Retracted: Obestatin Plays Beneficial Role in Cardiomyocyte Injury Induced by Ischemia-Reperfusion In Vivo and In Vitro.

The Editors of Medical Science Monitor wish to inform you that the above manuscript has been retracted from publication due to concerns with the credibility and originality of the study, the manuscript content, and the Figure images. Reference: Qin Zhang, Xin-wei Dong, Jia-ying Xia, Ke-ying Xu, Zhe-rong Xu. Obestatin Plays Beneficial Role in Cardiomyocyte Injury Induced by Ischemia-Reperfusion In Vivo and In Vitro. Med Sci Monit, 2017; 23: 2127-2136. DOI: 10.12659/MSM.901361.

Ultrasound for Measuring the Cross-Sectional Area of Biceps Brachii Muscle in Sarcopenia.

Background: Ultrasound is emerging as an effective method for measuring muscle mass in elderly people. It has been applied in numerous studies to obtain measurement of lower limbs. The study aims to explore the relationship between sarcopenia and ultrasound measurements of biceps brachii. Methods: Participants (n=179) aged over 60 years were enrolled from the first affiliated hospital of Zhejiang University. The muscle thickness (MT), cross-sectional area (CSA) and fat thickness (FT) of these participants were recorded. Spearman test and partial correlation test was used to determine the correlation between indicators. Mann-Whitney U test was performed to compare ultrasonic parameters between sarcopenia group and non-sarcopenia group. The binary logistic regression analysis was employed to detect the potential indicators and prediction equation of sarcopenia. Receiver operating characteristic (ROC) curve analysis was performed for the accuracy of equation. Results: The prevalence of sarcopenia were 16.3% and 10.8% respectively in men and women. CSA was significantly lower in sarcopenia group than non-sarcopenia group in women (P<0.05). CSA was positively correlated with skeletal muscle mass index (SMI) and grip strength (men: r=0.460, 0.433; women: r=0.267, 0.392). After controlling of age and BMI, these correlations disappeared. Binary logistic regression analysis showed that age (OR=1.149, 95%CI: 1.060-1.246; P=0.001) and CSA (OR=0.465, 95%CI: 0.225-0.963; P=0.039) was significant indicators associated with sarcopenia. Area Under Curve was 0.822 (95%CI: 0.725-0.919, P<0.001) for the prediction equation composed of age, gender and CSA for sarcopenia. Conclusion: CSA of the biceps brachii measured with ultrasound is an important indicator associated with sarcopenia.

Obestatin Plays Beneficial Role in Cardiomyocyte Injury Induced by Ischemia-Reperfusion In Vivo and In Vitro.

BACKGROUND Obestatin, primarily recognized as a peptide within the gastrointestinal system, has been shown to benefit the cardiovascular system. We designed this experiment to study the protective role and underlying mechanism of obestatin against ischemia-reperfusion(I/R) injury in myocardial cells. MATERIAL AND METHODS In an In vivo experiment, LAD was ligated for 0.5 h and then opened for reperfusion with obestatin for 24 h. Then, the infarction area was shown with TTC staining, and inflammation factors in serum were analyzed by qRT-PCR. In primary cultured cardiomyocytes, we measured the level of LDH, MDA, GSH, and SOD. Finally, we assessed cells apoptosis using flow cytometry and detected the concentrations of caspase-3, Bax, and Bcl-2 using Western blot analysis. RESULTS TTC staining showed that in the 3 obestatin groups, the infarct area became smaller with the increase of obestatin concentration. Obestatin also inhibited LDH expression in rat serum and decreased mRNA levels of TNF-α, IL-6, ICAM-1, and iNOS in rat cardiomyocytes after reperfusion. In primary cultured cardiomyocytes, obestatin decreased LDH content and increased GSH level after I/R injury. Obestatin was also found to antagonize the apoptosis of cardiomyocytes in a dose-dependent manner. Western blot analysis showed that obestatin downregulated the expression of caspase-3 and Bax and upregulated the expression of Bcl-2. CONCLUSIONS Obestatin can protect cardiomyocyte from I/R-induced injury in vitro and in vivo. This beneficial effect is closely related with its properties of anti-inflammation, anti-cytotoxicity, and anti-apoptosis. The protective effect of obestatin might be associated with activation of Bcl-2 and inhibition of caspase-3 and Bax.

