[Distribution and drug resistance of pathogens at hematology department of Jiangsu Province from 2014 to 2015: results from a multicenter, retrospective study].

Objective: To describe the distribution and drug resistance of pathogens at hematology department of Jiangsu Province from 2014 to 2015 to provide reference for empirical anti-infection treatment. Methods: Pathogens were from hematology department of 26 tertiary hospitals in Jiangsu Province from 2014 to 2015. Antimicrobial susceptibility testing was carried out according to a unified protocol using Kirby-Bauer method or agar dilution method. Collection of drug susceptibility results and corresponding patient data were analyzed. Results: The separated pathogens amounted to 4 306. Gram-negative bacteria accounted for 64.26%, while the proportions of gram-positive bacteria and funguses were 26.99% and 8.75% respectively. Common gram-negative bacteria were Escherichia coli (20.48%) , Klebsiella pneumonia (15.40%) , Pseudomonas aeruginosa (8.50%) , Acinetobacter baumannii (5.04%) and Stenotropho-monas maltophilia (3.41%) respectively. CRE amounted to 123 (6.68%) . Common gram-positive bacteria were Staphylococcus aureus (4.92%) , Staphylococcus hominis (4.88%) and Staphylococcus epidermidis (4.71%) respectively. Candida albicans were the main fungus which accounted for 5.43%. The rates of Escherichia coli and Klebsiella pneumonia resistant to carbapenems were 3.5%-6.1% and 5.0%-6.3% respectively. The rates of Pseudomonas aeruginosa resistant to tobramycin and amikacin were 3.2% and 3.3% respectively. The resistant rates of Acinetobacter baumannii towards tobramycin and cefoperazone/sulbactam were both 19.2%. The rates of Stenotrophomonas maltophilia resistant to minocycline and sulfamethoxazole were 3.5% and 9.3% respectively. The rates of Staphylococcus aureus, Enterococcus faecium and Enterococcus faecalis resistant wards vancomycin were 0, 6.4% and 1.4% respectively; also, the rates of them resistant to linezolid were 1.2%, 0 and 1.6% respectively; in addition, the rates of them resistant to teicoplanin were 2.8%, 14.3% and 8.0% respectively. Furthermore, MRSA accounted for 39.15% (83/212) . Conclusions: Pathogens were mainly gram-negative bacteria. CRE accounted for 6.68%. The rates of Escherichia coli and Klebsiella pneumonia resistant to carbapenems were lower compared with other antibacterial agents. The rates of gram-positive bacteria resistant to vancomycin, linezolid and teicoplanin were still low. MRSA accounted for 39.15%.

Characteristics of immune cell changes before and after immunotherapy and their clinical significance in patients with unexplained recurrent spontaneous abortion.

To investigate the characteristics of immune cells before and after immunotherapy and their clinical significance in patients with unexplained recurrent spontaneous abortion (URSA), an analysis of 67 URSA patients, 67 sporadic spontaneous abortion (SA) patients, and 22 normal nonpregnant women (as controls) was conducted. URSA patients underwent immunotherapy using paternal lymphocytes. Peripheral blood from patients and controls was examined for lymphocytes and other markers of immune status. Before the immunotherapy, lymphocyte counts, CD4:CD8 cell ratios, and the relative proportion of natural killer (NK) cells were significantly higher in the URSA patient group than in the SA patient and control groups (P < 0.05). After the therapy, all of these three measures were decreased, whereas the percentage of T cells was increased, and statistically significant differences before and after the immunotherapy were detected (P < 0.05). Therefore, the immune system appears to be activated in the URSA patients, and the abnormal immunologic state in the URSA patients is more severe than in the SA patients. The alterations in T and NK cells may be involved in the etiopathogenesis of URSA. Lymphocyte immunotherapy appears to be an effective treatment for URSA patients.

Fetal fibronectin detection for preterm birth prediction.

To study preterm birth prediction based on fetal fibronectin (fFN) in pregnant women, we randomly selected 124 patients. Vaginal posterior fornix secretions were analyzed using fFN quick test strips. Leucorrhea routine samples were collected to detect bacterial vaginosis, mycoplasma, and chlamydia. Delivery data at 7 days, 14 days, 34 weeks, and 37 weeks were documented and the sensitivity, specificity, positive predictive value, and negative predictive value were analyzed. Of the 124 cases, we found 2, 4, 10, and 18 cases of maternity within 7 days, 14 days, 34 weeks, and 37 weeks, respectively. The sensitivity, specificity, positive predictive value, and negative predictive value were as follows: 100, 77.8, 6.9, and 100% for 7 days; 75, 78.3, 10.3, and 98.9% for 14 days; 50.0, 78.9, 17.2, and 94.7% for 34 weeks; 33.3, 78.3, 20.7, and 87.4% for 37 weeks, respectively. Except for 18 preterm births, 23 cases were fFN-positive, 17 cases had lower genital tract infection. Eighty-three cases were fFN-negative, of which 18 cases had the lower genital tract infections. This difference was statistically significant (P < 0.05). Eighteen cases (14.5% of the pregnant women) had preterm birth. Ten cases delivered within 34 weeks. The negative predictive value and recent predictive value of fFN testing were higher; the positive predictive value was limited due to the impact of lower genital tract infection. The fFN-positive patients need timely clinical processing. During the pregnancy, monitoring of fFN changes and early detection of abnormalities help to reduce perinatal morbidity and mortality.

