A mathematical model for the first derivative wave analysis of the volumetric capnogram from the perspective of erythrocyte motion profiles.

Current trends in monitoring system are leading to the adoption of volumetric capnogram (Vcap). The first derivative wave analysis (FDWA) of Vcap represented the cardiogenic oscillations (CarO) as a propagated wave and the slope of phase III (SIII) as a constant. Until today the genesis of CarO and SIII is however under debate. In this study, we defined motion profiles of erythrocytes in the pulmonary parenchyma as pulsated-run and random-walk, on the basis of which we obtained a new mathematical expression describing FDWA of Vcap. The mathematical model of Vcap provided theoretical explanation concerned with motion profiles of erythrocytes about the genesis of CarO and SIII. As the results, the mathematical model predicted the close relationship between SIII and the transfer factor of carbon monoxide, which will be used for estimating validity of this mathematical model. In addition, the velocity of propagated wave in the phase III was suggested as a new physiological variable to estimate elastic properties of pulmonary arterioles, and a new measuring method of VD was proposed based on the theoretical reason, as well. Clinical investigations of the new VD to test its efficacy of monitoring are needed.

[Primary Spontaneous Pneumothorax with an Azygos Lobe].

A-21-year old man presented with dyspnea and a chest radiograph showed a right pneumothorax. Chest computed tomography revealed a collapsed lung and floating membrane, which was the lowermost part as a tear-shaped shadow. After the chest tube was inserted and surgical management was performed using a video-assisted thoracoscopic approach. At surgery, the visceral and parietal layers of pleura forming the mesoazygos were not fused, and azygos vein had a partial mobility. There was no adhesion between an upper lobe and visceral pleura. A stapling bullectomy was performed. The azygos lobe is a common malformation and has a reported incidence of 0.05~0.4% on health screening. The presence of an azygos lobe is usually assumed to be of no significance. We report a case and discuss the problems that it posed for surgical management.

[Bilateral Pneumothorax due to Pulmonary Metastasis from Angiosarcoma of the Forehead；Report of a Case].

Angiosarcoma is rare but highly malignant tumor arising from vascular endothelial cells. A 85-year-old man with difficulty in breathing for 3 days was referred to our hospital. He had a history of angiosarcoma of forehead 4 months before. A chest computed tomography (CT) scan showed left pneumothorax with multiple cystic changes and ground grass attenuations of bilateral lungs, which had obviously increased in recent 2 months. Pulmonary metastases with secondary pneumothorax was highly suspected by the serial CT findings. He was treated with tube thoracostomy and the instillation of a sclerosing agent (minocycline hydrochloride 200 mg). Seven weeks after his initial presentation, he died from obstructive pneumonia and an autopsy was held. Histologic examinations revealed that the tumor foci were peripheral, multiple and generally formed nodules. These cells were cluster differentiation (CD)31 and CD34 positive and negative for calretinin, cytokeratin, carcinoembryonic antigen (CEA), thyroid transcription factor (TTF-1) and epithelial membrane antigen (EMA). These findings were compatible with pulmonary metastases of angiosarcoma of forehead.

Pleural vasculitides of microscopic polyangiitis with asbestos-related plaques.

A 69-year-old man who had been exposed to asbestos for approximately 40 years presented with the complaint of fever and pleuritic chest pain on the right side on deep inspiration. Chest X-ray films showed pleural effusion in the right side. Initial antibiotic treatment was ineffective. The hyaluronic acid level was high in the pleural effusion but no malignant mesotheliomal cells were seen with blind pleural biopsy. Blood chemistry showed a remarkable high titer of myeloperoxidase anti-neutrophil cytoplasmic antibody (MPO-ANCA) and open renal biopsy suggested crescentic glomerulonephritis. The precise pathological examination on the pleura obtained by the open pleural biopsy showed vasculitides and plaque leading to diagnosis of microscopic polyangiitis (MPA). This is a rare case of MPA seen in the pleural arteries.

[A New Method of Analyzing the Closing Volume (CV) Curve: "N2 First Derivative Wave Method"].

Evaluation of the lung function involves the measurement of many factors. The closing volume (CV) curve is clinically important as an index of uneven alveolar ventilation and airway closure. Although conventional methods for CV measurement are usually based on the pattern of the exhaled nitrogen (N2) concentration curve with respect to the lung volume, it is often difficult to measure the steep pattern of patients with chronic obstructive pulmonary disease (COPD). In this paper, we proposed a new method called the "N2 first derivative (fdN) wave method" for measuring CV. The N2 concentration of the CV curve was transformed to a derivative with respect to the lung volume, which revealed the existence of cardiogenic oscillations. Discrimination between phases III and IV was straightforward based on the difference in the slope or in the amplitude of oscillations of the fdN wave. Our new method was able to distinguish phase IV from phase III using the difference in amplitude of the oscillation of the fdN wave even in the presence of COPD with steep patterns of the CV curve. Close relationships were seen among normal subjects including COPD patients in both the slope of the alveolar plateau (ΔN2) and the CV values measured with the conventional and new methods. In conclusion, the new method we propose in this paper was able to provide measurements of CV for all subjects including those with COPD. [Original]

Multiple cytokines-producing pleomorphic carcinoma of lung with metastasis to the small intestine.