The effectiveness of leucine on muscle protein synthesis, lean body mass and leg lean mass accretion in older people: a systematic review and meta-analysis.

In the present study, we performed a meta-analysis to assess the ability of leucine supplementation to increase the muscle protein fraction synthetic rate and to augment lean body mass or leg lean mass in elderly patients. A literature search was conducted on Medline, Cochrane, EMBASE and Google Scholar databases up to 31 December 2013 for clinical trials that investigated the administration of leucine as a nutrient that affects muscle protein metabolism and muscle mass in elderly subjects. The included studies were randomised controlled trials. The primary outcome for the meta-analysis was the protein fractional synthetic rate. Secondary outcomes included lean body mass and leg lean mass. A total of nine studies were included in the meta-analysis. The results showed that the muscle protein fractional synthetic rate after intervention significantly increased in the leucine group compared with the control group (pooled standardised difference in mean changes 1·08, 95% CI 0·50, 1·67; P< 0·001). No difference was found between the groups in relation to lean body mass (pooled standardised difference in mean changes 0·18, 95% CI - 0·18, 0·54; P= 0·318) or leg lean mass (pooled standardised difference in mean changes 0·006, 95% CI - 0·32, 0·44; P= 0·756). These findings suggest that leucine supplementation is useful to address the age-related decline in muscle mass in elderly individuals, as it increases the muscle protein fractional synthetic rate.

[Therapeutic effects and mechanisms of androgen and simvastatin on osteoporosis in castrated rats].

OBJECTIVE: To study the therapeutic effects and mechanisms of androgen and simvastatin on osteoporosis in castrated rats. METHODS: Fifty 12-month-old male SD rats were divided into five groups randomly: castrated group (A), sham operated group (B), androgen group (C), simvastatin group (D), androgen+ simvastatin group (E). Each group has 10 rats. In this study, osteoporosis model was established by castration.All the groups were given testis and epididymis resection except sham operated group. The drugs were administrated on 9 weeks after operation. C, D and E group were treated by the different drugs lavage for 12 weeks. A and B group were given normal saline at the same time. Lumbar spine bone mineral densities (BMD) of rats were measured on pre-operation, before administration, 6 weeks and 12 weeks after administration.All rats were sacrificed on 12 weeks after administration. Serum osteocalcin (BGP), interleukin-6 (IL-6) and Ca2+ were measured. Bone histology was observed. RESULTS: After the treatment by simvastatin or androgen for 12 weeks, BMD of the group C and group D was significantly higher than that of group A (P<0.01). After the treatment by simvastatin and androgen for 6 weeks, BMD of the group E was significantly higher than that of group A, C and D (P<0.05). The level of serum BGP in group A was significantly lower than that in group B (P<0.05) and the level of serum BGP in group E was significantly higher than that in group B (P<0.05). The serum IL-6 in each treated group were significantly lower than that in group A (P<0.05). CONCLUSION: The combination of simvastatin and androgen could inhibit bone absorption and promote bone formation, which could improve the osteoporosis.

Pain Characteristics and Progression to Sarcopenia in Chinese Middle-Aged and Older Adults: A 4-Year Longitudinal Study.