Effect of bcl-2 deficiency on the radiation response of clonogenic cells in small and large intestine, bone marrow and testis.

PURPOSE: Overexpression of bcl-2 protects against radiation induced apoptosis in lymphohaematopoietic cell types in vivo, whilst bcl-2 deficiency radiosensitizes murine T-lymphocytes in vitro. However, there are few data regarding the influence of bcl-2 deficiency on the radiosensitivity of non-lymphoid cell types. The purpose of this study was to investigate the role of bcl-2 in the clonogenic radiation response of intestinal crypts, bone marrow progenitor cells and testicular stem cells. METHOD: Survival curves were obtained for each cell type from bcl-2 null (-/-), heterozygote (+/-) and wild type (+/+) mice. Crypt survival in the small and large intestine was assessed using the crypt microcolony assay. Committed haemopoietic progenitors were assayed using in vitro colony-forming cell (CFC) assays and survival of clonogenic spermatogonia was assessed by scoring regenerative tubules at 35 days post-irradiation. RESULTS: There was no difference in small intestine crypt survival between the three genotypes. In the colon, there was a tendency towards lower clonogen survival in the +/- and -/- animals. Haemopoietic in vitro CFC from -/- animals showed lower survival in comparison to +/+ mice, but spermatogonial stem cells were comparatively more radioresistant. CONCLUSIONS: Deficiencies in bcl-2 affect the radiation response of different cell populations in small but different ways. This may be due to variations between cells in their innate capacity for apoptosis, their dependence on different members of the bcl-2 family gene and their cell-cycle status and p53 expression.

p53 deficiency sensitizes clonogenic cells to irradiation in the large but not the small intestine.

The role of p53 in the survival of irradiated crypts in the small intestine and three regions of the large intestine (cecum, mid-colon and rectum) was assessed by comparing the responses in p53 null, p53 heterozygous and wild-type mice. There was no difference in the levels of crypt survival in the small intestine between the three genotypes, although the rate of cell depletion and regeneration in the null mice appeared slower. In the large intestine, crypt survival was lowest in the null mice compared to the other genotypes, in particular after high doses. The levels of crypt survival in the heterozygotes were not significantly different from those in the wild-type mice. Hence the greater radioresistance of crypts in the colon than in the small intestine, reported previously by us and others using various other mouse strains, may be partly attributable to the presence of p53. This effect is not readily explained by current knowledge concerning the decreased p53 expression and the greater expression of the survival gene Bcl2 in the stem cell zone of crypts in the colon compared to those in the small intestine. Reduced repair associated with the lack of a G2-phase checkpoint delay, the predominant arrest point for intestinal cells, is a possible explanation for the decrease in survival.

The number of clonogenic cells in crypts in three regions of murine large intestine.

Data are presented for the kinetics of repair of sub-lethal damage in the large intestine of mice. The results are based on experiments using the crypt microcolony assay with two equal sized doses which were delivered with a variable interval of time between the doses. These show that this split-dose repair was largely complete after 5 h, and that there were no significant differences between three regions of the large intestine. Overall the half-time for the repair was 2.3 +/- 0.8 h, and the maximum split-dose repair ratio (the proportion of damage recovered by splitting the dose into two fractions) was 22 +/- 2% and the mean recovery factor (the ratio of the number of surviving crypts using long interfraction intervals to that at zero time) was 11 +/- 2. The split-dose approach (Hendry 1979) using a 5 h interval has been used to estimate the number of clonogenic cells in large intestinal crypts. A range of single and paired doses between 7 Gy and 10.5 Gy were used. There were significant differences between the three regions of the large intestine, the caecum, mid-colon and rectum. The estimate of the number of clonogens also depended in a significant way on the dose of radiation used to make the estimate. At low doses large intestinal crypts contain between 5 and 10 clonogenic cells while if high doses were used they contain an estimated 16 to 36 clonogenic cells. Considerable similarity exists between the small intestine and the large intestine for; (a) the repair kinetics (b), the clonogenic estimates, and (c) their dependence on dose.

Differential survival of murine small and large intestinal crypts following ionizing radiation.

Radiation survival curves have been obtained for crypts in the small and large intestine of male BDF1 mice using the microcolony assay. Four regions of the small intestine and three regions of the large intestine were studied. One of the major objectives was to determine the optimal conditions for the microcolony assay in the large bowel. Various times post-irradiation were studied using different approaches and threshold criteria for surviving crypts. Small, but statistically significant, differences were observed along the length of the small intestine, but no differences were observed between different regions of the large intestine. There was a marked difference (p < 0.001) in the response in the large compared with the small intestine (D0 = 291 +/- 14 compared with 151 +/- 4 cGy respectively with corresponding extrapolation numbers of 18 +/- 4 and 377 +/- 65). The use of tritiated thymidine or vincristine helped in the identification of true survivors in the large bowel, but these approaches are not necessary in the small bowel. The longer the time after irradiation that the samples were fixed the easier it was to identify survivors in the colon. However, the longer the time the more animals died. The optimum compromise in these studies was to use partial-body irradiation (abdomen only) and to sample on the fifth day after irradiation. With these criteria the mid-colon survival curve had a D0 = 274 +/- 28 cGy and an extrapolation number of 22 +/- 10. The results can be considered in relation to published data on the levels of p53 and bcl-2 expression and apoptosis in murine small and large bowel.