Aging has less effect on adipose-derived mesenchymal stem cells (ADSCs) than on bone marrow-derived mesenchymal stem cells (BMSCs), but whether the fact holds true in stem cells from elderly patients with osteoporotic fractures is unknown. In this study, ADSCs and BMSCs of the same donor were harvested and divided into two age groups. Group A consisted of 14 young patients (36.4 ± 11.8 years old), and group B consisted of eight elderly patients (71.4 ± 3.6 years old) with osteoporotic fractures. We found that the doubling time of ADSCs from both age groups was maintained below 70 hrs, while that of BMSCs increased significantly with the number of passage. When ADSCs and BMSCs from the same patient were compared, there was a significant increase in the doubling time of BMSCs in each individual from passages 3 to 6. On osteogenic induction, the level of matrix mineralization of ADSCs from group B was comparable to that of ADSCs from group A, whereas BMSCs from group B produced least amount of mineral deposits and had a lower expression level of osteogenic genes. The p21 gene expression and senescence-associated β-galactosidase activity were lower in ADSCs compared to BMSCs, which may be partly responsible for the greater proliferation and differentiation potential of ADSCs. It is concluded that the proliferation and osteogenic differentiation of ADSCs were less affected by age and multiple passage than BMSCs, suggesting that ADSCs may become a potentially effective therapeutic option for cell-based therapy, especially in elderly patients with osteoporosis.

The EAL regimen can achieve an efficacy similar to that of the standard EBTM therapy. It may be very useful in countries where bismuth salts are not available. Compliance, CYP2C19 genotype and resistances to antibiotics may influence the outcome of levofloxacin-based rescue therapy. It seems advisable to reserve levofloxacin for rescue treatment to avoid an increase in the resistance phenomenon.

No abstract

The presence of class 1 integrons in clinical isolates of Escherichia coli was detected by PCR. Of 104 E. coli isolates from Kaohsiung, 54 (52%) carried class 1 integrons, with inserted DNA regions of 1±3 kb. These integrons were located on plasmids, as demonstrated by Southern hybridisation. DNA sequencing was used to identify the genetic content of the integron-variable regions. Different class 1 integrons contained various numbers, kinds and combinations of gene cassettes within their variable regions. These gene cassettes included those encoding resistance to trimethoprim (dfrIa, dfrV, dfr12 and dfr17), aminoglycosides (aadA1a, aadA2, aadA4 and aadB), chloramphenicol (cmlA), erythromycin (ereA2) and â-lactams (blaP1). An integron carrying three inserted cassettes ± dfr12-orfF-aadA2 ± was present in 33 (61%) of the 54 isolates with class 1 integrons. Gene cassettes encoding resistance were expressed phenotypically. The results indicate that class 1 integrons are widespread in clinical E. coli isolates in Taiwan. The types, combinations and frequency of the gene cassettes in integrons may re¯ect the speci®c selective pressures to which the isolates were exposed and could provide useful surveillance data for relation to antibiotic usage information.

Objectives: Polymicrobial bloodstream infection (BSI) is a critical condition and has been increasingly reported; however, the authors were unable to find an emergency department (ED) patient-based study in the literature.Methods: A retrospective matched case-control study with a ratio of 1:3 among patients with polymicrobial BSIs in an ED was conducted. The case group was patients aged > 16 years with polymicrobial BSIs. Patients matched for age and sex with monomicrobial BSIs were sampled as the control group. Demographic information, underlying conditions, microbiologic data, and outcomes were collected for further analysis.Results: From January 2005 to December 2007, a total of 112 episodes of polymicrobial BSIs among 109 patients were included. Two pathogens were isolated among 87 (77.7%) episodes and three were found among 25 (22.3%) episodes. A history of hospitalization within 90 days was an independent risk factor for polymicrobial BSIs (p = 0.003). Intraabdominal infection (p < 0.001) and respiratory tract infection (p = 0.017) were more likely to be associated with polymicrobial BSIs. Gram-negative and Gram-positive bacteria were documented in 95.5 and 46.4% episodes of polymicrobial BSIs, respectively. Inappropriate antimicrobial treatment was observed in 53.6% of polymicrobial BSIs, but only accounted for 23.8% of monomicrobial BSIs (p < 0.001). The overall 30-day mortality rate of the polymicrobial group was significantly higher than those with monomicrobial BSIs (30.3 and 11.6%, respectively; p < 0.001).Conclusions: Patients with polymicrobial BSIs had a high mortality rate. Acknowledgment of the clinical and microbiologic characteristics and recognition of patients at risk for polymicrobial BSIs are critical in EDs.

Diabetic rats showed hindpaw mechanical allodynia for 6 months. Persistent mechanical allodynia was positively associated with sustained increased activation of Nav1.3 and increased p38 phosphorylation in activated microglia.

ADP‐ribosylation factor 6 (ARF6) is a well‐studied protein that is involved in multiple biological functions including cell migration and invasion. The mechanism by which ARF6 regulates the migration and invasion of upper tract urothelial carcinoma (UTUC) is still unknown. MiR‐145‐5p is a tumor suppressor microRNA, which is downregulated in several cancer types. We aimed to elucidate the molecular mechanism underlying the regulation of ARF6 by miR‐145‐5p in UTUC. ARF6 expression was observed to be higher in UTUC tissues than paired adjacent normal tissues. A reverse correlation between ARF6 and miR‐145‐5p was found in UTUC tissues. MiR‐145‐5p inhibited ARF6 expression by directly targeting its 3′‐UTR. The functional studies indicated that ARF6 expression reversed the miR‐145‐5p‐reduced tumor cell migration and invasion. Notably, miR‐145‐5p reduced MMP2, N‐cadherin, FAK and MMP7, and elevated E‐cadherin protein levels in vitro; however, the above effects were reversed by ARF6. Further, the expression of epithelial‐to‐mesenchymal transition (EMT) markers and cell invasion was suppressed by knocking down MMP7 in UTUC cells. These findings suggest that miR‐145‐5p may suppress UTUC cell motility and invasion by targeting ARF6/MMP7 through EMT.

Results indicate that p14ARF is a primary target of homozygous deletion, whereas p16INK4a is the hot spot of hypermethylation on the 9p21 region in bladder cancer. The frequent inactivation of the p14ARF and p16INK4a genes may be an important mechanism for the dysfunction of p53 and Rb growth regulatory pathways during bladder cancer development.