Tumorous calcification causing carpal tunnel syndrome.

PURPOSE: There is little information on solitary tumorous calcification causing carpal tunnel syndrome in the literature. This study describes our experience with surgically treated cases of solitary tumorous calcification causing carpal tunnel syndrome. METHODS: Seven patients with symptomatic carpal tunnel syndrome who had tumorous calcification in the carpal tunnel confirmed by radiographical examinations and had then undergone open incisional carpal tunnel release were reviewed. The precise location and the appearance of the calcified mass were confirmed with the preoperative radiographic examinations and the operative records. The additional histology and the composition analysis of the calcified mass were also reviewed in five removed calcifications. RESULTS: Radiographs of each hand revealed a mass of calcification lying anterior to the capitate bone in the carpal tunnel. Intraoperatively, an oval calcified nodule, measuring 10 x 10 x 10 - 18 mm, was observed overlying the capitate, attached firmly to the palmar radiocarpal extrinsic ligament. A composition with an average of 60 % basic calcium phosphate was revealed by infrared absorption spectrometry. Histological sections showed a calcified deposit surrounded by fibrocartilagenous tissue in three cases. CONCLUSION: These facts suggest that the pathogenesis of tumorous calcification causing carpal tunnel syndrome is comparable with that of calcifying tendinitis of the rotator cuff in which a cell-mediated reactive process plays an important role at the tendon insertion.

Protective effects of murine recombinant interferon-beta administered by intravenous, intramuscular or subcutaneous route on mouse hepatitis virus infection.

The significance of the route for administration of murine recombinant interferon-beta (IFN-beta) for inducing its therapeutic effects has been studied. BALB/c mice were daily injected intravenously, intramuscularly or subcutaneously with 1.5x10(3), 1. 5x10(4), or 1.5x10(5) IU of IFN-beta, from one day before to 8th day after mouse hepatitis virus (MHV-2) challenge. All mice received IFN-beta survived significantly longer than those without IFN. In the liver of those IFN-treated mice, viral growth and the histopathological damages were extremely alleviated. These results suggest that, irrespective of the differences in the route of administration, IFN-beta markedly suppressed viral activity when its administration was started prior to viral infection. For clinical use, however, further studies are needed on the optimal route for administration if IFN-beta is given after viral infection.

[Microscopic polyangiitis accompanying interstitial pneumonia with aluminum lung].

A 67-year-old man who had worked as an aluminum grinder had been given a diagnosis of pneumoconiosis. Ten years later, he was admitted with fever, dyspnea on exertion, and numbness. Chest roentgenograms showed linear-reticular shadows in both lower lung fields. ELISA-based tests were positive for perinuclear anti-neutrophil cytoplasmic antibody (P-ANCA). Renal biopsy specimens disclosed crescentic glomerulonephritis and angiitis of small arteries. Our diagnosis was microscopic polyangiitis accompanying interstitial pneumonia with aluminum lung. The results of high-energy dispersion X-ray microanalysis indicated that the patient's lungs contained aluminum. His general condition improved with the administration of corticosteroid and immunosuppressive agents, and his chief symptoms disappeared.

Cromakalim-induced membrane current in guinea-pig tracheal smooth muscle cells.

The characteristics of the cromakalim-induced membrane current were examined in single tracheal myocytes of the guinea-pig under voltage-clamp conditions. When K(+) concentrations in the pipette and bathing solutions were approximately 140 mM, cromakalim activated a membrane current (I(crom)) which was inward at -60 mV and reversed at -2 mV. I(crom) was blocked by 10 microM glibenclamide and potentiated when the ATP concentration in the pipette solution was decreased. The K(d) and Hill coefficient of glibenclamide for I(crom) block were 200 nM and 1.05, respectively. Application of the tyrosine kinase inhibitors, genistein and alpha-cyano-3-ethoxy-4-hydroxy-5-phenylthiomethylcinnamamid (ST638), reduced I(crom) in a concentration-dependent manner. Daidzein, which does not inhibit tyrosine kinase, was about 10 times less effective than genistein. Herbimycin A had no effect on I(crom). Internal application of these inhibitors from the pipette did not affect I(crom). In conclusion, cromakalim is a potent activator of the ATP-sensitive K(+) channel (K(ATP) channel) in guinea-pig tracheal myocytes. The inhibition of I(crom) by genistein and ST638 may be due to the direct block of the channel from outside.

[Churg-Strauss syndrome with pulmonary eosinophilia and intrapulmonary lymph nodes 2 years before the onset of vasculitis].

