Planned Overreaching and Subsequent Short-term Detraining Enhance Cycle Sprint Performance.

We investigated the effect of a training program consisting of planned overreaching and subsequent short-term detraining on sprint performance. 24 physically active men participated in an 18-day sprint-training program. They were divided into 2 groups: the overreaching-detraining (OR-DT) and the control (CON) groups. Subjects in the OR-DT group performed 12 consecutive days of maximal cycle sprint training followed by 6 days of detraining, whereas a rest day was provided after every 2 successive training days for the CON group. Peak power output during maximal pedaling increased significantly after 6 days of detraining in the OR-DT group compared with the baseline (P<0.05), whereas no change was observed in CON group. Intramuscular phosphocreatine concentration increased significantly after 12 days of daily training in the OR-DT group (69.3±45.8% increase vs. baseline, P<0.05), and it was maintained after the detraining period (46.6±33.6% increase vs. baseline, P<0.05). However, no change was observed in CON group. No significant changes in blood variables were observed after the training period except significant reduction of serum cortisol in the CON group. Daily sprint training and subsequent short-term detraining enhanced peak power output after the detraining period.

Multiple brain gas embolism after ingestion of concentrated hydrogen peroxide.

We present a 63-year-old man who developed multiple brain infarction after ingesting a 35% hydrogen peroxide solution. Neurologic examination revealed left hemiparesis, primarily affecting the lower limb, and mild weakness of the right lower limb. Gadolinium-enhanced MRI revealed patchy bilateral brain lesions. Oxygen gas embolization is the likely cause of the brain infarctions.

Vacuolar myositis with expression of both MHC class I and class II antigens on skeletal muscle fibers.

We describe here a 10-year-old patient with high levels of serum IgE and inflammatory myopathy whose muscle fibers exhibit excessive autophagy. Previous studies have demonstrated surface expression of class I MHC antigens on muscle fibers from patients with inflammatory myopathy. The muscle fibers of this patients showed marked expression of both class I and class II MHC antigens. The reaction products were demonstrated not only on sarcolemma but also in and around some vacuoles. Both CD4-positive and CD8-positive T-lymphocytes were noted in inflammatory exudates surrounding these fibers but B-lymphocytes were rare. We hypothesize that myocyte expression of both class I and class II antigens may play a role in the pathogenesis of this new type of inflammatory myopathy.

Myasthenia gravis, acute transverse myelitis, and HTLV-I.

We present the unusual case of a 49-year-old female carrier of HTLV-I with myasthenia gravis who presented with acute transverse myelitis. Laboratory data suggested a recent infection with varicella zoster virus and demyelination by an autoimmune process in the central nervous system. Adult T-cell leukemia-like cells were observed in the cerebrospinal fluid. T-cell-mediated immune responses modulated by HTLV-I infection may be involved in the pathogenesis of myasthenia gravis and acute transverse myelitis in this case.

Lymphocyte subsets in muscle biopsies of human T-lymphotropic virus type I carriers with polymyositis.

Recent epidemiologic studies have shown that human T-lymphotropic virus type I (HTLV-I) is associated with polymyositis. To clarify the histological features of HTLV-I positive polymyositis, we studied muscle tissue from two groups of patients with polymyositis, those seropositive for HTLV-I (5 patients) and those seronegative (5 patients). We examined the lymphocyte subsets in muscle biopsies using monoclonal antibodies. In the endomysium, a variable number of T-lymphocytes and macrophages and a smaller proportion of B-lymphocytes were found in both groups. In both HTLV-I positive and negative patients a variable number of T-lymphocytes and macrophages, with a smaller number of B-lymphocytes, were found in the perimysium. As a whole, the T-lymphocytes were predominantly of the helper/inducer phenotype in both groups. We failed to find any specific phenotype distribution among T-cells infiltrating the muscle of HTLV-I carriers with polymyositis.

Fungemia caused by Hansenula anomala: successful treatment with fluconazole.

Fungemia, due to Hansenula anomala, developed in an adult patient with small cell lung cancer who received anti-cancer chemotherapy and plasmapheresis for a sensori-motor neuropathy complication. Treatment with intravenous infusion of fluconazole in addition to the removal of the central venous catheter was successful in treating the fungemia. Pathogenic Hansenula anomala infections are rare, but reports of this infection have been increasing. The use of fluconazole treatment for this infection has not been reported in the literature, and this is the first case of an adult infection of Hansenula anomala in Japan.

