ABSTRACT
Objective To explore the effect of Omaha system nursing model on nutritional status and disease condition of patients with low body mass and chronic obstructive pulmonary disease (COPD). Methods Sixty COPD patients with low body mass who were admitted to the First Affiliated Hospital of Huzhou University from January 2015 to November 2016 were enrolled, and they were randomly divided into an Omaha system nursing model group and a routine care intervention group, with 30 cases in each group. The Delphi expert consultation method was used to construct the Omaha nursing problem system and intervention system for COPD patients with low body mass. The patients in the routine care intervention group were given routine care intervention; the patients in the Omaha system nursing model group underwent nutritional intervention according to the Omaha system nursing model. The Mini Nutritional Assessment (MNA), COPD Assessment Test (CAT) and the modified Medical Research Council Dyspnea Scale (mMRC) were used to be the evaluation system of the Omaha system nursing model, the changes of MNA, CAT and mMRC evaluation scores on admission and in 1, 3, and 6 months after discharge in the two groups were recorded, and the correlations between MNA score and CAT, mMRC scores were analyzed. Results Omaha system analysis showed that the main health problems of the Omaha system nursing model group were distributed in the environmental (17.86%), social psychological (8.93%), physiological (19.64%), and health-related behavioral (53.57%) aspects, among which health-related behaviors were mostly common. There were no statistical significant differences in the scores of CAT, mMRC, and MNA between the two groups on admission (all P > 0.05). The CAT and mMRC scores of the Omaha system nursing model group in 1, 3, and 6 months after discharge were significantly lower than those on admission (CAT score: 16.98±2.39, 16.67±2.55, 15.36±2.17 vs. 25.76±3.67; mMRC score: 2.35±0.57, 1.97±0.52, 1.49±0.51 vs. 3.07±0.55, all P < 0.05), MNA scores were significantly higher than those on admission (11.89±3.57, 13.97±3.52, 15.49±3.51 vs. 10.33±3.02, all P < 0.05), and along with the prolongation of time the decrease and increase in scores were more significant. The scores of the Omaha system nursing model group were improved more significantly in 1, 3 and 6 months after discharge than those of the routine care intervention group (CAT score: 16.98±2.39, 16.67±2.55, 15.36±2.17 vs. 23.01±2.67, 21.15±2.79, 19.06±2.61; mMRC score: 2.35±0.57, 1.97±0.52, 1.49±0.51 vs. 3.06±0.65, 3.06±0.61, 2.65±0.67;MNA score: 11.89±3.57, 13.97±3.52, 15.49±3.51 vs. 9.96±3.15, 10.06±3.09, 8.55±3.17, all P < 0.05]. Pearson correlation analyses showed that MNA score was significantly negatively correlated with CAT score (r = -0.493, P = 0.001) and with mMRC score (r = -0.594, P = 0.001) respectively. Conclusion Using the Omaha system nursing model for nutrition intervention in COPD patients with low body mass can significantly improve their nutritional status and disease condition as well as quality of life.
ABSTRACT
SUMOylation is recently found to function as a targeting signal for the degradation of substrates through the ubiquitin-proteasome system. RNF4 is the most studied human SUMO-targeted ubiquitin E3 ligase. However, the relationship between SUMO proteases, SENPs, and RNF4 remains obscure. There are limited examples of the SENP regulation of SUMO2/3-targeted proteolysis mediated by RNF4. The present study investigated the role of SENP3 in the global protein turnover related to SUMO2/3-targeted ubiquitination and focused in particular on the SENP3 regulation of the stability of Sp1. Our data demonstrated that SENP3 impaired the global ubiquitination profile and promoted the accumulation of many proteins. Sp1, a cancer-associated transcription factor, was among these proteins. SENP3 increased the level of Sp1 protein via antagonizing the SUMO2/3-targeted ubiquitination and the consequent proteasome-dependent degradation that was mediated by RNF4. De-conjugation of SUMO2/3 by SENP3 attenuated the interaction of Sp1 with RNF4. In gastric cancer cell lines and specimens derived from patients and nude mice, the level of Sp1 was generally increased in parallel to the level of SENP3. These results provided a new explanation for the enrichment of the Sp1 protein in various cancers, and revealed a regulation of SUMO2/3 conjugated proteins whose levels may be tightly controlled by SENP3 and RNF4.
