Effect of preoperative sleep disorders on delirium in proximal femoral surgery patients aged 60 or older.

OBJECTIVE: To examine the effect of preoperative sleep disorders on delirium in patients older than 60 years of age who underwent surgery for proximal femoral fracture. METHODS: This is a prospective observational study. We prospectively selected 143 patients with proximal femoral fracture who underwent surgery between April 2021 and April 2022. The primary outcome was postoperative delirium (PD). Multiple logistic regression analyses were performed and a receiver operating characteristic (ROC) curve was generated. The preoperative sleep quality of all eligible participants was assessed through the Pittsburgh Sleep Quality Index (PSQI). The Confusion Assessment Method (CAM) was used to assess PD from the first to the seventh day postoperatively. Patients were divided into two groups according to the PD diagnosis: (1) the no PD (NPD) group and (2) the PD (PD) group. RESULTS: Of 143 eligible patients, 43 (30.1%) were diagnosed with PD. Multiple logistic regression analysis demonstrated that postoperative ICU admissions (OR = 2.801, p = 0.049) and preoperative sleep disorders (OR = 1.477 p < 0.001) were independently associated with PD. A receiver operating characteristic (ROC) curve demonstrated that the preoperative PSQI score was predictive of PD (AUC 0.808, 95% CI 0.724 ~ 0.892, p < 0.001). CONCLUSION: Preoperative sleeping disorders may be an independent risk factor leading to PD and an independent predictive factor for the development of delirium in proximal femoral surgery patients aged 60 or older.

Modifiable risk factors of acute kidney injury after liver transplantation: a systematic review and meta-analysis.

BACKGROUND: Acute kidney injury (AKI) is a common and critical complication of liver transplantation (LT), which is associated with increased morbidity, mortality and health care cost. We aimed to identify modifiable risk factors of AKI after LT. METHODS: A literature search of Pubmed, EMBASE and Cochrane Databases was performed to identify studies investigating risk factors of AKI after LT. The Newcastle-Ottawa Scale was used to rate study quality. Effect size and 95% confidence interval were pooled using a random-effect model with inverse-variance method. RESULTS: Sixty-seven articles with 28,844 patients were included in the meta-analysis. Seventeen modifiable risk factors were found, including overweight, preoperative use of diuretic, preoperative anemia, donation after cardiac death organ, donor BMI ≥ 30 kg/m2, ABO-incompatible LT, low graft to recipient body weight ratio, intraoperative hypotension, major bleeding, intraoperative use of vasopressor, large RBC transfusion, postreperfusion syndrome, postoperative use of vasopressors, overexposure to calcineurin inhibitor, calcineurin inhibitor without mycophenolate mofetil, graft dysfunction and infection. A total of 38 articles were included in the systematic review, in which 8 modifiable risk factors and 1 protective factor were additionally associated in single studies with the incidence of AKI after LT. CONCLUSIONS: Effective interventions based on identified modifiable risk factors in the perioperative management and graft allocation and preservation may be promising to reduce the incidence of AKI after LT. TRIAL REGISTRATION: The protocol for this systematic review is registered with PROSPERO (No. CRD42020166918 ).

Association of overweight with postoperative acute kidney injury among patients receiving orthotopic liver transplantation: an observational cohort study.

