A Case of Paraplegia Treated with Cerebrospinal Fluid Drainage and Permissive Hypertension after Graft Replacement of the Ascending Aorta and the Total Aortic Arch for Acute Aortic Dissection Stanford Type A

Paraplegia after an operation for acute aortic dissection Stanford type A (AADA) is fairly uncommon, and there is no consensus about optimal treatment. We present a case in which cerebrospinal fluid drainage (CSFD) and permissive hypertension were used for treatment of paraplegia. When the patient showed complete bilateral paraplegia after operation for AADA, we immediately began CSFD and maintained mean arterial blood pressure at over 90 mmHg. His neurological deficit gradually recovered, and he was eventually able to walk without support. The combination of CSFD and permissive hypertension could be a first-line emergent treatment for postoperative paraplegia after AADA surgery

Role of the Transcription Factor BTB and CNC Homology 1 in a Rat Model of Acute Liver Injury Induced by Experimental Endotoxemia

Hepatic oxidative stress plays an important role in the pathogenesis of several acute liver diseases, and free heme is thought to contribute to endotoxemia-induced acute liver injury. The heme oxygenase 1 (HO-1) gene is upregulated and the δ-aminolevulinate synthase (ALAS1) gene is downregulated in the rat liver following lipopolysaccharide (LPS) treatment. BTB and CNC homology 1 (Bach1) is a heme-responsive transcription factor that normally represses HO-1 expression. In this study, we evaluated the changes in HO-1, ALAS1, and Bach1 expression and nuclear Bach1 expression in rat livers following intravenous LPS administration (10 mg/kg body weight). LPS significantly upregulated HO-1 mRNA and downregulated ALAS1 mRNA in the rat livers, suggesting that hepatic free heme concentrations are increased after LPS treatment. Bach1 mRNA was strongly induced after LPS injection. In contrast, nuclear Bach1 was significantly but transiently decreased after LPS treatment. Rats were also administered hemin (50 mg/kg body weight) intravenously to elevate heme concentrations, which decreased nuclear Bach1 levels. Our results suggest that elevated hepatic free heme may be associated with a decline of nuclear Bach1, and induction of Bach1 mRNA may compensate for the decreased nuclear Bach1 after LPS treatment in the rat liver

Protective effect of tin chloride on rhabdomyolysis-induced acute kidney injury in rats

The heme component of myoglobin plays a crucial role in the pathogenesis of rhabdomyolysis-associated acute kidney injury (RM-AKI). Heme oxiganenase-1 (HO-1) is the rate-limiting enzyme of heme catabolism, and its metabolites, iron, biliverdin, and carbon monoxide, have antioxidant properties. Tin chloride (SnCl2) is a kidney specific HO-1 inducer. In this study, we examined whether the induction of HO-1 in the kidney by SnCl2 pretreatment ameliorates RM-AKI in rats and if the effect is due to the degradation of excess renal free heme. We developed an RM-AKI rat (male Sprague-Dawley rats) model by injecting glycerol (Gly) in the hind limbs. RM-AKI rats were pretreated with saline or SnCl2 or additional SnMP (tin mesoporphyrin, a specific HO inhibitor) followed by Gly treatment. Serum blood urea nitrogen (BUN) and creatinine (Crea) were measured as indicators of renal function. Renal free heme level was assessed based on the levels of delta-aminolevulinate synthase (ALAS1), a heme biosynthetic enzyme, and nuclear BTB and CNC homology 1 (Bach1), an inhibitory transcription factor of HO-1. Elevated free heme levels lead to decreases in ALAS1 and nuclear Bach1. After 24 h of Gly injection, serum BUN and Crea levels in saline-pretreated rats were significantly higher than those in untreated control rats. In contrast, SnCl2-pretreated rats showed no significant increase in the indices. However, additional treatment of SnMP abolished the beneficial effect of SnCl2. Renal ALAS1 mRNA levels and renal nuclear Bach1 protein levels in the saline pretreated rats were significantly lower than those in control rats 3 h after Gly injection. In contrast, the levels in SnCl2-pretreated rats were not altered. The findings indicate that SnCl2 pretreatment confers protection against RM-AKI by virtue of HO-1 induction in the renal system, at least in part through excess free heme degradation

VENTRICULAR ENLARGEMENT AND WATER INTOXICATION IN SCHIZOPHRENIA

To determine the extent to which atrophy was related to water intoxication in schizophrenic patients, ventricular enlargement in polydipsic schizophrenic patients with hyponatremia and schizophrenic controls without hyponatremia was measured in a linear way. Ventricular enlargement was found in both schizophrenic patient groups, and larger ventricles were associated with water intoxication. It is suggested that ventricular enlargement may reflect a developmental or degenerative pathological process involving the occurrence of water intoxication in schizophrenia

エンチュウ タイショウセイ オ ユウスル POINCARE ゲージ リロン ノ ゲンミツカイ

この論文において我々は, 複素Einstein-Yang-Mills理論に帰着し得るPoincareゲージ理論の一つのモデルを取り上げ, 円柱対称性の仮定の下に, 通常のEinstein-Maxwell(EM)理論における軸対称解の解法を応用して, Poincareゲージ理論のーつの厳密解が得られることを示す。また, 我々の求めた解は, 特別な場合として通常のEM理論においてMelvin解として知られる厳密解を含むことを示す。In this paper we consider a model of Poincare gauge theory which is reducible to the complex Einstein-Maxwell (CEM) theory via the complex Einstein-Yang-Mills theory, and investigate the possibility of exact solutions under the condition of cylindrical symmetry. In this purpose we apply a method by which one has gotten some solutions for the ordinary Einstein-Maxwell (OEM) theory. As a result, we get a general solution which includes Melvin solution known in OEM theory

Dynamic changes in Bach1 expression in the kidney of rhabdomyolysis-associated acute kidney injury.

Free heme, a pro-oxidant released from myoglobin, is thought to contribute to the pathogenesis of rhabdomyolysis-associated acute kidney injury (RM-AKI), because renal overexpression of heme oxygenase-1 (HO-1), the rate-limiting enzyme in heme catabolism, confers protection against RM-AKI. BTB and CNC homology 1 (Bach1) is a heme-responsive transcription factor that represses HO-1. Here, we examined the changes with time in the gene expression of Bach1, HO-1, and δ-aminolevulinate synthase (ALAS1, a heme biosynthetic enzyme) in the rat kidney using an RM-AKI model induced by the injection of 50% glycerol (10 mL/kg body weight) into bilateral limbs. We also examined the protein expression of Bach1 in the nucleus and cytosol, and HO-1 in the rat kidney. Glycerol treatment induced significant elevation of serum creatinine kinase and aspartate aminotransferase levels followed by the marked elevation of serum blood urea nitrogen and creatinine levels, which caused serious damage to renal tubules. Following glycerol treatment, HO-1 mRNA and protein levels were significantly up-regulated, while ALAS1 mRNA expression was down-regulated, suggesting an increase in the free renal heme concentration. The Bach1 mRNA level was drastically increased 3 h after glycerol treatment, and the increased level was maintained for 12 h. Nuclear Bach1 protein levels were significantly decreased 3 h after treatment. Conversely, cytosolic Bach1 protein levels abruptly increased after 6 h. In conclusion, we demonstrate the dynamic changes in Bach1 expression in a rat model of RM-AKI. Our findings suggest that the increase in Bach1 mRNA and cytosolic Bach1 protein expression may reflect de novo Bach1 protein synthesis to compensate for the depletion of nuclear Bach1 protein caused by the induction of HO-1 by free heme

Oxygen Permeability through Silicone Liquid Membranes

小特集：膜工