Self-Assembly of a Graphene Oxide Liquid Crystal for Water Treatment.

Adsorbents, especially those with high removal efficiency, long life, and multi-purpose capabilities, are the most crucial components in an adsorption system. By taking advantage of the liquid-like mobility and crystal-like ordering of liquid crystal materials, a liquid crystal induction method is developed and applied to construct three-dimensional graphene-based adsorbents featuring excellent shape adaptability, a distinctive pore structure, and abundant surface functional groups. When the monoliths are used for water restoration, the large amount of residual oxygen-containing groups is more susceptible to electrophilic attack, thus contributing to cation adsorption (up to 705.4 mg g-1 for methylene blue), while the connected microvoids between the aligned graphene oxide sheets facilitate mass transfer, e.g., the high adsorption capacity for organic pollutants (196.2 g g-1 for ethylene glycol) and the high evaporation rate for water (4.01 kg m-2 h-1). This work gives a practical method for producing high-performance graphene-based functional materials for those applications that are sensitive to surface and mass transfer properties.

Diagnosis and Treatment of Esophageal Candidiasis: Current Updates.

Esophageal candidiasis (EC) is the most common type of infectious esophagitis. In the gastrointestinal tract, the esophagus is the second most susceptible to candida infection, only after the oropharynx. Immunocompromised patients are most at risk, including patients with HIV/AIDS, leukemia, diabetics, and those who are receiving corticosteroids, radiation, and chemotherapy. Another group includes those who used antibiotics frequently and those who have esophageal motility disorder (cardiac achalasia and scleroderma). Patients complained of pain on swallowing, difficulty swallowing, and pain behind the sternum. On physical examination, there is a plaque that often occurs together with oral thrush. Endoscopic examination is the best approach to diagnose this disease by directly observing the white mucosal plaque-like lesions and exudates adherent to the mucosa. These adherent lesions cannot be washed off with water from irrigation. This disease is confirmed histologically by taking the biopsy or brushings of yeast and pseudohyphae invading mucosal cells. The treatment is by systemic antifungal drugs given orally in a defined course. It is important to differentiate esophageal candidiasis from other forms of infectious esophagitis such as cytomegalovirus, herpes simplex virus, gastroesophageal reflux disease, medication-induced esophagitis, radiation-induced esophageal injury, and inflammatory conditions such as eosinophilic esophagitis. Except for a few complications such as necrotizing esophageal candidiasis, fistula, and sepsis, the prognosis of esophageal candidiasis has been good.

Growth hormone used to control intractable bleeding caused by radiation-induced gastritis.

Intractable bleeding caused by radiation-induced gastritis is rare. We describe a 69-year-old man with intractable hemorrhagic gastritis induced by postoperative radiotherapy for the treatment of esophageal carcinoma. Although anti-secretory therapy with or without octreotide was initiated for hemostasis over three months, melena still occurred off and on, and the patient required blood transfusions to maintain stable hemoglobin. Finally growth hormone was used in the treatment of hemorrhage for two weeks, and hemostasis was successfully achieved. This is the first report that growth hormone has been used to control intractable bleeding caused by radiation-induced gastritis.

Protective effect of salvianolic acid B on chronic pancreatitis induced by trinitrobenzene sulfonic acid solution in rats.

OBJECTIVES: To investigate the effects of salvianolic acid B (Sal-B) on pancreatic damage in experimental chronic pancreatitis. METHODS: Chronic pancreatitis was induced by infusion of trinitrobenzene sulfonic acid into the pancreatic duct in male Sprague-Dawley rats. From the beginning of 5 weeks, the rats in group 2 were treated with Sal-B by gavage for 8 weeks. Salvianolic acid B was given at a daily dose of 10 mg/kg body weight. At the end of 12 weeks, the levels of serum biochemical indexes were measured on an automatic biochemical analyzer; serum hyaluronic acid and laminin levels were determined by radioimmunoassay; pancreatic tissue malondialdehyde (MDA) was analyzed, and the degree of pancreatic damage was determined. RESULTS: The level of serum biochemical indexes were similar in all groups (P > 0.05 for all). Salvianolic acid B treatment did not obviously reduce hyaluronic acid and laminin concentration in blood (P > 0.05). Salvianolic acid B treatment decreased MDA concentration in pancreatic tissue (P < 0.01). Salvianolic acid B clearly improved pancreatic histological findings and prevented the activation of pancreatic stellate cells. CONCLUSIONS: Sal-B treatment decreased MDA concentration in pancreatic tissue, attenuated morphological pancreatic damage, and prevented the activation of pancreatic stellate cells in experimental chronic pancreatitis.

Endoscopic removal of an accidentally swallowed toothbrush.

