Epidemiological characteristics and factors influencing hospitalization burden among trauma patients: a retrospective analysis.

PURPOSE: This investigation aimed to understand the epidemiological characteristics and hospitalization burden and its possible influencing factors of patients with different injury mechanisms. METHODS: All trauma patients admitted via the emergency department at a trauma center from November 1, 2020, to April 30, 2022, were identified. The hospitalization burden, including the number of hospitalizations, deaths and in-hospital mortality, length of stay (LOS), and medical costs, was calculated. Univariate and multivariate logistic regression models were used to analyze the factors influencing the hospitalization burden of trauma. The receiver-operating characteristic (ROC) curves were drawn to evaluate the predictive value of the multivariate model. RESULTS: 16 485 trauma patients with 16 552 hospitalizations were included, with an in-hospital mortality rate of 1.269‰, median LOS of 7 days, and median hospitalization costs of 54 725.28 CNY. The median age was 52 years. 62.54% were hospitalized due to falls. The upper and lower extremities were the most common injury regions. There are differences between the demographic, injury, and hospitalization characteristics and factors influencing hospitalization burden across injury mechanisms, but there were also common influencing factors. Injury region, surgery, transfusion, and ICU treatment are influential factors for prolonged LOS. Age, injury region, surgery, and transfusion were influential factors for high hospitalization costs. CONCLUSIONS: This study provided primary evidence on the hospitalization burden of trauma. Considering demographics, injury and hospitalization characteristics as additional discriminators could further intervene in LOS and medical costs. Targeted efforts to use more early prevention measures could potentially lower future hospitalization burden.

Incidence and risk factors of postoperative hyperamylasemia and pancreatitis following total knee arthroplasty: a retrospective study.

BACKGROUND: Postoperative hyperamylasemia and pancreatitis are recognized complications after abdominal and spinal surgeries. The aim of this study is to investigate the incidence and identify risk factors for postoperative hyperamylasemia and pancreatitis following total knee arthroplasty. METHODS: 170 patients undergoing total knee arthroplasty were retrospectively identified from our database from January 2017 to January 2021. Patients were divided into normal and hyperamylasemia groups based on the presence of serum amylase level within or greater than the normal range. The diagnosis of postoperative pancreatitis was based on the 2012 revised Atlanta Classification of Acute Pancreatitis. Patient demographics, perioperative parameters were investigated with student t test, chi square test and multivariate logistic regression analysis. RESULTS: 43 patients (25.3%) exhibited postoperative hyperamylasemia while eight patients (4.7%) exhibited serum amylase < 5 times the normal upper limit. One patient (0.6%) was designated as having postoperative pancreatitis. More patients with Hypertriglyceridemia (HTG) were noted in hyperamylasemia group (P = 0.009) compared with normal group. Hyperamylasemia group showed higher preoperative serum amylase (74.95 vs. 55.62 IU/L, P < 0.001), higher intra-operative blood loss (IBL) (117.67 vs. 77.01 mL, P = 0.040) and longer surgical duration (132.98 vs. 107.01 min, P = 0.041). Multivariate logistic analysis revealed that HTG (OR = 0.189, P = 0.006), preoperative serum amylase (OR = 1.042, P < 0.001) and IBL (OR = 1.004, P = 0.022) were independent risk factors for postoperative hyperamylasemia. CONCLUSIONS: A significant percentage of patients developed hyperamylasemia after total knee arthroplasty. Patients with HTG, higher preoperative serum amylase and higher IBL had an increased risk of developing postoperative hyperamylasemia and pancreatitis.

[Tendency analysis of incidence and mortality of mechanical injuries among Chinese residents from 1990 to 2019].

