Transpyloric prolapse of a pedunculated polypoid gastric carcinoma

A patient with transpyloric prolapse of a pedunculated polypoid gastric carcinoma is reported. Only three previous cases have been reported in the international literatures. However, in Japan, 33 cases of prolapsed gastric carcinoma have been reported during the past 30 years. Prolapsed gastric carcinoma should be included in the differential diagnosis of localized intraluminal filling defects in the duodenal bulb. Endoscopy and biopsy are essential for correct diagnosis.     

Effects of endoscopic sinus surgery on nasal spray deposition using dye-based methods for humans and a human silicone sinonasal cavity model

ObjectiveWe have evaluated that the deposition patterns of corticosteroid nasal spray in the sinonasal cavity of both post-operated human cases, which were further compared with a computed tomography-based sinonasal airway model.MethodsFifty-one patients with chronic rhinosinusitis following an endoscopic sinus surgery were enrolled in this study. Nasal spray mometasone furoate hydrate (Nasonex®) containing 0.1% indigocarmine was applied to the patients' nasal cavities and the sinonasal cavity was observed by endoscopy and video documentation. A single plaster sinonasal model was used to quantify the sinonasal deposition of nasal sprays containing 10% red ink solution using 12 round paper strips.ResultsThe predominant areas of the spray deposition of the operated sinonasal cavities were recognized in the ethmoid sinus and the olfactory cleft in the human study. The droplets were mainly deposited in the inferior turbinate followed by the posterior part of the ethmoid sinus, the olfactory cleft, and anterior part of the ethmoid sinus in a sinonasal model.ConclusionThe corticosteroid nasal spray efficiently reached the olfactory cleft and the ethmoid sinus in post-operative conditions, which was demonstrated by post-operated human cases and a computed tomography-based sinonasal airway model.     

Renal Dysfunction is an Independent Risk Factor for Rebleeding After Endoscopic Hemostasis in Patients with Peptic Ulcer Bleeding

BackgroundDespite the progress in endoscopic hemostasis and pharmacological treatment, the mortality rate of peptic ulcer bleeding remains at 5–10%. Rebleeding after peptic ulcer bleeding is believed to be a risk factor for mortality. This study aimed to evaluate whether renal dysfunction is a predictor of rebleeding after endoscopic hemostasis in patients with peptic ulcer bleeding.Methods: In this retrospective study, consecutive patients with peptic ulcer bleeding who underwent endoscopic hemostasis at our Hospital from January 2010 to December 2018 were enrolled. The relationship between rebleeding within 30 days after endoscopic hemostasis and the patients’ admission and endoscopic characteristics were analyzed using univariate and multivariate regression models.ResultsOut of 274 patients with peptic ulcer bleeding, 17 (6.2%) patients experienced rebleeding. In the analysis of the patients’ admission characteristics, estimated glomerular filtration rate (eGFR) < 30 mL/min/1.73 m² was an independent risk factor for rebleeding (odds ratio 4.77, 95% confidence interval 1.168-18.211, p = 0.03). Patients with eGFR < 15 mL/min/1.73 m² with or without hemodialysis had the highest rebleeding rate at 36.8%. With respect to endoscopic characteristics, the rate of rebleeding was associated with combination therapy (p < 0.0001) and active bleeding (p = 0.03).Conclusion: Renal dysfunction might be an independent risk factor for rebleeding after endoscopic hemostasis in patients with peptic ulcer bleeding.     

Improvement of physical activity in chronic obstructive pulmonary disease by pulmonary rehabilitation and pharmacological treatment

