Objective To explore the value of magnetic resonance relaxation time quantitative imaging in predicting molecular subtypes of invasive ductal carcinoma(IDC)of breast.Methods A total of 79 IDC patients underwent routine magnetic resonance imaging(MRI)scanning and relaxation time quantitative imaging.According to immunohistochemical results of lesions,patients were divided into different immunohistochemical index groups and molecular subtype groups.The differences in MRI signs,T1 values and T2 values of lesions were statistically compared between each group.Patient operating characteristic(ROC)curve was used to evaluate values of T1 and T2 alone and the combination of them in differential diagnosis of IDC molecular subtypes.Results There were 82 samples of lesion in 79 patients,in which,Luminal A type 16(19.51%),Luminal B1 type 11(13.41%),Luminal B2 type 27(32.93%),tyrosine kinase receptor-2 overexpression type(Erb-B2)14(17.07%)and TNBC 14(17.07%).There were no significant differences in patient age,lesion distribution,maximum diameter,morphology,margin and enhancement performance between patients with various molecular subtypes(P>0.05).Among the immunohistochemical indexes,only the Ki-67 positive group had higher T1 value than the negative group(P<0.05).In ROC analysis,the critical T1 value of Ki-67 positive lesions was 2 145 ms,Yoden index was 0.368,the sensitivity was 53.47%,the specificity was 83.33%and the area under the curve(AUC)was 0.640(95%CI:0.527-0.744).There were no significant differences in T1 and T2 values between Luminal A,Luminal B1,Luminal B2,Erb-B2 enriched and TNBC subtypes(P<0.05).T1 and T2 values were lower in Luminal type lesion than those of TNBC type lesion(P＜0.05).ROC curve analysis showed that the combined T1 and T2 values were more effective in differentiating Luminal/TNBC type than those of T1 and T2 values alone.Conclusion T1 mapping can be used as one of the methods to predict the high or low expression levels of Ki-67 in IDC tumors.The combination of T1 and T2 values can improve the ability to predict Luminal/TNBC subtypes.

Since December 2019, a novel coronavirus (2019-nCoV, SARS-CoV-2) pneumonia (COVID-19) outbreak has occurred in Wuhan, Hubei Province, and the epidemic situation has continued to spread. Such cases have also been found in other parts of the country. The spread of the novel coronavirus pneumonia epidemic has brought great challenges to the clinical practice of thoracic surgery. Outpatient clinics need to strengthen the differential diagnosis of ground glass opacity and pulmonary plaque shadows. During the epidemic, surgical indications are strictly controlled, and selective surgery is postponed. Patients planning to undergo a limited period of surgery should be quarantined for 2 weeks and have a nucleic acid test when necessary before surgery. For patients who are planning to undergo emergency surgery, nucleic acid testing should be carried out before surgery, and three-level protection should be performed during surgery. Patients who are planning to undergo emergency surgery in the epidemic area should be confirmed with or without novel coronavirus pneumonia before operation, and perform nucleic acid test if necessary. Surgical disinfection and isolation measures should be strictly carried out. Among postoperative patients, cases with new coronavirus infection were actively investigated. For the rescue of patients with novel coronavirus infection, attention needs to be paid to prevention and treatment and related complications, including mechanical ventilation-related pneumothorax or mediastinal emphysema, and injury after tracheal intubation.

Objective To explore the levels of serum adiponectin (ADPN) and retinol-binding protein 4 (RBP4) in patients with type 2 diabetes mellitus (T2DM) and obstructive sleep apnea-hypopnea syndrome (OSAHS).Methods A total of 155 patients with T2DM and OSAHS were selected and divided into mild group (n=62),moderate group (n=53) and severe group (n=40) according to apnea-hypopnea index (AHI),35 OSAHS patients were designed as OSAHS group,42 T2DM patients were selected as T2DM group,and 38 healthy controls were selected as control group.Serum ADPN and RBP4 levels were detected by ELISA.Results Compared with healthy controls,the serum level of RBP4 significantly increased and the ADPN level significantly decreased in the other three groups (P<0.01).In subgroups of OSAHS and T2DM group,the level of RBP4 increased with increasing of AHI level,ADPN level is on the contrary (P<0.01).Conclusion The serum levels of ADPN and RBP4 are closely related with the severity of T2DM patients with OSAHS.

