Medical laboratories provide test data and consultation services and are engaged in ensuring test results being timely,accurate and reliable,which are satisfactory for their service recipients.A summary of the customer satisfaction theory and quality management system,and an analysis of problems found in the quality management of such laboratories,attempt to pinpoint underlying causes of service quality setbacks.Based on such studies,the quality management system is built in accordance with customer satisfaction theory and CNAS-CL02 Accreditation Criteria for the Quality and Competence of Medical Laboratories (ISO 15189:2007).Such efforts aim to continuously improve service quality and ensure customer satisfaction.

Objective To investigate the differential expression of proteins in the serum of diabetic patients quantitative proteomics technologies, and to identify specific protein biomarkers. Methods Serum samples from three diabetic patients and three healthy controls in Shenzhen in 2023 were collected. Immunoprecipitation and nano liquid chromatography-quadrupole-electrostatic orbitrap-linear ion trap mass spectrometry (easy-nanoLC-Q-orbitrap-fusion) were employed to perform fraction and no-fraction-based quantitative analysis of the serum proteome in diabetic patients and healthy controls. The mass spectrometry data were analyzed by MaxQuant1.6.1.0, and the differential proteins identified by the fraction-based method were subjected to gene ontology (GO) functional clustering and kyoto encyclopedia of genes and genomes (KEGG) pathway analysis. Results A total of 251 reliable proteins were identified by the no-fraction-based method, among which 17 differentially expressed proteins were selected. In contrast, 494 reliable proteins were identified by the fraction-based method, and 74 differentially expressed proteins were selected. Among them, seven proteins showed consistent changes in both methods. Five proteins were downregulated, including pregnancy zone protein (PZP), carbonic anhydrase 1 (CAH1), mannose-binding protein C (MBL2), fibrinogen alpha chain (FIBA), and haptoglobin (HPT). Two proteins were upregulated, including apolipoprotein(a) (LPA) and complement factor H-related protein 4 (CFH4). GO analysis revealed that the differentially expressed proteins were mainly involved in molecular functions such as glycosaminoglycan binding and heparin binding. KEGG pathway analysis showed that the differentially expressed proteins were mainly associated with complement and coagulation cascades, cell adhesion, PI3K-Akt signaling pathway, and other pathways. Conclusions Fraction-based no-fractional quantitative proteomics analysis provides an effective approach for analyzing differential protein expression in the serum of diabetic patients, and offers a valuable technique for screening specific protein biomarkers of serum samples in large-scale cohorts of disease.

Stranging the communication between the clinical laboratory and clinical department,is useful to promote and enhance the quality of tests and clinical examination.The communication work organization and implementation has been effectively guaranteed by managing communication theories and multiple pathways of communication means to strengthen clinical laboratory and clinical department communication.

In this study, we obtained the TiO2 films with different thickness by micro-are oxidation (MAO) on commercially available pure titanium. By altering the duration time, we got the films 5 microm, 10 microm, and 20 microm in thickness, respectively. XRD and SEM were employed to characterize the phase, composition and microstructure of the films. The MAO film, which was about 5 microm thick, was porous and even with the pore size about 1 microm. No other crystalline phase except anatase was detected by XRD. The film, which was 10 microm thick, was similar to the former. The pores were well separated and homogeneously distributed over the surface. The XRD pattern indicated that the film was composed of anatase and a minor amount of rutile, whereas the pore size of 20 microm film was about 4-6 microm and was bigger than the others. Furthermore, the small cracks were easy to observe. XRD pattern showed that the Ti peak was significantly reduced and new Ca, P, O containing compound was formed in addition to rutile and anatase with the film thickness increasing. There were significant differences in regard to surface roughness of the three groups. These findings suggest that the film thickness has an intense effect on the quality of the MAO coating. By changing the film thickness, we can extensively change the composition, structure and chemical properties of the surface layer on titanium.
Coated Materials, Biocompatible ; chemistry ; Oxidation-Reduction ; Porosity ; Surface Properties ; Titanium ; chemistry

OBJECTIVETo explore the characteristics in CFHR1 concentration and the frequency of CFHR1 gene polymorphisms of patients with type 2 diabetes mellitus (T2DM) based on the high level of complement factor H (CFH) expression among such patients and the similarity between CFHR1 and CFH in terms of sequence and functions.

