A study of five cases of traumatic diaphragmatic rupture

During the last 5 years, 5 cases of traumatic diaphragmatic rupture were surgically treated. These cases were reported and the literature concerning traumatic diaphragmatic hernia in the last one decade in Japan, including 80 cases was studied. The purpose of this study is to discuss the most important early diagnostic tools and to consider the choice of incision and approach. The following two results were gotten. (1) Plain chest X-ray, computed tomography and ultrasonography were the most valuable diagnostic tools. (2) The choice of incision and approach depends on the stage at which the rupture is recognized (early or late), the site of rupture and associate injuries.     

Amlodipine-induced reduction of oxidative stress in the brain is associated with sympatho-inhibitory effects in stroke-prone spontaneously hypertensive rats.

Amlodipine is a dihydropyridine calcium channel blocker that is widely used for the treatment of hypertensive patients and has an antioxidant effect on vessels in vitro. The aim of the present study was to examine whether treatment with amlodipine reduced oxidative stress in the brains of stroke-prone spontaneously hypertensive rats (SHRSP). The animals received amlodipine, nicardipine or hydralazine for 30 days in their drinking water. Levels of thiobarbituric acid-reactive substances (TBARS) in the brain (cortex, cerebellum, hypothalamus, and brainstem) were measured before and after each treatment. Systolic blood pressure decreased to similar levels in the amlodipine-, nicardipine-, and hydralazine-treated groups. Urinary norepinephrine excretion was significantly reduced in SHRSP after treatment with amlodipine, but not with nicardipine or hydralazine. Levels of TBARS in the cortex, cerebellum, hypothalamus, and brainstem were significantly higher in SHRSP than in Wistar-Kyoto rats (WKY), and were reduced in amlodipine-treated, but not in nicardipine- or hydralazine-treated, SHRSP. Electron spin resonance spectroscopy revealed increased levels of reactive oxygen species in the brains of SHRSP, which were reduced by treatment with amlodipine. Intracisternal infusion of amlodipine also reduced systolic blood pressure, urinary norepinephrine excretion, and the levels of TBARS in the brain. These results suggested that oxidative stress in the brain was enhanced in SHRSP compared with WKY rats. In addition, antihypertensive treatment with amlodipine reduced oxidative stress in all areas of the brain examined and decreased blood pressure without a reflex increase in sympathetic nerve activity in SHRSP.     

Right ventricular thrombosis due to familial heparin cofactor II deficiency

This case report was with regard to familial heparin cofactor II (HC II) deficiency. The patient was a 14-years-old female, having complaints of chest pain, fever and swelling of right lower extremity. Echocardiography and DSA showed a pediculated mass at the right ventricular outflow tract which highly suggested a ventricular myxoma. At surgery, a large pediculated thrombus was removed from the RV conus septum aun pulmonary valve. The mass was identified as thrombus by histological examination. Two months later, the RV thrombi recurred with additional pulmonary embolus to the left lung. HC II was discovered by hemo-coagulation tests. Her HC II antigen value was 48%, and 32% on repeat study. Her brother's HC II antigen value was 53%. At reoperation, small thrombi less than phi 10 mm, were removed from the RV outflow tract and pulmonary valve. Fresh frozen plasma was given and intravenous urokinase therapy was taken. She is doing well with therapy of oral warfarin, aspirin and ticlopidine for anticoagulation.     

Aneurysms of the anterior communicating artery and subclavian artery in association with congenital absence of unilateral internal carotid artery]

We encountered a rare case of unilateral internal carotid arterial defect complicated with anterior communicating aneurysm and subclavian artery aneurysm. The patient was a 56-year-old man in whom cerebral angiography and 3D-CTA revealed defects in the right internal carotid artery and the right carotid canal, and an unruptured aneurysm in the anterior communicating artery. In addition, the patient was also found to have an unruptured aneurysm in the right subclavian artery. As both the aneurysms were considered to have a high risk of rupture and such subclavian aneurysms were likely to cause an embolism, radical surgery was performed for each aneurysm. The postoperative course was uneventful, and the patient was discharged without ambulatory limitations. Although the defect in the internal carotid artery is a relatively rare vascular deformity, the incidence of cerebral aneurysm is about 30% in such cases due to the marked hemodynamic stress involved. On the other hand, there have been only two previous case reports of internal carotid arterial defect complicated with a subclavian aneurysm. Moreover, there have been no previous reports of internal carotid arterial defect complicated with both an intracranial aneurysm and a subclavian aneurysm, as observed in the present case. Thus, this case was very rare and is reported here.     

INTRAOPERATIVE BLEEDING IN ENDOSCOPIC SUBMUCOSAL DISSECTION IN THE STOMACH AND STRATEGY FOR PREVENTION AND TREATMENT

To control intraoperative bleeding is an important key to successful endoscopic submucosal dissection. The distribution of submucosal vessels encountered during the procedure differ in places in the stomach and are roughly categorized into three groups: those located in the antrum, those in the lesser curvature, and those on the anteroposterior corpus wall which consists of oblique muscle layers. Therefore, knowledge of a suitable setting of diathermy and adjusted depth of dissection in the submucosal layer for each site is imperative. The combination of utilizing the distal attachment forced or swift coagulation (trimming with coagulation mode) have enable the treatment with an insulation tipped knife safer.     

MANAGEMENT TO PREVENT BLEEDING DURING ENDOSCOPIC SUBMUCOSAL DISSECTION USING THE FLUSH KNIFE FOR GASTRIC TUMORS

The gastric vasculature responsible for intraoperative bleeding in endosocpic submucosal dissection (ESD) is the ramified vascular network occupying the middle of the submucosal layer and large vessels penetrating the muscle layer. Appropriate management for these vessels must be addressed. The trimming of the ramified vascular network can be safely performed with coagulation mode following shallow mucosal cutting. A large penetrating vessel usually requires precoagulation prior to dissection. These procedures are effectively performed with the water jet short needle knife (Flush knife).     