Objective To explore the levels of serum adiponectin (ADPN) and retinol-binding protein 4 (RBP4) in patients with type 2 diabetes mellitus (T2DM) and obstructive sleep apnea-hypopnea syndrome (OSAHS).Methods A total of 155 patients with T2DM and OSAHS were selected and divided into mild group (n=62),moderate group (n=53) and severe group (n=40) according to apnea-hypopnea index (AHI),35 OSAHS patients were designed as OSAHS group,42 T2DM patients were selected as T2DM group,and 38 healthy controls were selected as control group.Serum ADPN and RBP4 levels were detected by ELISA.Results Compared with healthy controls,the serum level of RBP4 significantly increased and the ADPN level significantly decreased in the other three groups (P<0.01).In subgroups of OSAHS and T2DM group,the level of RBP4 increased with increasing of AHI level,ADPN level is on the contrary (P<0.01).Conclusion The serum levels of ADPN and RBP4 are closely related with the severity of T2DM patients with OSAHS.

Objective To test whether glucagon like peptide-1 (GLP-1) would regulate the expression of visfatin in adipocytes,and to explore the mechanism of this effect.Methods Fully differentiated 3T3-L1 adipocytes were treated with GLP-1.Total RNA was extracted for analyzing the level of visfatin mRNA by quantitative RT-PCR.The media were collected for measuring the level of visfatin protein by enzyme linked immuno-assay (ELISA).In order to test the involvement of PKA pathway,the adipocytes were pretreated with a specific pharmacological PKA inhibitor H89 for 30 min before GLP-1 was added.Results GLP-1 increased visfatin expression in a time-and dose-dependent manner.The level of visfatin significantly increased at the concentration of 10 10 mol/L GLP-1 (P＜0.05),and reached the peak at 10-9 mol/L (P＜0.01).After incubation for 18 hours,GLP-1 dominantly increased the level of visfatin (P＜0.05).Inhibition of PKA pathway by H89 partially blocked the effect of GLP-1 on visfatin expression.Conclusions GLP-1 may enhance the expression of visfatin in 3T3-L1 adipocyte via the PKA pathway,which might contribute to the improvement in glucose homeostasis.

Heparinase III (HepIII) is a 73-kDa polysaccharide lyase (PL) that degrades the heparan sulfate (HS) polysaccharides at sulfate-rare regions, which are important co-factors for a vast array of functional distinct proteins including the well-characterized antithrombin and the FGF/FGFR signal transduction system. It functions in cleaving metazoan heparan sulfate (HS) and providing carbon, nitrogen and sulfate sources for host microorganisms. It has long been used to deduce the structure of HS and heparin motifs; however, the structure of its own is unknown. Here we report the crystal structure of the HepIII from Bacteroides thetaiotaomicron at a resolution of 1.6 Å. The overall architecture of HepIII belongs to the (α/α)₅ toroid subclass with an N-terminal toroid-like domain and a C-terminal β-sandwich domain. Analysis of this high-resolution structure allows us to identify a potential HS substrate binding site in a tunnel between the two domains. A tetrasaccharide substrate bound model suggests an elimination mechanism in the HS degradation. Asn260 and His464 neutralize the carboxylic group, whereas Tyr314 serves both as a general base in C-5 proton abstraction, and a general acid in a proton donation to reconstitute the terminal hydroxyl group, respectively. The structure of HepIII and the proposed reaction model provide a molecular basis for its potential practical utilization and the mechanism of its eliminative degradation for HS polysaccarides.
Amino Acid Sequence ; Bacteroides ; enzymology ; Catalytic Domain ; Crystallography, X-Ray ; Heparitin Sulfate ; metabolism ; Kinetics ; Models, Molecular ; Molecular Sequence Data ; Polysaccharide-Lyases ; chemistry ; metabolism ; Substrate Specificity