METHODSFifty T2DM patients and 30 healthy controls were selected. The plasma samples were separated by pI with OFFGEL electrophoresis following solution digestion. Further separation and identification were carried out on a Nano HPLC-Chip-MS/MS system. Differentially expressed proteins were identified by comparison. Enzyme-linked immunosorbent assay (ELISA) was used to validate the result. Genomic DNA of the two groups was extracted. Polymerase chain reaction and sequencing were used to determine the single nucleotide polymorphisms in the 6 exons of the CFHR1 gene.

RESULTSThe CFHR1 level in plasma of T2DM patients were significantly higher than that of the healthy controls (P=2.78× 10). A significant difference in allelic frequencies of rs12406079 of the fifth exon of the CFHR1 gene was found between the two groups (χ=5.692, P=0.017).

CONCLUSIONThe concentration of CFHR1 and frequencies of CFHR1 gene polymorphisms among patients with T2DM differ significantly from healthy subjects. Polymorphisms of the CFHR1 gene are associated with T2DM.

Complement C3b Inactivator Proteins ; genetics ; metabolism ; Diabetes Mellitus, Type 2 ; genetics ; metabolism ; Female ; Genotype ; Humans ; Male ; Middle Aged ; Polymorphism, Single Nucleotide

Objective To explore the effects of lncRNA HULC on hepatocellular carcinoma (HCC) growth by down?regulating miR?29. Methods The expression levels of HULC and miR?29 in HCC tissues and cells were detected by real?time quantitative PCR ( RT?qPCR ), and the correlation analysis was performed. After HCC cells were transfected with HULC overexpressed plasmid or siRNA, the expressions of miR?29 and its target gene SETDB1 were determinate by RT?qPCR. According to the bioinformatic prediction of the miR?29 binding site in the HULC sequence, the report gene plasmids were constructed.The HCC cells were co?transfected with miR?29 mimics or miR?29 inhibitor, and the HULC targeted regulation of miR?29 was verified by dual luciferase reporter assay. The effect of miR?29 on the HULC?mediated proliferation in HCC cells was detected by cell count kit 8 ( CCK?8) experiment. Expression of tumor proliferation antigen Ki?67 was detected by RT?qPCR.The Hep3B cells were inoculated in mice and miR?29 mimics and miR?29 negative control (NC) further injected into the lesions. The tumor volume was observed, and the expressions of tumor proliferation antigen ki?67 in tumor tissues were detected by immunohistochemical staining. Results The expression of HULC was significantly up?regulated while the expression of miR?29 was significantly down?regulated in HCC tissues and cells (P＜0.01). The level of HULC was negatively correlated with miR?29 in tumor tissues (r＝－0.754, P＜0.01) and HCC cells ( r＝－0.865, P＜0.05).The in vitro experiments showed that, compared with the blank control group, the expression of miR?29 in HULC overexpressed Huh7 cells was significantly reduced, while the mRNA level of miR?29 target gene SETDB1 was increased ( P＜0.01). The expression of miR?29 was significantly increased in HULC deleted Hep3B cells, while the mRNA expression of SETDB1 was decreased (P＜0.01). Double luciferase reporter gene assay showed that miR?29 mimics significantly inhibited the luciferase activity of Hep3B cells transfected with HULC wide type ( psi?HULC?WT) plasmid but had no effect on Hep3B cells transfected with mutant plasmid ( psi?HULC?Mut). However, the miR?29 inhibitor antagonized the inhibitory effect of miR?29 mimics on luciferase activity of psi?HULC?WT (P＜0.01).Cell proliferation experiments showed that, compared with the control group, the proliferation ability of miR?29 mimics overexpressed Huh7 cells was significantly reduced.After 24, 48 and 72 hours of treatment, the proliferation rates of Huh7 cells in the HULC overexpressed group were (43.87± 3.82)%, (83.45±7.46)% and (123.34±8.67)%, respectively, significantly higher than (13.45±1.77)%, (23.54±1.37)% and (38.21±2.09)% of control group (P＜0.05).After treatment for 48 and 72 hours, the proliferation rates of miR?29 mimics transfected Huh7 cells were ( 57.10 ± 1.94)% and ( 73.76± 3.46)%, respectively, significantly lower than (83.45±7.46)% and ( 123.34±8.67)% of control group ( P＜0.05). After treatment for 48 and 72 hours, the proliferation rates of Huh7 cells transfected with miR?29 mimics and miR?29 inhibitor group were (76.45± 3.24)% and ( 89.37± 4.37)%, respectively, significant higher than (57.10%±1.94)% and ( 73.76 ± 3.46)% of the control group ( P＜0.05). After 48 h transfection, the expression of Ki?67 in Huh7 transfected with miR?29 mimics was significantly inhibited compared with the control group (P＜0.01). However, the expression of Ki?67 mRNA was increased in Huh7 cells transfected with miR?29 inhibitor (P＜0.01). The results of in vivo experiments showed that the tumor volumes of the control group, miR?29 mimics group and miR?29 mimics + miR?29 inhibitors group were ( 504.0± 19.6) mm3, (310.0±24.3) mm3 and (483.7±21.2) mm3, respectively. Injection of miR?29 mimics reduced while miR?29 inhibitor promoted tumorigenesis ability of Huh7 in nude mice (P＜0.01). The immunohistochemical staining showed that the average optical density values of Ki?67 protein in tumor tissues of the control group, miR?29 mimics group and miR?29 analogue+miR?29 inhibitor group were 0.65±0.08, 0.36±0.07 and 0.56±0.06, respectively. The expression level of Ki?67 protein in miR?29 mimics group was significantly reduced ( P＜0.01) while increased in the miR?29 mimics+miR?29 inhibitor group ( P＜0.01). Conclusion LncRNA HULC promotes HCC growth by down?regulating miR?29.

