[Identification of B(A) Blood Group Serology Combined with Molecular Biology and Blood Transfusion Strategy].

OBJECTIVE: To analyze the reasons for ABO blood group forward typing and reverse typing incompatibility of the proband by serological and molecular biological tests, so as to clarify the blood group and genetic rules and determine the reasonable transfusion strategy. METHODS: On the basis of serological testing results, PCR-SSP method was utilized for the ABO exon sequencing in the peripheral blood of the proband and 5 family members, and blood group results were comprehensively analyzed. RESULTS: The serological results of ABO blood group of the proband were incompatibility, and the molecular biological test results showed that there was a c.700C>G mutation compared with B101, which was consistent with B(A)02 subtype, and the genotype was B(A)02/O02. The results of the elder brother was the same as the proband. The nephew of the proband also detected c.700C>G, genotype A102/B(A) 02. CONCLUSION: When the result of standard serological test for ABO blood group incompatibility occurs, using molecular biology detection technology to explore mutation is an effective method to confirm ABO subtype, and ensures the safety of clinical blood transfusion.

Chinese Consensus Report on Family-Based Helicobacter pylori Infection Control and Management (2021 Edition).

OBJECTIVE: Helicobacter pylori infection is mostly a family-based infectious disease. To facilitate its prevention and management, a national consensus meeting was held to review current evidence and propose strategies for population-wide and family-based H. pylori infection control and management to reduce the related disease burden. METHODS: Fifty-seven experts from 41 major universities and institutions in 20 provinces/regions of mainland China were invited to review evidence and modify statements using Delphi process and grading of recommendations assessment, development and evaluation system. The consensus level was defined as ≥80% for agreement on the proposed statements. RESULTS: Experts discussed and modified the original 23 statements on family-based H. pylori infection transmission, control and management, and reached consensus on 16 statements. The final report consists of three parts: (1) H. pylori infection and transmission among family members, (2) prevention and management of H. pylori infection in children and elderly people within households, and (3) strategies for prevention and management of H. pylori infection for family members. In addition to the 'test-and-treat' and 'screen-and-treat' strategies, this consensus also introduced a novel third 'family-based H. pylori infection control and management' strategy to prevent its intrafamilial transmission and development of related diseases. CONCLUSION: H. pylori is transmissible from person to person, and among family members. A family-based H. pylori prevention and eradication strategy would be a suitable approach to prevent its intra-familial transmission and related diseases. The notion and practice would be beneficial not only for Chinese residents but also valuable as a reference for other highly infected areas.

Clinical value of serum cancer antigen 19-9 as a tumor screening marker among healthy individuals.

PURPOSE: To investigate the clinical value of serum cancer antigen 19-9 (CA 19-9) as a tumor screening marker among healthy individuals. METHODS: CA 19-9 levels were measured in 1921 healthy individuals and were compared to reference values. Analysis based on gender was also carried out. Individuals who had higher CA 19-9 values were advised to undergo imaging examinations and start follow-up. The incidence rate of tumors in these individuals and their prognoses were monitored. RESULTS: High CA 19-9 levels were found in 30 -1.5%- individuals without tumor diagnosis at that time. The overall positive detection rate was 15.62 per 1000 population; the rate was higher in males than in females -9.29 and 32.56 per 1000 population, respectively; p<0.01-. Tumors were diagnosed in 7 -0.36%)cases -6 men and 1 woman-; 6 of 30 individuals had CA 19-9 levels that were 5-fold higher than the highest reference value, without tumor specificity. CONCLUSION: CA 19-9 has a low positive rate and is non-specific; routine screening is not recommended for healthy individuals.

Upregulation of microRNA 181c expression in gastric cancer tissues and plasma.

OBJECTIVE: To test the microRNA-181c (miR-181c) expression in tissues and plasma of gastric cancer (GC) cases, analyze any correlations, and explore the possibility of miR-181c as a potential molecular marker for GC diagnosis. MATERIALS AND METHODS: Relative miR-181c expression levels in cancers and plasma from 30 GC patients was tested using reverse transcription?real-time fluorescent quantitation PCR and compared to that in samples from 30 gastric ulcer and 30 chronic gastritis patients. RESULTS: The miR-181c expression level in the GC tissues was significantly higher than that in the gastric ulcer and chronic gastritis tissues (P = 0.000), as was the miR-181c expression level in the GC plasma (P = 0.000). We determined that miR-181c expression in GC plasma was positively correlated to its expression in the GC tissues (P = 0.000). CONCLUSIONS: The expression of miR-181c is upregulated in GC tissues and plasma, and the miR-181c expression level in GC plasma is positively correlated to that in the corresponding cancer tissues. Plasma miR-181c is possibly a new serological marker for GC diagnosis.