A rare case is reported with a large foreign body in the upper gastrointestinal tract. A 19-year-old girl accidentally swallowed her toothbrush which was successfully removed via endoscopy using a polypectomy snare under topical pharyngeal anesthesia. The extracted toothbrush was 20 cm long, and it had the characteristic radiographic image.

Ascorbic acid alleviates pancreatic damage induced by dibutyltin dichloride (DBTC) in rats.

PURPOSE: Because previous studies have reported depleted antioxidant capacity in patients with chronic pancreatitis (CP), prevention of free radical production has gained importance in antifibrotic treatment strategies for CP. The aim of this study was to investigate the effects of ascorbic acid on oxidative capacity and pancreatic damage in experimental CP. MATERIALS AND METHODS: CP was induced in male Sprague-Dawley rats by infusion of dibutyltin dichloride (DBTC) into the tail vein. Ascorbic acid was given intraperitoneally at a daily dose of 10 mg/kg body weight. The treatment groups were as follows: group 1, DBTC plus intraperitoneal physiologic saline; group 2, DBTC plus intraperitoneal ascorbic acid; group 3, solvent plus intraperitoneal physiologic saline; group 4, no operation plus intraperitoneal physiologic saline. Each group contained 15 animals. Treatment was started after CP was established. After 4 weeks of treatment, serum hyaluronic acid and laminin levels were determined by radioimmunoassay, pancreatic tissue oxidative stress was analyzed, and the degree of pancreatic damage was determined. RESULTS: Ascorbic acid treatment markedly increased superoxide dismutase (SOD) activity and decreased malondialdehyde (MDA) concentrations in pancreatic tissue (p < 0.01 for both). Significant serum hyaluronic acid and laminin reductions were observed in group 2 as compared with group 1 (p < 0.05). However, the serum hyaluronic acid and laminin levels remained elevated when compared with those of groups 3 and 4 (p < 0.05). Histopathologic scores were also lower in animals with CP that underwent ascorbic acid-treatment (p < 0.05). CONCLUSION: Ascorbic acid treatment alleviated the degree of oxidative stress and pancreatic damage in rat CP. Antioxidant treatment might be considered a potential option to improve the pathologic process in CP.

Plasma level of thrombomodulin is an early indication of pancreatic necrosis in patients with acute pancreatitis.

BACKGROUND: The potential to predict pancreatic necrosis within the first 48 h by using plasma soluble thrombomodulin (sTM) in 104 patients with acute pancreatitis (AP) was analyzed in a prospective 5-year investigation performed at a single institution. METHODS: According to Balthazar CT grade, pancreatitis was classified as no necrosis in 72 patients, one-third necrotic in 18 patients, one-half necrotic in 10 patients and more than one-half necrotic in 4 patients. Blood was collected at the first 48 hours after the onset of pain and analyzed for sTM. RESULTS: In the healthy volunteers, plasma levels of TM were 16.49+/-5.24 microg/L. By comparison, the mean plasma levels of TM in each group of pancreatitis patients were as follows: CT grade A group, 34.21+/-10.73 microg/L; CT grade B group, 36.18+/-12.50 microg/L; CT grade C group, 49.39+/-18.38 microg/L; CT grade D group, 114.46+/-39.44 microg/L; CT grade E group, 100.22+/-15.97 microg/L (p<0.01). And for the patients, the Pearson correlation coefficient between the CT grade and TM values was 0.784 (p<0.01). No necrosis group, 39.22+/-13.75 microg/L; one-third necrotic group, 71.44+/-18.02 microg/L; one-half necrotic group, 123.50+/-28.57 microg/L; more than one-half necrotic group, 129.00+/-33.28 microg/L (p<0.01); And for the patients, the Pearson correlation coefficient between the degree of necrosis and TM values was 0.888 (p<0.01). ROC analysis indicated the area under the ROC curve (AUC +/- SE) for sTM was 0.949+/-0.020, clearly supportive of the high accuracy of this index in predicting the necrosis of AP. CONCLUSION: Plasma soluble thrombomodulin (sTM) is a potential marker to predict pancreatic necrosis within the first 48 h, and further investigation in a multicentre study is necessary.

[Harmine induces apoptosis in human SGC-7901 cells].

OBJECTIVE: [corrected] To investigate the effect of apoptosis induced in human SGC-7901 cells by Harmine. METHODS: The effect of Harmine on human SGC-7901 cell survival and apoptosis was determined by MTT assay, light microscopy and flow cytometry. Cell genomic DNA was detected by agarose electrophoresis. RESULTS: The survival of human SGC-7901 cells decreased; Apoptotic cells were observed by fluorescent microscope; FCM analysis showed that the peak of apoptosis increased. Typical DNA Ladder were detected in DNA agarose gel electrophoresis. CONCLUSION: HM can induce apoptosis in human SGC-7901 cells.