Objective To explore the effects of lncRNA HULC on hepatocellular carcinoma (HCC) growth by down?regulating miR?29. Methods The expression levels of HULC and miR?29 in HCC tissues and cells were detected by real?time quantitative PCR ( RT?qPCR ), and the correlation analysis was performed. After HCC cells were transfected with HULC overexpressed plasmid or siRNA, the expressions of miR?29 and its target gene SETDB1 were determinate by RT?qPCR. According to the bioinformatic prediction of the miR?29 binding site in the HULC sequence, the report gene plasmids were constructed.The HCC cells were co?transfected with miR?29 mimics or miR?29 inhibitor, and the HULC targeted regulation of miR?29 was verified by dual luciferase reporter assay. The effect of miR?29 on the HULC?mediated proliferation in HCC cells was detected by cell count kit 8 ( CCK?8) experiment. Expression of tumor proliferation antigen Ki?67 was detected by RT?qPCR.The Hep3B cells were inoculated in mice and miR?29 mimics and miR?29 negative control (NC) further injected into the lesions. The tumor volume was observed, and the expressions of tumor proliferation antigen ki?67 in tumor tissues were detected by immunohistochemical staining. Results The expression of HULC was significantly up?regulated while the expression of miR?29 was significantly down?regulated in HCC tissues and cells (P＜0.01). The level of HULC was negatively correlated with miR?29 in tumor tissues (r＝－0.754, P＜0.01) and HCC cells ( r＝－0.865, P＜0.05).The in vitro experiments showed that, compared with the blank control group, the expression of miR?29 in HULC overexpressed Huh7 cells was significantly reduced, while the mRNA level of miR?29 target gene SETDB1 was increased ( P＜0.01). The expression of miR?29 was significantly increased in HULC deleted Hep3B cells, while the mRNA expression of SETDB1 was decreased (P＜0.01). Double luciferase reporter gene assay showed that miR?29 mimics significantly inhibited the luciferase activity of Hep3B cells transfected with HULC wide type ( psi?HULC?WT) plasmid but had no effect on Hep3B cells transfected with mutant plasmid ( psi?HULC?Mut). However, the miR?29 inhibitor antagonized the inhibitory effect of miR?29 mimics on luciferase activity of psi?HULC?WT (P＜0.01).Cell proliferation experiments showed that, compared with the control group, the proliferation ability of miR?29 mimics overexpressed Huh7 cells was significantly reduced.After 24, 48 and 72 hours of treatment, the proliferation rates of Huh7 cells in the HULC overexpressed group were (43.87± 3.82)%, (83.45±7.46)% and (123.34±8.67)%, respectively, significantly higher than (13.45±1.77)%, (23.54±1.37)% and (38.21±2.09)% of control group (P＜0.05).After treatment for 48 and 72 hours, the proliferation rates of miR?29 mimics transfected Huh7 cells were ( 57.10 ± 1.94)% and ( 73.76± 3.46)%, respectively, significantly lower than (83.45±7.46)% and ( 123.34±8.67)% of control group ( P＜0.05). After treatment for 48 and 72 hours, the proliferation rates of Huh7 cells transfected with miR?29 mimics and miR?29 inhibitor group were (76.45± 3.24)% and ( 89.37± 4.37)%, respectively, significant higher than (57.10%±1.94)% and ( 73.76 ± 3.46)% of the control group ( P＜0.05). After 48 h transfection, the expression of Ki?67 in Huh7 transfected with miR?29 mimics was significantly inhibited compared with the control group (P＜0.01). However, the expression of Ki?67 mRNA was increased in Huh7 cells transfected with miR?29 inhibitor (P＜0.01). The results of in vivo experiments showed that the tumor volumes of the control group, miR?29 mimics group and miR?29 mimics + miR?29 inhibitors group were ( 504.0± 19.6) mm3, (310.0±24.3) mm3 and (483.7±21.2) mm3, respectively. Injection of miR?29 mimics reduced while miR?29 inhibitor promoted tumorigenesis ability of Huh7 in nude mice (P＜0.01). The immunohistochemical staining showed that the average optical density values of Ki?67 protein in tumor tissues of the control group, miR?29 mimics group and miR?29 analogue+miR?29 inhibitor group were 0.65±0.08, 0.36±0.07 and 0.56±0.06, respectively. The expression level of Ki?67 protein in miR?29 mimics group was significantly reduced ( P＜0.01) while increased in the miR?29 mimics+miR?29 inhibitor group ( P＜0.01). Conclusion LncRNA HULC promotes HCC growth by down?regulating miR?29.