BACKGROUND: Acute kidney injury (AKI) is a common postoperative complication of orthotopic liver transplantation (OLT). So far, little attention has been paid on the association between overweight and AKI after OLT, and animal models or clinical studies have drawn conflicting conclusions. The objective of our study was to determine whether overweight (BMI [Body Mass Index] ≥ 25 kg/m2) is associated with an increased risk of AKI after OLT. METHODS: This retrospective cohort study included 244 patients receiving OLT in the Affiliated Hospital of Qingdao University between January 1, 2017, and August 29, 2019. Preoperative, intraoperative, and postoperative data were collected retrospectively. The primary outcome was the development of AKI as defined by Kidney Disease, Improving Global Outcome (KIDGO) staging system. Logistic regression analysis was used to determine the relationship between overweight and the occurrence of postoperative AKI. Data analysis was conducted from September to October 2019, revision in April 2020. RESULTS: Among 244 patients receiving OLT (mean [standard deviation] age, 54.1 [9.6] years; 84.0% male) identified, 163 patients (66.8%) developed postoperative AKI. Overweight (BMI ≥ 25 kg/m2) was associated with a higher rate of postoperative severe AKI (stage 2/3) compared with normal weight (18.5 ≤ BMI < 25 kg/m2) (41 [47.7%] vs 39 [28.7%]; adjusted odds ratio [OR], 2.539; 95% confidence interval [CI], 1.389-4.642; P = 0.002). Furthermore, patients with obese were at even higher risk of postoperative severe AKI after controlling for confounding factors (adjusted OR: 3.705; 95% CI: 1.108-12.388; P = 0.033). CONCLUSIONS: Overweight is independently associated with an increased risk of postoperative severe AKI among patients receiving OLT. The association of BMI with severe AKI after OLT is J-shaped.

Effects of ultrasound-guided paravertebral block on MMP-9 and postoperative pain in patients undergoing VATS lobectomy: a randomized, controlled clinical trial.

BACKGROUND: Local anesthesia can reduce the response to surgical stress and decrease the consumption of opioids, which may reduce immunosuppression and potentially delay postoperative tumor recurrence. We compared paravertebral block (PVB) combined with general anesthesia (GA) and general anesthesia regarding their effects on postoperative pain and matrix metalloproteinase-9 (MMP-9) after video-assisted thoracoscopic surgery (VATS) lobectomy. METHODS: 54 patients undergoing elective VATS lobectomy at a single tertiary care, teaching hospital located in Qingdao between May 2, 2018 and Sep 28, 2018 were randomised by computer to either paravertebral block combined with general anesthesia or general anesthesia. The primary outcomes were pain scores at rest and on cough at 1, 4, 24, and 48 h after surgery. The secondary outcome were plasma concentrations of MMP-9, complications, and length of postoperative hospital stay. RESULTS: 75 were enrolled to the study, of whom 21 were excluded before surgery. We analyzed lobectomy patients undergoing paravertebral block combined with general anesthesia (n = 25) or general anesthesia (n = 24). Both groups were similar regarding baseline characteristics. Pain scores at rest at 4 h and 24 h, on cough at 4 h were lower in PVB/GA group, compared with GA group (P < 0.05). There were no difference in pain scores at rest at 1 h, 48 h and on cough at 1 h, 24 h, and 48 h between groups. Patients in the PVB/GA group showed a greater decrease in plasma MMP-9 level at T1 and T2 after VATS lobectomy (P < 0.05). Postoperative complications and length of stay did not differ by anesthetic technique. CONCLUSIONS: The paravertebral block/general anesthesia can provide statistically better pain relief and attenuate MMP-9 response to surgery and after VATS lobectomy. This technique may be beneficial for patients to recover rapidly after lung surgery and reduce postoperative tumor recurrence. TRIAL REGISTRATION: Chinese Clinical Trial registration number ChiCTR1800016379. Registered 28 May 2018.

Ulk1/FUNDC1 Prevents Nerve Cells from Hypoxia-Induced Apoptosis by Promoting Cell Autophagy.