[Ilaprazole based bismuth-containing quadruple regimen for the first-line treatment of Helicobacter pylori infection: a multicenter, randomized, controlled clinical study].

OBJECTIVE: To explore the effects of 7-day quadruple regimen as the first-line therapy strategy for Helicobacter pylori(H. pylori)infection and compare the eradication rate of ilaprazole versus esoprazole-based regimen. METHODS: A total of 440 patients with H. pylori infection, who had never received H. pylori eradication treatment, were enrolled from 10 domestic hospitals from October 2010 to July 2011. Diagnosed as chronic gastritis or duodenal ulcer according to their endoscopic examination results, they were randomized into ilaprazole and(or) esoprazole-based bismuth-containing quadruple regimen group with amoxicillin and clarithromycin (n = 110 each). After a 7-day eradication treatment, all patients with duodenal ulcer received PPI (ilaprazole and(or) esoprazole) treatment for 14 days and (13)C urea breath test was performed at least 28 days after the end of therapy. The patients with failed eradication treatment underwent endoscopy examination and biopsy. H. pylori culture and detection of antibiotic-resistant genes were also performed. RESULTS: In gastritis patients, the eradication rate (per-protocol, PP value) were 78.2% (79/101) and 82.0% (82/100) in ilaprazole and esoprazole groups (P = 0.50) while the (intention-to-treat) ITT value of eradication rate were 71.8% (79/110) and 74.5% (82/110) in ilaprazole and esoprazole groups respectively (P = 0.65). And there was no statistical difference (P > 0.05). In duodenal patients, the eradication rate (PP) were 92.1% (93/101) and 91.4% (96/105) in ilaprazole and esoprazole group (P = 0.86) while the ITT value of eradication rate were 84.5% (93/110) and 87.3% (96/110) in ilaprazole and esoprazole groups respectively (P = 0.56). And no significant difference existed between two groups in gastritis and duodenal ulcer patients (P > 0.05). In total, the eradication rate was 80.1% (161/201) (PP) and 73.2% (161/220) (ITT), 91.7% (189/206) (PP) and 85.9% (189/220) (ITT) in chronic gastritis and duodenal ulcer patients respectively. The symptomatic improvements of stomachache, burning, belching and nausea remained almost unchanged. No severe side effect was observed. The point mutations for clarithromycin resistance were detected in all 53 H. pylori strains (100%) isolated from the patients with failed eradication treatment. CONCLUSIONS: The eradication rate of PPI based bismuth-containing quadruple regimen as the first-line treatment is satisfactory in chronic gastritis and duodenal ulcer patients. No significant difference exists between the effects of ilaprazole and esoprazole-based groups. And the treatment failure may be attributed mainly to the clarithromycin resistance of H. pylori.

[Expression of peroxiredoxin 6 in gastric cancer and its clinical significance].

OBJECTIVE: To elucidate the significance of anti-oxidant protein peroxiredoxin 6 (Prx6) expression in gastric cancer (GC) tissue. METHODS: Eighty-six GC tissues and 69 para-cancer tissues from surgically resected specimens were included. And the clinico-pathological data were collected by reviewing medical records. Tissue microarray and immunohistochemistry (IHC) were used to detect Prx6 protein expression in tissues. RESULTS: Prx6 protein was predominantly expressed in cytoplasm. Its expression rate in GC tissues (32.6%, n = 28) was significantly lower than that in para-cancer normal tissues (94.2%, n = 65, P < 0.05). And its protein overexpression rate in well and moderately-differentiated GC tissues was significantly higher than that in lowly-differentiated ones (39.6% (21/53) vs 6.1% (2/33), P < 0.05). Prx6 expression in gastric cancer tissues was not significantly related to age and sex of patients, lesion site, depth of invasion, clinical staging, vascular invasion and liver metastasis. CONCLUSIONS: The level of Prx6 protein is lower in GC tissues than that in normal para-cancer ones. And it is significantly correlated with the differentiation degree of GC.