Distribution of H.pylori antigens in gastric mucosa and its significance.

OBJECTIVE: To investigate the distribution of H.pylori antigens in the gastric mucosa in patients with H.pylori infection, and the relationship between the distribution and gastric cancer. METHODS: Of 112 patients confirmed by pathological study to have chronic superficial gastritis, precancerous changes (chronic atrophic gastritis, intestinal metaplasia or atypical hyperplasia) and gastric cancer, 28 were H.pylori negative and 84 were H.pylori positive. H.pylori antigens in the gastric mucosa were detected by immunohistochemistry. RESULTS: The H.pylori positive group, comprised 12 of 22 (50.0%) in the chronic superficial gastritis group, 22 of 25 (88.0%) in the precancerous changes group and 13 of 35 (37.1%) in the gastric cancer group. The positive rates of H.pylori antigens in the cytoplasm progressively increased, respectively at 0.0% (0/12), 63.6% (14/22) and 84.6% (11/13) for the same groups (chi(2)=19.76, P=0.000); H.pylori antigens were located in the mucus layer and above the neck of the mucosal gland in 9 of 12 (75.0%) cases with chronic superficial gastritis, at the neck of the mucosal gland and the isthmus in 12 of 22 (54.5%) cases with precancerous changes, below the isthmus in 9 of 13 (69.2%) cases with gastric cancer (chi(2)=25.30, P=0.000). In the H.pylori negative group, no H.pylori antigen was observed. CONCLUSION: With the progression of chronic superficial gastritis-->precancerous changes-->gastric cancer, H.pylori antigens progressively migrated from the outer part to the inner part of the cell, and from the superficial to the deep gastric mucosa.

[Plasma levels of ascorbic acid and vitamin E in patients with liver cirrhosis].

OBJECTIVE: To investigate the plasma levels of ascorbic acid and vitamin E in patients with liver cirrhosis and to explore their significance. METHODS: The plasma levels of ascorbic acid,vitamin E and lipoperoxides in patients with liver cirrhosis were measured, and the results were compared with those of sex-and age-matched healthy subjects. RESULT: The plasma levels of ascorbic acid, vitamin E and lipoperoxides in the patients group were (42.94 +/-6.99)micromol/L, (17.99 +/-3.51)micromol/L and (14.09 +/-1.28)micromol/L, respectively, while those in the control group were (53.30 +/-9.45)micromol/L (t=9.50, P=0.000), (24.59 +/-7.22)micromol/L (t=7.94, P=0.000) and (12.11 +/-1.20)micromol/L (t=17.21, P=0.000), respectively. CONCLUSION: The levels of ascorbic acid and vitamin E in patients with liver cirrhosis decrease significantly,which may indicates the disturbance of balance between oxidation and antioxidation.

Detection of H.pylori DNA in gastric epithelial cells by in situ hybridization.

AIM: To investigate the presence of H.pylori DNA within gastric epithelial cells in patients with H.pylori infection and its possible carcinogenic mechanism. METHODS: Total 112 patients, with pathologically confirmed chronic superficial gastritis, chronic atrophic gastritis, intestinal metaplasia, atypical hyperplasia or gastric cancer were studied. Among them, 28 were H.pylori negative and 84 H.pylori positive. H.pylori DNA in gastric epithelial cells was detected by GenPoint catalyzed signal amplification system for in situ hybridization. RESULTS: In the H.pylori positive group, zero out of 24 chronic superficial gastritis (0.0%), four out of 25 precancerous changes (16.0%) and thirteen out of 35 gastric cancers (37.1%) showed H.pylori DNA in the nucleus of gastric epithelial cells, the positive rates of H.pylori DNA in the nucleus of gastric epithelial cells were progressively increased in chronic superficial gastritis, precancerous changes and gastric cancer groups (chi(2)=12.56, P=0.002); One out of 24 chronic superficial gastritis (4.2%), eleven out of 25 precancerous changes (44.0%) and thirteen out of 35 gastric cancers (37.1%) showed H.pylori DNA in the cytoplasm of gastric epithelial cells (chi(2)=10.86, P=0.004). In the H.pylori negative group, only one patient with gastric cancer was found H.pylori DNA in the nucleus of gastric epithelial cells; Only two patients, one patient with precancerous changes and another with gastric cancer, showed H.pylori DNA in the cytoplasm of gastric epithelial cells. Furthermore, H.pylori DNA must have been in the cytoplasm as long as it existed in the nucleus of gastric epithelial cells. CONCLUSION: H.pylori DNA exists both in the nucleus and the cytoplasm of gastric epithelial cells in patients with H.pylori infections. The pathological progression from chronic superficial gastritis, precancerous changes to gastric cancer is associated with higher positive rates of H.pylori DNA presence in the nucleus of gastric epithelial cells.