Decrypting the skeletal toxicity of vertebrates caused by environmental pollutants from an evolutionary perspective: From fish to mammals.

The rapid development of modern society has led to an increasing severity in the generation of new pollutants and the significant emission of old pollutants, exerting considerable pressure on the ecological environment and posing a serious threat to both biological survival and human health. The skeletal system, as a vital supportive structure and functional unit in organisms, is pivotal in maintaining body shape, safeguarding internal organs, storing minerals, and facilitating blood cell production. Although previous studies have uncovered the toxic effects of pollutants on vertebrate skeletal systems, there is a lack of comprehensive literature reviews in this field. Hence, this paper systematically summarizes the toxic effects and mechanisms of environmental pollutants on the skeletons of vertebrates based on the evolutionary context from fish to mammals. Our findings reveal that current research mainly focuses on fish and mammals, and the identified impact mechanisms mainly involve the regulation of bone signaling pathways, oxidative stress response, endocrine system disorders, and immune system dysfunction. This study aims to provide a comprehensive and systematic understanding of research on skeletal toxicity, while also promoting further research and development in related fields.

Multigenerational effects of combined exposure of triphenyltin and micro/nanoplastics on marine medaka (Oryzias melastigma): From molecular levels to behavioral response.

In natural environments, micro/nanoplastics (MNP) inevitably coexist with various pollutants, making it essential to examine their combined toxicity and intergenerational effects on marine organisms. This study investigated the combined toxicity and intergenerational effects of exposure to triphenyltin (T), microplastics (M), nanoplastics (N), a combination of microplastics and triphenyltin (MT), and a combination of nanoplastics and triphenyltin (NT) on marine medaka. The results showed that all treatments had adverse and intergenerational effects on marine medaka. Regarding oxidative stress and energy metabolism, smaller sized plastic particles caused more significant damage to the organisms. However, MT inflicted greater gonadal system damage than NT, leading to imbalanced sex hormone levels. Additionally, T induced hyperactivity in fish, whereas MNP tended to induce behavioral depression. Notably, large plastic particles in the F0 generation had a more pronounced impact on depressive behaviors compared to smaller particles. These findings suggest that both individual and combined exposures to TPT and MNP can detrimentally affect marine medaka from the molecular to behavioral levels, posing risks to population sustainability. This study provided a robust theoretical foundation and deeper insights into the ecotoxicological impacts and risk assessments of coexisting pollutants.

Long-term tralopyril exposure results in endocrinological and transgenerational toxicity: A two-generation study of marine medaka (Oryzias melastigma).

This study aims to investigate the impact of tralopyril, a newly developed marine antifouling agent, on the reproductive endocrine system and developmental toxicity of offspring in marine medaka. The results revealed that exposure to tralopyril (0, 1, 20 µg/L) for 42 days resulted in decreased reproductive capacity in marine medaka. Moreover, it disrupted the levels of sex hormones E2 and T, as well as the transcription levels of genes related to the HPG axis, such as cyp19b and star. Sex-dependent differences were observed, with females experiencing more pronounced effects. Furthermore, intergenerational toxicity was observed in F1 offspring, including increased heart rate, changes in retinal morphology and cartilage structure, decreased swimming activity, and downregulation of transcription levels of relevant genes (HPT axis, GH/IGF axis, cox, bmp4, bmp2, runx2, etc.). Notably, the disruption of the F1 endocrine system by tralopyril persisted into adulthood, indicating a transgenerational effect. Molecular docking analysis suggested that tralopyril's RA receptor activity might be one of the key factors contributing to the developmental toxicity observed in offspring. Overall, our study highlights the potential threat posed by tralopyril to the sustainability of fish populations, as it can disrupt the endocrine system and negatively impact aquatic organisms for multiple generations.

[Control study on colonoscopy skills acquiring from endoscopic simulation system transfering to patients].

