Recurrent pulmonary edema associated with obstructive sleep apnea syndrome]

A 70-year-old non-obese man with no history of cardiopulmonary disease presented 4 times to the emergency room because of sudden onset of seizure during sleep. Each time he recovered within a few hours without any medication. Nocturnal polysomnographic recording revealed severe obstructive sleep apnea syndrome (OSAS, AHI 52.4/Hr). Nasal continuous positive airway pressure (n-CPAP) therapy was performed with 10cmH2O of pressure. His symptoms of severe daytime sleepiness and seizure were diminished. CPAP was decreased from 10cmH2O to 6 cmH2O later, because the patient complained with its high pressure. He then felt daytime sleepiness and suffered seizures during sleep again, and was re-admitted to our hospital. Chest roentgenogram taken at this admission showed remarkable pulmonary edema. We found that the pulmonary edema was recognized every time on his chest roentgenogram taken when he complained seizure. In addition, subsequesnt roentgenograms also showed that the pulmonary edema was diminished soon. On the other hand, his AHI was high (24.7/hr) even when he was under 6cmH2O of n-CPAP. We concluded that incompletely treated OSAS might lead not only to pulmonary edema, but also to seizures in this patient.     

Rationale and design of a large-scale trial using atrial natriuretic peptide (ANP) as an adjunct to percutaneous coronary intervention for ST-segment elevation acute myocardial infarction: Japan-Working groups of acute myocardial infarction for the reduction of Necrotic Damage by ANP (J-WIND-ANP).

BACKGROUND: The benefits of percutaneous coronary intervention (PCI) in acute myocardial infarction (AMI) are limited by reperfusion injury. In animal models, atrial natriuretic peptide (ANP) reduces infarct size, so the Japan-Working groups of acute myocardial Infarction for the reduction of Necrotic Damage by ANP (J-WIND-ANP) designed a prospective, randomized, multicenter study, to evaluate whether ANP as an adjunctive therapy for AMI reduces myocardial infarct size and improves regional wall motion. METHODS AND RESULTS: Twenty hospitals in Japan will participate in the J-WIND-ANP study. Patients with AMI who are candidates for PCI are randomly allocated to receive either intravenous ANP or placebo administration. The primary end-points are (1) estimated infarct size (Sigmacreatine kinase and troponin T) and (2) left ventricular function (left ventriculograms). Single nucleotide polymorphisms (SNPs) that may be associated with the function of ANP and susceptibility of AMI will be examined. Furthermore, a data mining method will be used to design the optimal combinational therapy for post-MI patients. CONCLUSIONS: J-WIND-ANP will provide important data on the effects of ANP as an adjunct to PCI for AMI and the SNPs information will open the field of tailor-made therapy. The optimal therapeutic drug combination will also be determined for post-MI patients.     

alpha1-Adrenergic receptor in rat ovary: presence and localization

Noradrenaline modulates ovarian steroidogenesis, stimulates ovulation, and probably promotes follicular development in the ovary. It has been suggested that these effects of noradrenaline are mediated by - and/or β-adrenergic receptors (ARs) in the ovary. The purpose of the present study was to examine whether ₁-AR is present in the rat ovary. In Western blotting, antibody against ₁-ARs recognized a major protein in the ovary of adult (10-week-old) rats with a molecular weight of 80 kDa, which is similar to that of the _1B-AR subtype. Immunohistochemistry using this antibody showed that ₁-AR was detected at various sites in the ovary, including large antral follicle, germinal epithelium at the circumference of large antral follicle, corpus luteum, and interstitial tissue. These results confirm that the ovary contains ₁-AR (probably _1B-subtype), and suggest that this receptor mediates some of the activities of noradrenaline in the regulation of ovarian functions. Furthermore, we found that ₁-AR is present in oocyte of large antral follicle, suggesting that noradrenaline acts on oocyte via this receptor.     

