Objective To research the effect of alimentary tract reconstruction after gastrectomy on the treatment of type 2 diabetes mellitus(non-insulin-dependent diabetes mellitus, NIDDM). Methods From January 2005 to January 2008, perioperative blood glucose level and insulin therapy in 24 gastric cancer or periampullary carcinoma patients with non-obesity type 2 diabetes were retrospectively analyzed. These patients underwent different alimentary tract reconstruction, including 8 patients for Billroth I, 10 for standard Whipples operation, 6 for esophageal Roux-en-Y jejunostomy after total gastrectomy. Glucose level and insulin dosage of thease patients were compared. Results In the patients underwent Billroth I operation, change of blood glucose level before and after operation was not significant(P＞0.05). The level of blood glucose in patients underwent Whipples operation and total gastrectomy were significant changed 1 and 2 months after the operation (P<0.001). In Billroth I group, 5 patients used insulin to control hyperglycemia preoperatively. After the operation, 2 patents maintained preoperative insulin dosage, 2 had to increase the use of insulin and 1 decreased the insulin dosage. In Whipples group, 6 patients used insulin preoperatively. Interestingly, 4 patents needed less insulin to control hyperglycemia and 2 were free of insulin dependance. In total gastrectomy group, there were 4 patients using insulin to control hyperglycemia. After the operation, 2 patents needed less insulin dosage and 2 stopped using insulin. Conclusions Both Whipples operation and total gastrectomy lead to decreased blood glucose level in NIDDM patients and less need of insulin.The effect of some types of alimentary tract reconstruction after gastrectomy on treatment of type 2 diabetes mellitus is assertive.

Objective To evaluate the effect of recombinant human tumor necrosis factor receptor type Ⅱ:IgG Fc fusion protein (rhTNFR:Fc,trade name Etanercept) combined with methotrexate on levels of interleukin-17A (IL-17A) and tumor necrosis factor-α (TNF-α) in the serum and mononuclear cells of patients with moderate to severe plaque psoriasis.Methods A total of 30 patients with moderate to severe plaque psoriasis were enrolled from Department of Dermatology of Tenth People's Hospital of Tongji University between August 2014 and February 2016,and then were randomly and equally divided into Etanercept group and Etanercept + methotrexate group.The treatment lasted 24 weeks.Fifteen healthy blood donors served as healthy control group.Enzyme-linked immunosorbent assay (ELISA) and real-time quantitative PCR were performed to measure the serum levels and mRNA expression of IL-17A and TNF-α,respectively,in the patients of the above two groups before and after the treatment.Results Before the treatment,the serum levels of IL-17A and TNF-ct,as well as the mRNA expression of IL-17A and TNF-α in peripheral blood mononuclear cells (PBMCs),were all significantly higher in all the patients than in the healthy controls (all P ＜ 0.05).After the treatment,compared with the Etanercept group,the Etanercept + methotrexate group showed significantly lower serum levels of IL-17A (142.67 ± 14.82 vs.163.54 ± 23.18,P ＜ 0.05) and TNF-α (70.07 ± 25.02 vs.91.98 ± 14.62,P ＜ 0.05),as well as lower mRNA expression of IL-17A (1.12 ± 0.33 vs.1.56 ± 0.77,P ＜ 0.05) and TNF-α in PBMCs (2.50 ± 1.04 vs.3.61 ± 2.14,P ＜ 0.05).Conclusion Etanercept combined with methotrexate is superior to Etanercept alone in the treatment of psoriasis,and can reduce treatment duration and improve therapeutic effect,likely by down-regulating the expression of IL-17A and TNF-α.

OBJECTIVETo explore the molecular basis of 4 cases with weak D variant of Rh blood type.

METHODSRoutine serological testing was applied to determine the D, C, c, E and e antigens of the Rh blood group. The D antigen was further detected with an indirect antiglobulin test. RHD zygosity was detected by sequence-specific primer PCR method. All exons and flanking intron regions of the RHD gene were sequenced.

RESULTSThe samples were determined as weak D phenotype by serological testing. DNA sequencing showed that the 4 cases were heterozygous for 17C>T mutation in exon 1, 29G>C mutation in exon 1, 1212C>A mutation in exon 9, and IVS4+5G>A mutation in intron 4 of the RHD gene, respectively. According to the rule of Rhesus Base Nomenclature, the 4 samples were respectively named as weak D type 31, weak D type 71, weak D type 72, and weak D type 82.