Cell autophagy and cell apoptosis are both observed in the process of hypoxia-induced ischemic cerebral infarction (ICI). Unc-51 like autophagy activating kinase 1 (Ulk1) and FUN14 Domain-containing Protein 1 (FUNDC1) are both involved in the regulation of cell autophagy. This study aimed to investigate the regulatory effects of Ulk1 and FUNDC1 on hypoxia-induced nerve cell autophagy and apoptosis. Cell viability was measured using cell counting kit-8 (CCK-8) assay. Cell apoptosis was detected using Annexin V-PE/7-ADD staining assay. qRT-PCR was used to quantify the mRNA levels of Ulk1 and FUNDC1 in PC-12 cells. Cell transfection was performed to up-regulate the expression of Ulk1. 3-Methyladenine (3-MA) was used as autophagy inhibitor and rapamycin was used as autophagy activator in our experiments. SP600125 was used as c-Jun N-terminal kinase (JNK) inhibitor. Western blotting was performed to analyze the expression levels of key factors that are related to cell autophagy, apoptosis and JNK pathway. We found that hypoxia simultaneously induced apoptosis and autophagy of PC-12 cells. The activation of Ulk1 and FUNDC1 were also found in PC-12 cells after hypoxia induction. Overexpression of Ulk1 promoted the activation of FUNDC1 and prevented PC-12 cells from hypoxia-induced apoptosis. Suppression of Ulk1 had opposite effects. Furthermore, we also found that JNK pathway participated in the effects of Ulk1 overexpression on PC-12 cell apoptosis reduction. To conclude, Ulk1/FUNDC1 played critical regulatory roles in hypoxia-induced nerve cell autophagy and apoptosis. Overexpression of Ulk1 prevented nerve cells from hypoxia-induced apoptosis by promoting cell autophagy.

Morphine Postconditioning Protects Against Reperfusion Injury: the Role of Protein Kinase C-Epsilon, Extracellular Signal-Regulated Kinase 1/2 and Mitochondrial Permeability Transition Pores.

BACKGROUND/AIMS: The purpose of this study was to investigate the implications of protein kinase C-epsilon (PKCε), Extracellular Signal-regulated Kinase 1/2 (ERK1/2) and mitochondrial permeability transition pore (mPTP) in myocardial protection induced by morphine postconditioning (MpostC). METHODS: The isolated rat hearts were randomly assigned into one of eight groups. Hearts in time control (TC) group were constantly perfused for 105min. Hearts in ischemia-reperfusion (I/R) group were subjected to 45 min of ischemia followed by 1 h of reperfusion. MpostC was induced by 10 min of morphine administration at the onset of reperfusion. εV1-2 (an inhibitor of PKCε) and PD (an inhibitor of ERK1/2) was administered with or without morphine during the first 10 min of reperfusion following the 45 min of ischemia. I/R injury was assessed by functional parameters, creatine kinase-MB (CK-MB) release and infarct size (IS/AAR). Additional hearts were excised at 20 min following reperfusion to detect the membrane-specific translocation of PKCε, ERK1/2 phosphorylation, mitochondrial permeability transition (MPT) and cytochrome C (Cyt-c) release. RESULTS: MpostC markedly reduced infarct size (IS/AAR), CK-MB release, and improved cardiac function recovery. However, these protective effects were partly abolished in the presence of εV1-2 or PD. Compared to TC group, the membrane translocation of PKCε, ERK1/2 phosphorylation, mPTP opening, and Cyt-c release were significantly increased in I/R hearts. MpostC further increased the membrane translocation of PKCε and ERK1/2 phosphorylation, and significantly inhibited mPTP opening and Cyt-c release. However, those protective effects induced by MpostC were abolished by εV1-2 or PD, which, used alone, showed no influence on reperfusion injury. CONCLUSIONS: These findings suggest that MpostC protects isolated rat hearts against ischemia-reperfusion injury via activating PKCε-ERK1/2 pathway and inhibiting mPTP opening.

Morphine enhances IL-1ß release through toll-like receptor 4-mediated endocytic pathway in microglia.

