH.

The effect of ultraviolet rays on the prevention of exit-site infections.

The aim of this study was to show that ultraviolet (UV) irradiation to the skin around the catheter exit site (ES) could inhibit its infection. First, bacterial cultures of swabbed fluid from the ES were obtained from 68 continuous ambulatory peritoneal dialysis (CAPD) outpatients six times during the 24-month observation period. Second, the bactericidal effects of UV irradiation on the catheter ES were examined. The results were as follows: (1) In spite of disinfection of the catheter ES by the strict application of povidone-iodine once or twice a day, 23%-45% of the cases were found to be micro-organism positive. The most prevalent micro-organisms from the catheter ES were, in order of highest to lowest prevalence, Staphylococcus epidermidis (SE), Staphylococcus aureus (SA), and Pseudomonas aeruginosa (PA). (2) In the nasal cavity SA was detected in 20%-25% of patients. There was a high incidence of ES infection among the SA nasal carriers. (3) UV irradiation was performed in 18 cases that constantly revealed bacteria on culture at the catheter ES. Ten cases (55%) became culture-negative, 3 cases showed a microbial decrease, and 5 cases remained unchanged. These results suggest that UV irradiation can eliminate bacteria and can be of prophylactic use for ES infections.

[Usefulness of T2* weighted magnetic resonance image in the diagnosis of head injury on chronic stage].

T2* weighted gradient echo image has heightened diagnostic sensitivity to hemorrhage, which is attributed to magnetic susceptibility-induced static field inhomogeneities arising from paramagnetic blood breakdown products such as hemosiderin, which shorten T2*. We examined 4 cases of head injury in chronic stage by T2* weighted images and assessed the clinical application of this sequence for diagnosis of the intracranial lesion. All patients underwent CT scan on acute stage and long-term follow up was performed. In all cases, abnormally low signals in the brain and subarachnoid space were more conspicuous with the T2* weighted image than with any of the conventional sequences. In 2 cases with diffuse axonal injury, of which lesions were not detected on acute stage CT scan, hypointensity area was clearly demonstrated in the cerebral peduncle and corpus callosum on T2* weighted images. Selection of T2* weighted image into the routine MR examination of patients with chronic stage of the head injury is recommended.

[Schizencephaly: clinical and MRI features].

We report the clinical and neuroimaging features of 4 cases with schizencephaly. Case 1 had bilateral schizencephaly with open-lip on the right and closed-lip on the left. Case 2 had unilateral schizencephaly with closed-lip on the left and subcortical heterotopia on the right. Case 3 had unilateral schizencephaly with closed-lip on the left. Case 4 had bilateral closed-lip schizencephaly. Although all cases except for Case 3 had bilateral lesions, neurodevelopmental outcome was generally good; Case 1 and 3 had mild hemiparesis. All patient have epilepsy which are well-controlled with antiepileptic drugs. Thus, the clinical presentation of schizencephaly, even if bilateral lesions, are quite variable.

Catecholamines in experimental spinal cord lesions associated with spinal arachnoiditis.

Catecholamines in the spinal cord and cerebrospinal fluid of dogs with arachnoiditis induced by cisternal kaolin injection were measured by radioenzymatic assay. The levels of noradrenaline in the gray matter of the cervical cord and the cerebrospinal fluid were highest in 1st week (mean values, 127.8 ng/g and 856.0 pg/ml), whereas those in the gray matter of the thoracic and thoracolumbar cord increased to 175.0 and 210.0 ng/g in average respectively in 12th week. The increase in the level of noradrenaline in the gray matter seemed to be related with degenerative cord lesions in almost all segments, while most segments with cavitation indicated low noradrenaline level.

In vivo and in vitro effects of growth hormone on the incorporation of [14C]leucine into protein of liver and muscle of the eel.

In vivo administration of ovine GH (2 micrograms/g body wt) increased [14C]leucine incorporation into protein of the liver, skeletal muscle, and opercular muscle of hypophysectomized eels. Addition of ovine GH into the medium (5 micrograms/ml) slightly increased [14C]leucine incorporation into protein of liver slices during 5 hr in vitro incubation, but did not affect protein synthesis from [14C]leucine in opercular muscle. In vivo pretreatment with ovine GH (2 micrograms/g body wt) 48 hr prior to tissue preparation clearly increased [14C]leucine incorporation into protein of liver slices in vitro. However, no statistically significant change was observed for in vitro incorporation of [14C]leucine into protein of opercular muscle of hypophysectomized eels which had been previously treated with ovine GH (2 micrograms/g body wt). These results indicate that ovine GH has a protein anabolic action in the liver and muscle of the eel and that compared to mammals a rather long lag period is needed to elicit such protein anabolic actions of GH in these animals.