Relationship of high-density lipoprotein cholesterol and red blood cell filterability: cross-sectional study of healthy subjects.

The deformability of red blood cells (RBCs) is an important rheologic factor in the maintenance of normal blood flow in the microcirculation. Contrary to the well-known relationship between hyperlipidemia and atherosclerosis, the relationship between RBC rheology and the serum lipid profile has remained controversial and obscure. Moreover, the correlation of high-density lipoprotein (HDL)-cholesterol and RBC deformability has not been fully understood. In the present cross-sectional study of 139 apparently healthy subjects, we investigated whole-cell deformability (filterability) of RBCs in relation to the lipid profile, using a nickel mesh filter with 3.2-microm pores. RBC filterability was independent of gender, age and serum levels of low-density lipoprotein (LDL)-cholesterol. The filterability was significantly proportional to the HDL-cholesterol values (r = 0.382, p < 0.01), whereas it was inversely proportional to the triglyceride levels (r = -0.259, p < 0.01). These findings may provide new insight into the role of HDL-cholesterol not only in preventing atherosclerotic progression but also in improving RBC filterability.

[Two cases of HTLV-I associated myelopathy (HAM) complicated with Sjögren's syndrome, T-lymphocyte alveolitis and arthropathy].

Two cases of HTLV-I-associated myelopathy (HAM) complicated with Sjögren's syndrome (SjS), T-lymphocyte alveolitis and arthropathy were reported. Case 1 was a 55-year-old woman. Since 40 years of age she had been suffering from repetitive pulmonary infection. She also noted polyarthralgia since 42 years of her age and was diagnosed as SjS at her age 43. She developed gait disturbance since April 1988. Case 2 was a 65-year-old woman. She began to have gait disturbance at 62 years of age. A right knee joint pain started in December 1988. The two cases have the following features in common: 1. The diagnosis of HAM is definite because of pyramidal signs and positive anti-HTLV-I antibody in both serum and cerebrospinal fluid. 2. The histological findings of the minor salivary glands are compatible with SjS. 3. Differential cell count in bronchoalveolar lavage fluid (BALF) showed an increase in lymphocytes which suggested the presence of clinical or subclinical T-lymphocyte alveolitis. 4. A mono-or polyarthropathy is observed. These findings are suggestive that HAM is not the disease restricted within the central nervous system but the disease with systemic involvement which may be caused by the activated T-lymphocytes. Thus the two cases are interesting for the understanding of the pathogenesis of HAM.

[Peripheral neuropathy involving cranial nerves in a patient with hepatitis C virus infection and mixed cryoglobulinemia].

A 75-year-old man developed subacute progressive muscle weakness and painful paresthesia of the left upper and right lower limbs. The patient had no history of diabetes mellitus. On physical examination, there was no evidence of icterus or hepatosplenomegaly. Palmar erythema without rash was noted. Neurologic examination revealed muscle atrophy and weakness in the left upper limb and mild muscle weakness in the right proximal lower limb. Dysesthesia, severe hypesthesia, and hypalgesia were found in the left upper limb. The tendon reflexes were decreased in the left upper limb and absent in the lower limbs. The cranial nerves were preserved on the day of admission, followed by the involvement of the right oculomotor nerve. Serological examination revealed a mixed IgG/IgM cryoglobulinemia and hepatitis C virus (HCV) infection with evidence of HCV virus replication by PCR for HCV RNA. The patient was diagnosed as having a mixed cryoglobulinemic neuropathy associated with HCV infection. Interferon-alpha therapy with 3 million units subcutaneously was initiated three times per week; however, there was no clinical improvement, although cryoglobulins became undetectable and the level of serum HCV RNA decreased remarkably. Intravenous immunoglobulin therapy 20 g per day for 5 days was also ineffective. The patient developed right facial nerve palsy, followed by right abducens nerve palsy. Treatment with prednisolone 40 mg per day improved and stabilized neurologic symptoms. Although interferon-alpha is considered to be a promising therapy for neurologic complications of HCV infection with mixed cryoglobulinemia, the optimal treatment remains unestablished.

