Total Glucosides of Paeony Attenuates Ulcerative Colitis via Inhibiting TLR4/NF-κB Signaling Pathway.

The therapeutic effects and mechanisms of action of total glucosides of paeony (TGP) in treating ulcerative colitis remain to be clarified. Mouse model of ulcerative colitis was treated with TGP and the indexes including scores of disease activity index, gross morphologic damage and histological damage, and inflammatory and oxidative stress markers were determined. Patients with ulcerative colitis received TGP capsule therapy and the indexes including efficacy of colonoscopy and histology, scores of Ulcerative Colitis Activity Index (UCAI) and Short Inflammatory Bowel Disease Questionnaire (SIBDQ), and inflammatory parameters were assessed. The expressions of toll-like receptor 4 (TLR4) and nuclear factor-kappa B (NF-κB) were measured in colonic tissues of mice and patients. TGP treatment significantly increased weight, decreased scores of disease activity index, gross morphologic damage and histological damage, and reduced the levels of tumor necrosis factor-α, interleukin-1ß, malondialdehyde and myeloperoxidase in mouse model. Patients treated with TGP capsule had significantly higher relief rates of diarrhea, abdominal pain, and bloody purulent stool, decreased UCAI and increased SIBDQ scores, and lower levels of erythrocyte sedimentation rate, C-reactive protein and CD4+/CD8+ T-cell ratio than those patients with routine therapy. The overall response rate of TGP capsule was significantly higher than that of routine therapy. TGP treatment significantly suppressed the expressions of TLR4 and NF-κB in colonic tissues of both mouse model and patients with UC. TGP shows a good therapeutic effect on ulcerative colitis in animals and human patients, and the underlying mechanisms may be related to the inhibition of TLR4/NF-κB signaling by TGP.

The Study of Maslow's Hierarchy of Needs Theory in the Doctor-Nurse Integration Teaching Method on Clinical Interns.

The student's attitude towards the doctor-nurse integrated teaching model and Maslow's hierarchy of needs theory is an important topic in clinical teaching. In this study, choosing 134 intern doctors and practice nurses who intern from January to December 2020. 67 students are selected as the control group, and the traditional interns teaching mode is adopted. 67 students are selected as the experimental group and Maslow's hierarchy of needs theory to apply in the doctor-nurse integrated teaching mode. The results show that the doctor-nurse integrated teaching model are accepted by most students, and the application of Maslow's hierarchy of needs theory in the clinical interns has advantages over the traditional model.

Pneumatosis cystoides intestinalis: A case report.

RATIONALE: Pneumatosis cystoides intestinalis (PCI) is a rare condition characterized by multiple gas-filled cysts in the intestinal wall, and can be caused by many conditions. PATIENT CONCERNS: We reported a-69-year-old man with a long history of chronic obstructive pulmonary disease was admitted to the gastroenterology department because of alternating bowel movement and intermittent bloody stool. DIAGNOSES: Colonoscopy revealed multiple nodular protuberances covered with normal-looking mucosa in the ascending and proximal transverse colon. Abdominal computed tomography scan and endoscopic ultrasound revealed multiple gas-filled cystic lesions in the submucosa. The diagnosis of PCI was confirmed by cyst collapse after puncturing with a fine needle. INTERVENTIONS AND OUTCOMES: Considering that the patient had no peritonitis or other complications, conservative approaches, including oxygen inhalation and oral probiotics, were used. The patient was transferred to the anorectal department after 5days of clinical observation in good condition to further treat hemorrhoids. LESSONS: PCI is a rare condition that may be secondary to many other diseases. Because of its atypical clinical manifestations, it can be misdiagnosed as other diseases, such as polyps, inflammatory bowel disease, and even cancer. The diagnosis of PCI depends on computed tomography, colonoscopy, and endoscopic ultrasonography. Fine-needle aspiration may be helpful in the diagnosis and treatment of PCI.