OBJECTIVE: To analyze the tendency of incidence and mortality of mechanical injuries among Chinese residents from 1990 through 2019 and to estimate the age-period-cohort effect. METHODS: Based on the Global Burden of Disease (GBD) 2019 database, the incidence and mortality data of mechanical injuries among Chinese residents from 1990 to 2019 were extracted. The trends of age-standardized incidence rate (ASIR) and age-standardized death rate (ASDR) of mechanical injuries among Chinese residents by gender was analyzed using the joinpoint regression model, and the annual percent change (APC) and average annual percent change (AAPC) were calculated. The age-period-cohort model was used to quantitatively assess the effects of age, period, and cohort on ASIR and ASDR for mechanical injuries. RESULTS: (1) Overall tendency: from 1990 to 2019, the ASIR of mechanical injuries showed an increasing trend (540.95/100 000 in 1990 vs. 815.34/100 000 in 2019), and the ASDR first increased slightly and then decreased (2.62/100 000 in 1990 vs. 2.87/100 000 in 2005 vs. 1.77/100 000 in 2019) among Chinese residents. During the observation period, ASIR and ASDR for mechanical injuries of male were higher than female. (2) Joinpoint regression model analysis showed that the ASIR of mechanical injuries had a fluctuating trend of increasing first and then decreasing and then rising rapidly among Chinese residents from 1990 to 2019 (AAPC = 1.42%, t = 9.59, P < 0.001). The ASIR of the Chinese male showed a slight decrease and then continued to increase (AAPC = 1.47%, t = 8.72, P < 0.001), while the ASIR of the Chinese female showed a rapid rising at first, then rapidly declining and then rising again (AAPC = 1.31%, t = 12.11, P < 0.001). From 1990 to 2019, the ASDR of mechanical injuries showed a fluctuating downward trend of first decreasing, then increasing, and then rapidly decreasing among Chinese residents (AAPC = -1.39%, t = -6.72, P < 0.001). The decrease rate of ASDR among male was as same as that among all population (AAPC = -1.44%, t = -7.29, P < 0.001), but the decrease rate of ASDR in female was relatively slow (AAPC = -1.08%, t = -4.54, P < 0.001). (3) Age-period-cohort model analysis showed that, with the increase of age, the risk of mechanical injuries among the overall population, male and female in China increased, then decreased, and then increased rapidly. The first small peak was at the age of 45-49 years old in male and 65-69 years old in female. The overall death risk showed an increasing trend with age, with a slowly increasing trend before 75 years old, and a sudden increase after 75 years old. The peak age of death risk was between 90 and 94 years. In terms of period effect, the risk of mechanical injuries showed a gradually increasing trend with time among the overall population, male, and female in China, and the risk of death showed a trend of decreasing first and then rapidly increasing and then decreasing. In terms of cohort effect, the risk of mechanical injuries among the overall population, male, and female in China showed a gradual upward trend with the increase in the birth year, and the risk of death showed an M-shaped trend. CONCLUSIONS: From 1990 to 2019, the incidence of mechanical injuries showed an increasing trend, and the mortality increased first and then decreased. Although the disease burden has improved, it is still high. More attention needs to be paid to the prevention and control of mechanical injuries, especially in the young population.

Fur Protein Regulates the Motility of Avian Pathogenic Escherichia coli AE17 Through Promoter Regions of the Flagella Key Genes flhD.

Avian pathogenic Escherichia coli (APEC) is an important pathogen causing several diseases in birds. It is responsible for local and systemic infections in poultry, seriously impeding the development of the poultry industry, and poses a potential risk to public health. The iron absorption regulatory protein Fur and the noncoding RNA, RyhB, that it negatively regulates are important factors in bacterial iron uptake, but the regulation of bacterial virulence genes varies greatly among different bacteria. We found that Fur is very important for the mobility of APEC. The expression of fur and RyhB is extensively regulated in APEC, and RyhB expression is also negatively regulated by Fur. A transcriptomic analysis showed that the genes significantly differentially regulated by Fur are related to cell movement, including pilus- or flagellum-dependent cell motility. To verify these results, we examined the effects of fur knockdown on cell movement by measuring the diameter of the bacteria colonies. Consistent with the RNA sequencing results, the mobility of AE17Δfur was significantly reduced compared with that of the wild type, and it had almost lost its ability to move. Using an electrophoretic mobility assay, we confirmed that the Fur protein directly binds to the promoter region of the key flagellum-related gene flhD, thereby affecting the assembly and synthesis of the APEC flagellum. This study extends our understanding of gene regulation in APEC.