A 58-year-old man underwent upper lobectomy for primary pleomorphic carcinoma of the lung. Nine months later, the pleomorphic carcinoma was recurred with marked peripheral leukocytosis and an elevated C-reactive protein. Chest and abdominal computed tomography (CT) revealed enlarged mediastinal lymph nodes and a bulky tumor in the small intestine. An enterectomy was performed and the intestinal tumor was removed. Immunostaining revealed tumor cells positive for G-CSF and TNF-α as well as an increased level of serum G-CSF and TNF-α. We describe a rare case of G-CSF and TNF-α producing pleomorphic carcinoma of the lung with metastasis to the small intestine.

Biologically variable respiration as a stochastic process in ventilation - a stochastic model study.

Based on the fractal bronchial tree, we introduced a function of "asynchronous phasic contractions of lobular bronchiole", which would generate fluctuations in tidal volumes. Stochastic control theory was able to describe a genesis of biological variability in spontaneous respirations using a Schroedinger wave function.

Cell shrinkage evoked by Ca2+-free solution in rat alveolar type II cells: Ca2+ regulation of Na+-H+ exchange.

The effects of intracellular Ca2+ concentration, [Ca2+]i, on the volume of rat alveolar type II cells (AT-II cells) were examined. Perfusion with a Ca2+-free solution induced shrinkage of the AT-II cell volume in the absence or presence of amiloride (1 microm, an inhibitor of Na+ channels); however, it did not in the presence of 5-(N-methyl-N-isobutyl)-amiloride (MIA, an inhibitor of Na+-H+ exchange). MIA decreased the volume of AT-II cells. Inhibitors of Cl(-)-HCO3- exchange, 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS) and 4-acetamido-4'-isothiocyanatostilbene-2,2'-disulfonic acid (SITS) also decreased the volume of AT-II cells. This indicates that the cell shrinkage induced by a Ca2+-free solution is caused by a decrease in NaCl influx via Na+-H+ exchange and Cl(-)-HCO3- exchange. Addition of ionomycin (1 microm), in contrast, induced cell swelling when AT-II cells were pretreated with quinine and amiloride. This swelling of the AT-II cells is not detected in the presence of MIA. Intracellular pH (pHi) measurements demonstrated that the Ca2+-free solution or MIA decreases pHi, and that ionomycin increases it. Ionomycin stimulated the pHi recovery after an acid loading (NH4+ pulse method), which was not noted in MIA-treated AT-II cells. Ionomycin increased [Ca2+]i in fura-2-loaded AT-II cells. In conclusion, the Na+-H+ exchange activities of AT-II cells, which maintain the volume and pHi, are regulated by [Ca2+]i.

Delayed shrinkage triggered by the Na+-K+ pump in terbutaline-stimulated rat alveolar type II cells.

Terbutaline (10 microm) induced a triphasic volume change in alveolar type II (AT-II) cells: an initial shrinkage (initial phase) followed by cell swelling (second phase) and a gradual shrinkage (third phase). The present study demonstrated that the initial and the third phases are evoked by the activation of K+ and Cl- channels and the second phase is evoked by the activation of Na+ and Cl- channels. Ouabain blocked the third phase, although it did not block the initial and second phases. This suggests that the third phase is triggered by the Na+-K+ pump. Tetraethylammonium (TEA, a K+ channel blocker) decreased the volume of AT-II cells and enhanced the terbutaline-stimulated third phase, although quinidine, another K+ channel blocker, increased the volume of AT-II cells. The TEA-induced cell shrinkage was inhibited by ouabain, suggesting that TEA increases Na+-K+ pump activity. Ba2+, 2,3-diaminopyridine and a high [K+]o (30 mm) similarly decreased the volume of AT-II cells. These findings suggest that depolarization induced by TEA increases Na+-K+ pump activity, which increases [K+]i. This [K+]i increase, in turn, hyperpolarizes membrane potential. Valinomycin (a K+ ionophore), which induces hyperpolarization, decreased the volume of AT-II cells and enhanced the third phase in these cells. In conclusion, in terbutaline-stimulated AT-II cells, an increase in Na+-K+ pump activity hyperpolarizes the membrane potential and triggers the third phase by switching net ion transport from NaCl entry to KCl release.