Morphine creates a neuroinflammatory response and enhances release of the proinflammatory cytokines like interleukin-1ß (IL-1ß), which compromises morphine analgesia as well as induces morphine tolerance. In this study, we attempted to investigate the mechanisms of morphine induced IL-1ß synthesis and release. Microglial cells were treated with morphine (100 µM) once daily for 3 days. Control groups underwent the same procedure but received sterile saline injection instead of morphine. Toll-like receptor 4 (TLR4) and P2X4 receptor (P2X4R) signaling were analyzed using Western blot; immunofluorescence was used to detect the signaling of CD68; real-time RT-PCR and ELISA kit was used to measure the messenger RNA and protein synthesis and release level of IL-1ß. Morphine enhanced IL-1ß synthesis and P2X4R protein expression. TLR4 were responsible for morphine-induced IL-1ß synthesis, while morphine-induced IL-1ß release was via P2X4R. Morphine-induced IL-1ß release is mediated by endocytosis of TLR4. These results indicated that TLR4 and P2X4R pathways mediated IL-1ß synthesis and release in microglia followed chronic morphine. TLR4 internalization is the main mechanism of morphine-induced microglia activation and IL-1ß release.

The µ-opioid receptor-mediated Gi/o protein and ß-arrestin2 signaling pathways both contribute to morphine-induced side effects.

The µ-opioid receptor-biased agonist theory holds that Gio protein signaling mediates the analgesic effect of opioids and the related side effects via the ß-arrestin2 signaling pathway. A series of µ-opioid-biased agonists have been developed in accordance with this theory, and the FDA has approved TRV130 (as a representative of biased agonists) for marketing. However, several reports have raised the issue of opioid side effects associated with the use of agonists. In this study, five permeable peptides were designed to emulate 11 S/T phosphorylation sites at the µ-opioid receptor (MOR) carboxyl-terminal. In vitro experiments were performed to detect the activation level of G proteins from the cAMP inhibition assay and the ß-arrestin2 recruitment by the BRET assay. Designed peptides might effectively interfere with the activation of the Gio and ß-arrestin2 pathways when combined with morphine. The resulting morphine-induced tolerance, respiratory inhibition, and constipation in mice showed that the ß-arrestin2 pathway was responsible for morphine tolerance while the Gio signaling pathway was involved with respiratory depression and constipation and that these side effects were significantly related to phosphorylation sites S363 and T370. This study may provide new directions for the development of safer and more effective opioid analgesics, and the designed peptides may be an effective tool for exploring the mechanism by which µ-opioid receptors function, with the potential of reducing the side effects that are associated with clinical opioid treatment.

Effect of Serum Bilirubin Levels on Contrast-induced Acute Kidney Injury: A Systematic Evaluation and Meta-analysis.

Contrast-induced acute kidney injury (CI-AKI) is an important complication following the use of iodinated contrast media. Bilirubin has a protective effect but may also aggravate CI-AKI. The purpose of this systematic review was to assess whether bilirubin is a risk factor for CI-AKI. We searched the databases PubMed, Embase, Web of Science, Cochrane Library, Scopus, Ovid Medline, CNKI (China National Knowledge Infrastructure), VPCS (Vip Paper Check System), Wanfang, and CBM (Chinese BioMedical Literature Database) from the initial date to May 6, 2023. We summarized the results by directly combining the effect-size odds ratio (OR) and 95% confidence interval (CI) and identified sources of heterogeneity through subgroup analysis, sensitivity analysis, and meta-regression analysis. A total of 10 studies (14 data sets) were included: 7 retrospective studies (10 data sets) and 3 prospective studies (4 data sets), involving 12776 participants. The incidence of CI-AKI of 16% (95% CI: 14-19%). Total bilirubin was positively associated with the occurrence of CI-AKI (OR = 1.80; 95% CI: 1.36-2.38). Both low and high bilirubin concentrations were risk factors for CI-AKI. The incidence of CI-AKI was higher in the low bilirubin group than in the high bilirubin group.

Melanocortin 4 receptor mediates neuropathic pain through p38MAPK in spinal cord.