Diameters of left gastric vein and its originating vein on magnetic resonance imaging in liver cirrhosis patients with hepatitis B: Association with endoscopic grades of esophageal varices.

AIM: To determine whether diameters of the left gastric vein (LGV) and its originating vein are associated with endoscopic grades of esophageal varices. METHODS: Ninety-eight liver cirrhotic patients with hepatitis B undergoing magnetic resonance (MR) portography, and upper gastrointestinal endoscopy for grading esophageal varices were enrolled. Diameters of the LGV and its originating vein - the splenic vein (SV) or portal vein (PV) - were measured on MR imaging. Statistical analyses were performed to identify the association of the diameters with the endoscopic grades. RESULTS: Univariate analysis showed that the SV was predominantly the originating vein of the LGV, and diameters of the LGV and SV were associated with grades of esophageal varices. Diameters of the LGV (P = 0.023, odds ratio [OR] = 1.583) and SV (P = 0.012, OR = 2.126) were independent risk factors of presence of the varices. Cut-off LGV diameters of 5.1 mm, 5.9 mm, 6.6 mm, 7.1 mm, 7.8 mm and 5.8 mm; or cut-off SV diameters of 7.3 mm, 7.9 mm, 8.4 mm, 9.5 mm, 10.7 mm and 8.3 mm, could discriminate grades 0 from 1, 0 from 2, 0 from 3, 1 from 3, 2 from 3, and 0-1 from 2-3, respectively. CONCLUSION: Diameters of the LGV and SV are associated with endoscopic grades of esophageal varices.

[Chemoprevention of Barrett's esophagus by celecoxib in rats].

OBJECTIVE: To examine the chemopreventive effect of selective cyclooxygenase-2 (COX-2) inhibitor celecoxib for Barrett's esophagus in rats. METHODS: Fifty 8-week-old male Sprague Dawley rats underwent esophagojejunostomy to induce Barrett's esophagus model. Four weeks after operation the animals were given celecoxib 10 mg/(kg*d(-1))(celecoxib group), or saline 1 ml (control group). Another 10 rats were sham operation group. All animals were sacrificed at 20 week after surgery. The degree of inflammation, Barrett's esophagus, adenocarcinoma, COX-2 expression and PGE(2) of animals were assessed. RESULT: Among 60 rats, 6 rats died in celecoxib group, 8 rats died in control group, 1 rat died in sham operation group, and 45 (75%) rats completed the study. The incidence of mild, moderate and severe degree esophageal inflammation in celecoxib group and control group was 14/19(73.68%), 4/19(21.05%), 1/19(5.26%); 4/17(23.53%), 5/17(29.41%), 8/17(47.06%)(P<0.05), respectively. The incidence of Barrett's esophagus was 7/19(36.84%), 13/17(76.47%) in two group respectively(P<0.05); The incidence of Barrett's esophagus with dysplasia was 2/19(10.53%), 8/17(47.06%)(P<0.05), respectively. The expression of COX-2 was 1/7(14.29%), 10/13(76.92%)(P<0.05) in two groups. PGE2 content was significantly lower in the celecoxib group than that in control group(P<0.001). No esophageal pathological changes were found in sham operation group. CONCLUSION: Selective COX-2 inhibitors celecoxib can inhibit inflammations, development of Barrett's esophagus and esophagus adenocarcinoma.

[Establishment of reflux esophagitis models in rats].