OBJECTIVE: To explore the feasibility of transferring the skills from the AccuTouch flexible endoscopy simulator colonoscopy training to clinical practices. METHODS: The novice colonoscopies were divided into 2 groups.Group A (control group) including 4 trainees for traditional training, Group B (experimental group) including 4 trainees for simulator training. After training, we compared the number of cases for achieving independent competence, assisted competence and incompetence in the first ten patients. RESULTS: No significant differences existed between two groups in terms of age and gender (both P > 0.05). Significant differences existed in educational background and the controlled group was better than the experimental group (Z = -2.005, P = 0.04). The cases of independent completion, assisted competence and incompetence of the control and experimental groups were 2, 4, 9 and 21, 29, 15 respectively. Rank tests show that the simulator training was better than the traditional counterpart (average rank: 56.14 vs 24.86, Z = -6.393, P = 0.00). CONCLUSIONS: The skills acquired from AccuTouch Endoscopy Simulator may be well transferred into the clinical colonoscopy environment. It clearly supports the scheme of integrating simulator training into colonoscopic education curricula.

Effects of peri-operative glucose levels on adverse outcomes in infants receiving open-heart surgery for congenital heart disease with cardiopulmonary bypass.

OBJECTIVE: Studies designed to evaluate the association of hyperglycemia and adverse events in pediatric patients receiving open cardiac surgery have yielded inconsistent results. The aim of this retrospective, observational study was to evaluate the effects of peri-operative glucose levels on adverse events in infants receiving open-heart surgery with CPB. METHODS: From Nov 2009 through Dec 2009, 100 infants undergoing open-heart surgery were enrolled. All glucose values during the operation and intensive care unit stay were documented. Metrics of glucose control, including mean, peak and minimum glucose levels were calculated. Hyperglycemia was defined as a mean glucose above 150 mg/dl. Hypoglycemia was defined as minimum glucose below 65 mg/dl. Multivariable regression analyses were used to determine relationships between these metrics of glucose control and a composite morbidity-mortality outcome after controlling for multiple variables known to influence early outcomes after congenital heart surgery. RESULTS: According to our definition, 43 patients (43%) developed hyperglycemia and 9 patients (9%) developed at least one episode of hypoglycemia. A total of 58 patients reached the overall composite morbidity-mortality end point at some point during the study period. After adjusting the effects of age, cross-clamp time and pre-operative percutaneous oxygen saturation by multivariable analysis, euglycemia, defined as mean glucose ≤150 mg/dl, was found to be a significant predictor for morbidity, with an odds ratio of 5.1(95% confidence interval 1.5-17.5). CONCLUSION: In contrast to adult critically ill patients, data from the present study did not prove that hyperglycemia was detrimental to infants receiving open-heart surgery with CPB. The existing literature and findings of our present study warranted future clinical studies of strict glycemic control in critically ill children, considering a more permissive glycemic range as a desirable target.

Spinal Ninjurin2 contributes to the neuropathic pain via NF-κB-mediated neuroinflammation in the spared sciatic nerve injury rats.