Beta 2-adrenergic regulation of ciliary beat frequency in rat bronchiolar epithelium: potentiation by isosmotic cell shrinkage.

Single bronchiolar ciliary cells were isolated from rat lungs. The beta(2)-adrenergic regulation of ciliary beat frequency (CBF) was studied using video-optical microscopy. Terbutaline (a beta(2)-adrenergic agonist) increased CBF in a dose-dependent manner, and it also decreased the volume of the ciliary cells. These terbutaline actions were inhibited by a PKA inhibitor (H-89) and mimicked by forskolin, IBMX and DBcAMP. Ion transport inhibitors were used to isosmotically manipulate the volume of the terbutaline-stimulated bronchiolar ciliary cells. Amiloride (1 microM) and bumetanide (20 microM) potentiated cell shrinkage and the CBF increase, and they shifted the terbutaline dose-response curve to the lower-concentration side. Quinidine (500 microM), in contrast, increased cell volume and suppressed the CBF increase. Moreover, a KCl solution containing amiloride (1 microM) and strophanthidin (100 microM) increased cell volume and suppressed the CBF increase, and then the subsequent removal of either amiloride or strophanthidin decreased cell volume and further increased CBF. NPPB (10 microM) or glybenclamide (200 microM) had no effect on the action of terbutaline. Thus, in terbutaline-stimulated ciliary cells, cell shrinkage enhances the CBF increase; in contrast, cell swelling suppresses it. However, the results of direct manupulation of cell volume by applying osmotic stresses (hyperosmotic shrinkage or hyposmotic swelling) were the opposite of the findings of the isosmotic experiments: hyposmotic cell swelling enhanced the CBF increase, while isosmotic swelling suppressed it. These results suggest that isosmotic and non-isosmotic volume changes in terbutaline-stimulated bronchiolar ciliary cells may trigger different signalling pathways. In conclusion, terbutaline increases CBF and decreases the volume of rat bronchiolar ciliary cells via cAMP accumulation under isosmotic conditions, and the isosmotic cell shrinkage enhances the CBF increase by increasing cAMP sensitivity.

Thymic carcinoma presenting as cranial metastasis with intradural and extracranial extension: case report.

OBJECTIVE AND IMPORTANCE: Thymic carcinoma is an uncommon malignant tumor that is different from thymoma. Cranial and brain metastases from this tumor are extremely rare. We report a thymic carcinoma with cranial metastasis and discuss the behavior of this tumor. CLINICAL PRESENTATION: A 50-year-old man presented with headache and a palpable scalp tumor. Computed tomographic scans and magnetic resonance images revealed an osteolytic tumor with intradural and extracranial extension in the right occipital bone. INTERVENTION: After gross total resection and histological diagnosis, further investigation revealed a primary thymic tumor in the anterior upper mediastinum and liver metastases. The patient received multiple-cycle chemotherapy (cisplatin and gemcitabine) for primary and metastatic lesions. CONCLUSION: Thymic carcinoma has a poor prognosis because of a high degree of malignancy, early metastasis, and delayed diagnosis. Thus, treatment of a patient with this tumor calls for prompt diagnosis, surgical treatment, and optimal adjuvant therapy.

Terbutaline-induced triphasic changes in volume of rat alveolar type II cells: the role of cAMP.

Changes in the volume of rat alveolar type II cells (AT-II cells) induced by terbutaline, a beta(2)-agonist, were measured using video-enhanced contrast microscopy. The changes consisted of three phases: initial cell shrinkage, cell swelling, and gradual cell shrinkage. The initial cell shrinkage was Ca(2+)-dependent and was inhibited by quinine (a K+ channel blocker). The subsequent cell swelling was cAMP-dependent and was inhibited by amiloride (a Na+ channel blocker). The final cell shrinkage was cAMP-dependent and was inhibited by 5-nitro-2-(3-phenylpropylamino)-benzoate (NPPB, a Cl- channel blocker). Thus, terbutaline-induced cell volume changes were regulated by both Ca2+ and cAMP. Accumulation of cAMP alone, however, induced the Ca2+ -dependent cell shrinkage of AT-II cells and H-89 (a PKA inhibitor) inhibited terbutaline-induced cell volume changes. This suggests that cAMP accumulation stimulates the Ca2+ signal during terbutaline stimulation. In conclusion, terbutaline stimulates not only Na+ influx, but also K+ and Cl- release mediated via cAMP accumulation in rat AT-II cells, which induces the triphasic cell volume changes.