Underwater endoscopic submucosal dissection for colorectal tumors decreases the incidence of post-electrocoagulation syndrome.

BACKGROUND AND AIMS: Underwater endoscopic submucosal dissection (U-ESD) is a recently developed procedure that has the potential to prevent post-ESD coagulation syndrome (PECS) owing to its heat-sink effect. We aimed to clarify whether U-ESD decreases the incidence of PECS compared with conventional ESD (C-ESD). METHODS: A total of 205 patients who underwent colorectal ESD (C-ESD: 125; U-ESD: 80) were analyzed. Propensity score matching analysis was performed to adjust for patient backgrounds. Ten C-ESD and two U-ESD patients with muscle damage or perforation during ESD were excluded when comparing PECS. The primary outcome was to compare the incidence of PECS between the U-ESD and C-ESD groups (54 matched pairs). Secondary outcomes were to compare procedural outcomes between the C-ESD and U-ESD groups (62 matched pairs). RESULTS: Among the 78 patients who underwent U-ESD, PECS occurred in only one patient (1.3%). Adjusted comparisons between the U-ESD and C-ESD groups demonstrated a significantly lower incidence of PECS in the U-ESD group (0% vs 11.1%; P = 0.027). Median dissection speed was significantly faster in the U-ESD than in the C-ESD group (10.9 mm2 /min vs 6.9 mm2 /min; P < 0.001). En bloc and complete resection rates were 100% in the U-ESD group. Although perforation and delayed bleeding occurred in one patient each (1.6%) as adverse events in the U-ESD group, there were no differences compared with the C-ESD group. CONCLUSIONS: Our study demonstrates that U-ESD effectively decreases the incidence of PECS and is a faster and safer method for colorectal ESD.

Effects of liposome-encapsulated hemoglobin on learning ability in tokai high-avoider rat after total brain ischemia and reperfusion.

Liposome-encapsulated hemoglobin with low O2 -affinity (l-LEH) was shown to be protective in focal brain ischemia and reperfusion (I/R) in rats and primates. We tested l-LEH in the transient whole brain ischemia in the Tokai high-avoider rat (THA), which has been selected, mated, and bred over 77 generations for a high and consistent learning ability determined by the Sidman avoidance test (SAT). Young/naïve (before SAT) and adult/parent (after SAT) THA rats underwent acute and complete four-vessel occlusion in the chest for 3 or 5 min, administration of 2 mL/kg of l-LEH, saline, or homologous washed red blood cells (RBCs), reperfusion, and resuscitation. One week later, all rats underwent SAT, open-field behavioral observation, Morris water maze tests, and morphological study. Whereas young/naïve rats treated with l-LEH retained a rapid and consistent learning curve as in nonischemic controls, THA rats treated with RBCs or saline had retarded learning response on SAT as well as reduced cellularity in the amygdala. Adult/parent rats with established memory on SAT maintained perfect achievement even after I/R. In contrast, l-LEH-treated rats showed no better performance on Morris water maze (function) or cellularity of the CA1 sector of the hippocampus (morphology) compared with the rats treated with RBCs. Although task performance on SAT and Morris water maze appeared antithetical, morphological observations corresponded to the respective functions, suggesting that l-LEH was protective only for the amygdala on SAT tasks but not for the CA1 sector of the hippocampus on spatial orientation as in our previous studies on focal brain I/R, where the cortex was preserved better than basal ganglia.

[Study of cumulative head injury in high shock avoider rat (THA rat)].