[Jinghuaweikang capsules combined with triple therapy in the treatment of Helicobacter pylori associated gastritis and duodenal ulcer and analysis of antibiotic resistance: a multicenter, randomized, controlled, clinical study].

OBJECTIVE: To explore the efficacy of Jinghuaweikang capsules plus triple therapy (LACJ) in treatment of Helicobacter pylori (H. pylori) associated gastritis or duodenal ulcer, compare it with bismuth-containing quadruple therapy (LACB) and standard triple therapy (LAC) and analyze the antibiotic sensitivity of gastric mucosal H. pylori strains from the failed patients. METHODS: A total of 565 patients with H. pylori infection were recruited from 11 hospitals from January 2010 to June 2011. There were 336 males and 229 females. They underwent gastroendoscopy examination due to upper gastrointestinal symptoms and had never received H. pylori eradication therapies. Duodenal ulcer patients were divided randomly into LACJ therapy group, LACB therapy group and LAC therapy group while gastritis patients LACJ therapy group and LACB therapy group. Group LAC received lansoprazole 30 mg + amoxicillin 1000 mg + clarithromycin 500 mg, twice a day, for 7 d (d1-7). Group LACJ: LAC therapy plus Jinghuaweikang, 3 capsules, twice a day, for 7 d (d1-7) then Jinghuaweikang, 3 capsules, twice a day, for 14 d (d8-21). Group LACB: LAC plus bismuth potassium citrate 220 mg, twice a day, for 7 d (d1-7) and then bismuth potassium citrate 220 mg, twice a day, for 14 d (d8-21). All duodenal ulcer patients received lansoprazole (30 mg, once a day) for 14 days after the first 7-day of treatment (d 8-21). At least 28 days after the end of treatment, all patients underwent (13)C urea breath test. Gastric mucosa was collected under endoscopy from the failed patients. The detection technique of gene chip was employed to detect antibiotics resistant gene from mucosa. RESULTS: The eradication rates of duodenal ulcer patients in groups LACJ, LACB and LAC were as follows: per-protocol (PP), 80.2% (77/96), 89.9% (89/99) and 72.2% (70/97) (P = 0.007), intention-to-treat (ITT), 78.6% (77/98), 88.1% (89/101) and 70.0% (70/100) (P = 0.007). No statistical differences existed between groups LACJ and LACB or LAC (all P > 0.05). But there were statistical differences between groups LACB and LAC (both P = 0.002). The eradication rates of PP and ITT of chronic gastritis patients in groups LACJ and LACB were as follows: 75.8% (97/128), 74.6% (97/130) vs 83.8% (109/130), 80.1% (109/136) (both P > 0.05). The symptomatic improvements of abdominal pain, burning and acid reflux of duodenal ulcer patients in group LACJ were higher than those in groups LACB and LAC. There were statistical differences between groups LACJ and LAC (all P < 0.05). The symptomatic improvements of bloating and belching for chronic gastritis patients in group LACJ were higher than those of group LACB. But no significant difference existed between two groups (all P > 0.05). Sixty samples of gastric mucosa were collected from the failed patients. The detection rates of antibiotic-resistant gene to clarithromycin and amoxicillin were 60.0% (36/36) and 18.3% (11/60) respectively. CONCLUSIONS: The efficacy of LACJ for the treatment of H. pylori infection patients is similar to LACB and superior to LAC. And the symptomatic improvement of patients is better than the other two regimens. The main cause of treatment failure is antibiotic resistance of H. pylori strains.

Di-µ-sulfato-κO:O'-bis-{bis-[3-(2-pyrid-yl)pyrazole]cobalt(II)}.

In the centrosymmetric binuclear title molecule, [Co(2)(SO(4))(2)(C(8)H(7)N(3))(4)], the Co(II) ion is coordinated by two N,N'-bidentate 3-(2-pyrid-yl)pyrazole ligands and two sulfate ions, generating a distorted cis-CoO(2)N(4) octa-hedral geometry for the metal atom. The dihedral angles between the pyridine and pyrazole rings in the two ligands are 10.5 (2) and 7.38 (19)°. The bridging sulfate ions generate an eight-membered ring and intra-molecular N-H⋯O hydrogen bonds help to establish the mol-ecular conformation.

