Sepsis is a life-threatening organ dysfunction caused by dysregulated host response to infection. Immunosuppression is an important factor of secondary infection in the late state of sepsis, including multi-drugs resistant bacteria, which ultimately leads to the death of patients. The aim of this article was to help clinical staffs better manage patients with sepsis, improve long-term survival rate of the patients, and reduce their re-hospitalization rate by reviewing the relationship between sepsis-induced immunosuppression and multi-drugs resistant bacteria through three aspects: the mechanism of sepsis-induced immunosuppression, the mechanism of antibiotic resistance and the relationship between sepsis-induced immunosuppression and secondary infections.

OBJECTIVETo quantitatively analyze the temporal and spatial pattern of RhoA expression in injured spinal cord of adult mice.

METHODSA spinal cord transection model was established in adult mice. At 1, 3, 7, 14, 28, 56 and 112 days after the surgery, the spinal cords were dissected and cryosectioned for RhoA/NF200, RhoA/GFAP, RhoA/CNPase or RhoA/IBA1 double fluorescent immunohistochemistry to visualize RhoA expressions in the neurons, astrocytes, oligodendrocytes and microglia. The percentages as well as the immunostaining intensities of RhoA-positive cells in the parenchymal cells were quantitatively analyzed.

RESULTSRhoA was weakly expressed in a few neurons and oligodendrocytes in normal spinal cord. After spinal cord injury, the percentage of RhoA-positive cells and RhoA expression intensity in the spinal cord increased and peaked at 7 days post injury (dpi) in neurons, oligodendrocytes and astrocytes, followed by a gradual decrease till reaching a low level at 112 dpi. In the microglia, both the RhoA-positive cells and RhoA expression intensity reached the maximum at 14 dpi and maintained a high level till 112 dpi.

CONCLUSIONTraumatic spinal cord injury can upregulate RhoA expression in the neurons as well as all the glial cells in the spinal cord. RhoA expression patterns vary with post-injury time, location and among different parenchymal cells in the injured spinal cord.

Animals ; Astrocytes ; metabolism ; Female ; Mice ; Mice, Inbred Strains ; Microglia ; metabolism ; Neuroglia ; metabolism ; Neurons ; metabolism ; Spinal Cord ; metabolism ; Spinal Cord Injuries ; metabolism ; rho GTP-Binding Proteins ; metabolism

OBJECTIVE: To investigate the effect of human bone morphogenetic protein (hBMPs) 2/3/6 and 12 on osteosarcoma cell UMR106. METHODS: Adenovirus-BMP2/3/6 and 12 (AdBMP2/3/6 and12) were used to treat the cell line. Their proliferation, apoptosis, and transmigration were detected by Trypan blue exclusion test, TdT-mediated biotinylated-dUTP nick end labeling (TUNEL), acridine orange-ethidium bromide (AO/EB) double fluorescent dye staining, and transwell-room test, respectively. The alkaline phosphatase (ALP) activity was detected to reflect the differentiation of tumors. RESULTS: Compared with the control groups, the cell survival rate of the experimental groups treated with AdBMP2/3/6 and 12 showed a significant time-dependent decrease (P<0.01). The apoptosis indexes were increased significantly (P<0.01) and the results from TUNEL and AO/EB method were consistent. The cell numbers of transmembrane significantly decreased at 24,48, and 72 h (P<0.01). AdBMP2/3/6 and 12 treatment enhanced the activity of ALP activity from day 3 and this effect might still be observed up to day 9 of the treatment (P<0.01). CONCLUSION hBMPs2/3/6 and 12 can inhibit the proliferation and transmigration, and induce their apoptosis and differentiation in osteosarcoma cell line UMR106.
Adenoviridae ; genetics ; metabolism ; Apoptosis ; drug effects ; Bone Morphogenetic Protein 2 ; pharmacology ; Bone Morphogenetic Protein 3 ; pharmacology ; Bone Morphogenetic Protein 6 ; pharmacology ; Bone Morphogenetic Proteins ; pharmacology ; Bone Neoplasms ; pathology ; Cell Line, Tumor ; Cell Transformation, Neoplastic ; drug effects ; Growth Differentiation Factors ; pharmacology ; Humans ; Osteosarcoma ; pathology ; Recombinant Proteins ; pharmacology

Objective: To examine whether presepsin level can serve as a distinguishing marker between G- bacteria and G+ bacteria, fungal infection in sepsis patients. Methods: A prospective observation study was conducted on the consecutive patients with positive bacterial cultures in intensive care unit (ICU) from June 2017 to November 2018. The patients were divided into the G- group, G+ group and fungal group. Blood samples were collected upon admission to measure the levels of presepsin and procalcitonin (PCT). Results: (1) Of the 156 patients met the inclusion criteria. 96 (62% G- rods, 25 (16%) G+ microbes, and 35 (22%) fungi were detected. (2) Presepsin concentrations were significantly higher in the G- group compared with the G+ and fungal groups (P = 0.000). (3) Presepsin level has a higher accuracy in differentiating G- sepsis from Gram+ and fungal sepsis than PCT level [area under the curve (AUC): 0.809 vs 0.712]. The AUC value of a combination of presepsin and PCT level was significantly larger than that of presepsin level alone in differentiating G- sepsis from Gram+ and fungal sepsis (AUC: 0.866 vs 0.809). Conclusions In contrast to PCT, presepsin is a good discriminative biomarker in different infections.