OBJECTIVE: To establish animal models of reflux esophagitis in rats. METHODS: Seventy male Sprague Dawley rats aged 8 weeks were randomly divided into 4 groups: in Group A (n=20) esophagojejunostomy was performed to induce a gastro-jejuno-esophageal reflux; in Group B (n=20) esophagoduodenostomy was performed to induce a gastro-duodeno-esophageal reflux; in Group C (n=20) total gastrectomy plus esophagojejunostomy was performed to induce a jejuno-esophageal reflux; in Group D (n=10) only was performed sham operation (control). RESULT: Among 70 rats, 6 died in Group A, 7 died in Group B, 6 died in Group C, and 72.9 %(51/70) animals were completed in the study. After 12 weeks the incidence of esophageal inflammation was 100.0%; in Groups A, B and C erosion occurred in 11/14 (78.6%), 10/13 (76.9%), 3/14 (21.4%) of animals, respectively; squamous dysplasia was in 10/14 (71.4%), 10/13 (76.9%), 5/14 (35.7%) of rats, respectively; Barrett's esophagus was in 6/14 (42.9%), 5/13 (38.5%), 1/14 (7.1%), respectively. One esophageal adenocarcinoma was found in Group A; no histological changes were observed in Group D. CONCLUSION: The animal models of reflux esophagitis can be induced by esophagojejunostomy, esophagoduodenostomy or total gastrectomy plus esophago-jejunostomy in rats; and the former two surgical modalities are better than the later.

Clinical value of fecal calprotectin in determining disease activity of ulcerative colitis.

AIM: To investigate possibility and clinical application of fecal calprotectin in determining disease activity of ulcerative colitis (UC). METHODS: The enzyme-linked immunosorbent assay (ELISA) was used to measure the concentrations of calprotectin in feces obtained from 66 patients with UC and 20 controls. C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), acid glycoprotein (AGP) were also measured and were compared with calprotectin in determining disease activity of UC. The disease activity of UC was also determined by the Sutherland criteria. RESULTS: The fecal calprotectin concentration in the patients with active UC was significantly higher than that in the inactive UC and in the controls (402.16 +/- 48.0 microg/g vs 35.93 +/- 3.39 microg/g, 11.5 +/- 3.42 microg/g, P < 0.01). The fecal calprotectin concentration in the inactive UC group was significantly higher than that in the control group (P < 0.05). A significant difference was also found in the patients with active UC of mild, moderate and severe degrees. The area under the curve of the receiver operating characteristics (AUCROC) was 0.975, 0.740, 0.692 and 0.737 for fecal calprotectin, CRP, ESR and AGP, respectively. There was a strong correlation between the fecal calprotectin concentration and the endoscopic gradings for UC (r = 0.866, P < 0.001). CONCLUSION: Calprotectin in the patient's feces can reflect the disease activity of UC and can be used as a rational fecal marker for intestinal inflammation in clinical practice. This kind of marker is relatively precise, simple and noninvasive when compared with other commonly-used markers such as CRP, ESR and AGP.

[Significance of fecal lactoferrin in evaluation of disease activity in ulcerative colitis].

OBJECTIVES: To explore the possibility and clinical application value of fecal lactoferrin as a marker of the activity of ulcerative colitis (UC). METHODS: Specimens of feces were collected from 66 UC patients and 20 healthy persons or irritable bowel syndrome patients. ELISA was used to measure the concentration of lactoferrin in feces, and CRP and ESR were also measured. The disease activity of UC was determined by Mayo criteria. RESULTS: The fecal lactoferrin concentration of the patients with active UC was (61.6 +/- 4.8) microg/g, significantly higher than that of the patients with inactive UC and the controls [(7.9 +/- 1.1) microg/g and (3.0 +/- 0.5) microg/g, both P < 0.01], and the fecal lactoferrin concentration of the patients with inactive UC group was also significantly higher than that of the controls (P < 0.05). The higher the grade of activity of disease the higher the concentration of lactoferrin (P < 0.05 or P < 0.01). The area under curve of receiver operating characteristic (AUCROC) of fecal lactoferrin was 0.982, significantly larger than those of the CRP and ESR (0.740 and 0.692 respectively, both P < 0.01). However, there was no significant difference in AUCROC between CPR and ESR. The fecal lactoferrin concentration was positively correlated with the endoscopic grades of UC (r = 0.871, P < 0.01). CONCLUSION: Lactoferrin in feces reflects the disease activity of UC and is a rational fecal marker of intestinal inflammation for clinical application. A precise, simple, and noninvasive method, lactoferrin examination is better than common clinically used markers, such as CRP and ESR.