Diaqua-1κO,3κO-di-µ-cyanido-1:2κN:C;2:3κC:N-dicyanido-2κN-bis-{4,4'-dibromo-2,2'-[propane-1,2-diylbis(nitrilo-methyl-idyne)]diphenolato}-1κO,N,N',O';3κO,N,N',O'-1,3-dimanganese(III)-2-nickel(II).

In the title compound, [Mn(2)Ni(C(17)H(14)Br(2)N(2)O(2))(2)(CN)(4)(H(2)O)(2)] or [{Mn(C(17)H(14)Br(2)N(2)O(2))(H(2)O)}(2)(µ-CN)(2){Ni(CN)(2)}], each Mn(III) atom is chelated by a Schiff base ligand via two N and two O atoms and is additionally coordinated by a water mol-ecule to give a slightly distorted octa-hedral geometry. Two such Mn(III) ions are linked by a square-planar Ni(CN)(4) unit, which lies on an inversion centre. A two-dimensional network is formed by O-H⋯O and O-H⋯N hydrogen bonds.

Diazido-bis{2-[3-(dimethyl-amino)propyl-imino-meth-yl]phenol}manganese(III) perchlorate.

The title compound, [Mn(N(3))(2)(C(12)H(18)N(2)O)(2)]ClO(4), was synthesized from manganese(III) acetate, sodium azide and 2-[3-(dimethyl-amino)propyl-imino-meth-yl]phenol by a hydro-thermal reaction. The Mn(III) ion is hexa-coordinated by two N and two O atoms from two phenolate ligands and two N atoms from two azide ligands. The Mn(III) cation lies on an inversion centre and, as a result, the asymmetric unit comprises one half-mol-ecule.

[Preventive effects of teprenone on gastric mucosal lesions induced by Helicobacter pylori in mice].

OBJECTIVE: To determine the preventive effect of teprenone on gastric mucosal injury induced with Helicobacter pylori concentrated culture supernatant (CCS) in Balb/c mice. METHODS: Gastric mucosa lesions were induced with intragastrical administration of Helicobacter pylori CCS. Sixty Balb/c mice were divided into control group, injury group, sucralfate protective group and teprenone protective group. Mice of two protective groups were pretreated with sucralfate or teprenone respectively before induction of gastric mucosa lesions. Mucosal changes were assessed by microscopic examination, quantitative histology and electron microscopy. RESULTS: Histologic and ultrastructural lesions in protective groups were less severe than those in injury group. Epithelial damage scoring (EDS) of teprenone protective group (1.68 +/- 0.69) and sucralfate protective group (1.72 +/- 0.73) were significantly decreased than injury group (2.47 +/- 0.58, P < 0.05). CONCLUSION: Teprenone as well as sucralfate reduces gastric mucosal lesions induced by Helicobacter pylori CCS in mice.

[Proliferative changes of human gastric mucosa cells in different pathological lesions and their clinical significance].

