The complement system acts to removal exogenous pathogens, immune complexes and apoptotic cells. However, complement activation often induces tissue injury near the removal site. Complement components and these substances circulate to the kidney, and are filtrated or trapped at the glomerulus. The complement cascade is comprised of the three following pathways: the classical pathway, which is activated by the immune complex, the alternative pathway, which is activated by the inhibition of complement regulatory proteins, and the lectin pathway, which is activated by the carbohydrate terminus of glycoproteins. C5b-9 complex and C9 polymer are formed at the target tissue via any of the three pathways. Immune complexes are formed in situ within the glomerular capillary membrane, and the classical complement pathway is activated in glomerulonephritis. Circulatory C3b reacts with C3b receptors of exogenous pathogens, and the alternative complement pathway is also activated in vivo. Mannose-binding lectin and related proteins bind to the carbohydrate terminals, and the lectin pathway is activated simultaneously. Glomerular injury occurs during complement activation. Autoantibodies and circulating immune complexes are recognized in sera from systemic lupus erythematosus. Complement components in sera are consumed by complement activation. Moreover, hereditary deficiency of complement receptor 1 and the production of autoantibody against C1q are recognized in lupus nephritis. These pathological states reduce the ability to clear the immune complex, and increase the suceptibility to glomerular injury.Complement components are mainly produced in hepatocytes. The active adipocyte also produces the early components of the alternative pathway such as C3, Factor D (Adipsin), and Factor B. Thus, hypocomplementemia is recognized in emaciation and partial lipodystrophy. While hypercomplementemia is recognized in massive obesity or type 2 diabetes mellitus, and sometimes proteinuria is also recognized in these patients. In obese or diabetic patients, postprandial chylomicron activates the alternative pathway very slowly. This delayed activation, so-called ‘C3 tick over’, produces proinflammatory cytokines and induces oxidative stress in glomeruli. Complement activation is relevant in glomerular injury, not only through formation of the membrane attack complex, but also through continueous glomerular stress.

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We present the annual report of the department of surgery at the Itabashi Hospital of the Nihon University School of Medicine from January to December 2007. Compared with last year, the volume of surgical cases increased in the divisions of digestive surgery, cardiovascular surgery, breast and endocrine surgery, and pediatric surgery.

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We have previously elucidated that a bell-shaped relationship exists between the central blood volume and spontaneous arterial-cardiac baroreflex function, over stepwise widespread changes in central blood volume with lower body negative pressure (LBNP) and isotonic saline infusion. However, to precisely reveal that central hypovolemia is the essential factor underlying reduced spontaneous baroreflex function in the bell-shaped relationship, it is necessary to show that not only LBNP but also plasma volume reduction can reduce spontaneous baroreflex function, as assessed by both transfer function analysis and sequence method. We therefore examined whether both spontaneous baroreflex indices of these analytical methods decrease simultaneously with central hypovolemia due to dehydration. Seven individuals were treated with 0.4 mg/kg furosemide to reduce plasma volume. We then estimated the degree of central hypovolemia and dehydration as the central venous pressure and plasma volume changed. Spontaneous baroreflex function was assessed before (Baseline) and approximately 1 hour after furosemide administration (Dehydration). Both central venous pressure (about 4 mmHg) and plasma volume (about 10%) decreased after furosemide administration. Both spontaneous baroreflex indices of high-frequency transfer function gain (Baseline 21.5 ± 3.2; Dehydration 14.9 ± 2.9 ms/mmHg) and of the sequence slope (Baseline 18.5 ± 2.8; Dehydration 14.3 ± 2.7 ms/mmHg) were significantly reduced by plasma volume reduction, similar to our previous findings during LBNP without plasma volume reduction. Thus, the results of transfer function analysis and the sequence method together suggest that central hypovolemia due to dehydration would reduce spontaneous arterial-cardiac baroreflex function via mechanisms similar to LBNP.

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Experimental studies have demonstrated that augmentation of the magnitude of the phase 1 notch, which results in a decrease or loss of the action potential dome leading to phase 2 reentry, plays an important role in the pathogenesis of ventricular arrhythmias in Brugada syndrome. We recorded monophasic action potential (MAP) and measured the effective refractory period (ERP) from the right ventricular outflow tract (RVOT) in Brugada syndrome (BS) and compared the MAP duration (MAPD), its restitution property, and ERP with those in healthy controls. The subjects of this study were consisted of 9 patients with BS and 8 control patients. VF was induced by programmed ventricular stimulation from the RVOT in all the patients with BS. The MAPD of the RVOT at basic cycle lengths (600 ms) did not differ between the BS and control groups. However, the ERP and MAPD at the shortest diastolic interval were shorter in the BS group compared with the control group. The maximum slope of the restitution curve in the BS group tended to be steeper than that in the control group. In patients with BS, abnormal APD repolarization properties in the RVOT might contribute to the initiation and maintenance of VF.

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Previous reports have demonstrated that the implantable cardioverter defibrillator is the only proven treatment to prevent sudden death in patients with Brugada syndrome (BS). However, several recent reports have shown that oral quinidine (QND) administration prevented ventricular fibrillation (VF) storm and VF induction by programmed ventricular stimulation (PVS); thus, it might be a potential alternative therapy for BS. We investigated the effects of intravenous administration of QND on the refractoriness and the action potential duration restitution kinetics at the right ventricular outflow tract (RVOT) in patients with BS. The subjects of this study included 5 asymptomatic patients with BS. One patient exhibited Brugada-type-1 ST-segment elevation, three patients exhibited type-2 ST-segment elevation, and the other exhibited type-3 ST-segment elevation. All patients had inducible VF at baseline PVS. In 4 of 5 patients, VF could not be induced after intravenous administration of QND. In these 4 patients, QND increased the effective refractory period (ERP) of the RVOT and decreased the maximum slope of the action potential duration restitution curve of the RVOT. Intravenous QND test might be useful for evaluating the efficacy of oral QND to prevent sudden cardiac death/ VF in BS.

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Rotavirus is a common cause of severe gastroenteritis in children. It is known that rotavirus gastroenteritis can accompany some neurological manifestations, including encephalitis/encephalopathy or seizures. We report a case of a 5-year- old boy with acute encephalopathy associated with rotavirus gastroenteritis. He was admitted to our hospital because of unconsciousness, diarrhea, and vomiting. Rotavirus antigen in his feces was positive. Cell counts in the cerebrospinal fluid were normal. However, brain CT showed cerebral edema, and electroencephalogram showed generalized, high- voltage slow waves. Therefore, he was diagnosed with acute encephalopathy associated with rotavirus infections. However, the patient’s prognosis was good, and he exhibited no abnormal sequelae. When encephalitis/encephalopathy associated with rotavirus infection occurs, it may not be accompanied with convulsions. Head CT should be utilized in rotavirus infection when patients exhibit unconsciousness.

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