PURPOSE: Small but repeated head trauma, as represented by boxing-related punch-drunk syndrome and dementia pugilistica, occasionally cause dyskinesia and marked brain dysfunction following long-term post-traumatic follow-up, despite the absence of intracranial lesions, such as cerebral contusion and intracranial hemorrhage. We defined this condition as "cumulative head injury." To clarify its mechanism, we conducted an experiment involving appliciation of continuous head trauma of Tokai High Avoider (THA) rats, and examined subsequent marked function/histopathological changes. METHODS: THA rats were divided into 3 categories based on the frequency of impact exposure: a control group (Group A), a group exposed to 1 impact set (Group B), and a group exposed to 3 impact sets (Group C). In each group, histopathological, spontaneous motility, and learning tests were conducted. RESULTS: Histopathologically, no marked tissue destruction was observed in Group B or C. In Group C, the number of GFAP-positive cells were increased in acute-phase specimens of the hippocampus, cerebral cortex, and basilar cortex. With respect to chronic-phase histological changes, the numbers of GFAP-positive cells were increased in the hippocampus and the basilar cortex in Group C; however, these changes were less marked than in the acute stage. A marked function test identified emotional suppression in the acute stage and bimodal learning reduction in the acute to chronic stages in Group C. CONCLUSION: The results of this experiment revealed that the repetition of low-level trauma which did not lead to brain injury as revealed on pathological examination, induced emotional suppression and the bimodal reduction in learning results; further, this disorder exacerbated with an increase in impact frequency. The influence on marked brain function could be verified using a specific experimental system of THA rats. This model may be useful for evaluating the cumulative effects of repeated head trauma.

[Case of pollinosis to grass pollens who presented with dyspnea successfully treated by rush immunotherapy].

We present a 15 years old boy who experienced unusual symptoms for pollen allergy, and successfully treated by rush immunotherapy. The patient started to complain erythema and edema on his face and serous rhinorrhea at 10 years old when going out. He entered baseball team at junior high school, and subsequently experienced choking sensation, dyspnea, face edema, and it was sometimes impossible to continue play. He was diagnosed as bronchial asthma at some hospital, and prescribed many anti-asthma medications including inhaled corticosteroid, which did not take effect. His symptoms deteriorated in summer and ameliorated in winter. When he was 15 years old, he was referred to us by a pediatrician for reassessment of his symptoms. Flow-volume curve was normal, and bronchial provocation test (acetylcholine and histamine), and exercise challenge were negative. IgE antibodies specific to grass pollens were highly positive. We made a diagnosis of pollinosis to grass pollens instead of bronchial asthma. Oral antihistamines and intranasal corticosteroid partially improved his symptoms. We started rush-immunotherapy of grass-pollens (oats and bromegrass), Japanese cedar, and ragweed. His symptoms improved dramatically on the next season of grass pollens.

Perceived sleepiness of non-shift working men in two different types of work organization.

Increased sleepiness at work is increasingly being focused on as a safety and health issue. However, research on workers' sleepiness is very limited in scope and the characteristics of work organization, including the impact of job stress, have not been fully addressed. A questionnaire survey was conducted to investigate the prevalence of daytime sleepiness and its associated factors among non-shift working men at two manufacturing businesses: Company A, having a rapid rate of development and growth, with 564 workers (19-61 yr old, mean age: 32.7, response rate: 81.4%); and Company B, long established, possessing a huge production facility, with 1,654 workers (20-63 yr old, mean age: 37.1, response rate: 78.2%). The prevalence of daytime sleepiness was 11.3% in company A and 16.8% in company B. Multivariate logistic regression analysis revealed that, in company A, perceived sleepiness was associated with long sleep duration on non-working days and high cognitive demands and, in company B, with insufficient daily sleep, single, and depression. Psychosomatic exhaustion resulting from jobs requiring high adaptivity due to rapid frequency of operational change as in company A may have the potential to become an important factor in perceived sleepiness. However, in a comparatively stable work organization, as in company B, increased sleepiness may be mainly linked to factors outside work. It is suggested that not only lifestyle and sleep habits, but also the characteristics and dynamics of a work organization should be a focus of attention when planning measures to prevent sleepiness at work.

Vascular dysfunction in patients with chronic arsenosis can be reversed by reduction of arsenic exposure.

