Background: Inflammation is involved in the pathophysiology of postoperative acute kidney injury (AKI). We investigated whether preoperative platelet-to-white blood cell ratio (PWR), a novel serum biomarker of systemic inflammation, was associated with postoperative AKI following cerebral aneurysm treatment. We also compared the discrimination power of preoperative PWR with those of other preoperative systemic inflammatory indices in predicting postoperative AKI. Methods: Perioperative data including preoperative systemic inflammatory indices and cerebral aneurysm-related variables were retrospectively analyzed in 4,429 cerebral aneurysm patients undergoing surgical clipping or endovascular coiling. Based on the cutoff value of preoperative PWR, patients were divided into the high PWR (≥39.04, n=1,924) and low PWR (<39.04, n=2,505) groups. After propensity score matching (PSM), 1,168 patients in each group were included in the data analysis. AKI was defined according to the Kidney Disease Improving Global Outcomes guidelines. Results: Postoperative AKI occurred more frequently in the low PWR group than in the high PWR group before PSM (45 [1.8%] vs. 7 [0.4%], P<0.001) and after (17 [1.5%] vs. 5 [0.4%], P=0.016). A low preoperative PWR was predictive of postoperative AKI before PSM (odds ratio [95% CI], 3.93 [1.74–8.87]; P<0.001) and after (3.44 [1.26–9.34], P=0.016). Preoperative PWR showed the highest area under the curve for postoperative AKI (0.713 [0.644–0.782], P<0.001), followed by preoperative platelet-to-neutrophil ratio (0.694 [0.619–0.769], P<0.001), neutrophil percentage-to-albumin ratio (0.671 [0.592–0.750], P<0.001), white blood cell-to-hemoglobin ratio (0.665 [0.579–0.750], P<0.001), neutrophil-to-lymphocyte ratio (0.648 [0.569–0.728], P<0.001), and systemic inflammatory index (0.615 [0.532–0.698], P=0.004). Conclusions A low preoperative PWR was associated with postoperative AKI following cerebral aneurysm treatment.

Peripheral neurodegenerative diseases induced by irreversible peripheral nerve degeneration (PND), such as diabetic peripheral neuropathy, have a high prevalence worldwide and reduce the quality of life. However, there is no agent effective against the irreversible PND. After peripheral nerve injury, Schwann cells play an important role in regulating PND. However, because PND involves multiple biochemical events in Schwann cells, a one-drug-single-target therapeutic strategy is not feasible for PND. Here, we suggested that fascaplysin (Fas), a compound with multiple targets (CDK4/6), could overcome these problems. Fas exerted a significant inhibitory effect on axonal degradation, demyelination, and Schwann cell proliferation and dedifferentiation during in vitro and ex vivo PND. To discover the most likely novel target for PND, a chemo-bioinformatics analysis predicted the other on-targets of Fas and identified androgen receptor (AR) which were involved in Schwann cell differentiation and proliferation.AR interacted with Fas, and nuclear import of the AR/Fas complex was inhibited in Schwann cells, altering the expression patterns of transcription factors during PND. Therefore, Fas may have therapeutic potential for irreversible peripheral neurodegenerative diseases.

Peripheral neurodegenerative diseases induced by irreversible peripheral nerve degeneration (PND), such as diabetic peripheral neuropathy, have a high prevalence worldwide and reduce the quality of life. However, there is no agent effective against the irreversible PND. After peripheral nerve injury, Schwann cells play an important role in regulating PND. However, because PND involves multiple biochemical events in Schwann cells, a one-drug-single-target therapeutic strategy is not feasible for PND. Here, we suggested that fascaplysin (Fas), a compound with multiple targets (CDK4/6), could overcome these problems. Fas exerted a significant inhibitory effect on axonal degradation, demyelination, and Schwann cell proliferation and dedifferentiation during in vitro and ex vivo PND. To discover the most likely novel target for PND, a chemo-bioinformatics analysis predicted the other on-targets of Fas and identified androgen receptor (AR) which were involved in Schwann cell differentiation and proliferation.AR interacted with Fas, and nuclear import of the AR/Fas complex was inhibited in Schwann cells, altering the expression patterns of transcription factors during PND. Therefore, Fas may have therapeutic potential for irreversible peripheral neurodegenerative diseases.

