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Background Anorectal manometry ( ARM) is typically preformed in a lateral position. This non-physiological testing position has produced an unexpected negative rectoanal pressure gradient ( RAPG, i.e. difference between rectal and anal pressure) with normal defecation. This study was designed (i) to study differences in ARM parameters between water-perfused and solid-state sensors and between lateral and seated positions and (ii) to investigate the roles of ARM parameters in predicting balloon expulsion. Methods ARM was performed in 18 healthy volunteers ( HV) and 60 patients with functional constipation ( FC) under three randomized conditions: water-perfused in lateral position, solid-state in lateral position, and solid-state in seated position, followed by a balloon expulsion test in seated position. Key Results i) Under the same lateral position, solid-state sensors produced higher rectal resting pressure and RAPG than water-perfused sensors. ii) Using the solid-state sensors, ARM in the seated position revealed higher resting rectal pressure (34.9 vs 10.9 mmHg in HV, 30.9 vs 10.6 mmHg in FC, both P<.001) and higher RAPG (22.6 vs −6.2 mmHg in HV, 17.1 vs −8.1 mmHg in FC, both P<.001) than the lateral position. iii) When ARM was performed using solid-state sensors in seated position, RAPG was predictive of balloon expulsion; using 10 mmHg as a threshold, RAPG could predict balloon expulsion with specificity of 82% and sensitivity 77%. Conclusions and Inference ARM performed in a seated position using solid-state sensors seems more accurate in assessing rectal pressure, and the RAPG measured under these conditions is predictive of balloon expulsion in FC patients. [ABSTRACT FROM AUTHOR]

Varicocele-associated apoptosis has been recognised as a cause of male infertility. Thus, we assessed the expression of somatic apoptosis-related proteins (the typical protein-dependent apoptosis markers) in ejaculated sperm plasma from both patients with varicocele and normal donors. We evaluated the relationships between certain apoptosis-related proteins and normal semen quality. Semen samples were obtained from 25 patients with varicocele and from 10 normal fertile controls. These samples were compared using computer-assisted semen analysis for motion parameters and manual analysis for morphology, and were also assayed for apoptosis-related protein activation including caspase-3, poly-ACP-ribose polymerase (PARP), the Bcl-2 family (Bcl-2, Bak) and p53 by means of immunoblot analysis. PARP, Bak and p53 were expressed substantially more in the sperm cells of the varicocele group when compared with the normal group ( P < 0.05). The expression of caspase-3 and Bcl-2 did not appear to differ between these two study groups. An increased expression of PARP, Bak and p53 for varicocele-afflicted individuals indicated an increased participation by these agents in the regulating of apoptosis in the ejaculated semen from patients with varicocele, suggesting that certain protein-development apoptotic mechanisms might originate in the cytoplasmic droplet or within mitochondria of spermatocytes and then might function within the nucleus of the cell. [ABSTRACT FROM AUTHOR]

Background: It has been proposed that the volatile anesthetic isoflurane induces neuroprotection and that the endogenous opioid peptide dynorphin induces neurocytotoxicity in cells. The levels of dynorphin are often significantly elevated in neuropathophysiological conditions, and dynorphin can directly induce toxicity. However, the neuroprotective effects of isoflurane on dynorphin-induced cytotoxicity are still unclear. Methods: In order to determine the effect of isoflurane on dynorphin-induced cytotoxicity in neuronal cells, we have designed a device wherein cultured human neuroblastoma SH-SY5Y cells can be exposed to isoflurane. Fully differentiated SH-SY5Y cells were obtained by treating the cells with retinoic acid for 6 days. We examined SH-SY5Y cell survival, apoptosis, and antiapoptotic protein expression by cell viability, terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling stain, and Western blot analysis, respectively. Results: After 16 h of dynorphin (10 μM) treatment, the SH-SY5Y cells showed significant cytotoxicity, apoptosis, and downregulation of the antiapoptotic Bcl-2 protein expression. These effects of dynorphin were significantly inhibited by isoflurane exposure for 32 h [pretreatment for 16 h and posttreatment (after dynorphin treatment) for 16 h]. Conclusion: Thus, our results suggest that isoflurane exerts neuroprotective effects in the case of dynorphin-induced pathophysiological disruption. [ABSTRACT FROM AUTHOR]

Background: It is well known that long-term morphine administration results in tolerance, which limits the clinical use of this drug in pain management. Methods: Male Wistar rats were randomly assigned to receive one of four different infusions: morphine [15 μg/h, intrathecal (i.t.)], saline, MK-801 (5 μg/h, i.t.) plus morphine (15 μg/h, i.t.), or MK-801 (5 μg/h, i.t.) alone. Results: Morphine infusion induced a maximal antinociceptive effect on day 1 and tolerance on day 3, and the maximal anti-receptive tolerance was observed on day 5. Co-infusing MK-801 with morphine attenuated morphine's anti-receptive tolerance. Two-dimensional gel electrophoretic analysis of spinal proteins revealed that eight protein spots were up-regulated in morphine-tolerant rats, and that they were significantly inhibited by MK-801 co-infusion. Among the up-regulated proteins, glial fibrillary acid protein (GFAP), a glial-specific maker, was identified by mass spectrometry. This finding was also confirmed by Western blot analysis. Conclusion: Using proteomic analysis, we identified eight GFAP protein spots that were up-regulated in the dorsal horn of morphine-tolerant rat spinal cords. This up-regulation was partly inhibited by N-methyl-d-aspartate receptor antagonist MK-801 co-infusion, which suggests that GFAP protein can be considered to be a pathogenesis marker of morphine tolerance. [ABSTRACT FROM AUTHOR]

Postoperative ileus (PI) is the transient impairment of bowel motility due to surgical trauma and the associated physiological responses. Postoperative ileus results in patient discomfort, increases gastrointestinal risks, prolongs hospital stay and increases medical expenses. In this study, we investigated the effect of patient-controlled analgesia (PCA) morphine with or without ketorolac on bowel functions in patients after colorectal surgeries.A total of 79 patients who received elective colorectal resection were randomly allocated into two groups receiving either intravenous PCA morphine (M group) or intravenous PCA morphine plus ketorolac (K group). Recovery of bowel functions (bowel movement, passage of flatus, and soft diet intake), pain scores, morphine consumption, time for first ambulation, and opioid-related side-effects were recorded.Patients in the K group received 29% less morphine than patients in the M group with comparable pain scores. The first bowel movement (1.5[0.7–1.9] vs. 1.7[1.0–2.8] days,P < 0.05) and the first ambulation (2.2 ± 1.0 vs. 2.8 ± 1.2 days,P < 0.05) were significantly earlier in the K group than in the M group. The time of the first flatus passing, the first intake of soft diet, and duration of hospital stay were not significantly different between the two groups.The results of this study suggest that addition of ketorolac to intravenous morphine PCA provides an opioid-sparing effect but has limited benefit in shortening the duration of bowel immobility and time to first ambulation. These findings imply that postoperative ileus is attributable to multiple factors in addition to morphine consumption. [ABSTRACT FROM AUTHOR]