The Clinical Outcomes of Lower Gastrointestinal Bleeding Are Not Better than Those of Upper Gastrointestinal Bleeding

The incidence of lower gastrointestinal bleeding (LGIB) is increasing; however, predictors of outcomes for patients with LGIB are not as well defined as those for patients with upper gastrointestinal bleeding (UGIB). The aim of this study was to identify the clinical outcomes and the predictors of poor outcomes for patients with LGIB, compared to outcomes for patients with UGIB. We identified patients with LGIB or UGIB who underwent endoscopic procedures between July 2006 and February 2013. Propensity score matching was used to improve comparability between LGIB and UGIB groups. The clinical outcomes and predictors of 30-day rebleeding and mortality rate were analyzed between the two groups. In total, 601 patients with UGIB (n = 500) or LGIB (n = 101) were included in the study, and 202 patients with UGIB and 101 patients with LGIB were analyzed after 2:1 propensity score matching. The 30-day rebleeding and mortality rates were 9.9% and 4.5% for the UGIB group, and 16.8% and 5.0% for LGIB group, respectively. After logistic regression analysis, the Rockall score (P = 0.013) and C-reactive protein (CRP; P = 0.047) levels were significant predictors of 30-day mortality in patients with LGIB; however, we could not identify any predictors of rebleeding in patients with LGIB. The clinical outcomes for patients with LGIB are not better than clinical outcomes for patients with UGIB. The clinical Rockall score and serum CRP levels may be used to predict 30-day mortality in patients with LGIB.

Association between Serum Fibroblast Growth Factor-21 Levels and Nonalcoholic Fatty Liver in Korean Men with Type 2 Diabetes / 대한내과학회지

BACKGROUND/AIMS: Serum fibroblast growth factor-21 (FGF-21) levels are elevated in obesity, metabolic syndrome, and type 2 diabetes. Clinical studies have demonstrated an association between FGF-21 and nonalcoholic fatty liver (NAFL) in the general population. This study investigated the association between FGF-21 and NAFL in Korean men with type 2 diabetes. METHODS: Clinical and biochemical metabolic parameters were measured in 135 Korean men with type 2 diabetes (mean age: 56.2 +/- 9.2 years; HbA1C: 7.6 +/- 1.5%). Serum FGF-21 was determined by enzyme-linked immunosorbent assay. NAFL severity was assessed by ultrasound of the liver. High-grade (hg) NAFL was defined as moderate or severe fatty liver. RESULTS: The patients were divided into three subgroups according to NAFL severity: normal (17.0%), low-grade (50.4%), and high-grade (32.6%). Patients with hgNAFL had a larger waist circumference and higher body mass index (BMI), homeostatic model assessment-estimated insulin resistance (HOMA-IR) score, and triglyceride (TG), liver enzyme, and FGF-21 levels than those with a normal liver. FGF-21 correlated positively with BMI, serum creatinine (Cr), TG, liver enzymes, and high-sensitivity C-reactive protein, but negatively with high density lipoprotein (HDL). In multivariate regression analysis, Cr and TG were independently associated with FGF-21. BMI, TG, HDL, HOMA-IR, and FGF-21 correlated strongly with hgNAFL. The odds ratio (OR) of a 1-standard-deviation increase in FGF-21 predicting hgNAFL was 2.39 (95% confidence interval, 1.55-3.68). The OR remained significant after adjustment for Cr, TG, BMI, and HOMA-IR. CONCLUSIONS: Our findings suggest an independent association of serum FGF-21 with NAFL in Korean men with type 2 diabetes.

Effects of H2O2 on Cardiac Rate and Apoptosis of Primary Rat Cardiomyoblasts in in Vitro Culture Systems

PURPOSE: This work was intended to establish experimental conditions for monitoring the effect of ischemic/reperfusion injury on the beating capability of and apoptotic damage to primary rat cardiomyoblasts. METHODS: In an in vitro system, cardiac rate differed depending on the number of days after birth that the cells were isolated. We maintained a mean rate of 62 times per min until 4 or 5 days in culture. To generate ischemic/reperfusion injury, primary rat cardiomyoblasts were treated with hydrogen peroxide (H2O2). RESULTS: Treatment with H2O2 significantly decreased the cardiac rate of primary rat cardiomyoblasts in a time- and dose-dependent manner. Interestingly, the cardiac rate of primary rat cardiomyoblasts abruptly dropped prior to the decrease in cell viability. H2O2 also induced a decrease in the expression of heme oxygenase-1 (HO-1) protein in P2 primary rat cardiomyoblasts in a time-dependent manner. Moreover, treatment with H2O2 resulted in an increase in the proportion of cells in the sub-G0/G1 phase, indicating that H2O2 induces the apoptotic death of P2 primary rat cardiomyoblasts. However, the intracellular level of calcium was markedly decreased under the same experimental conditions. CONCLUSION: An in vitro culture system is useful for investigating the mechanism underlying the beating capability of rat heart cells and the mechanism underlying apoptotic damage to primary rat cardiomyoblasts induced by ischemic/reperfusion injury, including ROS-induced damage.