OBJECT: Ninjurin2 (nerve injury induced protein 2, NINJ2) is a molecule which mediates cell-to-cell and cell-to-extracellular matrix interactions in the nervous system. Clinical study shows NINJ2 is associated with the development of postherpetic neuralgia. However, it is lack of direct evidence that NINJ2 participated in neuropathic pain. In this study, we aim to investigate the role of NINJ2 in the development of neuropathic pain in spared sciatic nerve injury rats and the underlying mechanism. METHOD: Spared sciatic nerve injury (SNI) models were established. The level of NINJ2 and p-p65 (a NF-κB family member) were measured in SNI rats by western blots and immunofluorescent staining. Lentivirus encoding small interfering RNA targeting NINJ2 (RNAi) was intrathecally injected into rats. Then the change of pain behavior of rats induced by NINJ2 RNAi was tested by Von-Frey hairs. The change of p-p65 in the spinal cord in rats after NINJ2 RNAi treatment was also measured by western blots. inhibitor of p-p65-induced change of TNF-α, IL-1ß, and IL-6 levels were measured by ELISA. RESULTS: NINJ2 and p-p65 were increased in the spinal cord of SNI rats on the 3, 7, 14th days after modeling. NINJ2 were mainly expressed in neurons, and co-located with p-p65 in the spinal dorsal horn. When down regulating the level of NINJ2 by RNAi, the development of pain in SNI rats was partially blocked. Phosphorylation of p65 was also inhibited by NINJ2 RNAi. Blocking the phosphorylation of NF-κB pathway could inhibit the increase of TNF-α, IL-1ß, and IL-6 in the spinal cord of SNI rats. CONCLUSION: NINJ2 protein was increased in the spinal cord of SNI rats. It participated in the development of nerve injury-induced neuropathic pain by activating neuroinflammation in the spinal cord via NF-κB pathway. This study provides a new target to investigate the mechanism of neuropathic pain.

The Roles of Chemokine CXCL13 in the Development of Bone Cancer Pain and the Regulation of Morphine Analgesia in Rats.

Chemokines are important regulators of immune, inflammatory, and neuronal responses in peripheral and central pain pathway. The aim of this study was to investigate whether chemokine (C-X-C motif) ligand 13 (CXCL13) and its receptor (C-X-C chemokine receptor type 5, CXCR5) involve in the development of bone cancer pain (BCP) and the regulation of morphine analgesia in rats. The change of pain behaviors in BCP rats were measured by testing paw withdrawal threshold (PWT). The levels of CXCL13, CXCR5 and signal pathway proteins (p-p38, p-ERK and p-AKT etc.) in the spinal cord were measured via western blots. The expression of CXCL13 and CXCR5 in spinal cord was increased in BCP rats. The BCP rats showed decrease of PWTs, which was relieved by CXCR5i. Intrathecally injection of murine recombinant CXCL13 (mrCXCL13) decreased the PWTs of BCP rats and opposed morphine-induced analgesia in BCP rats. In BCP rats, the signal pathway proteins (p38, ERK and AKT) in the spinal cord were activated. CXCL13 and morphine had contrary effect on the phosphorylation of these proteins. MrCXCL13 directly increased the levels of p-p38, p-ERK and p-AKT in BCP rats. However, morphine decreased the levels of these proteins in BCP rats. While blocking the activation of p-p38, p-ERK and p-AKT, morphine analgesia was enhanced. These results suggest CXCL13 participated in bone cancer pain and opposed morphine analgesia via p38, ERK and AKT pathways. It may be a target to enhance pain management in cancer pain patients.

[Clinical features of unexpected sudden death clustered in 7 families in Yunnan Province].

OBJECTIVE: To investigate the clinical features of unexpected sudden death (SUD) clustered in families in Yunnan province. METHODS: This retrospective study analyzed the clinical features of SUD occurred between July to September 2005 in 7 families in Yunnan province. RESULTS: All 16 SUD patients shared common clinical features such as fatigue and repeated syncope and one group of SUD patients (n = 8 from 4 families) presented with the gastric intestinal tract manifestations including nausea, vomiting, abdominal pain and diarrhea with suspected dietary history and abnormal laboratory enzyme findings (GOT/GPT, CK/CKMB, LDH/LDH1 etc.). In SUD patients without gastric intestinal tract manifestations (n = 8 from 3 families), there were no clear symptoms before death and repeated ventricular tachycardia and ventricular fibrillation were recorded in one survivor. There was no clear evidence for the involvements of hereditary and infectious factors for observed SUD. CONCLUSION: The reason for the unexpected sudden death clustered in 7 families in Yunnan remains unclear. Repeated syncope and fatigue served as the common clinical features in the presence or absence of gastric intestinal tract manifestations in all SUD cases. Further studies are needed to clarify the pathology and detailed clinical manifestations of SUD occurred in this area.