Parathyroid cell growth in patients with advanced secondary hyperparathyroidism: vitamin D receptor, calcium sensing receptor, and cell cycle regulating factors

The parathyroid gland (PTG) is a unique endocrine organ in which the quiescent glandular cells begin to proliferate in response to the demand for maintaining calcium (Ca) homeostasis in the progressive course of renal failure, leading to secondary hypereparathyroidism (SHPT). SHPT is characterized with continuous over-secretion of parathyroid hormone (PTH) and high turn-over bone disease, osteitis fibrosa, and the major factors include a deficiency of active vitamin D, hypocalcemia, and phosphate retention. With long-term end-stage renal failure, SHPT becomes resistant to conventional medical treatment such as phosphate binders and active vitamin D supplementation, and the growth of the PTG accelerates with the pattern of hyperplasia changing from diffuse to nodular type. In this process, the sigmoid curve between extracellular Ca concentration (exCa) and the plasma level of PTH shifts to the upper-rightward, indicating both an absolute increase in PTH secretion and the resistance of PT cells to exCa. Many experimental and human studies have revealed down-regulation of vitamin D receptor (VDR), calcium-sensing receptor (CaSR), and retinoid X receptor (RXR) in PT cells. The sustained proliferation of PT cells after obtaining autonomicity is another characteristic feature of SHPT. In this context, it has been demonstrated that the cell cycle is markedly progressed, where the expression of cyclin-dependent kinase inhibitor (CDKI), p21 and p27, is depressed in a VDR-dependent manner. These pathological features are most evident in nodular hyperplasia, in which monoclonal proliferation is obvious, indicating the phenotypic changes have occured in PT cells. It has been observed by Fukagawa and colleagues that pharmacologically high dose of active vitamin D administered orally can cause small-size PTG hyperplasia to regress in patients with advanced SHPT. Successful renal transplantation may also restore VDR and CaSR expressions in the diffuse type, in association with increasing TUNEL-positive cells. Thus, it is important to vigorously treat SHPT when the PT cell proliferation is in the reversible stage of diffuse hyperplasia.     

Esophageal intramural spreading from an adenocarcinoma of the esophagogastric junction

Although intramural spreading from gastric carcinoma to the esophageal wall is occasionally reported, longitudinal intramural lesion of the esophagus is very rare. We herein report the case of a patient found to have a carcinoma of the gastric cardia with intramural spreading to the esophagus approximately 7.0 cm in length. A 65-year-old man was admitted to our department suffering from a persistent midthoracic pain and mild dysphagia during the previous 3 months. Upper gastrointestinal studies revealed an oval submucosal tumor of the lower esophagus and a flare irregular lesion on the esophagogastric junction. An endoscopic ultrasonography showed the main tumor was in the submucosal layer and invaded beyond the muscularis propria. Histopathological examination of the resected specimen confirmed a poorly differentiated adenocarcinoma, 7.0 cm in length, which penetrated through the gastric wall, and invaded the submucosal layer of the esophagus. When only a few scattered carcinoma cells infiltrate only the mucosa or submucosa, it is difficult to diagnose the extent of esophageal invasion. In treating patients with gastric cancer with esophageal invasion, it is important to determine the safety of the proximal margin for esophageal resection. Histological examination using frozen sections obtained during surgery is essential for deciding the operative safety margin.     

Two cases of lupus cystitis with no bladder irritation symptoms

Lupus cystitis is a rare manifestation in systemic lupus erythematosus (SLE); it usually occurs in association with gastrointestinal manifestations. We report two cases of lupus cystitis without bladder irritation symptoms. Both cases developed severe abdominal pain, nausea, and diarrhea and showed no bladder irritation symptoms. The diagnosis of lupus cystitis was made by abdominal ultrasonography and bladder biopsy. The patients were treated with intravenous methylprednisolone pulse therapy followed by oral prednisolone. Their symptoms were ameliorated, and hydroureteronephrosis improved. Thus, when a patient with SLE shows gastrointestinal symptoms, further examinations are required to determine whether the patient has lupus cystitis.     

Ionic mechanisms underlying region-specific remodeling of rabbit atrial action potentials caused by intermittent burst stimulation.