Objective: To explore the effects of lncRNA HULC on hepatocellular carcinoma (HCC) growth by down-regulating miR-29. Methods: The expression levels of HULC and miR-29 in HCC tissues and cells were detected by real-time quantitative PCR (RT-qPCR), and the correlation analysis was performed. After HCC cells were transfected with HULC overexpressed plasmid or siRNA, the expressions of miR-29 and its target gene SETDB1 were determinate by RT-qPCR. According to the bioinformatic prediction of the miR-29 binding site in the HULC sequence, the report gene plasmids were constructed. The HCC cells were co-transfected with miR-29 mimics or miR-29 inhibitor, and the HULC targeted regulation of miR-29 was verified by dual luciferase reporter assay. The effect of miR-29 on the HULC-mediated proliferation in HCC cells was detected by cell count kit 8 (CCK-8) experiment. Expression of tumor proliferation antigen Ki-67 was detected by RT-qPCR.The Hep3B cells were inoculated in mice and miR-29 mimics and miR-29 negative control (NC) further injected into the lesions. The tumor volume was observed, and the expressions of tumor proliferation antigen ki-67 in tumor tissues were detected by immunohistochemical staining. Results: The expression of HULC was significantly up-regulated while the expression of miR-29 was significantly down-regulated in HCC tissues and cells (P<0.01). The level of HULC was negatively correlated with miR-29 in tumor tissues (r=-0.754, P<0.01) and HCC cells (r=-0.865, P<0.05). The in vitro experiments showed that, compared with the blank control group, the expression of miR-29 in HULC overexpressed Huh7 cells was significantly reduced, while the mRNA level of miR-29 target gene SETDB1 was increased (P<0.01). The expression of miR-29 was significantly increased in HULC deleted Hep3B cells, while the mRNA expression of SETDB1 was decreased (P<0.01). Double luciferase reporter gene assay showed that miR-29 mimics significantly inhibited the luciferase activity of Hep3B cells transfected with HULC wide type (psi-HULC-WT) plasmid but had no effect on Hep3B cells transfected with mutant plasmid (psi-HULC-Mut). However, the miR-29 inhibitor antagonized the inhibitory effect of miR-29 mimics on luciferase activity of psi-HULC-WT (P<0.01). Cell proliferation experiments showed that, compared with the control group, the proliferation ability of miR-29 mimics overexpressed Huh7 cells was significantly reduced.After 24, 48 and 72 hours of treatment, the proliferation rates of Huh7 cells in the HULC overexpressed group were (43.87±3.82)%, (83.45±7.46)% and (123.34±8.67)%, respectively, significantly higher than (13.45±1.77)%, (23.54±1.37)% and (38.21±2.09)% of control group (P<0.05). After treatment for 48 and 72 hours, the proliferation rates of miR-29 mimics transfected Huh7 cells were (57.10±1.94)% and (73.76±3.46)%, respectively, significantly lower than (83.45±7.46)% and (123.34±8.67)% of control group (P<0.05). After treatment for 48 and 72 hours, the proliferation rates of Huh7 cells transfected with miR-29 mimics and miR-29 inhibitor group were (76.45±3.24)% and (89.37±4.37)%, respectively, significant higher than (57.10%±1.94)% and (73.76±3.46)% of the control group (P<0.05). After 48 h transfection, the expression of Ki-67 in Huh7 transfected with miR-29 mimics was significantly inhibited compared with the control group (P<0.01). However, the expression of Ki-67 mRNA was increased in Huh7 cells transfected with miR-29 inhibitor (P<0.01). The results of in vivo experiments showed that the tumor volumes of the control group, miR-29 mimics group and miR-29 mimics + miR-29 inhibitors group were (504.0±19.6) mm³, (310.0±24.3) mm³ and (483.7±21.2) mm³, respectively. Injection of miR-29 mimics reduced while miR-29 inhibitor promoted tumorigenesis ability of Huh7 in nude mice (P<0.01). The immunohistochemical staining showed that the average optical density values of Ki-67 protein in tumor tissues of the control group, miR-29 mimics group and miR-29 analogue+ miR-29 inhibitor group were 0.65±0.08, 0.36±0.07 and 0.56±0.06, respectively. The expression level of Ki-67 protein in miR-29 mimics group was significantly reduced (P<0.01) while increased in the miR-29 mimics+ miR-29 inhibitor group (P<0.01). Conclusion LncRNA HULC promotes HCC growth by down-regulating miR-29.

