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Although intussusception in adults generally results from malignant tumors and polyps, intussusception caused by chronic diverticulitis is extremely rare. We present the case of a 59-year-old man treated with steroids and biopharmaceuticals at the Department of Dermatology for psoriasis vulgaris. Cecal diverticulitis frequently recurred, for which he was treated during follow-up. This time, endoscopy showed a circumferential stenosis in the ascending colon, and computed tomography showed the appearance of a target sign in the right colon. As a result, the patient was preoperatively diagnosed as having intussusception of the ascending colon triggered by diverticulitis of the cecum and underwent laparoscopic right colectomy. Pathological findings of the specimen revealed multiple diverticulitis of the cecum. Therefore, we thought that the intussusception was caused by chronic inflammation of the diverticula and surrounding fibrosis. Among intussusception in adults, chronic diverticulitis should be considered as a target of surgical treatment on rare occasions. [ABSTRACT FROM AUTHOR]

Among synchronous colorectal cancers (SCRCs) reported previously, the incidence of quadruple advanced SCRCs is very rare. We present the case who underwent laparoscopic two-segment resection of the colon requiring two anastomoses that was performed for quadruple advanced cancers, and four tumors were curatively removed. There were no signs of recurrence at 64 months after surgery. Laparoscopic surgery provided less invasiveness even for quadruple advanced SCRCs in terms of early recovery with an acceptable long-term outcome. [ABSTRACT FROM AUTHOR]

Background: Human herpesvirus 6 (HHV-6) causes life-threatening central nervous system disorders after allogeneic hematopoietic stem cell transplantation (allo-HSCT). Recent studies implicated CD134 as a specific receptor of HHV-6B and demonstrated that its expression levels in CD4-positive T cells after allo-HSCT could be related to the reactivation of HHV-6. We prospectively evaluated the relationship between HHV-6 reactivation and CD134+ T cells in the recipients of allo-HSCT.Methods: HHV-6 viral load in plasma was quantitatively measured weekly after allo-HSCT by digital polymerase chain reaction in 34 patients. The ratio of CD134 in CD4+ T cells (CD134/CD4 ratio) was serially measured by flow cytometry before and after transplantation.Results: HHV-6 reactivation was detected in 23 patients (68%). The CD134/CD4 ratio before conditioning was significantly higher in patients with HHV-6 reactivation than in those without (median, 3.8% vs 1.5%, P < .01). In multivariate analysis, a higher CD134/CD4 ratio before conditioning was significantly associated with the incidence of HHV-6 reactivation (odds ratio, 10.5 [95% confidence interval, 1.3-85.1], P = .03).Conclusions: A higher CD134/CD4 ratio before conditioning was associated with a higher risk of HHV-6 reactivation, suggesting that the rate may be a promising marker for predicting HHV-6 reactivation after allo-HSCT. [ABSTRACT FROM AUTHOR]

According to a systematic review on the measurement of frailty as an outcome, the frailty index (FI) score is introduced as the most appropriate outcome measure, although its clinimetric properties need to be further considered ([2]). When discussing frailty outcome, no change in frailty may indicate a positive result, as the mean deficit accumulation rate in community-dwelling older adults has been reported to be close to 3% per year ([6]), which shows frailty proceeding its natural course. [Extracted from the article]

Aims Although atrial-tachycardia remodelling is a significant atrial fibrillation (AF) promoting factor, little information is available about how atrial-tachycardia rate determines remodelling effects. This study assessed the effects of atrial tachypacing (ATP) over a range of clinically relevant rates on atrial electrophysiology and AF. Methods and results Chronically instrumented dogs underwent sequential 7 day ATP at 400, 300, 200, and 160 bpm in random order with 2 day recovery intervals between periods of ATP. ATP at 400, 300, and 200 bpm significantly decreased atrial effective refractory period (ERP) by 41 ± 2, 37 ± 3, and 7 ± 1 ms, respectively, with no significant effects at 160 bpm. Mean duration of induced AF was increased by 400 and 300 bpm ATP (404 ± 284 and 410 ± 283 s on day 4, respectively, vs. 12 ± 4 s at baseline, P Conclusion There is a non-linear relationship between atrial rate and the extent of atrial electrical remodelling. Remodelling at rates equivalent to paroxysmal supraventricular tachycardias in man is insufficient to promote AF alone or in the presence of an atrial fibrotic substrate, but can accelerate the remodelling and stabilization of AF when followed by faster atrial tachyarrhythmias. [ABSTRACT FROM AUTHOR]