BACKGROUND: Neuropathic pain is characterised by spontaneous ongoing or shooting pain and evoked amplified pain responses after noxious or non-noxious stimuli. Neuropathic pain develops as a result of lesions or disease affecting the somatosensory nervous system either in the periphery or centrally. Melanocortin 4 receptor (MC4R) plays an important role in the initiation of neuropathic pain but the underlying mechanisms are still unclear. METHODS: Adult male Wistar rats were given chronic constriction injury (CCI) or sham operations. Part of CCI rats were intrathecally treated with HS014 (MC4R antagonist) or SB203580 (p38MAPK inhibitor). On the third, seventh and fourteenth day, the thermal threshold of operated paws was tested. In addition, the MC4R or phosphorylated p38MAPK (p-p38MAPK) levels of lumbar spinal cord were tested with ELISA (enzyme-linked immunosorbent assay), western blot and immunohistochemistry. RESULTS: Here we demonstrate that (1) both HS014 and SB203580 reduced CCI reduced hyperalgesia (2) p-p38MAPK was increased after CCI with a time course parallel to that of the MC4R change, (3) The p38 activation was prevented by blocking MC4R with an antagonist HS014, but MC4R-IR was not prevented by SB203580. (4) MC4R and p-p38MAPK were located in the same cells. CONCLUSION: The mechanisms of neuropathic pain mediated by MC4R is related to the inhibition of p38MAPK activation. P38MAPK may be a downstream of MC4R.

Melanocortin 4 receptor induces hyperalgesia and allodynia after chronic constriction injury by activation of p38 MAPK in DRG.

Melanocortin 4 receptor (MC4R) is implicated in the initiation and maintenance of neuropathic pain. Although the effect of MC4R on neuropathic pain is known, it remains unclear how MC4R mediates neuropathic pain. In vitro MC4R activates mitogen-activated kinase (MAPK). Accordingly, we investigate whether MC4R activates the p38MAPK cascade in vivo to trigger pain behavior of Wistar rats after chronic constriction injury (CCI). Intrathecal injection of MC4R antagonist HS014 (5 µg/day) at the moment of CCI for seven days attenuated thermal hyperalgesia and mechanical allodynia. Similarly, intrathecal injection of a p38 inhibitor (SB203580, 10 mg/day) at the moment of CCI for seven days was also effective. To assess whether the effects of HS014 were mediated via increased p38MAPK activation, ipsilateral L4 and L5 dorsal root ganglion (DRG) were analyzed for MC4R and phosphorylated p38MAPK (p-p38MAPK) after CCI alone or CCI combined with HS014 treatment or SB203580 treatment. After CCI, DRG p-p38MAPK and MC4R were elevated by three, seven, and 14 days. Treatment with SB203580 blocked p38 activation. Both MC4R and phosphorylated p38 localized in DRG neurons. These data suggest a sequential role for MC4R and p38 in the induction and maintenance of neuropathic pain. MC4R plays an important role in the establishment of neuropathic pain following CCI, seemingly dependent on p38 activation.

A prospective randomized study of intraoperative thoracic epidural analgesia in off-pump coronary artery bypass surgery.

OBJECTIVE: The purpose of this study was to test the hypothesis that general anesthesia (GA) plus thoracic epidural anesthesia (TEA) has no impact on the outcomes of off-pump coronary artery bypass surgery (OPCABs) compared to GA followed by patient-controlled TEA (PCTEA), while GA plus TEA leads to a higher requirement for vasoactive drug use. METHODS: Sixty-four patients, American Society of Anesthesiologists physical status II and III, who were scheduled for elective OPCABs, were offered an epidural catheter inserted at the T2-3 interspace and then randomized into 1 of 2 groups according to whether TEA was applied intraoperatively. The TEA(perio) group received GA plus TEA, while the TEA(post) group received GA alone. All groups had postoperative PCTEA. The number of requirements for vasoactive drugs and the extubation times were recorded. The analgesic effect was monitored by visual analog scale (VAS) pain scores. Heart rate, blood pressure, and blood gases were also monitored. The data are presented as mean values ± standard deviation, or medians with quartiles. RESULTS: The proportion of vasoactive drug use was significantly higher in the TEA(perio) group intraoperatively (before or during completion of anastomoses: 59.4 vs. 20.7%, p = 0.004; after completion of anastomoses: 53.1 vs. 17.2%, p = 0.007). There was no statistically significant difference in extubation times or VAS scores between the 2 groups. CONCLUSIONS: We conclude that GA plus TEA has no impact on the outcomes of OPCABs, while its use leads to a higher requirement for vasoactive drug use. GA followed by PCTEA facilitates the anesthesia administration, while it does not affect the extubation time and the postoperative analgesic effect.