Objective:To investigate the efficacy and safety of daratumumab in relapsed and refractory multiple myeloma (RRMM).Methods:The efficacy and adverse events (AEs) of daratumumab based regimens were retrospectively analyzed in 37 patients with RRMM from Peking University People′s Hospital, Beijing Hospital and Fu Xing Hospital affiliated to Capital Medical University in China. The deadline for inclusion was December, 2019.Results:Among the 37 patients, 35 patients were available for response evaluation. The overall response rate (ORR) was 68.6%, which was better in patients receiving 16 mg/kg daratumumab than in those with fixed doses of 800 mg daratumumab [ORR: 78.3%(18/23) vs. 40.0%(4/10)]. The percentage of infusion related reactions of daratumumab was 27.0%(10/37). The most common hematological AEs were lymphocytopenia and thrombocytopenia, with the incidences of grade 3 or more severe 59.5%(22/37) and 43.2%(16/37) respectively. Pulmonary infections(37.8%, 14/37) were the most common non-hematological AEs. One patient with positive hepatitis B surface antigen (HBsAg) and two patients dependent on dialysis were safely treated with daratumumab.Conclusion:Daratumumab is highly effective in relapsed and refractory multiple myeloma. Adverse reactions are mild and well tolerable.

Objective To explore the feasibility and safety of kidney transplantation for pre-sensitized infants using deceased donors and summarize the relevant literature reports .Methods A second kidney transplantation was successfully performed for an 8-month-old pre-sensitized girl in July 2017 .She had a low level of donor specific antibody (DSA ) against human leucocyte antigen (HLA ) B62 due to severe acute rejection (AR) after her first kidney transplantation .For desensitization , plasmapheresis and intravenous immunoglobulin plus anti-CD20 antibodies were offered on operative day .Clinical data and outcomes were retrospectively analyzed .Results Renal graft regained immediate function after transplantation .Preformed DSA could be detected at 1 week .However ,there was no de novo DSA .At 1 year post-transplantation ,preformed DSA turned negative .During a follow-up period of 2 years ,renal graft showed an excellent function with a serum creatinine of 31 μmol/l and eGFR of 110 ml/min/1 .73m2 .No AR episode or proteinuria occurred .DSA stayed negative .Simultaneously physical development also caught up .Her height of 93 cm tall and weight of 13 .5 kg at month 24 & 8 months corresponded to normal grow th curve of her age .Conclusions Pre-sensitized infant could tolerate desensitization therapy well and achieve satisfactory outcomes .With surgical precisions and optimized managements ,kidney transplantation provides excellent renal functions and survivals for infants with organs from deceased donors .