BACKGROUND: It is imperative for public health to identify the factors that contribute to the progression of sarcopenia among middle-aged and older adults. Our study aimed to investigate the association between pain characteristics and the progression to sarcopenia and its subcomponents among middle-aged and older adults in China. METHODS: We included 5 568 participants from the China Health and Retirement Longitudinal Study. All participants completed assessments for pain characteristics and sarcopenia. Pain assessment included pain status (baseline pain, incident pain, and pain persistence) and pain distribution (single-site pain and multisite pain) using a self-report questionnaire. Diagnosis of sarcopenia followed The Asian Working Group for Sarcopenia 2019 consensus. The odds ratios (ORs) and 95% confidence intervals (CIs) were obtained by logical regression analysis. RESULTS: Participants who reported baseline pain, multisite pain, pain persistence, or multisite pain persistence were more likely to progress to sarcopenia than those without pain, with ORs of 1.33 (95% CI: 1.08-1.65), 1.44 (95% CI: 1.15-1.80), 1.63 (95% CI: 1.23-2.14), and 1.59 (95% CI: 1.19-2.11), respectively. Even after adjusting for other covariates such as gender, age, residential area, education level, marital status, smoking, alcohol consumption, comorbidities, and falls, these associations remained significant. Additionally, pain persistence and multisite pain persistence were significantly associated with low grip strength and clinically meaningful Short Physical Performance Battery decline, but not with low muscle mass. CONCLUSIONS: Our study showed that pain, especially pain persistence, was closely correlated to the increased risk of progression to sarcopenia in Chinese middle-aged and older adults.

The Relationship Between Chronic Pain and Cognitive Impairment in the Elderly: A Review of Current Evidence.

Chronic pain and cognitive impairment are prevalent geriatric syndromes in the population of older adults, and they are the main cause of disability in people over sixty-five years of age. As the global population continues to age, chronic pain and cognitive impairment will affect an increasing number of older adults. While numerous studies in recent years have shown that chronic pain is associated with cognitive decline, the exact mechanisms linking the two remain unclear. In this review, we aim to present the available evidence on the connection between chronic pain and cognitive impairment and to discuss the potential mechanisms by which chronic pain affects cognitive function. In addition, we review potential therapeutic interventions targeting psychological factors, microglia activation, and altered gut flora that may improve and prevent cognitive decline in people with chronic pain.

Sarcopenia and Chronic Pain in the Elderly: A Systematic Review and Meta-Analysis.

Objective: Sarcopenia and chronic pain are prevalent among older adults, and despite numerous studies, the potential epidemiological link between the two conditions remains a topic of controversy. Therefore, we performed a comprehensive systematic review and meta-analysis to assess the relationship between chronic pain and sarcopenia in the elderly. Methods: EMBASE, Web of Science, PubMed, and the Cochrane Library were searched through 22 March 2023 with additional manual searches of reference lists of included studies and relevant reviews. We used a random effects model to conduct the meta-analysis and evaluated heterogeneity across studies with Cochran's Q statistic and I2. Subgroup analyses were conducted based on income level, diagnostic criteria for sarcopenia, and pain site. Results: 17 observational studies (33,600 participants, 49% female) were included, of which 6 articles were retrieved for narrative review. The pooled prevalence of sarcopenia and the pooled odds ratios (OR) between chronic pain and sarcopenia were extracted from the remaining 11 studies. The pooled prevalence of sarcopenia among older adults suffering from chronic pain was 0.11 (95% CI, 0.08-0.18). Our analysis revealed a statistically significant positive association between chronic pain and an increased risk of sarcopenia, yielding a pooled OR of 1.52 (95% CI, 1.31-1.76). Furthermore, our subgroup analysis demonstrated that the low-income countries group showed a stronger association (OR, 1.73; 95% CI, 1.54-1.95) between chronic pain and sarcopenia than the high-income countries group (OR, 1.38; 95% CI, 1.20-1.60). Conclusion: Older adults with chronic pain have a significantly higher prevalence of sarcopenia and risk of developing sarcopenia compared to those without pain. These findings highlight the importance of prioritizing the assessment and early detection of chronic pain in older people, as well as implementing proactive intervention measures in clinical practice. In addition, our results suggest that older people with chronic pain should be actively screened for sarcopenia. Prospero Registration Number: CRD42021239807.

Cullin-3 intervenes in muscle atrophy in the elderly by mediating the degradation of nAchRs ubiquitination.