Subject(s)
Animals , Humans , Mice , Cysteine Endopeptidases , Genetics , Metabolism , Gene Expression Regulation, Neoplastic , Immunoenzyme Techniques , Immunoprecipitation , Mice, Inbred BALB C , Mice, Nude , Prognosis , Protein Processing, Post-Translational , Proteolysis , RNA, Messenger , Genetics , Real-Time Polymerase Chain Reaction , Reverse Transcriptase Polymerase Chain Reaction , Small Ubiquitin-Related Modifier Proteins , Genetics , Metabolism , Sp1 Transcription Factor , Genetics , Metabolism , Stomach Neoplasms , Genetics , Metabolism , Pathology , Sumoylation , Tumor Cells, Cultured , Ubiquitination , Ubiquitins , Genetics , Metabolism , Xenograft Model Antitumor AssaysABSTRACT
BACKGROUND: Liver cirrhosis is characterized by fibrous scarring and hepatocellular regeneration. Matrix metalloproteinases (MMPs) comprise a family of zinc-dependent enzymes that degrade the extracellular matrix (ECM) components. This study examined whether or not gene delivery of human MMP-3 can attenuate established liver cirrhosis in a rat. METHODS: Rat liver cirrhosis was induced by an intraperitoneal injection of dimethylnitrosamine (DMN) three times a week for 8 weeks. The rats were infected once with either a recombinant adenovirus, AdMMP3.GFP, or a control adenovirus, Ad.GFP, into a portal vein and followed up for 3 weeks. In the rat liver tissues, the collagen content, histopathology and immunohistochemical staining were measured. RESULTS: Liver fibrosis in the DMN induced cirrhotic rat was attenuated along with a diminished hydroxyproline content and increased dried liver weight after the gene delivery of AdMMP3.GFP. In addition, the number of activated hepatic stellate cells was lower whereas the proliferation of hepatocytes, which was confirmed by immunohistochemical staining using anti-proliferating cell nuclear antigen (PCNA) antibody, was observed in the AdMMP3.GFP infected rats, suggesting that human MMP-3 stimulated hepatocyte proliferation. CONCLUSIONS: These results suggest that the gene transfer of human MMP-3 in the liver attenuates established fibrosis and induces hepatocyte proliferation. Therefore, gene therapy using MMP-3 in liver cirrhosis might be a promising therapeutic option in the future.
Subject(s)
Animals , Humans , Rats , Adenoviridae , Cicatrix , Collagen , Dimethylnitrosamine , Extracellular Matrix , Fibrosis , Genetic Therapy , Hepatic Stellate Cells , Hepatocytes , Hydroxyproline , Injections, Intraperitoneal , Liver Cirrhosis , Liver , Matrix Metalloproteinases , Models, Animal , Portal Vein , RegenerationABSTRACT
<p><b>OBJECTIVE</b>To evaluate expressions of cyclooxygenase-2 (COX-2) and vascular endothelial growth factor (VEGF) in primary prostate cancer and its clinical significance.</p><p><b>METHODS</b>Expressions of COX-2 and VEGF were detected by immunohistochemical assay in tissues of 40 prostate cancer and 10 benign prostatic hyperplasia samples.</p><p><b>RESULTS</b>COX-2 and VEGF levels in prostate cancer were much higher than those in BPH. The degrees of cancer malignancy and invasion positively correlated with the expressions of COX-2 and VEGF. COX-2 level positively correlated with VEGF level.</p><p><b>CONCLUSION</b>The abnormal expression of COX-2 plays an important role in the development of primary prostate cancer. COX-2 and VEGF are good molecular markers of prostate cancer which are hopeful to be used for the assistant diagnosis and the prediction of prognosis of prostate cancer.</p>