Objective To explore the difference involved in the activation of inflammation pathway and the plasma level of inflammatory factors in the subjects with different sorts of insulin sensitivity. Methods The study was carried out in 38 women, consisting of obesity (n = 22 ) and control (n = 16 ) groups according to body mass index. The insulin sensitivity was assessed by homeostasis model assessment of insulin resistance (HOMAIR). Plasma concentrations of interleukin-6 (II-6) and IL-1β were determined by enzyme immunoassay. Western blot analysis was used to examine total protein expression and phosphorylation levels of IκB kinase (IKK) ,inhibitor of nuclear factor-κB ( IκB ) in peripheral blood leukcocytes. Electrophoretic mobility shift assay (EMSA)was used to detect the binding activity of NFκB. Results The levels of fasting plasma insulin[62.2 ( 20.0-127. 0) pmol/L vs 19. 15 ( 14. 2-47. 8 ) pmol/L, P<0. 01], HOMA-IR[2. 32 ( 0. 76-5.49 ) vs 0.70(0.53-1.7),P<0.0l], HbA1 C[(5.42±0. 45 ) % vs ( 5.08 ±0. 38) %, P<0. 05], triglyceride[( 1.75 ±0. 68 vs 1.22 ±0. 58 )mmol/L, P<0. 05], plasma IL-6[3. 15 (0. 03-22. 2) pg/ml vs 1.26 (0. 74-6.06 ) pg/ml, P<0. 01], and IL-1 β[6. 53 ( 0. 84-36 ) pg/ml vs 3. 16( 1.48-8. 86 ) pg/ml, P<0. 01]in obesity group were significantly higher than those in control group. Compared with control group, the levels of IKKo, IKKβ expression and IκBα serine phosphorylation in obesity group were markedly increased, while the expression of IκBα was significantly reduced. Accompanied with the degradation of IκBα protein, the binding activity of NFκB in obesity group was significantly increased. Conclusions The plasma levels of IL-6 and IL-1β were significantly raised in obesity group. The activation of IKK-IκB-NFκB pathway is closely associated with the genesis and development of insulin resistance in obese subjects.

To investigate the effects and the mechanism of visfatin on MIN6 cell signaling pathway and apoptosis induced by palmitate.Human recombinant visfatin promotes protein kinase B (Akt) and extracellularsignal regulating kinase (ERK)1/2 phosphorylation in dose-and time-dependent manner,and prevents MIN6 cell from apoptosis induced by palmitate (P<0.05 or P<0.01).The activation of Akt and ERK1/2 signaling pathway may be one of the molecular mechanisms of visfatin.

Objective To investigate the effects of differentiated 3T3-L1 adipoeytes on inflammation of rat islet cells,as well as the protective effect of a-lipoic acid on the inflammation in vitro.Methotis Rat islet cells were divided into three groups:the control group,the experimental co-culture system group(cocuhured with differentiated mature 3T3-LI adipoeytes)and the intervention group (cocuhured with mature 3T3-LI adipocytes containing 4 μg/ml a-lipoic acid).Insulin releasing lest wag performed for estinmting the function of islet cells in culture supernatant of difierent groups.At the same time,the expression level of IKKIβin islet cells Was detected by western blot and realtime PCR.Results There was significant decrease of insulin stimulation index (SI) in experimental co-culture system group compared with the control group and intervention group(1.0 ±0.1 vs 2.6±0.2,2.5±0.5 respectively;P<0.01),while,the mRNA(4.62±0.60 vs1.00±0.46 and 2.25±0.75;P<0.01)and protein expression of IKKβ were significandy increased in the experimental group as compared with the other two groups.Conclusions In the co-culture system of adipocytes/islet cells,impaired function of islet cells could be induced by IKKβ activation,IKKβ Was a key molecule in inflamnmtion signal pathway in islet cells and could be activated by 3T3-LI adipocytes.a-lipoic acid Was able to reverse the impaired function of islet cells by suppressing IKKβ expression.

Visfatin was expressed in rat anti mouse islets,as well as in MIN6 cells. The visfatin expression was affected by various concentrations of environmental glucose (5.5 and 33.3 mmoL/L) and palmitate(0.5 mmol/L). As compared with low-level glucose medium (5.5 mmol/L, 1.0±0.11) , visfatin expression increased in media with high glucose and palmitate (1.32 ±0. 18, 1. 33±0. 15,1.72±0.27, all P<0. 05). The result suggests that visfatin seems to be involved in the regulation of insulin secretion.