[Pathological study of unexpected sudden death clustered in family or village in Yunnan province: report of 29 cases of autopsy].

OBJECTIVE: To investigate the pathological features and causes of sudden death clustered in family or village in Yunnan province so as to provide the morphological basis for exploring its etiology and medical intervention. METHODS: Autopsy was performed on 29 cases of clustered in family or village in Yunnan province during the period 1991-2006, 16 males and 13 females, aged 32 (8-69), accounting for 10.2% of whole sudden unexpected deaths occurring in the same period. The heart, lung, liver, spleen, brain, kidney, intestinal tract, and other organs were examined macroscopically and histologically, including a study of cardiac conduction system in 5 cases. Pathological diagnosis of myocarditis was based on the Dallas Criteria and World Heart Federation's consensus while the histological evaluation of Keshan disease referred the China national guideline for pathological diagnosis of Keshan disease. RESULTS: Based on the main pathological changes and the causes of death, these cases were classified into seven groups (group A-G). Group A comprised 11 cases (38%) with lymphocytic myocarditis accompanied with focal myocardial necrosis or degeneration. Group B comprised 3 cases (10%) with neutrophil myocarditis accompanied with focal myocytolysis or coagulation necrosis. Group C comprised 4 cases (14%) with arrhythmogenic right ventricle cardiomyopathy in which fatty infiltration of myocardium was the only pathological finding. Group D comprised 2 cases (7%) with ischemic heart disease in which fresh or old foci of myocardial infarction were found but coronary stenosis was shown only in one case. Group E comprised 2 cases (7%) with left ventricle hypertrophy and obstructive muscle bundle in the outflow of left ventricle. Group F comprised 2 cases (7%) with allergic bronchitis or chronic bronchitis and pulmonary emphysema. Group G comprised the remaining 5 cases (17%) without any pathological finding that could explain sudden death. No cases suffered with Keshan disease and dilated cardiomyopathy. Focal but not diffuse inflammatory infiltration was the prominent histological feature of myocarditis in Yunnan cases. Among the five cases with histological examination of cardiac conduction system, 2 cases were detected to suffer from acute hemorrhage in His bundle and its left branching site, and the atrioventricular node of 1 case was involved. Different pathological changes coexisted in 4 pairs of family members as a cluster of sudden deaths. 3 of 4 first deaths had focal myocarditis and the other one had chronic infection. But 3 secondary deaths had myocardial ischemia and the other one had arrhythmogenic right ventricle cardiomyopathy. Pulmonary edema, acute respiratory infection and congestive or ischemic liver necrosis were found in some cases simultaneously. CONCLUSION: The pathological changes of the cases of clustered sudden death in Yunnan province are various, such as myocarditis, myocardial dysplasia and the other lethal heart-lung disorders. No case of Keshan disease has been found. Arrhythmogenic right ventricle cardiomyopathy and other foundational heart diseases might act as a background. It is very hard to contribute only one etiological factor to the clustering of sudden death in Yunnan. It was most likely that multiple factors cluster and trigger an outbreak of death in a definite time and space.

The complete mitochondrial genome of the Tamarisk gerbil, Meriones tamariscinus (Rodentia: Muridae).

The complete mitochondrial genome of the Tamarisk jird, Meriones tamariscinus, was sequenced. The 16,389bp genome contains 37 genes, typical for rodent mitogenomes, including 22 tRNA genes, 2 rRNA genes, and 13 protein-coding genes. The total GC content of the mitochondrial genome is 36.8%, with a base composition of 34.0% A, 24.5% C, 12.3% G, and 29.2% T. The phylogenetic analysis showed that M. tamariscinus was classified in the genus Meriones, Muridae.

[PCR amplification, cloning and protein expression of interferon-inducible transmembrane protein-1 gene].