Atrial fibrillation (AF) is the most common sustained clinical tachyarrhythmia. AF is a progressive condition as demonstrated by the finding that maintenance of normal rhythm and contractile function becomes more difficult the longer AF exists. AF causes cellular stress, which induces atrial remodelling, involving reduction in the expression of L-type Ca2+ channels and structural changes (myolysis), finally resulting in contractile dysfunction. Heat shock proteins (HSPs) comprise a family of proteins involved in the protection against different forms of cellular stress. Their classical function is the prevention of toxic protein aggregation by binding to (partially) unfolded proteins. Recent investigations reveal that HSPs prevent atrial remodelling and attenuate the promotion of AF in both cellular and animal experimental models. Furthermore, studies in humans suggest a protective role for HSPs against progression from paroxysmal AF to chronic, persistent AF. Therefore, manipulation of the HSP system may offer novel therapeutic approaches for the prevention of atrial remodelling. Such approaches may contribute to the maintenance or restoration of tissue integrity and contractile function. Ultimately, this concept may offer an additional treatment strategy to delay progression towards chronic AF and/or improve the outcome of cardioversion. [ABSTRACT FROM PUBLISHER]

Aims: Heat shock proteins (HSPs) are a set of endogenous cytoprotective factors activated by various pathological conditions. This study addressed the effects of geranylgeranylacetone (GGA), an orally active HSP inducer, on the atrial fibrillation (AF) substrate associated with acute atrial ischaemia (AI). [ABSTRACT FROM PUBLISHER]

Abstract: Background: Congestive heart failure (CHF) is a common cause of atrial fibrillation (AF). Oxidative stress and inflammation (profibrotic) and peroxisome proliferator-activated receptor-α (PPAR-α, antifibrotic) factors may be involved in CHF-related remodeling. We evaluated the effects of simvastatin (antioxidant, anti-inflammatory) and fenofibrate (PPAR-α activator) on CHF-related atrial remodeling. Methods and results: Dogs were subjected to 2-week ventricular tachypacing (VTP) in the absence and presence of simvastatin (20 or 80 mg/day) or fenofibrate. Induced AF duration (DAF) was increased by VTP from 36±14 (non-paced controls) to 1005±257 s (p <0.01). Simvastatin prevented VTP-induced DAF increases (147±37 and 84±37 s at 20 and 80 mg/day, respectively), but fenofibrate did not (1018±352 s). Simvastatin also attenuated CHF-induced conduction abnormalities (heterogeneity-index reduced from 1.5±0.1 to 1.1±0.1 and 1.0±0.1 at 20 and 80 mg/day, p <0.01) and atrial fibrosis (from 19.4±1.3% to 10.8±0.8% and 9.9±0.8% at 20 and 80 mg/day, p <0.01), while fenofibrate did not. Simvastatin (but not fenofibrate) also attenuated VTP-induced left-ventricular nitric-oxide synthase and nitrotyrosine increases, along with hemodynamic dysfunction. Atrial fibroblast proliferation increased with 24-h fetal bovine serum (FBS) stimulation from 654±153 to 7264±1636 DPM (p <0.001). Simvastatin, but not fenofibrate, suppressed fibroblast proliferation (664±192 DPM, p <0.001). Simvastatin also significantly attenuated transforming growth factor-β1-stimulated α-smooth muscle actin (α-SMA) expression (indicating myofibroblast differentiation) from 1.3±0.1 to 1.0±0.1 times baseline (p <0.05). Conclusions: CHF-induced atrial structural remodeling and AF promotion are attenuated by simvastatin, but not fenofibrate. Statin-induced inhibition of profibrotic atrial fibroblast responses and attenuation of left-ventricular dysfunction may contribute to preventing the CHF-induced fibrotic AF substrate. [Copyright &y& Elsevier]

Abstract: Objective: Acute atrial ischemia produces a substrate for atrial fibrillation (AF) maintenance, but the response of this substrate to antiarrhythmic-drugs has not been defined. The present study assessed the effects of class 1–4 antiarrhythmic-drugs on the electrophysiological consequences of acute atrial ischemia, and compared effects in ischemic AF with those in vagal AF. Methods and results: Isolated atrial ischemia was created by ligating a right coronary artery branch perfusing the right atrial free wall. Experiments were performed in dogs treated with loading and maintenance doses of flecainide (class 1; n =5), nadolol (class 2, n =7), dofetilide (class 3, n =5), or diltiazem (class 4, n =7) prior to coronary artery occlusion. Dogs subjected to coronary occlusion without pre-treatment (n =10) served as controls. Coronary artery occlusion substantially increased AF duration, e.g. from 7±4 s (pre-ischemic baseline) to 876±245 s at 3 h of ischemia, and caused substantial ischemic zone conduction slowing. Diltiazem and nadolol prevented AF promotion (AF durations 12±8 s and 4±1 s at 3 h of ischemia respectively; each p <0.001 vs control) and suppressed ischemic conduction slowing. Flecainide and dofetilide failed to prevent ischemia-induced AF promotion (e.g. AF duration at 3-hour ischemia 779±417 and 801±414 respectively, p =NS vs control) and failed to alter ischemia-induced conduction slowing. A different pattern of response occurred with vagal AF: flecainide was highly effective in reducing vagal AF duration; dofetilide, diltiazem, and nadolol were ineffective. Conclusions: Beta-blockade and Ca2+ antagonism suppress the arrhythmic consequences of acute atrial ischemia, whereas Na+ channel or K+-channel block are ineffective. These results are relevant to understanding the effects of different classes of antiarrhythmic-drugs on AF occurring in coronary disease patients. [Copyright &y& Elsevier]