Prevention of inflammation-mediated acquisition of metastatic properties of benign mouse fibrosarcoma cells by administration of an orally available superoxide dismutase.

Weakly tumorigenic and nonmetastatic QR-32 cells derived from a fibrosarcoma in C57BL6 mouse are converted to malignant cells once they have grown after being coimplanted with a gelatine sponge which induces inflammation. We administered a newly developed peroral superoxide dismutase (SOD), oxykine, and as control vehicle, gliadin and saline, starting 2 days before the coimplantation and continued daily throughout the experiment. In the oxykine group, tumour incidence was lower (41%) than in the gliadin or saline group (83 and 79%, respectively). The inhibitory effect of oxykine was lost when an individual component of oxykine was administered, that is, SOD alone and gliadin alone. The effect was also abolished when administered by intraperitoneal route. When perfused in situ with nitroblue tetrazolium, an indicator of superoxide formation, the tumour masses from gliadin and saline groups displayed intense formazan deposition, whereas, those from oxykine group had less deposition. Enzymatic activity of SOD was also increased in oxykine group. Arising tumour cells in gliadin and saline groups acquired metastatic phenotype, but those in oxykine group showed reduced metastatic ability. These results suggested that the orally active SOD derivative prevented tumour progression promoted by inflammation, which is thought to be through scavenging inflammatory cell-derived superoxide anion.

Asymptomatic primary biliary cirrhosis in HTLV-I-associated myelopathy.

A 54-yr-old woman was admitted for complaints of slowly progressive gait and bladder disturbance, and HTLV-I-associated myelopathy (HAM/TSP) was diagnosed by positive antibodies to HTLV-I, both in her serum and cerebrospinal fluid. In the course of a diagnostic evaluation, she was found to have asymptomatic primary biliary cirrhosis. In immunohistochemistry, a fair number of her hepatocyte nuclei stained strongly positive for HTLV-I core protein, suggesting that HTLV-I may infect hepatocytes. The present case demonstrates that the spectrum of HTLV-I infection may be broad, and suggests the relationship between HTLV-I-associated myelopathy and primary biliary cirrhosis by autoimmune process.

Neuropathology of HTLV-I-associated myelopathy--a report of two autopsy cases.

A neuropathological analysis was performed in two autopsy cases of HTLV-I-associated myelopathy. The thoracic spinal cords were most severely affected and the histopathological findings consisted of mononuclear cell infiltration, marked destruction of myelin and axons and astrocytic gliosis. More than half the infiltrated cells were positive for pan-T cell marker; B cells were sparse in the parenchyma and subarachnoid spaces. CD4 and CD8 positive cells were found in the early stages of the lesions. CD8, however, predominated over CD4 in the other stages. It appeared that a chronic inflammatory process had started at the middle to lower thoracic cord and had extended gradually in both directions. The middle thoracic spinal cord is known to have the poorest blood supply, and the horizontal distribution of inflammatory cells at this region correlated with the most distal supply of the anterior spinal artery.

Brain lesions in the course of generalised tetanus.

A 47-year-old woman developed left hemiparesis primarily affecting the lower limbs during the course of severe generalised tetanus. MRI on the 82nd hospital day revealed cortical and subcortical lesions predominantly in the right frontal and parietal lobes in addition to marked brain atrophy. Three months later, the enhancing lesions were still present on follow up MRI. We postulate that structures above brainstem may be involved in severe generalised tetanus.

Multiple cranial neuritis associated with large granular lymphocytosis.

A patient with a unique form of large granular lymphocytosis and multiple cranial neuritis is reported. The patient presented with facial weakness, diplopia and dysarthria. An increase in large granular lymphocytes (LGLs) was seen in blood (1.8 x 10(9)/l), CSF (237/microliters) and bone marrow (20% in a normocellular bone marrow). The phenotype of the LGLs in CSF, blood and bone marrow was CD2+ CD3+ CD4+ CD8- CD16- CD56- and CD57-. The unique features of this case include the CD4+ phenotype, the relative abundance of CSF LGL and the clinical presentation.