Physical activity (PA) is defined as bodily movement produced by skeletal muscles with energy expenditure beyond resting levels. PA is closely related to reduced morbidity and mortality in chronic obstructive pulmonary disease (COPD). Self-report questionnaires are often subject to recall bias, correlating poorly with objectively qualified PA, and do not provide an accurate estimate of free-living energy expenditure. PA may be objectively evaluated by newly developed tri-axial accelerometers by quantifying steps or body movements over a period of time. Low-intensity, home-based pulmonary rehabilitation (PR) using pedometer feedback improves PA. Improvement in physiological factors correlates with increased walking time in stable elderly COPD patients.This review focuses on the effects of PR and pharmacological treatment on PA in COPD patients. We selected 32 studies from our literature search evaluating the effects of PR and 11 studies examining the effects of pharmacological treatment on PA. Findings in both categories were inconsistent. Nineteen studies showed a positive effect with PR whereas 13 showed no effect. Eight studies showed a positive effect, while three revealed no effect from pharmacological intervention. As both interventions increase exercise capacity without a consistent effect on PA, counseling with behavioral changes may be necessary to achieve a significant and lasting increase in PA. Changing PA behavior in COPD patients requires an interdisciplinary approach involving specialists in respiratory medicine, rehabilitation, social, and behavioral sciences. Future research in this area is warranted to advance our knowledge in this area, specifically with regard to the interaction of pharmacological and non-pharmacological interventions.     

A novel HLA class II alloantigen detected by an alloantiserum TK2

An alloantiserum, TK2, obtained from a kidney transplant patient, was investigated. TK2 reacted with B lymphocytes that had only one detectable DQ antigen. DQ "blank" homozygous cell lines were positive for TK2, but DQwl, DQw2, and DQw3 homozygous cell lines failed to react with TK2. Positive reactions for TK2 segregated with DQ "blank" haplotypes in the families studied. The reactivity of TK2 to B lymphocytes was strong, while its reactivity to monocytes was very weak. When TK2 was absorbed with DQ "blank" cells, it became unreactive to other lymphocytes. TK2 blocked the binding of an anti-DQ monoclonal antibody to DQ "blank" cells. It did not affect the binding of the antibody to DQw1 and DQw3 cells, nor did it affect the binding of an anti-DR monoclonal antibody to a DQ "blank" cell line. These findings suggest that TK2 can detect a new HLA class II alloantigen that corresponds to a DQ "blank" specificity.     

Mode of relaxing action of FK336, a new antianginal agent, in rabbit aorta.

1. FK336 (10(-6)-10(-4) M) inhibited contractile responses to norepinephrine (NE), KCl and Ca2+ in isolated rabbit aortas. 2. Relaxing effect of FK336 on KCl-response was inhibited by nitroglycerin (NG), but not by nifedipine or verapamil. 3. FK336 inhibited residual NE response and a subsequent Ca2+ response in Ca(2+)-free medium. FK336 did not affect the inositol monophosphate level. 4. Relaxing effect of FK336 on NE response was inhibited by methylene blue, NG, K(+)-channel inhibitors and acetylcholine (ACh), and potentiated by M&B 22,948 and theophylline. 8-Br cGMP and dibutyl cAMP had no effect. 5. FK336 increased cGMP level in rat aorta. 6. Potentiation of isoproterenol-relaxation by FK336 was inhibited by methylene blue. 7. The inhibitory effect of ACh on FK336-relaxation was eliminated by endothelium removal, nordihydroquaiaretic acid and guinacrine, but not by indomethacin. These treatments themselves did not affect FK336-relaxation. 8. The mode of vasorelaxing action of FK336 is discussed.     

The mode of vasorelaxing action of melatonin in rabbit aorta.

1. The vasorelaxing effect of melatonin on the contractile response to 5-hydroxytryptamine (5-HT) was investigated in rabbit isolated aorta. 2. Melatonin (10(-5)-10(-3) M) caused relaxation of the 5-HT (10 M) response in a concentration-dependent manner. Nifedipine (10(-6) M) did not affect the relaxing action of melatonin. 3. Pretreatment with methylene blue (10(-5) M) or nitroglycerin (3 x 10(-8) M) inhibited or potentiated, respectively, the relaxing action of melatonin. 4. Pretreatment with melatonin (10(-3) M) or M&B 22.948 (10(-3) M) potentiated the relaxing effect of nitroglycerin (10(-9)-10(-5) M) on the contraction induced by PGF2 alpha (4 x 10(-6) M). The effect of a combined treatment with melatonin and M&B 22.948 was not significantly different from that of a single treatment with M&B 22.948. 5. Melatonin (10(-5)-10(-3) M) inhibited the activity of cGMP-phosphodiesterase, in a concentration-dependent manner. 6. These results suggest that the vasorelaxing action of melatonin may be due to an increase in the level of cGMP.