OBJECTIVE: To investigate the variation of cell proliferation and growth in different pathological lesions of gastric mucosa and to assess the possible roles of expression of epidermal growth factor receptor (EGFR), transforming growth factor beta receptor type I and type II (TGF(beta)RI, TGF(beta)RII). METHODS: The proliferating cell nuclear antigen (PCNA), EGFR, TGF(beta)RIand TGF(beta)RII were studied in chronic superficial gastritis (CSG, n = 30), chronic atrophic gastritis (CAG, n = 26), intestinal metaplasia (IM,n = 40), Dysplasia (DYS, n = 22), early gastric cancer (EGC, n = 22), advanced gastric cancer (AGC, n = 26) by immunohistochemical methods and their relations with carcinogenesis were analyzed. RESULTS: (1) In different gastric mucosa lesions (CSG, CAG, IM, DYS, EGC, AGC), there were significantly different expression of PCNA (chi2 = 91.06, P < 0.0001), EGFR (chi2 = 52.82, P < 0.0001), TGF(beta)RI (chi2 = 15.93, P = 0.007) and TGF(beta)RII (chi2 = 40.48, P < 0.0001), PCNA and EGFR were increased, TGF(beta)RI and TGF(beta)RII were decreased. (2) In DYS stage, PCNALI (40.00 +/- 16.34) was higher than in CSG (16.63 +/- 10.52), CAG (16.92 +/- 8.50) and IM (23.25 +/- 18.64), but lower than EGC (53.09 +/- 13.51) and AGC (57.54 +/- 16.88) (P < 0.0001); (3) EGFR expression in IM (55.0%) and DYS (72.7%) were higher than in CSG (10.0%) and CAG (3.8%) (P < 0.0001), but no different with EGC (59.1%) and AGC (73.1%). (4) TGF(beta)RI expression in EGC (50.0%) and AGC (30.8%) were lower than in CSG (73.3%) (P = 0.007). (5) TGF(beta)RII expression in AGC (26.9%) was lower than in CSG (83.3%), CAG (82.8%), IM (65.0%), DYS (54.5%) and EGC (45.5%) significantly (P < 0.0001). (6) The expression of EGFR had positive correlation with PCNA, TGF(beta)RI and TGF(beta)RII had negative correlation with PCNA respectively, TGF(beta)RI and TGF(beta)RII had positive correlation. CONCLUSIONS: DYS is the key link in the change of cell proliferation during gastric carcinogenesis; The increase of EGFR and the decrease of TGF(beta)R may play important roles in promoting gastric carcinogenesis by affecting gastric cell proliferation.

[Effect of helicobacter pylori on gastric mucosal cell proliferation in gastritis].

OBJECTIVE: To study the effect of helicobacter pylori on gastric mucosal cell proliferation in gastritis. METHODS: Fifty-six gastritis patients with or without Helicobacter pylori infection (Hp+ 27; Hp- 29) were selected. The expression of proliferation cell nuclear antigen (PCNA), epidermal growth factor receptor (EGFR), transforming growth factor beta receptor type I and type II(TGFbetaRI, TGFbetaRII) in gastric mucosa were examined by immunohistochemical method. RESULTS: The PCNA and EGFR were significantly higher in Hp positive chronic gastritis patients than in Hp negative ones(P<0.05); The TGFbetaRI(P=0.16) and TGFbetaRII(P=0.97) were lower. CONCLUSION: Hp infection promotes over proliferation of gastric mucosal cells.

[The relation between Helicobacter pylori infection and p53 mutation, MG-7 antigen and AgNORs expression in the development of gastric mucosa lesions].

OBJECTIVE: To explore the relation between H. pylori infection and the development of gastric mucosa lesions, and to evaluate the effect of H. pylori infection on cell proliferation, p53 mutation, and MG-7 antigen expression in patients with gastric precancerous lesions. METHODS: One hundred and nine gastric biopsy specimens were divided into five groups of different gastric mucosa lesions according to pathologic findings and the results of mucosa histochemical staining: type I intestinal metaplasia (IM), type IIIM, type III IM, dysplasia (Dys) and gastric cancer (GC). H. pylori and its cagA status were assessed by microdissection/PCR method. Expression of P53 protein and MG-7 antigen were examined by immunohistochemical staining. AgNOR staining was performed for each specimen. RESULTS: (1) Expression of P53 increased in more severe gastric mucosa lesion groups. The P53 expression rate in GC group was significantly higher than other groups (P < 0.05). There was no difference in expression of P53 between groups of different H. pylori status as while as different cagA status. (2) The expression of MG-7 in GC group was significantly higher than that in other groups (P < 0.05). There were no difference of expression of MG-7 between subgroups of different H. pylori infection status or cagA status in all groups (P > 0.05). (3) The counts of argyrophil protein of the nucleolar organizer regions (AgNORs) were significantly increased in more severe gastric mucosa lesion groups (P < 0.05), and were significantly higher in H. pylori positive and cagA positive specimens than in other specimens (P < 0.05). CONCLUSIONS: Infection with H. pylori, particularly cagA-positive strains, is associated with the development of more severe gastric mucosa lesions; it seems to have effects on cell proliferation in patients with gastric precancerous lesions. Expression of P53 and MG-7 are earlier events in gastric cancer carcinogenesis.