Effects of H2O2 on Cardiac Rate and Apoptosis of Primary Rat Cardiomyoblasts in in Vitro Culture Systems

PURPOSE: This work was intended to establish experimental conditions for monitoring the effect of ischemic/reperfusion injury on the beating capability of and apoptotic damage to primary rat cardiomyoblasts. METHODS: In an in vitro system, cardiac rate differed depending on the number of days after birth that the cells were isolated. We maintained a mean rate of 62 times per min until 4 or 5 days in culture. To generate ischemic/reperfusion injury, primary rat cardiomyoblasts were treated with hydrogen peroxide (H2O2). RESULTS: Treatment with H2O2 significantly decreased the cardiac rate of primary rat cardiomyoblasts in a time- and dose-dependent manner. Interestingly, the cardiac rate of primary rat cardiomyoblasts abruptly dropped prior to the decrease in cell viability. H2O2 also induced a decrease in the expression of heme oxygenase-1 (HO-1) protein in P2 primary rat cardiomyoblasts in a time-dependent manner. Moreover, treatment with H2O2 resulted in an increase in the proportion of cells in the sub-G0/G1 phase, indicating that H2O2 induces the apoptotic death of P2 primary rat cardiomyoblasts. However, the intracellular level of calcium was markedly decreased under the same experimental conditions. CONCLUSION: An in vitro culture system is useful for investigating the mechanism underlying the beating capability of rat heart cells and the mechanism underlying apoptotic damage to primary rat cardiomyoblasts induced by ischemic/reperfusion injury, including ROS-induced damage.

The Benefit of Further Tests for Patients Presenting to the Emergency Department with Non-Specific Abdominal Pain

PURPOSE: Acute abdominal pain is the most common cause of visits to the emergency department (ED). Among these visits, 30% of patients have non-specific abdominal pain (NSAP). Although the actual number of such patients is large, there are few studies of NSAP. Our report is about the usefulness of results from additional diagnostic tests for patients who have NSAP. METHODS: Subjects in our study were patients who presented at our ED between January 1, 2007 and December 31,2008 with NSAP. We retrospectively investigated the relevance of several factors including general patient characteristic, associated symptoms, pain site, existence of tenderness, and whether additional diagnostic tests were done. RESULTS: A total of 470 patients visited our ED during the study period and 148 of them had additional tests. Among the 148 patients who had additional tests, 48 had an important change in their treatment plan. Abdominal-pelvic computed tomography scans were a most useful tool in plan change (in 37 patients). Diseases that changed the treatment plan included fatal diseases such as abdominal aortic dissection and pan-peritonitis. CONCLUSION: Among patients with NSAP, carrying out of additional diagnostic tests led to important changes in the treatment plan. Abdominal-pelvic CT scans were a useful diagnostic tool. Therefore, close observation of NSAP patients is necessary and it is clinically useful to carry out additional diagnostic tests to see if the patient's symptoms and signs are changing.

A Case of Recurrent Bowel Perforation in a Patient with Churg-Strauss Syndrome / 대한류마티스학회지

Churg-Strauss syndrome is a rare systemic disorder characterized by asthma, eosionphilia and necrotizing vasculitis affecting small-to-medium-sized vessels. Although it is frequently associated with gastrointestinal mucosal lesions, recurrent bowel perforation is rare and potentially life threatening. We report a case of a 66-year-old man with Churg-Strauss syndrome, who presented with recurrent small bowel perforation. He was admitted with abdominal pain developed previous night, who had a previous small bowel perforation history treated with laparoscopic closure 5 months ago. Laboratory data showed remarkable eosinophilia. Physical examination indicated positive signs of peritoneal irritation in the entire abdomen, and abdominal computed tomography scanning showed edematous small bowel with intra-abdominal free air, suggesting intestinal perforation. He underwent laparoscopic small bowel closure and was treated with steroid.

Glutamate Induces Endoplasmic Reticulum Stress-Mediated Apoptosis in Primary Rat Astrocytes

BACKGROUND: Glutamate is a well-known central nervous system (CNS) excitatory neurotransmitter that plays a role in memory and learning. However, in excess, it leads to a process called excitotoxicity resulting in cell death. To investigate the mechanism of glutamate cytotoxicity, the apoptosis signaling pathway of primary rat astrocytes was explored in vitro. With this study, we hope to improve the prevention and treatment of ischaemic strokes and various central nervous system disorders. METHODS: To produce a model of cell injury, primary rat astrocytes were treated with glutamate. RESULTS: Treatment with glutamate induced death by apoptosis in primary rat astrocytes. This was evidenced by an increase in sub-G0/G1 fraction of the cell cycle with a loss of cell viability. Glutamate also increased the intracellular accumulation of Ca2+ ions, the expression levels of glucose-regulated protein 78 (Grp78) and C/EBP homologous protein (CHOP) protein, and the phosphorylation of protein kinase r-like endoplasmic reticulum kianse (PERK). However, the expression pattern of activating transcription factor (ATF)4 protein did not change and the 90 kDa ATF6 was cleaved to 50 kDa along with a reduced amount of Bcl-2 protein in a time-dependent manner. Interestingly, pre-treatment with glutathione markedly suppressed the reactive oxygen species (ROS) generation and the sub-G0/G1 fraction. However, the intracellular concentration of Ca2+ did not change. CONCLUSION: Our findings suggest that glutamate injures primary rat astrocytes through the endoplasmic reticulum (ER) stress-mediated apoptotic signaling pathway, as well as, ROS generation. More specifically, through Grp78, PERK, and CHOP, glutamate activates the ER stress-mediated signaling pathway in astrocytes and activates ATF6 to reduce the expression of the Bcl-2 proteins contributing to apoptosis. In addition, the ER stress-mediated signaling pathway is closely related to the transformation of intracellular ROS. This information should be applied to research for the prevention and treatment of strokes and other CNS conditions.