Sarcopenia involves in the loss of muscle mass associated with aging, which is the major cause of progressive muscle weakness and deterioration in older adults. Muscle atrophy is a direct presentation of sarcopenia, and it greatly contributes to the decline in quality of life among older adults. Neuromuscular junction (NMJ) stability is the key link to maintain muscle function. Besides, the degenerative change of NMJ promotes the process of muscle atrophy in the elderly. Based on previous transcriptome sequencing and bioinformatics analyses of aged muscle, this study used the 18-month-old aged mouse model and the 6-month-old young mouse model to deliberate the role and underlying mechanisms of Cullin-3 (Cul3) in age-related muscle atrophy. The results of reverse transcriptase polymerase chain reaction (RT-PCR) and immunoblotting analysis showed that the expression of CUL3 increased in aged muscle tissue, while the expression level of postsynaptic membrane nicotinic acetylcholine receptors (nAChRs) decreased significantly, which manfested a negative correlation. Meanwhile, immunofluorescence demonstrated that Cul3 was highly expressed in senile muscle NMJ. The results of ubiquitin indicated that the ubiquitin level of aged muscle nAChRs was evidently increased. Co-immunoprecipitation furtherly verified the correlation between Cul3 and nAChRs. Taken together, Cul3 may mediate the ubiquitination degradation of nAChRs protein at the NMJ site in aged mice, leading to NMJ degeneration and accelerated atrophy of fast-twitch muscle fibers in aged muscle. As a prominent element to maintain the stability of NMJ, Cul3 is supposed to be one of candidate intervention targets in sarcopenia.

Lactobacillus rhamnosus GG Promotes Recovery of the Colon Barrier in Septic Mice through Accelerating ISCs Regeneration.

Disruption of the intestinal barrier is both the cause and result of sepsis. The proliferation and differentiation of intestinal stem cells (ISCs) promote the regenerative nature of intestinal epithelial cells, repairing the injured intestinal mucosal barrier; however, it is uncertain whether the recovery effects mediated by the ISCs are related to the gut microbiota. This research found that the survival rate of septic mice was improved with a Lactobacillus rhamnosus GG (LGG) treatment. Furthermore, an increased proliferation and decreased apoptosis in colon epithelial cells were observed in the LGG-treated septic mice. In vitro, we found that a LGG supernatant was effective in maintaining the colonoid morphology and proliferation under the damage of TNF-α. Both in the mice colon and the colonoid, the LGG-induced barrier repair process was accompanied by an increased expression of Lgr5+ and lysozyme+ cells. This may be attributed to the upregulation of the IL-17, retinol metabolism, NF-kappa B and the MAPK signaling pathways, among which, Tnfaip3 and Nfkbia could be used as two potential biomarkers for LGG in intestinal inflammation therapy. In conclusion, our finding suggests that LGG protects a sepsis-injured intestinal barrier by promoting ISCs regeneration, highlighting the protective mechanism of oral probiotic consumption in sepsis.

Phenotypes and clinical significance of circulating CD4(+)CD25(+) regulatory T cells (Tregs) in patients with acute-on-chronic liver failure (ACLF).