We report a case of a 55-year-old man who had been treated for bronchial asthma diagnosed at the age of 51. One year following diagnosis, chest X-ray films disclosed nodular shadows. Biopsy specimens obtained by video-assisted thoracoscopic surgery were histopathologically identified as intrapulmonary lymph nodes. Three years after the initial diagnosis, the patient experienced sensory disturbance of the lower extremities, low-grade fever, and weight loss. At this point he was admitted to our hospital. On admission, physical examination and clinical investigations showed peripheral eosinophilia and signs of vasculitis. Specimens obtained by transbronchial lung biopsy and bronchoalveolar lavage showed strong evidence of tissue damage with infiltration of eosinophils but no evidence of necrotizing vasculitis or extra-vascular granuloma. Churg-Strauss syndrome (CSS) was diagnosed, and treatment was initiated with prednisolone at a dose of 60 mg/day. Except for the sensory disturbances in the lower extremities, after a few days of treatment the patient's symptoms subsided and his clinical data improved. This case was clinically important because pulmonary eosinophilic infiltration into vessel walls was confirmed a year after the diagnosis of bronchial asthma, and 2 years before the patient demonstrated signs of vasculitis. Further, it was a very rare case of CSS in which intrapulmonary lymph nodes had developed beneath the visceral pleura despite the absence of a history of heavy smoking, thus suggesting continuous stimulation by some as yet unknown antigen.

Characteristics of Ca2+ release for activation of K+ current and contractile system in some smooth muscles.

Characteristics of Ca2+ release from stores were investigated in strips from ileum and portal vein and in isolated myocytes from ileum and urinary bladder of the guinea pig with use of caffeine and 9-methyl-7-bromoeudistomin D (MBED), a potent releaser of Ca2+ from skeletal muscle sarcoplasmic reticulum. In skinned strips, 1-30 mM caffeine elicited a transient contraction, but 10-300 microM MBED did not. Pretreatment with 100 microM MBED did not affect the subsequent caffeine-induced contraction. In single cells loaded with indo 1-acetoxymethyl ester, 10 mM caffeine increased cytoplasmic Ca2+ concentration, whereas 100 microM MBED elicited a small or no increase. Under whole cell clamp, spontaneous transient outward currents through Ca(2+)-dependent K+ (BK) channels were first enhanced and then suppressed by 30 microM MBED or 5 mM caffeine. The amplitude of Ca(2+)-dependent transient K+ current on depolarization was reduced by MBED and caffeine (50% inhibitory concentrations = 20 microM and 1 mM, respectively). Other currents and single BK channel activity were not significantly affected by MBED. The Ca2+ release from stores responsible for BK channel activation may be resolved from that for the activation of the contractile system by MBED in these smooth muscle cells.

Effects of ONO-1101, a novel beta-antagonist, on action potential and membrane currents in cardiac muscle.

Direct effects of ONO-1101 ¿(-)-[(S)-2,2-dimethyl-1,3-dioxolan-4-yl]methyl-3-[4-[(S) -2-hydroxy-3-(2-morpholino carbonylamino)ethylamino] propoxy]phenylpropionate monohydrochloride), a novel beta-antagonist, on action potential parameters and membrane currents, and its beta adrenoceptor antagonism were examined in cardiac muscle. Action potential-parameters in papillary muscle of reserpinized animals and membrane currents recorded from single myocytes obtained from guinea pig and rabbit hearts were not affected by 1 to 100 microM ONO-1101. On the other hand, ONO-1101 markedly inhibited the potentiation of Ca current by isoproterenol in single cardiac myocytes of the guinea pig. The concentration-response relationship of Ca current for isoproterenol was shifted to the right. This effect resembled that of esmolol, which is also a beta adrenoceptor antagonist. A Schild plot analysis revealed the slope and pA2 value of each antagonist (ONO-1101, 0.94, 8.0; and esmolol, 0.98, 7.3, respectively) and demonstrated that ONO-1101 is about 5 times more potent than esmolol as a beta-antagonist. Two other effects of isoproterenol: 1) potentiation of delayed rectifier K current and 2) activation of chloride current, were also inhibited by ONO-1101. The time required for 50% removal of beta-antagonism of ONO-1101 and esmolol after the washout was estimated as 4 and 6 min, respectively, in depolarized papillary muscle. These results suggest that ONO-1101 is a potent beta-antagonist whose effects were removed quickly by washout. When applied at what is thought to be a clinical dosage, ONO-1101 had no direct effects on action potential-parameters and membrane currents in cardiac muscle. These characteristics of ONO-1101 suggest that this agent may be effective in clinical use.

Time course of Ca(2+)-dependent K+ and Cl- currents in single smooth muscle cells of guinea-pig trachea.