Phosphorylation of Extracellular Signal-Regulated Kinase1/2 and Caldesmon in Rat Colon by Electrical Stimulation to Sacral Plexus Following Spinal Cord Injury

OBJECTIVE: To find out whether electrical stimulation affects intracellular signaling mechanisms that link the biochemical and mechanical events of smooth muscle contraction. METHOD: A total of 31 adult Sprague-Dawley female rats were divided into 3 groups: control group, spinal cord injury (SCI) only group, and spinal cord injury with electrical stimulation (SCI+ES) group. Complete spinal cord transection was performed surgically at T10 cord level. The electrode for electrical stimulation was implanted into sacral spinal cord region (S2-4). Electrical stimulation was applied 4 hours per day from the day of operation. RESULTS: In SCI+ES group, the weights of fecal pellet were significantly higher from the 3rd day of post-operation to the 6th day than the SCI only group. The numbers of pERK 1/2 immunoreactive cells significantly increased in all colon segments of the SCI+ES group but had decreased in the SCI only group. Western blot showed the stronger bands of phosphorylated ERK1/2 in all colon segments and also phosphorylated caldesmon in mid or distal colon segments in the SCI+ES group. CONCLUSION: These results suggest that electrical stimulation to sacral plexus region activate phosphorylation of ERK1/2 and caldesmon which leads to improvement of bowel function by promotion of secretion or motility in the colon.

Scoring Methods for Prognosis of Patients with Acute Severe Organophosphate Intoxication

PURPOSE: Although, there have been many reports about factors involved in the severity and prognosis of organophosphate toxicity, there are few reports on integrated application of scoring methods using those factors for prognosis. Our report is about the possible application of such scoring methods in the early stage of organophosphate intoxication. METHODS: This study included organophosphate intoxication patients who were admitted to the Emergency department (ED) between March 1, 2004 and February 28, 2008. We limited enrolment in the study to patients who had required assisted mechanical ventilation and used atropine for therapy. This was a retrospective study about age, drug toxicity, mental status, existence of metabolic acidosis and QT prolongation for each patient. RESULTS: Thirty seven patients were enrolled in this study. Among the 37, 22 survived and 15 died. For survivors, drug toxicity and mental status were correlated with total dose of atropine, and the existence of metabolic acidosis was correlated with the duration of mechanical ventilation. Survivors had lower total scores than non-survivors. CONCLUSION: Application of scoring methods that include five factors (age, drug toxicity, mental status, existence of metabolic acidosis, existence of QTc prolongation) when acute, severe, organophosphate poisoning patients arrive at an ED can be helpful for their prognosis.

Immunohistochemical Study of the Expression of pERK1/2 Protein in the Forebrains of Adult Rodents Following Hypoxia-ischemia injury

PURPOSE: The purpose of this study was to evaluate spatiotemporal evaluation of pERK1/2 protein expression in the forebrain following hypoxic-ischemic (HI) injury in adult Sprague-Dawley rats. METHODS: HI injury was induced by occlusion of the bilateral common carotid artery (CCA) and respiration with 5% O2 hypoxic gas for 8 minutes, followed by unilateral release of CCA. RESULTS: Immunoreactivity for pERK1/2 protein in the bilateral cortex began to increase at 2 hours, reached peak levels at 6 hours, and then decreased by 24 hours after HI injury. In a cortical neuron, the expression of pERK1/2 protein was observed in all cellular components and processes including dendrites, cell body and nuclei at 6 hours, but persisted only in the cell body by 24 hours after HI injury. Temporal changes in the immunoreactivity for pERK1/2 protein in the hippocampus was very similar to that of the cortex following HI injury. In contrast, the temporal changes in the cellular distribution of pERK12 protein in hippocampal neurons was largely different from that of the cortex following HI injury. CONCLUSION: The results of the present study suggest that HI injury causes an early activation of ERK1/2 signaling with a differential cellular distribution of pERK1/2 protein among different forebrain structures. Further study needs to be done in order to elucidate a possible role of ERK1/2 signaling for neural damage in the adult rodent HI model.