BACKGROUND: CD4(+)CD25(+) regulatory T cells (Tregs) play an important role in maintaining immunological tolerance to self and foreign antigens. T cell receptors (TCR) reflect the composition and function of T cells. It is not universally agreed that there is a relationship between CD4(+)CD25(+) Treg frequency and the severity of acute-on-chronic liver failure (ACLF). The repertoire of TCR beta chain variable (TCRBV) regions of peripheral Tregs in ACLF patients is not well understood. METHODS: Human PBMCs were separated and sorted into CD4(+)CD25(+) Treg subsets using density gradient centrifugation and magnetic activated cell sorting (MACS). The CD4(+)CD25(high) Treg frequency in peripheral blood of ACLF and chronic hepatitis B (CHB) patients was measured by flow cytometry. The molecular profiles of TCRBV CDR3 were determined using gene melting spectral pattern (GMSP) analysis. TCRBV gene families were cloned and sequenced when the GMSP profiles showed a single-peak. RESULTS: CD4(+)CD25(high) Treg prevalence in peripheral blood of ACLF patients is increased significantly compared to healthy donors (HDs) (P < 0.01) and CHB patients (P < 0.01). The prevalence of CD4(+)CD25(high) Tregs in ACLF or CHB patients is positively correlated with HBV DNA load. The TCRBV11, BV13.1, BV18, BV20 are the most prevalent TCRBV in CD4(+)CD25(+) Tregs in ACLF and CHB patients. In addition, the CDR3 motifs were relatively conserved in these four TCRBV gene families. CONCLUSIONS: The CD4(+)CD25(high) Tregs prevalence in peripheral blood is indicative of disease severity in ACLF or CHB patients. The relatively conserved TCRBV20 CDR3 motif "TGTGHSPLH" and TCRBV11 CDR3 motif "VYNEQ" may be used in helping diagnosis and treat patients with ACLF.

[Atorvastatin inhibits the H2O2-induced apoptosis of human vascular endothelial cells through a down-regulation of cleaved caspase-9/caspase-3].

OBJECTIVE: To investigate the effect and potential mechanism of atorvastatin against H2O2-induced apoptosis of human umbilical vein endothelial cells (ECV-304). METHODS: ECV-304 cells were pretreated with different concentrations of atorvastatin (0.1, 1 and 10 µmol/L) for 2 h, followed by an exposure to 100 µmol/L H2O2 for 18 h. Cellular morphology was observed under fluorescence microscope. Cellular viability and apoptosis were evaluated by methyl thiazolyl tetrazolium (MTT) and flow cytometry. Finally the expressions of cleaved caspase-3 and caspase-9 were measured by Western blot. RESULTS: H2O2 treatment caused an obvious apoptosis of ECV-304 cells and significantly decreased the cellular viability as characterized by a high percentage (50.71%) of apoptotic cells. Atorvastatin pretreatment inhibit cellular apoptosis induced by H2O2 (39.45%, 20.53% and 7.83%). Western blot assay showed that H2O2 treatment caused a high expression of cleaved caspase-3 and caspase-9 while atorvastatin pretreatment obviously inhibited the expression in a dose-dependent manner. CONCLUSIONS: Atorvastatin inhibits the H2O2-induced apoptosis of ECV-304 cells in a dose-dependent manner. This effect may be associated with the down-regulation of cleaved caspase-9/caspase-3.

[Plasma gamma-glutamyl transpeptidase level as a cardiovascular risk factor in elderly patients with hypertension or hypertension with diabetes mellitus].

OBJECTIVE: To investigate plasma gamma-glutamyl transpeptidase (γ-GGT) level as a cardiovascular risk factor in elderly patients with hypertension or hypertension with diabetes mellitus. METHODS: Forty-nine elderly patients of hypertension and 42 elderly patients of hypertension with diabetes mellitus and 39 healthy elderly subjects were enrolled in the study. The height, weight and blood pressure of patients were measured, serum C reactive protein and other biochemical indicators were detected. The relation between plasma γ-GGT and cardiovascular risk factors in three groups were analyzed. RESULTS: There was no significant difference in plasma γ-GGT levels among three groups. There was a positive correlation of plasma γ-GGT levels with systolic pressure, pulse pressure, hemoglobin A1c and CRP in control group. While in hypertension with diabetes mellitus group, plasma γ-GGT levels were correlated with systolic pressure, mean arterial pressure, fasting blood sugar and cystatin. CONCLUSION: Plasma γ-GGT might be a risk factor for cardiovascular diseases, and may be used as a predictive indicator for kidney injury in early patients with hypertension with diabetes mellitus.

CUL3 and COPS5 Related to the Ubiquitin-Proteasome Pathway Are Potential Genes for Muscle Atrophy in Mice.