Anesthetic management of hip fracture in geriatric patient with respiratory and heart failure using pericapsular nerve group block: A case report.

INTRODUCTION: Hip fracture with severe cardiopulmonary and cerebral dysfunction is a relatively common problem in the elderly population and poses a great challenge to anesthetic management. Pericapsular nerve group (PENG) block combined with nerve blocks of the hip region has recently attracted significant interest from anesthesiologists, and very few reports on its anesthetic management exist. PATIENT CONCERNS: Patient suffered from the right femoral neck fracture, combined with respiratory failure, heart failure, moderate-to-severe pulmonary hypertension, cerebral infarction, atrial fibrillation, and cognitive dysfunction. DIAGNOSIS: Because of right femoral neck fracture, artificial femoral head replacement was scheduled for this patient. INTERVENTIONS: Ultrasound-guided PENG block combined with sacral plexus, thoracic 11 to 12 paravertebral block, and lateral femoral cutaneous block were performed to a high-risk elderly patient. OUTCOMES: The patient successfully received artificial femoral head replacement with our effective anesthesia techniques and no postoperative complication was reported. CONCLUSIONS: Among elderly patients with multiple organ dysfunction undergoing hip surgery, PENG block combined with nerve blocks of the hip region is an ideal anesthesia method. This case demonstrated that these regional analgesia techniques had a stable hemodynamic process, satisfactory anesthetic effect, effective postoperative analgesia, and no effect on postoperative cognitive function. Further studies are needed to determine the appropriate doses of local anesthetics in the elderly with multiple organ system failure to reduce delayed local anesthesia systemic toxicity.

Sevoflurane diminishes neurogenesis and promotes ferroptosis in embryonic prefrontal cortex via inhibiting nuclear factor-erythroid 2-related factor 2 expression.

OBJECTIVE: Prenatal sevoflurane exposure may pose neurotoxicity to embryonic brain development and lead to cognitive dysfunction in offspring, but the underlying mechanism is still unclear. We aimed to investigate whether sevoflurane could cause neurogenesis abnormality and ferroptosis in embryonic prefrontal cortex (PFC) and to identify the role of nuclear factor-erythroid 2-related factor 2 (Nrf2) in the sevoflurane-related neurotoxicity. METHODS: We used the rodents and primary neural stem cells to examine whether sevoflurane impacted proliferation, differentiation, ferroptosis and apoptosis in the neural stem cells of embryonic PFC. In addition, the expression of Nrf2 and the intensity of reactive oxygen species (ROS) were also assessed to explore the underlying molecular mechanism. RESULTS: Our results showed that sevoflurane exposure in third trimester could lead to neurogenesis inhibition and ferroptosis in-vivo embryonic PFC, with little influence on apoptosis. Moreover, a significant decrease in the expression of Nrf2 as well as an increase in ROS accumulation were also found in neural stem cells after sevoflurane anesthesia. CONCLUSION: We conclude that Nrf2-related neurogenesis inhibition and ferroptosis are a central mechanism contributing to sevoflurane-induced neurotoxicity in embryonic brain. The results of the present study are the first to demonstrate that ferroptosis and the expression of Nrf2 are involved in sevoflurane-related neurotoxicity in embryonic brain, which provides new vision for consideration in anesthesia-associated neurological abnormalities.