BACKGROUND: Pulmonary veins (PVs) and the coronary sinus (CS) play pivotal roles in triggering some episodes of atrial fibrillation. In isolated rabbit right or left atrial preparations, a 3-hour intermittent burst pacing protocol shortens action potential duration (APD) in CS and PV, but not in sinus node (SN) and left Bachmann bundle (BB) regions. OBJECTIVE: The purpose of this study was to use patch clamp techniques to study the rapidly inactivating (I(to)) and sustained (I(sus)) K(+) currents as well as Ca(2+) currents (I(Ca)) in cells dispersed from intermittent burst pacing and sham PV, BB, CS, and SN regions to determine whether changes in these currents contributed to APD shortening. METHODS: Real-time polymerase chain reaction was performed for transient outward K(+) and Ca(2+) channel subunit mRNAs to determine if intermittent burst pacing affected expression levels. RESULTS: I(to) densities were unaffected by intermittent burst pacing in PV and Bachmann bundle cells. mRNA levels of K(V)4.3, K(V)4.2, K(V)1.4, and KChIP2 subunits of I(to) in both regions were stable. In CS cells, I(to) densities in intermittent burst pacing were greater than in sham (P <.05), but there were no parallel mRNA changes. I(Ca) density of PV cells was reduced from 14.27 +/- 2.08 pA/pF (at -5 mV) in sham to 7.52 +/- 1.65 pA/pF in intermittent burst pacing PV cells (P <.05) due to a significant shift in voltage dependence of activation. These results were seen in the absence of mRNA changes in alpha(1C) and alpha(1D) Ca(2+) channel subunits. In contrast, intermittent burst pacing had no effect on Ca(2+) current densities and kinetics of CS cells, but decreased alpha(1)C and alpha(1)D mRNA levels. CONCLUSION: There is region-specific remodeling of I(to) and I(Ca) by intermittent burst pacing protocols in rabbit atrium. Increased I(to) in CS cells could account for the APD shortening observed with intermittent burst pacing, whereas an intermittent burst pacing-induced shift in voltage dependence of activation may contribute to APD shortening in PV cells.     

Elevation of serum thioredoxin levels in patients with nonalcoholic steatohepatitis.

Thioredoxin (TRX) is induced by many oxidative stresses. Serum TRX levels were significantly elevated in nonalcoholic steatohepatitis (NASH) patients, as compared to simple fatty liver (FL) patients or healthy controls. Serum TRX levels in NASH patients were significantly correlated with serum ferritin levels, but not with other variables. Removal of hepatic excess iron by phlebotomy significantly decreased the serum levels of TRX and ALT in NASH patient. Therefore, the pathogenesis of NASH may be associated with iron-related oxidative stress. The serum TRX level is a parameter for discriminating NASH from FL.     

Electromyographic activity of human triangularis sterni muscles during thoracic rotation]

The triangularis sterni muscles (TS) have been recognized as expiratory muscles, but there is no information on their postural activity or their phasic electromyographic (EMG) activity during thoracic rotation. We examined the EMG activity of the right TS using fine-wire electrodes, in 5 healthy male subjects. With subjects breathing through a mouthpiece, airflow, raw and moving-averaged EMG signals were sampled with a computer during thoracic rotation and resting, accompanied by breathing with or without voluntary thoracic rotation. Maximum EMG (EMGmax) was defined as the greatest moving-averaged EMG activity recorded from each subject during the slow expiratory maneuver from functional residual capacity to residual volume. With leftward thoracic rotation without breathing, the tonic EMG activity of the right TS was observed in all subjects. During resting breathing without thoracic rotation, there were respiration-related phasic activities on TS EMG during expiration in all subjects. With leftward thoracic rotation, the respiration-related phasic activities on TS EMG significantly increased from 8.2 +/- 3.5 (mean +/- SE) %EMGmax to 15.2 +/- 6.1 %EMGmax. On the other hand, with rightward thoracic rotation, it decreased to 3.0 +/- 1.0 %EMGmax. We concluded that 1) TS has a postural function like that of the intercostal muscles, and that 2) the respiratory function of TS is affected by thoracic rotation.