Sarcopenia is a condition that reduces muscle mass and exercise capacity. Muscle atrophy is a common manifestation of sarcopenia and can increase morbidity and mortality in specific patient populations. The aim of this study was to identify novel prognostic biomarkers for muscle atrophy and associated pathway analysis using bioinformatics methods. The samples were first divided into different age groups and different muscle type groups, respectively, and each of these samples was analyzed for differences to obtain two groups of differentially expressed genes (DEGs). The two groups of DEGs were intersected using Venn diagrams to obtain 1,630 overlapping genes, and enrichment analysis was performed to observe the Gene Ontology (GO) functional terms of overlapping genes and the enrichment of the Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway. Subsequently, WGCNA (weighted gene coexpression network analysis) was used to find gene modules associated with both the age and muscle type to obtain the lightgreen module. The genes in the key modules were analyzed using PPI, and the top five genes were obtained using the MCC (maximum correntropy criterion) algorithm. Finally, CUL3 and COPS5 were obtained by comparing gene expression levels and analyzing the respective KEGG pathways using gene set enrichment analysis (GSEA). In conclusion, we identified that CUL3 and COPS5 may be novel prognostic biomarkers in muscle atrophy based on bioinformatics analysis. CUL3 and COPS5 are associated with the ubiquitin-proteasome pathway.

Colorectal Cancer Chemotherapy Drug Bevacizumab May Induce Muscle Atrophy Through CDKN1A and TIMP4.

The muscle in the organism has the function of regulating metabolism. Long-term muscle inactivity or the occurrence of chronic inflammatory diseases are easy to induce muscle atrophy. Bevacizumab is an antiangiogenic drug that prevents the formation of neovascularization by inhibiting the activation of VEGF signaling pathway. It is used in the first-line treatment of many cancers in clinic. Studies have shown that the use of bevacizumab in the treatment of tumors can cause muscle mass loss and may induce muscle atrophy. Based on bioinformatics analysis, this study sought the relationship and influence mechanism between bevacizumab and muscle atrophy. The differences of gene and sample expression between bevacizumab treated group and control group were studied by RNA sequencing. WGCNA is used to find gene modules related to bevacizumab administration and explore biological functions through metascape. Differential analysis was used to analyze the difference of gene expression between the administration group and the control group in different muscle tissues. The key genes timp4 and CDKN1A were obtained through Venn diagram, and then GSEA was used to explore their biological functions in RNA sequencing data and geo chip data. This study studied the role of bevacizumab in muscle through the above methods, preliminarily determined that timp4 and CDKN1A may be related to muscle atrophy, and further explored their functional mechanism in bevacizumab myotoxicity.

Cardiac troponin T and autoimmunity in skeletal muscle aging.

Age-related muscle mass and strength decline (sarcopenia) impairs the performance of daily living activities and can lead to mobility disability/limitation in older adults. Biological pathways in muscle that lead to mobility problems have not been fully elucidated. Immunoglobulin G (IgG) infiltration in muscle is a known marker of increased fiber membrane permeability and damage vulnerability, but whether this translates to impaired function is unknown. Here, we report that IgG1 and IgG4 are abundantly present in the skeletal muscle (vastus lateralis) of ~ 50% (11 out of 23) of older adults (> 65 years) examined. Skeletal muscle IgG1 was inversely correlated with physical performance (400 m walk time: r = 0.74, p = 0.005; SPPB score: r = - 0.73, p = 0.006) and muscle strength (r = - 0.6, p = 0.05). In a murine model, IgG was found to be higher in both muscle and blood of older, versus younger, C57BL/6 mice. Older mice with a higher level of muscle IgG had lower motor activity. IgG in mouse muscle co-localized with cardiac troponin T (cTnT) and markers of complement activation and apoptosis/necroptosis. Skeletal muscle-inducible cTnT knockin mice also showed elevated IgG in muscle and an accelerated muscle degeneration and motor activity decline with age. Most importantly, anti-cTnT autoantibodies were detected in the blood of cTnT knockin mice, old mice, and older humans. Our findings suggest a novel cTnT-mediated autoimmune response may be an indicator of sarcopenia.