CONCLUSIONSerological and molecular testing for the weak D can facilitate in-depth understanding of its immunology and genetics, and provide guidance for clinical blood transfusion and prevention of hemolytic disease in newborns.

Objective To analyze the effects of valproic acid(VPA),a histone deacetylase(HDAC)inhibitor,on macrophage polarization in?duced by paraquat(PQ)or lipopolysaccharide(LPS). Methods Mouse RAW264.7 cells were cultured at 37℃with 5%CO2,passaged,and then given one of the following treatments:(1)PQ;(2)PQ+VPA(classⅠandⅡa HDAC inhibitor);(3)PQ+apicidin(classⅠHDAC inhibitor);(4)PQ+MC1568(classⅡa HDAC inhibitor);(5)LPS;(6)LPS+VPA;(7)LPS+apicidin;(8)LPS+MC1568. The cells and culture supernatants were harvested after 8 h of treatment. RT?PCR,ELISA,and flow cytometry were conducted to assess the expression levels of macrophage phenotyp?ic markers. Results Both PQ and LPS skewed the macrophage functional polarity toward proinflammatory phenotype. VPA,apicidin,and MC1568 all inhibited PQ?and LPS?induced macrophages polarizing toward pro?inflammatory phenotype ,but the inhibitory effects were different in some ways. Conclusion VPA inhibits the proinflammatory function of macrophages induced by PQ and LPS ,but the effect of VPA on PQ?and LPS?induced macrophages has its own characteristics.

OBJECTIVE: To report on a novel weak D type identified in a Chinese individual. METHODS: Peripheral blood sample was collected for a voluntary blood donor with weakened expression of D antigen. Routine serological testing was carried out to determine the D, C, c, E and e antigens of the Rh blood group. A D-screening kit was used to analyze the RhD epitopes. The 10 exons and flanking intronic regions of the RHD gene were sequenced. The zygosity of RHD was determined with a sequence-specific primer PCR method. RESULTS: A novel RHD allele, RHD (1022T>A), was found in the subject with a weak D phenotype. Serological testing of the RhD epitopes has coined with the weak D phenotype. CONCLUSION A novel weak D allele has been identified in Chinese population.
Alleles ; Asian Continental Ancestry Group ; China ; Exons ; Genotype ; Humans ; Introns ; Rh-Hr Blood-Group System ; genetics

OBJECTIVE: To explore the molecular basis for an individual with para-Bombay phenotype of the H blood group. METHODS: Intron 5 to 3'-UTR of the ABO gene and exon 4 of the FUT1 gene were amplified with PCR and subjected to direct sequencing. Mutations of the FUT1 gene were identified by TOPO cloning sequencing. RESULTS: Direct sequencing showed that her ABO genotype was B101/O01. TOPO cloning sequencing found that this individual had three mutations of the FUT1 gene, including an heterozygous AG deletion (CAGAGAG→CAGAG) at position 547 to 552, and two C→T mutations at positions 35 (C35T) and 293 (C293T) on the other homologous chromosome. The two alleles comprised a new recombination of mutations c.35T>C and c.293C>T, and the sequence has been submitted to NCBI (No. MG597611). CONCLUSION A novel combination of FUT1 alleles with c.35 C>T and c.293C>T has been identified in an individual with para-Bombay phenotype.
ABO Blood-Group System ; Alleles ; Female ; Fucosyltransferases ; genetics ; Genotype ; Humans ; Phenotype

OBJECTIVETo identify a novel Bx13 allele.

METHODSSerological characteristics was determined with standard serological methods. All of the seven exons and flanking regions of the ABO gene were analyzed with PCR and direct sequencing. The amplicon of exon 7 was also cloned and sequenced.

RESULTSThe individual was determined as with a rare Bx phenotype by serological tests. Direct DNA sequencing showed that the individual was heterozygous for the B/O01 allele, while there was a novel 893C>T mutation in the B101 allele, which has led to an amino acid substitution Ala298Val in the α,3-D-galactosyl-transferase. The mutation was not found among 100 randomly selected blood donors.

CONCLUSIONA novel Bx13 allele has been identified. Substitution of amino acid in the conserved region of the enzyme may reduce the activity of α,3-D-galactosyl-transferase.