OBJECTIVE: To study the PCR amplification, cloning and protein expression of interferon-inducible transmembrane protein-1 (IFITMP-1) gene. METHODS: With the cDNA fragment containing IFITMP-1 gene as template, IFITMP-1 gene was amplified using Pfu enzyme by means of PCR. After EcoRI and HindIII digestion, the target gene fragment was linked to pUCm-T plasmid and sequenced. The IFITMP-1 gene was cloned into pET-Trx protein expression plasmid, and the condition for protein expression was optimized. RESULTS: The length of the PCR product of IFITMP-1 gene-containing cDNA fragment was about 1000 bp. The IFITMP-1 gene was successfully inserted into pUCm-T plasmid with correct sequence and cloning of the IFITMP-1 gene into the pET-Trx protein expression plasmid was achieved. Expression of the fusion protein of pUCm-T plasmid and IFITMP-1 gene was detected after IPTG induction. CONCLUSION: Successful amplification and cloning of the IFITMP-1 gene and its protein expression may facilitate further study of the role of IFITMP-1 gene in colorectal cancer.

[Outcome of extracorporeal membrane oxygenation support for adult patients in Fuwai Hospital during the last 10 years: treatment strategy and risk factors].

OBJECTIVE: To retrospectively review the clinical data of patients receiving extracorporeal membrane oxygenation (ECMO) during the last 10 years in Fuwai Hospital in order to assess the factors associated with the outcome of patients who had undergone ECMO, as well as to summarize the clinical experience, and to adopt a treatment strategy for future clinical decision. METHODS: The clinical data of adult patients undergoing ECMO admitted to Fuwai Hospital from December 2004 to December 2014 were retrospectively analyzed. Demographic characteristics, diagnosis, ECMO related data, including ECMO indication, operation, undergoing cardiopulmonary resuscitation (CPR) or not, and site of establishment, clinical parameters before and 24 hours after ECMO, duration of ECMO, and complications were collected to set up a database. The patients were divided into survival group and non-survival group according to the prognosis. The risk factors of mortality in hospital after ECMO were analyzed by logistic regression. RESULTS There were 142 adult patients who had received ECMO support, with 106 male and 36 female. All patients received veno-arterial ECMO (V-A ECMO). The indication of ECMO in 59 patients was unsuccessful weaning from extracorporeal circulation (41.5%), and that of 44 patients was low cardiac output cardiogenic shock (31.0%). CPR was necessary in 34 out of 142 patients undergoing ECMO. In 37 patients intra-aortic balloon pump (IABP) was necessary. ECMO was successfully weaned in 99 patients (69.7%), and 84 patients (59.2%) survived. The most frequent complication during ECMO support was bleeding from site of catheterization or operation (45.8%). Logistic regression revealed that high lactic acid levels [odds ratio (OR) = 1.469, 95% confidence interval (95%CI) = 1.170-1.843, P = 0.001] and high blood glucose (OR = 0.984, 95%CI = 0.969-0.999, P = 0.037) at 24 hours after ECMO, multiple organ dysfunction syndrome (MODS, OR = 17.243, 95%CI = 3.177-93.581, P = 0.001), gastrointestinal bleeding (OR = 8.774, 95%CI = 1.414-54.457, P = 0.020) were risk factors of in-hospital mortality in adult patients undergoing ECMO. CONCLUSIONS: ECMO can provide effective auxiliary support in patients with respiratory and circulatory failure, which 'shows good clinical effect. Strict indication, timely ECMO support and sophisticated management are the keys to the success of ECMO. The most frequent complications during ECMO support is bleeding from site of catheterization or operation. High lactic acid levels at 24 hours after ECMO, MODS and gastrointestinal bleeding are predictors of in-hospital mortality in adult patients, and appropriate control of blood sugar was beneficial for the recovery of patients.

Effects of probiotic on intestinal mucosa of patients with ulcerative colitis.

