Nomogram for predicting surgical site infections in elderly patients after open lumbar spine surgery: A retrospective study.

The aim of this study is to develop a nomogram to assess the risk of surgical site infection in elderly patients undergoing open lumbar spine surgery and explore related risk factors. We reviewed the records of 578 elderly patients who had undergone open lumbar spine surgery. The clinical parameters were subjected to lasso regression and logistic regression analyses. Subsequently, a nomogram was constructed to predict the risk of postoperative surgical site infection and validated using bootstrap resampling. A total of 578 patients were included in the analysis, of which 17 were diagnosed as postoperative surgical site infection. Following the final logistic regression analysis, obesity, hypoalbuminemia and drinking history were identified as independent risk factors and subsequently incorporated into the nomogram. The nomogram demonstrated excellent discrimination, with an area under the receiver-operating characteristic curve of 0.879 (95% CI 0.769 ~ 0.989) after internal validation. The calibration curve exhibited a high level of consistency. Decision curve analysis revealed that this nomogram had greater clinical value when the risk threshold for surgical site infection occurrence was >1% and <89%. We had developed a nomogram for predicting the risk of postoperative surgical site infection in elderly patients who had undergone open lumbar spine surgery. Validation using bootstrap resampling demonstrated excellent discrimination and calibration, indicating that the nomogram may hold potential clinical utility as a simple predictive tool for healthcare professionals.

Aerobic Exercise Ameliorates Liver Injury in Db/Db Mice by Attenuating Oxidative Stress, Apoptosis and Inflammation Through the Nrf2 and JAK2/STAT3 Signalling Pathways.

Objective: Diabetes mellitus (DM) implicates oxidative stress, apoptosis, and inflammation, all of which may contribute liver injury. Aerobic exercise is assured to positively regulate metabolism in the liver. This project was designed to investigate whether and how aerobic exercise improves DM-induced liver injury. Methods: Seven-week-old male db/db mice and age-matched m/m mice were randomly divided into a rest control group or a group that received 12 weeks of aerobic exercise by treadmill training (10 m/min). Haematoxylin and eosin (HE) staining, electron microscopy, Oil Red O staining and TUNEL assays were used to evaluate the histopathological changes in mouse liver. The serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), triglyceride (TRIG), cholesterol (CHOL) were analyzed by serum biochemical analysis. Interleukin-6 (IL-6), tumour necrosis factor-α (TNF-α), and tissue levels of malondialdehyde (MDA) and superoxide dismutase (SOD) were analyzed via ELISA. Nuclear factor E2-associated factor-2 (Nrf2), nuclear factor κB (NF-κB) and JAK2/STAT3 pathway-related proteins were measured by immunofluorescence, Western blotting and q-PCR. F4/80 expression in liver tissues was assessed by immunohistochemistry. Results: In diabetic mice, exercise training significantly decreased the levels of serum TRIG, CHOL, IL-6, TNF-α, ALT and AST; prevented weight gain, hyperglycaemia, and impaired glucose and insulin tolerance. Morphologically, exercise mitigated the diabetes-induced increase in liver tissue microvesicles, inflammatory cells, F4/80 (macrophage marker) levels, and TUNEL-positive cells. In addition, exercise reduced the apoptosis index, which is consistent with the results for caspase-3 and Bax. Additionally, exercise significantly increased SOD activity, decreased MDA levels, activated Nrf2 and decreased the expression of NF-kB, phosphorylated JAK2 and STAT3 proteins in the livers of diabetic mice. Conclusion: This study demonstrated that aerobic exercise reversed liver dysfunction in db/db mice with T2DM by reducing oxidative stress, apoptosis and inflammation, possibly by enhancing Nrf2 expression and inhibiting the JAK2/STAT3 cascade response.

Intraoperative use of low-dose dexmedetomidine for the prevention of emergence agitation following general anaesthesia in elderly patients: a randomized controlled trial.

OBJECTIVE: To clarify the effect of an intraoperative low-dose dexmedetomidine infusion on emergence agitation following general anaesthesia in elderly patients. METHODS: Eighty elderly patients (> 64-years-old) following elective general anaesthesia for radical cancer surgeries were randomly allocated into two groups (n = 40 each): the dexmedetomidine group (Group D) and the normal saline group (Group C). Anaesthesia was maintained with continuous intravenous infusion of dexmedetomidine at - 0.2 µg kg-1 h-1 in Group D, and an equal volume of normal saline (0.5 ml kg-1 h-1) was given in Group C. All patients were observed for 30 min in the post-anaesthesia care unit (PACU), AFPS and NRS were recorded every 2 min, and the total doses of nalbuphine and fentanyl were calculated in the PACU. MAP and HR were recorded at the time of 10 min (T1), 20 min (T2), 30 min (T3) after dexmedetomidine or saline pumping, and before extubation (T4), immediately after extubation (T5), and 5 min after extubation (T6). We also documented some durations, including anaesthesia duration (D1), surgery duration (D2), duration from the end of surgery to extubation (D3), and emergence agitation duration (D4). RESULTS: The MAP in Group C was significantly higher than that in Group D (P < 0.05), and there were no significant changes between the two groups in HR and MAP within each time point and D1, D2, D3, and D4. The incidence of agitation, NRS score and total dose of nalbuphine and fentanyl were all lower in Group D than in Group C (P < 0.05). CONCLUSION: An intraoperative low-dose dexmedetomidine continuous infusion can reduce emergence agitation following general anaesthesia in elderly patients (> 64-years-old), remain stable in terms of haemodynamics, and not lead to delays in anaesthesia recovery time and extubation time.