OBJECTIVE: To explore the molecular basis for an individual with Ax28 phenotype of the ABO subtype. METHODS: The ABO group antigens on red blood cells of the proband were identified by monoclonal antibodies. The ABO antibody in serum was detected by standard A, B, O cells. Exons 1 to 7 of the ABO gene were respectively amplified by PCR and directly sequenced. Amplicons for exons 5 to 7 were also sequenced after cloning. RESULTS: Weakened A antigen was detected on red blood cells from the proband. Both anti-A and anti-B antibodies were detected in the serum. Heterozygous 261G/del was detected in exon 6, while heterozygous 467C/T and 830T/C were detected in exon 7 by direct DNA sequencing. After cloning and sequencing, two alleles (O01 and Ax28) were obtained. Compared with A102, the sequence of Ax28 contained one nucleotide changes (T to C) at position 830, which resulted in amino acid change (Val to Ala) at position 277. CONCLUSION The novel mutation c.830T>C of the galactosaminyltransferase gene may give rise to the Ax28 phenotype.
ABO Blood-Group System ; genetics ; Alleles ; Amino Acid Substitution ; Exons ; Galactosyltransferases ; genetics ; Genotype ; Humans ; Phenotype ; Polymorphism, Single Nucleotide ; Sequence Deletion

OBJECTIVE: To explore the molecular basis of two individuals with weak D variant of the Rh blood type. METHODS: Routine serological testing was carried out to detect the D, C, c, E and e antigens of the Rh blood group. The D antigen was further detected with an indirect antiglobulin test. The presence of Rhesus box was detected by PCR to determine the homozygosity of the RHD gene. RESULTS: Both samples were determined as weak D phenotype by the indirect antiglobulin test. DNA sequencing revealed that case 1 harbored a heterozygous 208C>T variant in exon 2 and a heterozygous 1227G>A variant in exon 9; while case 2 harbored homozygous 779A>G variants of exon 5 of the RHD gene. Case 1 was determined as RHD+/RHD+, while case 2 was determined as RHD+/RHD-. The two samples were respectively named as weak D type 122 and weak D type 149 based on the rules of Rhesus Base Nomenclature. CONCLUSION D negative blood donors should subject to indirect antiglobulin testing and molecular analysis for safer transfusion.
Alleles ; Blood Donors ; Blood Grouping and Crossmatching ; Genotype ; Humans ; Molecular Biology ; Phenotype ; Rh-Hr Blood-Group System/genetics*

Objective:To investigate the current status of anticoagulant therapy and the incidence of ischemic and bleeding events in hospitalized patients aged 90 years and over with non-valvular atrial fibrillation(NVAF).Methods:We retrospectively collected clinical data, antithrombotic treatment strategies, in-hospital ischemic stroke and bleeding events from NVAF patients(≥90 years)who were admitted to our hospital from June 2014 to August 2018.Based on the CHA 2DS 2-VASc score(2, 3, and ≥4 respectively), patients were divided into three ischemic risk groups, and antithrombotic treatment strategies and in-hospital ischemic stroke events were compared between the three groups.Alternatively, patients were divided into the high bleeding risk group(HAS-BLED score ≥3, )and the non-high bleeding risk group(HAS-BLED score ≤2), and antithrombic treatment strategies and the major bleeding events were compared between the two groups. Results:Among the 223 hospitalized NVAF patients aged 90 years and over, 42.6% of them received anticoagulant treatment, 25.6% received antiplatelet drugs, and 31.8% received non-antithrombotic treatment.With the increase of the CHA 2DS 2-VASc score, there was a trend of declined rates of non-antithrombotic treatment among the three ischemic risk groups(47.4%, 42.9%, 26.4%, P=0.06), and the rates of in-hospital ischemic stroke were similar among groups(10.5%, 12.2%, 15.5%, P=0.75). Moreover, compared with the non-high bleeding risk group, patients in the high bleeding risk group more frequently received anticoagulant treatment(47.2% vs.38.3%)and less frequently received non-antithrombotic therapy(28.7% vs.34.7%). There was no significant difference in antithrombotic treatment strategies( P=0.39)or rate of in-hospital major bleeding events(13.0% vs.10.2%, P=0.51). However, the rate of in-hospital major bleeding events was significantly higher in those with concurrent infections(16.8% vs.6.4%, P=0.02)or respiratory failure(21.3% vs.8.0%, P=0.01). Conclusions:The rate of anticoagulant use in NVAF patients aged 90 years and over is too low during hospitalization, and anticoagulant therapy should be standardized.In addition to the HAS-BLED score, we should consider the complications that increase the bleeding risk, such as infections and respiratory failure, when evaluating the bleeding risk.