Uropathogenic Escherichia coli infection: innate immune disorder, bladder damage, and Tailin Fang II.

Background: Uropathogenic Escherichia coli (UPEC) activates innate immune response upon invading the urinary tract, whereas UPEC can also enter bladder epithelial cells (BECs) through interactions with fusiform vesicles on cell surfaces and subsequently escape from the vesicles into the cytoplasm to establish intracellular bacterial communities, finally evading the host immune system and leading to recurrent urinary tract infection (RUTI). Tailin Fang II (TLF-II) is a Chinese herbal formulation composed of botanicals that has been clinically proven to be effective in treating urinary tract infection (UTI). However, the underlying therapeutic mechanisms remain poorly understood. Methods: Network pharmacology analysis of TLF-II was conducted. Female Balb/C mice were transurethrally inoculated with UPEC CFT073 strain to establish the UTI mouse model. Levofloxacin was used as a positive control. Mice were randomly divided into four groups: negative control, UTI, TLF-II, and levofloxacin. Histopathological changes in bladder tissues were assessed by evaluating the bladder organ index and performing hematoxylin-eosin staining. The bacterial load in the bladder tissue and urine sample of mice was quantified. Activation of the TLR4-NF-κB pathway was investigated through immunohistochemistry and western blotting. The urinary levels of interleukin (IL)-1ß and IL-6 and urine leukocyte counts were monitored. We also determined the protein expressions of markers associated with fusiform vesicles, Rab27b and Galectin-3, and levels of the phosphate transporter protein SLC20A1. Subsequently, the co-localization of Rab27b and SLC20A1 with CFT073 was examined using confocal fluorescence microscopy. Results: Data of network pharmacology analysis suggested that TLF-II could against UTI through multiple targets and pathways associated with innate immunity and inflammation. Additionally, TLF-II significantly attenuated UPEC-induced bladder injury and reduced the bladder bacterial load. Meanwhile, TLF-II inhibited the expression of TLR4 and NF-κB on BECs and decreased the urine levels of IL-1ß and IL-6 and urine leukocyte counts. TLF-II reduced SLC20A1 and Galectin-3 expressions and increased Rab27b expression. The co-localization of SLC20A1 and Rab27b with CFT073 was significantly reduced in the TLF-II group. Conclusion: Collectively, innate immunity and bacterial escape from fusiform vesicles play important roles in UPEC-induced bladder infections. Our findings suggest that TLF-II combats UPEC-induced bladder infections by effectively mitigating bladder inflammation and preventing bacterial escape from fusiform vesicles into the cytoplasm. The findings suggest that TLF-II is a promising option for treating UTI and reducing its recurrence.

Morphological Variation and Recovery Mechanism of Residual Crude Oil by Biosurfactant from Indigenous Bacteria: Macro- and Pore-Scale Experimental Investigations.

Microbial enhanced oil recovery (MEOR) is being used more widely, and the biological contributions involved in MEOR need to be identified and quantified for the improvement of field applications. Owing to the excellent interfacial activity and the wide distribution of producing strains in oil reservoirs, lipopeptides have proved to be an essential part of the complex mechanisms in MEOR. In this study, crude lipopeptides were produced by a strain isolated from an indigenous community in an oil reservoir. It was found that crude lipopeptides can effectively reduce the IFT (interfacial tension) to 10(-1)~10(-2) mN/m under high salinity without forming stable emulsions, and the wettability of natural sandstone can be enhanced (Amott index, from 0.36 to 0.48). The results of core flooding experiments indicate that an additional 5.2% of original oil in place can be recovered with a 9.5% reduction of injection pressure. After the shut-in period, the wettability of the core, the reduction of injection pressure, and the oil recovery can be improved to 0.63, 16.2% and 9.6%, respectively. In the microscopic flooding experiments, the crude oil in membrane, cluster, and throat states contribute nearly 90% in total of the additional oil recovery, and the recovery of membranestate oil was significantly enhanced by 93.3% after shut in. Based on the results in macro and pore scale, the IFT reduction and the wettability alteration are considered primary contributors to oil recovery, while the latter was more dominant after one shut-in period.

[One family investigation and risk factors analysis of developmental dysplasia of the hip].

OBJECTIVE: To investigate the clinical manifestations and risk factors of the patients from developmental dysplasia of the hip(DDH) family. METHODS: Detailed epidemiology investigation, physical examination, functional movement assessment, lab test and X-ray examination were applied to the whole members of a DDH family. RESULTS: In the family with 9 generations and 218 persons, the incidence of DDH was 31.03% in 145 survivors. Patients mainly manifested bilateral knee and hip joint pain, flexion contracture of hip, limitation in internal and external rotation of hip; a few had arthritic functional disorder, deformation, and limp. The radiography illustrated shallow acetabulum with increased inclination, which encompassed the femoral head badly. Deformation of the femoral head, narrow joint space and osteophyte were also found by X-ray examination. The main risk factors of DDH were genetic factors, gender, birth season etc. The son or daughter with one or two DDH parents had a higher risk for developing DDH than those with no DDH parents. Furthermore, first-degree relatives of the DDH patients also had a greater chance to develop DDH than second-degree relatives and third-degree relatives. The incidence among females was higher than males, and the family member who was given birth in winter had a highest risk for developing DDH. However, there was no difference between incidence of DDH in children and youths and in adults; the incidence of DDH in the immigrants with no blood relationship also did not differ from the incidence of DDH in the family member. CONCLUSION: The genetic factors play an important role in the development of DDH, so do the environmental factors.