Inflammatory milieu cultivated Sema3A signaling promotes chondrocyte apoptosis in knee osteoarthritis.

Osteoarthritis (OA) is the leading degenerative joint disease and featured by articular cartilage destruction, where chondrocyte apoptosis plays a critical role. Semaphorin-3A (Sema3A) has been implicated in OA chondrocyte physiology. In this study we aimed to uncover how Sema3A signaling is regulated in chondrocytes and investigate its role in OA chondrocyte survival. Here, we report that Sema3A and its receptor neuropilin-1 (Nrp1) are synchronously upregulated in cartilage chondrocytes of knee OA patients. Their expressions in chondrocytes could be induced by the stimulation of proinflammatory cytokines IL-1ß and TNF-α and subsequent transcriptional activation orchestrated by C/EBPß. The resulting excessive Sema3A signaling promotes chondrocyte apoptosis through impairing PI3K/Akt prosurvival signaling. These findings indicate a regulatory mechanism and a proapoptotic function of aberrant Sema3A signaling in OA chondrocytes, and suggest that targeting Sema3A signaling might interfere OA pathogenesis.

Overexpression of suppressors of cytokine signaling 1 regulate the proliferation and differentiation of rat-derived neural stem cells.

Neural stem cells are a reliable resource in various neural tissue repair and neurodegenerative diseases. Increasing evidence has demonstrated that Suppressor of cytokine signaling proteins (SOCS) was involved in the nervous system development. The universality and diversity of SOCS also suggested their important roles in neurogenesis and nerve regeneration. In this study, we employed a lentiviral vector to investigate the impacts of overexpression SOCS1 on the proliferation and differentiation of rat-derived NSCs. Cells infected with LV-EGFP-SOCS1 showed a prominent increased cell number, diameter, and metabolic activity compared with other groups. Immunofluorescence analysis revealed the proportion of cells positive for microtubule associated protein-2 (MAP2) or myelin basic protein (MBP) was significantly increased in LV-EGFP-SOCS1 group while the proportion of glial fibrillary acidic protein (GFAP)-positive cells in LV-EGFP-SOCS1 group was significantly decreased compare to LV-EGFP and PBS group. Moreover, Western blot results were consistent with immunofluorescence results which indicated that overexpression of SOCS1 could promote neuronal and oligodendrocyte differentiations of NSCs but inhibit astrocyte differentiation of NSCs. In conclusion, our findings provided evidence that SOCS1 could promote the proliferation of NSCs and affect the differentiation of NSCs, providing a potential target for NSCs transplantation strategies.

Glutaredoxin 1 (GRX1) inhibits oxidative stress and apoptosis of chondrocytes by regulating CREB/HO-1 in osteoarthritis.

GRX1 (glutaredoxin1), a sulfhydryl disulfide oxidoreductase, is involved in many cellular processes, including anti-oxidation, anti-apoptosis, and regulation of cell differentiation. However, the role of GRX1 in the oxidative stress and apoptosis of osteoarthritis chondrocytes remains unclear, prompting the current study. Protein and mRNA expressions were measured by Western blot and RT-qPCR. Oxidative stress was detected by the measurement of MDA and SOD contents. Cells apoptosis were detected by Annexin V-FITC/PI and caspase-3 activity assays. We found that the mRNA and protein expressions of GRX1 were significantly down-regulated in osteoarthritis tissues and cells. GRX1 overexpression increased the mRNA and protein expression of CREB and HO-1. Meanwhile, GRX1 overexpression inhibited oxidative stress and apoptosis in osteoarthritis chondrocytes. Furthermore, we found that GRX1 overexpression regulated HO-1 by increasing CREB, and that HO-1 regulated oxidative stress and apoptosis in osteoarthritis chondrocytes. Thus, GRX1 overexpression constrains oxidative stress and apoptosis in osteoarthritis chondrocytes by regulating CREB/HO-1, providing a novel insight into the molecular mechanism and potential treatment of osteoarthritis.