Effects of insulin and glucagon on the incorporation of [14C]glycine into the protein of the liver and opercular muscle of the eel in vitro.

Effects of insulin and glucagon on the incorporation of [14C]glycine into the protein of liver slices and the opercular muscle of the eel were studied in vitro. Addition of insulin (0.1 IU/ml) to the medium increased the radioactivity both of the trichloroacetic acid (TCA)-soluble fraction and of the protein of the opercular muscle, indicating an acceleration by the hormone both of entry of the amino acid into the tissue and of protein synthesis. Insulin also increased the incorporation of [14C]glycine into the liver protein, while a decrease in the radioactivity of the TCA-soluble fraction was observed. These findings suggest that the hormone accelerated protein synthesis at the expense of an intracellular amino acid pool. In contrast, glucagon (5 micrograms/ml) did not affect the radioactivity either of the TCA-soluble fraction or of protein for either the opercular muscle or the liver. Thus, the present results highlight the importance of insulin in the regulation of protein synthesis in the eel both in muscle and in liver.

Effects of insulin and glucagon on amino acid transport into the liver and opercular muscle of the eel in vitro.

Effects of insulin and glucagon on amino acid transport in vitro into liver slices and the opercular muscle of the eel were studied using a labeled nonmetabolizable amino acid analog, alpha-[1-14C]aminoisobutyric acid (AIB). Addition of insulin (0.1 IU/ml) to the medium increased the radioactivity in the deproteinized fractions of both the liver slices and opercular muscle, indicating an accelerated movement of this amino acid analog into these tissues. Glucagon (5 micrograms/ml) also enhanced the entry of [14C]AIB into the liver slices; however, treatment of opercular muscle with glucagon did not alter the radioactivity in the deproteinized fraction. These findings clearly indicate that the entry of amino acids into eel tissues independent of protein synthesis can be altered by insulin and glucagon.

Effect of mammalian growth hormone on amino nitrogen mobilization in the eel.

Hypophysectomy decreased plasma amino nitrogen (PAN) levels of Japanese eels. In contrast, administration of bovine or ovine growth hormone (GH; 2 micrograms/g) produced a delayed increase in PAN levels of both intact and hypophysectomized eels 48 hr after GH injection. The minimum dose of GH required to elevate PAN levels was found to be 0.1-1 micrograms/g body wt. The fact that GH treatment also increased PAN of hepatectomized eels indicates that the increased PAN was at least partly caused by the increased mobilization of amino nitrogen from body protein. GH also increased plasma free fatty acid content of intact and hypophysectomized eels 48 hr after GH injection in one experiment of the present study, but this effect was not reproducible in other experiments. No effect of GH administration was observed either in plasma glucose and lipid of intact and hypophysectomized eels 48 hr after the injection.

The role of ATP-sensitive potassium channels in the mechanism of ischemic preconditioning.

We clarified the role of K(ATP) channels in the mechanism of ischemic preconditioning by using K(ATP) channel opener, nicorandil, and K(ATP) channel inhibitor, glibenclamide. Forty anesthetized dogs were divided into five groups: (a) control (C), (b) ischemic preconditioning (PC), (c) intravenous infusion of nicorandil before PC (Ni), (d) glibenclamide pretreated with PC (Gl + PC), and (e) glibenclamide pretreated with Ni (Gl + Ni). All groups were followed by 60-min ischemia and 60-min reperfusion and analyzed by the biochemical procedures. At the end of 60-min reperfusion, percentage of segment shortening in C indicated paradoxic bulging. This value was significantly recovered in PC and Ni, but it was still negative in Gl + PC and Gl + Ni. Ca2+ -adenosine triphosphatase (ATPase) activity of sarcoplasmic reticulum (SR) was significantly decreased in C. In PC and Ni, this activity was significantly maintained; however, in Gl + PC and Gl + Ni, it was similar to that in C. State III respiration of mitochondria showed similarity to the changes in SR. These results indicated that the K(ATP) channel opener enhanced the effects of ischemic preconditioning, and its blockade abolished these phenomena. We conclude that the ATP-sensitive potassium channel may play one of key roles in the mechanisms of ischemic preconditioning in the dog model.

Biochemical and ultrastructural evaluations of the effect of ischemic preconditioning on ischemic myocardial injury--role of the adenosine triphosphate-sensitive potassium channel.