Which BMI for Diabetes Patients is Better? From the View of the Adipose Tissue Macrophage-Derived Exosome.

PURPOSE: Diabetes, as a group of metabolic diseases, can elevate blood glucose, thus leading to the development of life-threatening complications. It is difficult to define the outcome for diabetics with different BMI. This review will illustrate the adipose tissue macrophage-derived exosome in the diabetics with different BMI. PATIENTS AND METHODS: Insulin resistance in peripheral tissues can cause diabetes. The peripheral tissues include liver, muscle, or the adipose depots. Communication between these organs is fatal to the maintenance of glucose homeostasis. This review will illustrate this communication. Obesity is closely linked with diabetes. There are different changes in fat distribution in diabetic patients. Adipose tissue macrophages can secrete various hormones, including adiponectin, leptin, resistin and other classical cytokines, such as TNF-α and IL-6. Studies illustrated that exosomes from the adipose tissue, can modulate inter-organ cross-talk by regulating gene expression in other tissues. RESULTS: Adipose tissue macrophages exosomes links thin and fat individuals in the development of diabetes. CONCLUSION: The molecular pathways initiated by exosomes such as miRNA in the situations of metabolic stress could help us gain a deeper knowledge of the pathophysiology of diabetes.

[Hyperbilirubinemia induced oxidative stress resulting in glomerular injury in rats].

OBJECTIVE: To observe the effect of hyperbilirubinemia on glomerulus of rats, and to explore its dose-response and mechanism. METHODS: Twenty-four adult male Sprague-Dawley (SD) rats were divided into four groups according to the random number table method, with 6 rats in each group. Hyperbilirubinemia rat model was reproduced by intraperitoneal injection of bilirubin once every 12 hours for 4 times, at doses of 50, 100, and 200 mg/kg in low, medium, and high dose bilirubin group (LB group, MB group, HB group), respectively. The rats in negative control group (NC group) were given the same solvent without bilirubin powder. Urine was collected 24 hours after administration, and total protein (TP) level was detected. Then the rats were sacrificed, the blood was collected by cardiac puncture, and the total bilirubin (TBil) and direct bilirubin (DBil) levels were measured by automatic biochemical analyzer. The renal tissue was collected and stained with periodic acid-Schiff (PAS) staine, the glomerular morphology was observed under light microscope, and the glomerular injury score was performed. Podocyte morphology was observed by transmission electron microscopy after uranium acetate and lead citrate double staining. The activity of superoxide dismutase (SOD) and content of malondialdehyde (MDA) were determined by colorimetric method. The expression level of podocyte specific marker Wilms tumor protein-1 (WT-1) was determined by Western blotting. RESULTS: With the increase of bilirubin dose, the contents of 24-hour urine TP, blood TBil, blood DBil and MDA content in kidney tissue were gradually increased, and the SOD activity and WT-1 expression in kidney tissue were gradually decreased. The differences between LB group, MB group, HB group and NC group were statistically significant [24-hour urine TP (mg): 24.85±2.22, 52.57±3.66, 56.84±3.49 vs. 7.50±1.33; blood TBil (µmol/L): 37.75±2.19, 81.37±2.13, 125.13±9.96 vs. 5.53±0.41; blood DBil (µmol/L): 15.50±1.96, 37.88±1.05, 64.53±2.89 vs. 2.38±0.35; kidney MDA (µmol/g): 3.14±0.65, 5.01±0.28, 7.50±1.08 vs. 2.30±0.20; kidney SOD (kU/g): 95.91±10.43, 57.06±15.90, 37.12±11.72 vs. 113.91±12.16; kidney WT-1 protein (WT-1/GAPDH): 0.280±0.006, 0.239±0.006, 0.198±0.001 vs. 0.361±0.005; all P < 0.05]. It was shown under light microscope that uneven thickness of mesangial membrane and basement membrane of the glomerulus, and some of them were accompanied by hyperplasia and widening. The glomerular injury score increased with the increase in bilirubin dose. The differences between LB group, MB group, HB group and NC group were statistically significant (17.50±1.05, 25.00±1.41, 34.00±1.41 vs. 11.67±0.82, all P < 0.05). Transmission electron microscopy showed that with the increase of bilirubin dose, the damage of glomerular podocytes was aggravated. CONCLUSIONS: Hyperbilirubinemia induced damage to glomerulus in a dose-dependent manner. In the lethal dose range, the higher the dose, the stronger the damage, which might be related to the oxidative stress promoted by bilirubin and the damage of glomerular podocytes.