Abstract: Background: There is evidence suggesting involvement of oxidative stress, inflammation, and calcineurin/nuclear factor of activated T cell pathways in atrial fibrillation. This study evaluated the efficacy of anti-inflammatory and calcineurin-inhibitory drugs on promotion of atrial fibrillation by atrial tachycardia-induced remodeling in dogs. Methods and results: Dogs were subjected to atrial tachypacing at 400 bpm in the absence and presence of treatment with prednisone (15 or 50 mg/day) or ibuprofen (anti-inflammatory) or cyclosporine-A (calcineurin inhibitor). Serial closed-chest electrophysiological studies were performed in each dog at baseline and 2, 4, and 7 days after tachypacing onset. A final open-chest study was performed on day 8. Serum C-reactive protein was measured by ELISA and nitric oxide synthase by Western blotting. The mean duration of induced atrial fibrillation was markedly increased by tachypacing alone, from 26±8 to 962±317 s (p <0.01), and the atrial effective refractory period was decreased from 117±4 to 73±7 ms (p <0.001; cycle-length 300 ms). Tachypacing-induced effective refractory period shortening and atrial fibrillation promotion were unaffected by ibuprofen or cyclosporine-A; however, both doses of prednisone suppressed tachypacing-remodeling effects (atrial fibrillation duration to 96±60 s and 28±11 s at higher and lower doses, respectively; effective refractory period to 101±6 ms for higher-dose and 105±3 ms for lower-dose group). In addition, prednisone (but not ibuprofen or cyclosporine) significantly decreased C-reactive protein concentrations and attenuated the increase in endothelial nitric oxide synthase expression caused by atrial tachypacing. Conclusions: Prednisone prevents the electrophysiological and atrial fibrillation-promoting effects of atrial tachycardia-remodeling, possibly by an anti-inflammatory action, whereas the less potent anti-inflammatory ibuprofen and the calcineurin inhibitor cyclosporine-A are without effect. [Copyright &y& Elsevier]

Examines the value of laparoscopically assisted distal gastrectomy in (LDG) the elderly. Comorbidity more common in elderly patients than in younger patients; Advantages offered by LDG to elderly patients with early gastric cancer, including rapid return of gastrointestinal function, fewer complications and a shorter hospital stay.

Background: Intravenous verapamil has been reported to prevent electrical remodeling induced by rapid atrial excitation of several minutes to several hours. However, the clinical efficacy of verapamil when taken orally and daily remains controversial. Purpose: We attempted to demonstrate our hypothesis that if verapamil prevents calcium (Ca) overload, its efficacy would be greater when taken before, rather than after, the onset of rapid atrial excitation. Methods: In 24 dogs, pacing and recording electrodes were sutured onto the right atrium. After a 5-day recovery period, rapid atrial pacing at 400 ppm was started, followed 2 days later by oral verapamil (8 mg/kg per day) in eight dogs (After group; A). In another eight dogs, oral verapamil administration was begun 1 week before the initiation of rapid pacing (Before group; B). In the remaining eight dogs, only rapid atrial pacing was started, without oral verapamil (Control group; C). We measured the effective refractory period (ERP) and conduction velocity (CV), and calculated wavelength (WL) at cycle lengths 200 and 300 ms on the day before (P0), and after 2 (P2), 7 (P7), 14(P14) days of rapid pacing. Results: In response to rapid atrial pacing, ERP, CV, WL decreased and progressively and comparably in A and C (P<0.05 vs. P0). In contrast, in B, these parameters did not change significantly and remained greater than those in A and C (P<0.05). Moreover, the adaptation of ERP to rate was preserved only in B. The duration of atrial fibrillation (AF) was shorter in B than in A and C (P<0.05). The inducibility of AF tended to be lower, and the fibrillation cycle length was longer in B than in A and C. Conclusions: Oral verapamil started before but not after rapid atrial excitation prevents electrical remodeling. Verapamil may exert beneficial effects when it is taken during sinus rhythm, but not after more than 2 days of atrial tachyarrhythmia. [Copyright &y& Elsevier]

We report the case of a 61-year-old woman with Kartagener syndrome who presented with a 3-month history of chronic watery diarrhoea and severe hypoalbuminaemia. Histopathological examination of duodenum and large intestine biopsies showed amyloid A (AA) amyloid deposition. Scintigraphy and alpha-1 anti-trypsin clearance evaluations revealed protein-losing gastroenteropathy. Computed tomography with contrast and positron emission tomography showed a pelvic mass with multiple para-aortic lymph node enlargement. We suspected protein-losing gastroenteropathy secondary to AA amyloid produced related to malignant tumours. Following tumour resection, histopathological examination of the lesion revealed undifferentiated carcinoma of unknown origin. Postoperatively, the patient's nutritional condition improved. There has been no recurrence of protein-losing gastroenteropathy 6 months postoperatively. This is the first report of protein-losing gastroenteropathy and AA amyloidosis secondary to undifferentiated carcinoma. Early recognition and intervention could increase the likelihood of amyloidosis remission. [ABSTRACT FROM AUTHOR]