Non-small cell lung cancer combination therapy: Hyaluronic acid modified, epidermal growth factor receptor targeted, pH sensitive lipid-polymer hybrid nanoparticles for the delivery of erlotinib plus bevacizumab.

Non-small cell lung cancer (NSCLC) is the leading cause of cancer-related mortality in China. This study aimed to develop a hyaluronic acid (HA) decorated, pH sensitive lipid-polymer hybrid nanoparticles (LPH NPs) to co-deliver erlotinib (ERL) and bevacizumab (BEV) (HA-ERL/BEV-LPH NPs) for targeting and suppressing NSCLC. HA contained pH sensitive nano-materials were synthesized by acylation reaction. HA-ERL/BEV-LPH NPs were prepared using a sonication method. To explore the efficiency of the system, we evaluated the physicochemical parameters and performed a release study, a cellular uptake assay, a cytotoxicity evaluation, and several in vivo anti-tumor studies in comparison with free drugs and single drug systems. All LPH NPs samples have particle sizes of about 100-120 nm, polydispersity index values range from 0.12 to 0.15, and negative zeta potentials. HA-ERL/BEV-LPH NPs contained pH sensitive adipic acid dihydrazide (ADH) showed fast drug release at pH 5.5 than pH 7.4. After 21 days, the tumor volume of the HA-ERL/BEV-LPH NPs group (229.2 ± 13.1 mm3) was significantly smaller than 0.9 % NaCl control group (1126.3 ± 39.4 mm3), with a tumor inhibition rate of 79.7 ± 3.2 %. The maximum plasma ERL concentrations, half life period, and area under the curve of HA-ERL/BEV-LPH NPs were 21.6 µg/mL, 7.57 h, and 290.3 mg/L·h). With the highest tumor tissue accumulation concentration (25.3 µg/mL) and low system toxicity, HA-ERL/BEV-LPH NPs. HA-ERL/BEV-LPH NPs could be used as a promising system for the combination therapy of NSCLC.

SATB1 expression is associated with biologic behavior in colorectal carcinoma in vitro and in vivo.

There is increasing evidence that Special AT-rich sequence-binding protein 1 (SATB1) is aberrantly expressed in several cancers and is correlated with clinicopathologic parameters in these tumors. In this study, we showed over-expression of SATB1 in 80 cases of colorectal cancer and in 3 colorectal cancer cell lines and found expression levels were strongly associated with tumor differentiation and stage. Expression levels of SATB1 protein were higher in poorly-differentiated as compared with well-differentiated cell lines, and both quantity and distribution patterns of SATB1 were associated with tumor differentiation and pTNM stage. Strikingly, we further investigated the effect of down regulation of SATB1 expression on malignant phenotypic features in colorectal cancer cells in vitro, and showed that SABT1 down-regulation negatively affected growth potential, anchorage-independent colony formation and cancer cell invasion, and resulted in increased apoptosis. SATB1 expression was positively associated with the expression of various biological and genetic markers, including Cyclin D1, MMP-2, NF-κB, and PCNA, and was associated with loss of APC and BRAF(V600E). These findings suggest that SATB1 is involved in the carcinogenesis, development and progression of colorectal cancer.

IgG expression in human colorectal cancer and its relationship to cancer cell behaviors.

Increasing evidence indicates that various cancer cell types are capable of producing IgG. The exact function of cancer-derived IgG has, however, not been elucidated. Here we demonstrated the expression of IgG genes with V(D)J recombination in 80 cases of colorectal cancers, 4 colon cancer cell lines and a tumor bearing immune deficient mouse model. IgG expression was associated with tumor differentiation, pTNM stage, lymph node involvement and inflammatory infiltration and positively correlated with the expressions of Cyclin D1, NF-κB and PCNA. Furthermore, we investigated the effect of cancer-derived IgG on the malignant behaviors of colorectal cancer cells and showed that blockage of IgG resulted in increased apoptosis and negatively affected the potential for anchor-independent colony formation and cancer cell invasion. These findings suggest that IgG synthesized by colorectal cancer cells is involved in the development and growth of colorectal cancer and blockage of IgG may be a potential therapy in treating this cancer.

Expression and distribution of immunoglobulin G and its receptors in an immune privileged site: the eye.

It has recently been demonstrated that not only mature B lymphocytes, but also non-lymphoid cells, including cancer cells and neurons, express IgG. In the eye, an important immune privileged site, the presence of IgG has been ascribed to IgG entering the eye through breaches of the blood­ocular barrier. Here we demonstrate that the eye itself can produce IgG intrinsically. Applying immunohistochemistry, in situ hybridization, and RT-PCR, several intraocular structures were found to express proteins and mRNA transcripts of IgG heavy chains, light chains, V(D)J rearrangements, and enzymes required for V(D)J recombination. IgG receptors were also detected in the intraocular epithelium and endothelium. The extensive distribution of IgG and its receptors in intraocular structures indicates that locally produced IgG could play a significant role in maintaining the ocular microenvironment and protection of the eyes, and it might also be involved in the pathogenesis of age-related macular degeneration and some inflammatory diseases.