STANDARD IMAGING TECHNIQUES OF ENDOSCOPIC ULTRASOUND‐GUIDED FINE‐NEEDLE ASPIRATION USING A CURVED LINEAR ARRAY ECHOENDOSCOPE

Standard imaging techniques using a curved linear array echoendocope are summarized to facilitate the attainment of expertise in endoscopic ultrasonography and endoscopic ultrasound‐guided fine needle aspiration, and to promote the widespread use of this diagnostic and therapeutic tool. Typical images of the mediastinal organs, the bilio‐pancreatic systems and neighboring organs by scanning from the esophagus, stomach, duodenal bulb, and descending portion of the duodenum, are shown in a sequential manner. The basic techniques of endoscopic ultrasound‐guided fine needle aspiration are also presented.     

Urine levels of CD46 (membrane cofactor protein) are increased in patients with glomerular diseases

Soluble membrane cofactor protein (MCP, CD46) has not been detected by conventional ELISA in human urine. Here, we established a highly sensitive assay method for determination of urinary MCP (uMCP) using monoclonal antibody-coated paramagnetic beads. This method enabled us to detect less than 0.05 ng/ml of purified membrane and recombinant soluble MCP, a sensitivity 10-fold higher than that of conventional ELISA. In normal subjects, the levels of uMCP were <0. 05 ng/ml. The levels of uMCP were elevated in patients with IgA nephropathy and more prominently in patients with rapidly progressive glomerulonephritis. The levels of uMCP were correlated significantly with those of serum MCP (sMCP) and N-acetyl-beta-glucosaminidase and nonsignificantly with those of beta(2)-microglobulin, total urine protein, or serum creatinine. The properties of uMCP were inconsistent with those of the reported sMCP, since uMCP showed three bands on SDS-PAGE/immunoblotting with molecular mass profiles different from those of sMCP. uMCP exhibited factor I cofactor activity for cleavage of C3b comparable to that of sMCP. The origin of uMCP, however, remains to be determined. These results, taken together with the parameter correlation profiles, suggested that uMCP is secreted or produced secondary to tubular or glomerular damage. The physiological role and clinical significance of uMCP are now within the scope of our investigation by establishment of this assay.     

Activation of brain neurons by circulating angiotensin II: direct effects and baroreceptor-mediated secondary effects

Circulating angiotensin II acts on neurons in circumventricular organs, leading to activation of central pathways involved in blood pressure regulation and body fluid homeostasis. Apart from this primary effect, an increase in the level of circulating angiotensin II may also activate brain neurons as a secondary consequence of the associated increase in blood pressure, which will stimulate arterial baroreceptors and thus activate central neurons that are part of the central baroreceptor reflex pathway. The aim of this study was to identify the population of neurons that are activated as a consequence of the direct actions of circulating angiotensin II on the brain, independent of secondary baroreceptor-mediated effects. For this purpose, we have mapped the distribution of neurons in the brainstem and forebrain that are immunoreactive for Fos (a marker of neuronal activation) following intravenous infusion of angiotensin II in conscious rabbits with chronically denervated carotid sinus and aortic baroreceptors. The distribution was compared with that evoked by the same procedure in two separate groups of barointact rabbits, in which angiotensin II was infused either at a rate similar to that in the barodenervated group, or at a rate approximately five times greater. In barodenervated rabbits, angiotensin II infusion evoked a significant increase in Fos expression, compared to control animals infused with the vehicle solution alone, in several forebrain nuclei (organum vasculosum of the lamina terminalis, subfornical organ, median preoptic nucleus, supraoptic nucleus, paraventricular nucleus, bed nucleus of the stria terminalis and suprachiasmatic nucleus), but little or no increase in Fos expression in any lower brainstem region. In barointact rabbits infused with angiotensin II at a similar rate to that in barodenervated rabbits, a similar degree of Fos expression was evoked in all of the above forebrain regions, but in addition a significantly greater degree of Fos expression was evoked in several medullary regions (nucleus tractus solitarius, area postrema, and ventrolateral medulla), even though the angiotensin II-evoked increase in mean arterial pressure (17 +/- 3 mmHg) was less than that evoked in the barodenervated rabbits (26 +/- 2 mmHg). In barointact rabbits infused with angiotensin II at the higher rate, the increase in mean arterial pressure was 29 +/- 3 mmHg. In these animals, the pattern of Fos expression was similar to that evoked in barointact rabbits infused at the lower rate, but the degree of Fos expression in all medullary regions and in some forebrain regions was significantly greater. The results of the present study, together with those of previous studies from our laboratory in which we determined the effects of phenylephrine-induced hypertension on brain Fos expression [Li and Dampney (1994) Neuroscience 61, 613-634; Potts et al. (1997) Neuroscience 77, 503-520], indicate that in conscious rabbits circulating angiotensin II activates primarily circumventricular neurons within the organum vasculosum of the lamina terminalis and subfornical organ, but not the area postrema, and this in turn leads to activation of neurons in other forebrain regions, including the median preoptic, supraoptic, paraventricular and suprachiasmatic nucleus as well as the bed nucleus of the stria terminalis. In contrast, the activation of neurons in medullary regions evoked by an increase in the level of circulating angiotensin II is primarily a secondary effect resulting from stimulation of arterial baroreceptors.     

The association between renal elasticity evaluated by Real-time tissue elastography and renal fibrosis

Clinical and Experimental Nephrology - The progression of chronic kidney disease (CKD) depends on the extent of fibrosis in the kidneys; however, a renal biopsy is necessary to evaluate the...