The Value of the Monocyte to High-Density Lipoprotein Cholesterol Ratio in Assessing the Severity of Knee Osteoarthritis: A Retrospective Single Center Cohort Study.

Background: Inflammatory responses and metabolic abnormalities play essential roles in the pathophysiology of osteoarthritis (OA). Our study aimed to evaluate the association between monocyte-to-high density lipoprotein-cholesterol ratio (MHR) and OA and compared it with other systemic inflammatory markers. Methods: This study recruited 323 OA cases and age- and sex-matched 283 control participants during the same period. Demographic, clinical, and imaging data and laboratory indicators were obtained from participants' records. Systemic inflammatory markers were calculated for both cohorts. The diagnostic effectiveness of each index for distinguishing patients with OA was analyzed using receiver operating characteristic (ROC) curves. Spearman's method and ordered logistic regression were used to analyze the association between each indicator and Kellgren and Lawrence (KL) grade. Results: MHR was significantly higher (0.38±0.18 vs 0.25±0.07, p < 0.0001) in OA patients than healthy controls. MHR had the largest area under the ROC curve for predicting OA. Analysis of ordered logistic regression indicated that MHR was a risk factor for OA radiological severity. Spearman correlation analysis indicated that MHR significantly correlates with the KL grade. Moreover, MHR was significantly higher in early stage patients than in healthy controls. Conclusion: These results suggest that an elevated MHR could reflect knee OA severity and might be a useful marker for diagnosis and monitoring of OA.

Serum interleukin-38 levels correlated with insulin resistance, liver injury and lipids in non-alcoholic fatty liver disease.

BACKGROUND: Insulin resistance, liver injury and dyslipidemia are reported in non-alcoholic fat liver disease (NAFLD) patients. Interleukin (IL)-38 may take part in the pathophysiology of insulin resistance. Nevertheless, the function of IL-38 in NAFLD is unknown. Herein, we determined whether serum IL-38 level might be utilised as a biochemical marker for diagnosing NAFLD. METHODS: NAFLD patients and healthy participants (n = 91 each) were enrolled. Circulating serum IL-38 levels were detected using enzyme-linked immunosorbent assay. Other metabolic and inflammatory indices related to NAFLD were also assessed. RESULTS: Patients with NAFLD had higher serum IL-38 levels than healthy individuals. Significantly higher serum IL-38 levels were found in patients with severe and moderate NAFLD than in patients with mild NAFLD. IL-38 showed a significant correlation with parameters of insulin resistance, inflammation, and liver enzyme in NAFLD cases. Anthropometric, insulin resistance, inflammatory parameters, lipids and frequency of NAFLD showed significant differences among the serum IL-38 level tertiles. Participants in the 2nd and 3rd tertiles of serum IL-38 levels had a greater risk of NAFLD than those in the 1st tertile. Furthermore, IL-38 ROC curve showed a high area under ROC with 0.861. CONCLUSIONS: It is possible for serum IL-38 to be a biomarker for NAFLD.

[Construction of Vectors Expressing Inhibiting Peptides for Nuclear Import and Its Effect on Growth and Migration of HeLa Cell].

OBJECTIVE: To construct the expression vectors for red fluorescent protein fused with inhibiting peptides for nuclear import (Bimax),and explore the location of Bimax and its potential effects on cell proliferation and migration in HeLa cells. METHODS: Two kinds of polynucleotide encoding inhibiting peptides for nuclear import were synthesis respectively and subsequently annealed for inserting into vector pDs-Red-C1. The recombinant plasmids were transfected into competent bacterial DH-5α. After transfection,the positive bacteria were picked up for DNA sequencing. The recombinant plasmids pDs-Red-Bimax2,pDs-Red-Bimax1 and negative plasmid pDs-Red-C1 were transfected into HeLa cells respectively according to Lipofectamine2000 protocol. After transfection,the expression and location of red fluorescent protein were observed with fluorescence microscope. Furthermore,MTT assay and cell-migration assay were used to detect the proliferation and migration of Bimax transducted cells. RESULTS: DNA sequencing showed that the polynucleotides encoding Bimax1 or Bimax2 were inserted into pDs-Red-C1 vector successfully. After transfected into HeLa cells,the inhibiting peptide induced red fluorescent protein locating in nuclear. Furthermore,either the fusion protein RFP-Bimax1 or RFP-Bimax2 can suppress the proliferation and migration of HeLa cells. CONCLUSION: The expression vectors for red fluorescent protein fused with inhibiting peptides for nuclear import were successfully constructed. In addition,the fusion proteins were expressed and located in nuclear and suppressed the proliferation and migration of tumor cells.

[Construction and identification of eukaryotic expression plasmid expressing siRNA targeting USP22 gene].

OBJECTIVE: To construct eukaryotic expression plasmid expressing siRNA targeting ubiquitin specific peptidase 22 gene (USP22), and to investigate its effect on the growth of hepatoma carcinoma cells HepG2. METHODS: siRNA templates were synthesized based on USP22 mRNA sequence and cloned into vector Pmscv/Hyg/U6. The resulting recombinant was identified by restriction enzyme digestion and DNA sequencing. Recombinants were than transfected into HepG2 cells mediated by liposome. The USP22 protein and mRNA in HepG2 cells were detected by western blot and RT-PCR, respectively. The cellular growth activity was evaluated with MTT assay. RESULTS: Recombinant plasmid expressing siRNA targeting USP22 was successfully constructed. The down-regulated protein and mRNA level of USP22 and decreased cellular growth in HepG2 cells transfected with recombinant plasmid were observed. CONCLUSION: The eukaryotic expression vector for RNA interference USP22 gene is constructed successfully, which inhibits the expression of USP22 in HepG2 cells and suppresses cell proliferation.

[Redox modulation of large conductance calcium-activated potassium channels in rat cultured trigeminal ganglion neurons].

AIM: To observe redox modulation of ion channel in trigeminal ganglion neurons by oxidants and reducing agents. METHODS: The effects of oxidants and reducing agents on maxi-conductance calcium-activated potassium channel in cultured rat trigeminal ganglion neurons by using whole-cell patch-clamp technique. RESULTS: Methionine-specific oxidant chloramine-T (Ch-T) 1 mmol/L slightly increased the current amplitude and this enhancement did not antagonized by DTT. In contrast, cysteine-specific reagent 5, 5'-dithio-bis(2-nitrobenzoic acid) (DTNB) 500 micromol/L significantly decreased current amplitude of BK(Ca) channels. The effect was reversed by the reducing agent 2 mmol/L 1, 4-dithio-DL-threitol (DTT). CONCLUSION: Reactive oxygen species were definitely involved in regulation of native neuronal function via redox modulation of BK(Ca) channels, which are suggested to play compensatory roles under oxidative stress-related conditions.