AIM: To investigate the effects of probiotic on intestinal mucosae of patients with ulcerative colitis (UC), and to evaluate the role of probiotic in preventing the relapse of UC. METHODS: Thirty patients received treatment with sulphasalazine (SASP) and glucocorticoid and then were randomly administered bifid triple viable capsule (BIFICO) (1.26 g/d), or an identical placebo (starch) for 8 wk. Fecal samples were collected for stool culture 2 wk before and after the randomized treatments. The patients were evaluated clinically, endoscopically and histologically after 2 mo of treatment or in case of relapse of UC. p65 and IkappaB expressions were determined by Western blot analysis. DNA-binding activity of NF-kappaB in colonic nuclear extracts was detected by electrophoretic mobility shift assay (EMSA). mRNA expressions of cytokines were identified by semi-quantitative assay, reverse transcriptase- polymerase chain reaction (RT-PCR). RESULTS: Three patients (20%) in the BIFICO group had relapses during 2-mo follow-up period, compared with 14 (93.3%) in placebo group (P<0.01). The concentration of fecal lactobacilli, bifidobacteria was significantly increased in BIFICO-treated group only (P<0.01). The expressions of NF-kappaB p65 and DNA binding activity of NF-kappaB were significantly attenuated in the treatment group than that in control (P<0.05). The mRNA expression of anti-inflammatory cytokines was elevated in comparison with the control group. CONCLUSION: The probiotic could impede the activation of NF-kappaB, decrease the expressions of TNF-alpha and IL-1beta and elevate the expression of IL-10. These results suggest that oral administration of this new probiotic preparation is effective in preventing flare-ups of chronic UC. It may become a prophylactic drug to decrease the relapse of UC.

[The effects of bifidobacterium on the intestinal mucosa of the patients with ulcerative colitis].

OBJECTIVE: To investigate the effects of bifidobacterium (Bf) on the intestinal mucosa of the patients with ulcerative colitis (UC). METHODS: Thirty patients in clinical and endoscopic remission by sulphasalazine and glucocorticoid were randomized to receive either Bifid Triple Viable capsule (BIFICO), 420 mg/d, or an identical placebo (starch) for 8 weeks. Fecal samples were collected for stool culture before and after treatment. Patients were assessed clinically endoscopically and histologically after 2 months or in the case of a relapse. p65 and IkappaB expression was determined by Western blot analysis DNA-binding activity of NF-kappaB in colonic nuclear extracts was detected by electrophoretic mobility shift assay. The mRNA expression of cytokines were identified by a semi-quantitative assay, reverse transcription-polymerase chain reaction. RESULTS: Three patients in the BIFICO group had relapses within the 2-month follow-up period, compared with 14 in the placebo group (P < 0.01). Fecal concentration of lactobacilli, bifidobacteria, increased significantly from baseline levels only in the BIFICO-treated group (P < 0.01). The expression of NF-kappaB p65 and DNA binding activity of NF-kappaB were significantly attenuated in the treat group than that in control (P < 0.05). The mRNA expression of anti-inflammatory cytokines elevated obviously comparable of control group. CONCLUSIONS: The Bf maybe impede the activation of NF-kappaB, decrease the expression of TNF-alpha and IL-1beta and elevate the expression of IL-10. These results suggest that oral administration of this new probiotic preparation is effective in preventing flare-ups of chronic UC. It will become a prophylactic drug delaying the relapse of UC.

[Serrated adenoma of large intestine: report of 7 cases].

From December 2000 to April 2001, 859 patients were examined with coloscopy in our endoscopy centre and 188 cases of adenoma were diagnosed. Among the 188 patients, 7 were found with serrated adenoma that had been confirmed pathologically, including 6 male and 1 female patients, aged 32 to 53 with an average of 44.7 years. All the 7 cases were identified as having single focal lesion, among which 3 were found in the rectum, 1 in the transverse colon, 2 in the ascending colon and 1 in the cecum. The diameter of the lesions ranged from 8 to 27 mm with an average of 15.4 mm.