The time course of two types of Ca(2+)-dependent currents were compared in single smooth muscle cells freshly isolated from guinea-pig trachea. When the pipette solution contained mainly 140 mM KCl, depolarization from -60 mV to 0 mV evoked an initial inward current followed by an outward current which consisted of transient (I(to)) and sustained components. In addition, a long-lasting inward tail current (Itail) was occasionally observed after the repolarization to -60 mV. Although I(to) often occurred repetitively during depolarization, the first I(to) reached the peak of approximately 50 ms after the start of depolarization and had the largest amplitude in most cells examined. The amplitude of Itail increased with the increase in depolarization period up to about 500 ms. Pharmacological analyses indicate that I(to) and Itail are Ca(2+)-dependent K+ and Cl- currents (IK-Ca and ICl-Ca), respectively, and suggest that not only Ca(2+)-influx through Ca2+ channels but also subsequent Ca2+ release from stores contributes to activate these currents. Spontaneous transient outward and inward currents, IK-Ca and ICl-Ca, respectively, were simultaneously recorded at -40 mV. In over 80% of the spontaneous current events, outward and inward currents coupled one to one and always occurred in this order. Puff-application of 10 mM caffeine also induced IK-Ca and ICl-Ca in this order at -40 mV. When caffeine was applied twice with various intervals, the current amplitude in the second application depended upon the period of the interval. The recovery of ICl-Ca during the interval was faster than that of IK-Ca. The results indicate that the activation and decay time courses of ICl-Ca are slower but its recovery is faster than those of IK-Ca.

Characteristics of caffeine-induced and spontaneous inward currents and related intracellular Ca2+ storage sites in guinea-pig tracheal smooth muscle cells.

Characteristics of caffeine-induced inward current (Icaf) and spontaneous transient inward current were examined in single smooth muscle cells isolated from guinea-pig trachea. When a pipette solution contained mainly CsCl, an application of 10 mM caffeine elicited transient Icaf at a holding potential of -60 mV. Spontaneous transient inward currents were recorded in about 15% of cells examined and were abolished by caffeine. Both were Cl- current activated by an increase in intracellular Ca2+ concentration (ICl-Ca). When 10 mM caffeine was puff-applied twice with various intervals, the amplitude of the second Icaf depended upon the period of the interval. The relationship between the amplitude and the interval represents the recovery time course of Icaf, which was significantly slowed by 30 microM cyclopiazonic acid. The Icaf was not significantly affected by addition of Cd2+. Removal of external Ca2+ did not affect the first Icaf but markedly reduced the second one, regardless of the presence of Cd2+. In conclusion, Icaf is evoked by activation of ICl-Ca via Ca2+ release. The recovery time course of Icaf indicates the refilling of Ca2+ storage sites by the cyclopiazonic acid-sensitive Ca2+ pump. The refilling at -60 mV depends strongly upon Ca2+ influx through the Cd(2+)-insensitive pathway. Spontaneous transient inward currents may be also due to ICl-Ca activated by spontaneous Ca2+ release from local storage sites.

[Physiological functions and regulation of K+ and Cl- channels in single smooth muscle cells].

The major functional roles of K channels in smooth muscle cells are as follows: (i) Keeping resting membrane potential (RMP). (ii) Induction of hyperpolarization (HP) in response to bioactive substances. (iii) Facilitation of action potential repolarization (APR). (iv) Induction of action potential after-hyperpolarization (AH). (v) Facilitation of slow wave repolarization. (vi) Inhibition of depolarization and/or action potential. Major background K channels responsible for RMP have not been identified yet, whereas it is been postulated that several K channels including Ca-dependent K channels and ATP-dependent K channels may co-contribute in part to RMP. Further activation of these channels by bioactive substances results in hyperpolarization and muscle relaxation. APR and AH in several types of smooth muscles are due to activation of mainly large conductance Ca-dependent K channels (BK) and additionally delayed rectifier K channels. Moreover, another type of delayed rectifier K channels and early inactivating K channels may also contribute to some of the functional roles shown above. Although activation of Ca-dependent Cl channels in response to agonists depolarizes the cell membrane in several types of smooth muscle cells, a single channel current has not been identified. Ca-dependent K and Cl currents can be regulated by intracellular Ca store sites, which may be exhausted after a large release induced by inositol 1,4,5-trisphosphate or caffeine. The Ca-pump activity in the store sites may also regulate indirectly but strongly the activity of the channels and consequently membrane excitability.

Transcribing chromatin is not preferentially enriched with acetylated histones.

Chromatin fragments of the RNA polymerase II-transcriptional complex were purified from the micrococcal nuclease digest of rat liver nuclei in the presence of n-butyrate, a potent histone deacetylase inhibitor. Polyacrylamide gel electrophoretic analysis in Triton acid-urea revealed that the extent of histone acetylation of the complex did not differ markedly from that of the total chromatin.