Expression, purification, and characterization of recombinant lumbrokinase PI239 in Escherichia coli.

Lumbrokinase (LK) is an important fibrinolytic enzyme derived from earthworms. It has been found that LK is composed of a group of isoenzymes. To construct and express the mature peptide of LK PI239 in Escherichia coli, we amplified and optimized the gene of LK which was then cloned into the prokaryotic expression vector pET-22b(-). The recombinant LK (rLK) protein was expressed as inclusion bodies and we have developed a purification process of rLK from these inclusion bodies. A step-down urea concentration strategy was applied to the rLK renaturation process. The purified and renatured rLK apparently ameliorated the conditions of the model thrombosis rats used, and may be developed into a therapeutic agent for thrombotic-associated diseases.

Construction of a recombinant adenovirus vector expressing IL-18BP/IL-4 fusion gene and the anti-inflammatory effect induced by this gene on lipopolysaccharide-stimulated synovial fibroblasts.

OBJECTIVE: To construct a recombinant adenovirus vector for expressing the IL-18 binding protein (IL-18BP)/IL-4 fusion gene and confirm the anti-inflammatory effect of this gene. MATERIALS AND METHODS: The recombinant virus expressing IL-18BP/IL-4 fusion protein (AD-IL-18BP/IL-4) was constructed. AD-IL-18BP/IL-4 was used to infect synovial fibroblasts (SF). ELISA and Western blot analysis were used to determine the expressions of the proteins IL-4 and IL-18BP. To investigate the protective effects of this vector on rheumatoid arthritis, SF were infected with AD-IL-18BP/IL-4 and stimulated by LPS (1 microg/ml) 4 h later. The expression levels of TNF-alpha, IL-6, IL-8, and IL-18 in the culture supernatant were detected by ELISA and production of PGE2 and NO was estimated. The protein expression of COX-2, iNOS, and NF-kappaB p50 in treated SF was analyzed by Western blot. RESULTS: AD-IL-18BP/IL-4 can effectively express the IL-18BP/IL-4 fusion protein. The expressions of TNF-alpha, IL-6, IL-8, and IL-18 were significantly inhibited in LPS-stimulated SF after treatment with AD-IL-18BP/IL-4. The production of PGE2 and NO was significantly decreased. Moreover, NF-kappaB p50, COX-2, and iNOS levels in SF were markedly suppressed by AD-IL-18BP/IL-4. CONCLUSION: AD-IL-18BP/IL-4 can suppress the production and expression of inflammatory cytokines such as COX-2, iNOS, and NF-kappaB in LPS-stimulated SF.

[Changes of blood pressure, blood glucose and blood lipids levels after intensive treatment in incipient diabetes II patients].

OBJECTIVE: To evaluate the effect of intensive treatment on the blood sugar, blood lipids and blood pressure levels in incipient diabetes II patients. METHODS: One hundred and sixty incipient diabetes patients were allocated into two groups according to chronological order: 80 cases received routine treatment and 80 cases received intensive treatment. Fasting blood-glucose (FBG), glycosylated hemoglobin (HbA1C), blood pressure, blood cholesterol (TC), triglyceride (TG), LDL cholesterol-C (LDL-C), alanine aminotransferase (ALT) and aspertate aminotransferase (AST) were tested before treatment. For intensive treatment group blood pressure, blood sugar and blood lipids were regularly tested, and the therapeutic protocols were adjusted according to the test results until the therapeutic target reached. After six months, HbA1C, blood pressure, TC, LDL-C, ALT and AST were tested again and comparison was made between the two groups. RESULTS: There was a significant decrease in TC and LDL-C in the intensive treatment group compared with those in the routine treatment group (P <0.05). CONCLUSION: The intensive treatment on the incipient diabetes II patients facilitate the control of the blood lipids and blood sugar.