[Endoscopic diagnosis and treatment of the early-stage malignant colorectal polyp and follow-up study].

In the past 20 years we have performed endoscopic removal of colorectal polyps in 4 000 cases, and thorough histological examination of the removed polyps identified 121 cases of early-stage malignant polyp. According to the depth of malignant invasion and whether malignant remnants were present after the initial surgical removal, conservative treatment or radical operation was implemented. During the follow-up study, endoscopy was performed once each year in all the patients with malignancies. No recurrence was found in the 33 patients with mucosa cancer or in the 27 patients with type I submucosa cancer who did not receive radical operation due to absence of malignant remnants or in the 38 patients with type II submucosa cancer who had the radical operation. Relapse occurred in 1 patient with malignant remnant and in another 3 cases of type II submucasa cancer without radical operation.

[Construction and application of colorectal polyp database].

OBJECTIVE: To study the construction and application of computerized database of colorectal polyp in the clinical management and research of this disease. METHOD: A colorectal polyp database and its management system was constructed on the basis of Microsoft Access 2000. Clinical, endoscopic and pathological data, which went through standardized and elemental processing, of 2 627 cases (4 850 records) of colorectal polyp collected from 1990 to 2000 in Nanfang Hospital was entered into this database. RESULTS: Using this new database, the information on the population and age distribution, location and clinical features of colorectal polyps were obtained. Comparative study of the clinical and pathological findings in the cases, evaluation of the therapeutic effects, statistical review of the identification of the polyp and its canceration in the previous years as well as the analysis of other relevant factors were successfully accomplished, which greatly facilitated the follow-up study of some chosen cases that may be of clinical significance. CONCLUSIONS: Applications of modern informatics and computer technology greatly facilitates case management and clinical research of colorectal polyps, and standardized and elemental processing of the clinical data offers a new possibility for easy case information management.

Establishment of dextran sulfate sodium-induced ulcerative colitis model in mice.

OBJECTIVE: To establish a model of ulcerative colitis in mice. METHODS: The mice were given 5% dextran sulfate sodium (DSS) solution freely for 7 consecutive days after which distilled water was given in stead for another 10 d, to complete one cycle of whole treatment plan that consisted of 4 such cycles. The symptoms were observed daily. At the end of the first and the fourth cycle respectively, the mice were killed for examining the whole colon under anatomic microscopy and serial tissue sections were prepared for histological observation. RESULTS: The symptoms observed in the mice including hematochezia diarrhea and loss of the body weight were similar to those of ulcerative colitis patients. Histological examination revealed infiltration of neutrocytophilia and lymphocythemia, with loss of integrity of the colon mucosa in the gland. CONCLUSION: This mouse model of ulcerative colitis can be easily induced and readily applied in various studies of ulcerative colitis.

[Expression of pro-inflammation cytokines and activation of nuclear factor kappab in the intestinal mucosa of mice with ulcerative colitis].

OBJECTIVE: To investigate the expression of pro-inflammation cytokines and activation of nuclear factor kappaB (NF-kappaB) in mouse models of ulcerative colitis. METHODS: Mouse models of ulcerative colitis were established by oral administration of 5% dextran sulfate sodium for 7 d, and the expression of tumor necrosis factor (TNF)- alpha and interleukin (IL)-1beta in the intestinal mucosa were detected by semi-quantitative reverse transcriptional (RT) PCR. The activation of NF-kappaB in the intestinal mucosa was evaluated by electrophoretic mobility shift assay (EMSA). RESULTS: The expressions of TNF-alpha and IL-1beta were increased in the intestinal mucosa (P=0.009), and the nuclear binding activity of NF-kappaB was also up-regulated after the onset of colitis. CONCLUSION: Pro-inflammatory cytokines play important roles in the pathogenesis of UC, and may exacerbate the inflammation of the intestinal mocosa and cause apoptosis of the epithelial cells, possibly under the regulation of NF-kappaB activation.