Chronic arsenic exposure causes vascular diseases associated with systematic dysfunction of endogenous nitric oxide. Replacement of heavily arsenic-contaminated drinking water with low-arsenic water is a potential intervention strategy for arsenosis, although the reversibility of arsenic intoxication has not established. In the present study, we examined urinary excretion of cyclic guanosine 3 ,5 -monophosphate (cGMP), a second messenger of the vasoactive effects of nitric oxide, and signs and symptoms for peripheral vascular function in 54 arsenosis patients before and after they were supplied with low-arsenic drinking water in an endemic area of chronic arsenic poisoning in Inner Mongolia, China. The arsenosis patients showed a marked decrease in urinary excretion of cGMP (mean +/- SEM: male, 37.0 +/- 6.1; female, 37.2 +/- 5.4 nmol/mmol creatinine), and a 13-month period of consuming low-arsenic drinking water reversed this trend (male, 68.0 +/- 5.6; female, 70.6 +/- 3.0 nmol/mmol creatinine) and improved peripheral vascular response to cold stress. Our intervention study indicates that peripheral vascular disease in arsenosis patients can be reversed by exposure cessation and has important implications for the public health approach to arsenic exposure.

Anesthesia and acoustic stress-induced intra-uterine growth retardation in mice.

Stress interferes with reproduction, adversely influencing implantation and fetal growth, and sometimes even leading to abortion. Here, we attempted to evaluate the early gestational effects of uncomfortable sound on pregnant mice and their offspring. Ten-week-old pregnant Jcl:ICR mice were exposed to sound (100 dB, random frequency between 9-34 kHz) for 8 hours on the 3(rd), 5(th) and 7(th) gestational days (GD). The effects of general anesthesia were also investigated, with or without acoustic stress. All groups were examined on the 18(th) GD for fetal growth. Fetal weight, number of ossified sacrococcygeal vertebrae and placental weight were all significantly reduced (P<0.0001) when stress was induced on the 7(th) GD, but not on the 3(rd) or 5(th) GD. This intra-uterine growth retardation (IUGR) was significantly inhibited by general anesthesia (P<0.0001), although general anesthesia alone induced significant IUGR (P<0.0001) when compared with control mice. This suggests that acoustic exposure indirectly exerts an effect on fetal growth, possibly via a psycho-maternal pathway. We also found that analysis of the number of ossified sacrococcygeal vertebrae is the most sensitive tool for the study of IUGR.

Evidence for induction of oxidative stress caused by chronic exposure of Chinese residents to arsenic contained in drinking water.

Exposure of experimental animals or cultured cells to arsenic induces oxidative stress, but, to date, no examination of this phenomenon in humans has been reported. In this study we conducted a cross-sectional study in Wuyuan, Inner Mongolia, China, to explore the relationship between chronic arsenic exposure from drinking water and oxidative stress in humans. Thirty-three inhabitants who had been drinking tube-well water with high concentrations of inorganic arsenic (mean value = 0.41 mg/L) for about 18 years constituted the high-exposure group, and 10 residents who lived nearby but were exposed to much lower concentrations of arsenic in their drinking water (mean value = 0.02 mg/L) were selected as the low-exposure comparison group. Results of the present study indicated that although the activity for superoxide dismutase (SOD) in blood did not differ significantly between the two groups, the mean serum level of lipid peroxides (LPO) was significantly higher among the high-exposed compared with the low-exposed group. Elevated serum LPO concentrations were correlated with blood levels of inorganic arsenic and its methylated metabolites. In addition, they showed an inverse correlation with nonprotein sulfhydryl (NPSH) levels in whole blood. The subjects in the high-arsenic-exposure group had mean blood NPSH levels 57.6% lower than those in the low-exposure group. Blood NPSH levels were inversely correlated with the concentrations of inorganic arsenic and its methylated metabolites in blood and with the ratio of monomethylarsenic to inorganic arsenic. These results provide evidence that chronic exposure to arsenic from drinking water in humans results in induction of oxidative stress, as indicated by the reduction in NPSH and the increase in LPO. Some possible mechanisms for the arsenic-induced oxidative stress are discussed.