The aim of this study was to clarify the role of the adenosine triphosphate (ATP)-sensitive potassium channel on the mechanism of ischemic preconditioning (IP). Thirty-five anesthetized dogs were divided into 5 groups: (1) Control (C), (2) IP, (3) intravenous infusion of nicorandil (Ni) prior to IP, (4) glibenclamide (G1) pretreated with IP (G1+IP), and (5) G1 pretreated with Ni (G1+Ni). All groups had 60 min ischemia followed by 60 min reperfusion, and were analyzed by biochemical and morphological procedures. At the end of the 60-min reperfusion, %segment shortening in C indicated paradoxical bulging. This value had significantly recovered in IP and Ni groups, but it was still negative in the G1+IP and G1+Ni groups. Ca++-ATPase activity of the sarcoplasmic reticulum (SR) was significantly decreased in C. In the IP and Ni groups, this activity was significantly maintained; however, in the G1+IP and G1+Ni groups it was similar to that in C. State 3 respiration of mitochondria showed similar changes in the SR. In the ultrastructural observations, severely damaged cells were not observed in the IP and Ni groups. These results indicated that an ATP-sensitive potassium channel opener enhanced the effects of IP and its blockade abolished these phenomena. It was conclude that the ATP-sensitive potassium channel may play a key role in the mechanism of IP.

Possible role of an endovascular provocative test in the diagnosis of glossopharyngeal neuralgia as a vascular compression syndrome.

We utilized endovascular provocative techniques to identify the indications for microvascular decompression surgery in a serious case of glossopharyngeal neuralgia. This is the first reported case in which an endovascular provocative test was applied for diagnosis of glossopharyngeal neuralgia as a vascular compression syndrome. A 68-year-old woman presented with severe paroxysmal facial pain which could not be controlled by medical therapy. Partial effectiveness to carbamazepine led us to wonder whether or not the selection of microvascular decompression surgery would be appropriate. Pre-operative angiography was performed. During the examination a microcatheter was inserted into the right posterior inferior cerebellar artery (PICA), and an attack of typical glossopharyngeal neuralgia occurred. The patient thus underwent microvascular decompression surgery. The PICA was verified to compress the glossopharyngeal nerve and therefore was moved to induce decompression. The patient has since experienced no further pain for one year postoperatively. The diagnosis of glossopharyngeal neuralgia is sometimes complex and it is difficult to select the most appropriate surgical modality. In such cases this endovascular provocative technique may thus be useful for making a definitive decision or microvascular decompression surgery.

Protective effect of captopril on ischemic myocardium.

The protective effect and mechanism of action of the angiotensin-converting enzyme inhibitor (ACE-I) captopril was investigated in organelles from ischemic myocardial cells in a canine coronary ligation model. Sarcoplasmic reticulum (SR) and mitochondrial fractions were extracted from ischemic and nonischemic myocardial cells from captopril- and saline-treated (control) hearts. Heart rate, cardiac output, and right ventricular systolic blood pressure were similar in the captopril-treated and control groups. Left ventricular systolic blood pressure (LVPs) decreased gradually to 89% of the baseline value after captopril administration, and to 78% of the baseline value after ligation. Ca-ATPase activity in the SR, the respiratory control ratio (RCR) in the mitochondria, and dinitrophenol (DNP)-stimulated ATPase activity were significantly higher in ischemic myocardium from the captopril-treated group than from the saline-treated (control) group. The SH group content of both organelles was higher in the captopril-treated group. Our results suggest that, in addition to their hemodynamic effects, ACE-I agents containing SH groups protect the myocardium from ischemic damage by preventing enzyme oxidation.

Generation of free radicals and the damage done to the sarcoplasmic reticulum during reperfusion injury following brief ischemia in the canine heart.

Free radical generation was studied by the electron spin resonance (ESR) technique using alpha-phenyl N tert butyl nitrone (PBN) in a brief ischemia-reperfusion model of the canine heart, and correlated with biochemical changes of the sarcoplasmic reticulum (SR). ESR spectra (aH=0.3-0.4mT, aN=1.43-1.58mT) were observed as PBN spin adducts, which peaked at levels 5-fold above the control levels at 5 min after reperfusion. The simulated coupling constants of PBN spin adducts suggested that the sample should contain at least 2 carbon-centered radicals at 5 min after reperfusion (radical A: aH=0.350mT, aN=1.485mT; radical B: aH=0.370mT, aN=1.615 mT). At this time point, a significant reduction in Ca-ATPase activity of the SR was found without degradation of the major ATPase protein. Superoxide dismutase (SOD) significantly reduced the intensity of the PBN spin adduct signals and preserved the Ca-ATPase activity of the SR to 80% of the control level. Reperfusion injury after brief ischemia may be the result of inactivation of intracellular Ca-ATPase by free radicals generated during reperfusion, and SOD contributes to the protective effect by scavenging the radicals.