Hyperglycemia may increase deep vein thrombosis in trauma patients with lower limb fracture.

Diabetes mellitus is associated with prothrombotic states and thrombotic events. This study examined the association between preoperative glucose levels and deep vein thrombosis (DVT) in trauma patients undergoing surgery for lower limb fracture. Data from 1,591 patients who underwent fracture surgery between January 2017 and March 2022 at the Affiliated Hospital of Qingdao University were queried from institutional electronic medical records. A total study population of 1,086 patients was identified, comprising 138 patients who experienced DVT and 948 controls. The primary outcome was DVT. Multiple logistic regression analyses were performed and a receiver operating characteristic (ROC) curve was generated. Age, D-dimer level, preoperative RBC count, and preoperative glucose level were independent predictors of DVT. The two highest categories of D-dimer level (≥ 960, < 2,102; ≥ 2,102 ng/ml) increased the odds ratio for DVT by 4.215 times [95% confidence interval (CI) 1.820-9.761] and 7.896 times (95% CI 3.449-18.074), respectively, compared with the lowest reference category (< 490 ng/ml). The area under the curve (AUC) for the preoperative glucose level was 0.605. Hyperglycemia (glucose ≥ 6.1, < 7.0 mmol/l) increased the odds of DVT by 1.889-fold [95% CI (1.085-3.291); p < 0.0001] compared with euglycemia (glucose < 6.1 mmol/l). We therefore observed an association between preoperative hyperglycemia and DVT in patients with lower limb fractures. There are several modalities for controlling hyperglycemia, offering potential targets for future improvement.

The impact of IPACK combined with adductor canal block under ultrasound guidance on early motor function after total knee arthroplasty.

BACKGROUND: This study aimed to evaluate the impact of Infiltration between the Popliteal Artery and Capsule of the posterior Knee (IPACK) combined with an adductor canal block under the guidance of ultrasound on early motor function after Total Knee Arthroplasty (TKA). METHODS: A sample of 60 cases who were scheduled for elective unilateral TKA were divided into two groups using random number table method: a group with IPACK combined with an adductor canal block (I group, n = 30), and a group with femoral nerve block combined with superior popliteal sciatic nerve block (FS group, n = 30). Before anesthesia induction was completed, the patients in I group received an ultrasound-guided adductor canal block with 15 mL of 0.375% ropivacaine and an IPACK block with 25 mL of ropivacaine, and the patients in FS group received a femoral nerve block and a superior popliteal sciatic nerve block with 20 mL of 0.375% ropivacaine under ultrasound guidance. Post-operation, all the patients received patient-controlled intravenous analgesia combined with an oral celecoxib capsule to relieve pain and maintain a visual analogue scale score of ≤ 3. RESULTS: The quadriceps femoris muscle strength score was significantly higher in Ⅰ group than in FS group (p = 0.001), while the modified Bromage score were significantly lower and walking distance results were significantly higher in Ⅰ group than in FS group (both p = 0.000). CONCLUSION: Compared with femoral nerve block combined with superior popliteal sciatic nerve block, IPACK combined with adductor canal block had a mild impact on early motor functions after TKA.