Tetrandrine prevents multidrug resistance in the osteosarcoma cell line, U-2OS, by preventing Pgp overexpression through the inhibition of NF-κB signaling.

The development of multidrug resistance (MDR) remains a major limitation to successful chemotherapy in osteosarcoma. Preventing the introduction of MDR has been a research hotspot in clinical and investigational oncology. The aim of this study was to evaluate the preventive effects of tetrandrine (TET) against MDR in osteosarcoma. For this purpose, U-2OS human osteosarcoma cells were treated with paclitaxel alone or a combination of paclitaxel with TET. The cells treated with paclitaxel alone eventually acquired MDR along with the overexpression of and highly activated P-glycoprotein (Pgp), while the cells treated with the paclitaxel-TET combination were sensitive to chemotherapeutic drugs and expressed decreased levels of Pgp and less Pgp activity. The promoter activities of MDR gene 1 (MDR1) and nuclear factor (NF)­κB, and the expression levels of NF-κB and p-IκB-α were all enhanced in the cells cultured with paclitaxel alone. NF-κB DNA-binding activity and the binding ability of NF-κB to the MDR1 promoter were also enhanced in the cells cultured with paclitaxel alone compared to the control cells. However, the expression and activity of NF-κB were significantly decreased in the paclitaxel-TET combination-treated group as compared with the cells treated with paclitaxel alone. On the whole, our findings suggest that TET prevents paclitaxel-induced MDR by inhibiting Pgp overexpression through a mechanism that may involve the inhibition of NF-κB signaling in osteosarcoma.

Effects of STAT3 inhibitors on neural functional recovery after spinal cord injury in rats.

Spinal cord injuries (SCIs) can induce primary and secondary injury, resulting in severe neurological damage and dysfunction in patients. Studies have reported that signal transducer and activator of transcription 3 (STAT3) plays an important role in the inflammatory immune response and neural stem cell differentiation. In order to examine whether a STAT3 inhibitor can prevent worsening of an SCI and promote neural stem cell differentiation, a rat model of surgically induced SCI was created and rats were treated with the STAT3 inhibitor S31-201. Tissue from the injured region was harvested and fixed in formalin and paraffin. H&E staining was used to look for morphological changes. The Basso, Beattie, and Bresnahan locomotor scale (BBB score), somatosensory evoked potentials (SEP), and motor evoked potentials (MEP) were examined. Western blotting was used to detect the expression of ß-tubulin ш, vimentin, GFAP, NF-200, and OX-42 protein. Results indicated that the STAT3 inhibitor S31-201 reduces the extent of SCI and it promotes neural stem cell differentiation.

miRNA-497 Negatively Regulates the Growth and Motility of Chondrosarcoma Cells by Targeting Cdc25A.

Chondrosarcoma (CHS) is the second most common malignant bone sarcoma with increased risk of invasion and metastasis. However, the regulatory mechanisms of CHS tumorigenesis remain unknown. Here we investigated the novel role of miR-497 in regulating chondrosarcoma cell growth and cell cycle arrest. RT-PCR analysis showed that the expression of miR-497 is aberrantly downregulated in human chondrosarcoma samples and cells. After transfection with miR-497 mimic or antagomir, the proliferation and apoptosis of JJ012 and OUMS-27 chondrosarcoma cells were determined by CCK-8 assay and flow cytometric analysis, respectively. Results showed that the proliferation capacity of JJ012 and OUMS-27 cells was significantly decreased by miR-497 overexpression but increased by miR-497 repression. Apoptosis in both cell types was remarkably enhanced by miR-497 mimic but inhibited by miR-497 antagomir. By bioinformatics and luciferase reporter analysis, Cdc25A was proven to be a direct target of miR-497 in chondrosarcoma cells. Further studies indicated that miR-497 modulates the growth of chondrosarcoma cells by targeting Cdc25A, in which the cell cycle inhibitor p21 is involved through a p53-independent pathway. In conclusion, we demonstrated that miR-497 represents a potential tumor suppressor in human chondrosarcoma that regulates the growth of chondrosarcoma cells by targeting Cdc25A. This may provide a novel therapeutic target for chondrosarcoma.