Peripheral neurodegenerative diseases induced by irreversible peripheral nerve degeneration (PND), such as diabetic peripheral neuropathy, have a high prevalence worldwide and reduce the quality of life. However, there is no agent effective against the irreversible PND. After peripheral nerve injury, Schwann cells play an important role in regulating PND. However, because PND involves multiple biochemical events in Schwann cells, a one-drug-single-target therapeutic strategy is not feasible for PND. Here, we suggested that fascaplysin (Fas), a compound with multiple targets (CDK4/6), could overcome these problems. Fas exerted a significant inhibitory effect on axonal degradation, demyelination, and Schwann cell proliferation and dedifferentiation during in vitro and ex vivo PND. To discover the most likely novel target for PND, a chemo-bioinformatics analysis predicted the other on-targets of Fas and identified androgen receptor (AR) which were involved in Schwann cell differentiation and proliferation.AR interacted with Fas, and nuclear import of the AR/Fas complex was inhibited in Schwann cells, altering the expression patterns of transcription factors during PND. Therefore, Fas may have therapeutic potential for irreversible peripheral neurodegenerative diseases.

Peripheral neurodegenerative diseases induced by irreversible peripheral nerve degeneration (PND), such as diabetic peripheral neuropathy, have a high prevalence worldwide and reduce the quality of life. However, there is no agent effective against the irreversible PND. After peripheral nerve injury, Schwann cells play an important role in regulating PND. However, because PND involves multiple biochemical events in Schwann cells, a one-drug-single-target therapeutic strategy is not feasible for PND. Here, we suggested that fascaplysin (Fas), a compound with multiple targets (CDK4/6), could overcome these problems. Fas exerted a significant inhibitory effect on axonal degradation, demyelination, and Schwann cell proliferation and dedifferentiation during in vitro and ex vivo PND. To discover the most likely novel target for PND, a chemo-bioinformatics analysis predicted the other on-targets of Fas and identified androgen receptor (AR) which were involved in Schwann cell differentiation and proliferation.AR interacted with Fas, and nuclear import of the AR/Fas complex was inhibited in Schwann cells, altering the expression patterns of transcription factors during PND. Therefore, Fas may have therapeutic potential for irreversible peripheral neurodegenerative diseases.

In addition to cellular damage, ischemia-reperfusion (IR) injury induces substantial damage to the mitochondria and endoplasmic reticulum. In this study, we sought to determine whether impaired mitochondrial function owing to IR could be restored by transplanting mitochondria into the heart under ex vivo IR states. Additionally, we aimed to provide preliminary results to inform therapeutic options for ischemic heart disease (IHD). Healthy mitochondria isolated from autologous gluteus maximus muscle were transplanted into the hearts of Sprague–Dawley rats damaged by IR using the Langendorff system, and the heart rate and oxygen consumption capacity of the mitochondria were measured to confirm whether heart function was restored. In addition, relative expression levels were measured to identify the genes related to IR injury. Mitochondrial oxygen consumption capacity was found to be lower in the IR group than in the group that underwent mitochondrial transplantation after IR injury (p < 0.05), and the control group showed a tendency toward increased oxygen consumption capacity compared with the IR group. Among the genes related to fatty acid metabolism, Cpt1b (p < 0.05) and Fads1 (p < 0.01) showed significant expression in the following order: IR group, IR + transplantation group, and control group. These results suggest that mitochondrial transplantation protects the heart from IR damage and may be feasible as a therapeutic option for IHD.

Nanoscale biomaterials have garnered immense interest in the scientific community in the recent decade. This review specifically focuses on the application of three nanomaterials, i.e., graphene and its derivatives (graphene oxide, reduced graphene oxide), carbon nanotubes (CNTs) and nanocellulose (cellulose nanocrystals or CNCs and cellulose nanofibers or CNFs), in regenerating different types of tissues, including skin, cartilage, nerve, muscle and bone. Their excellent inherent (and tunable) physical, chemical, mechanical, electrical, thermal and optical properties make them suitable for a wide range of biomedical applications, including but not limited to diagnostics, therapeutics, biosensing, bioimaging, drug and gene delivery, tissue engineering and regenerative medicine. A state-of-the-art literature review of composite tissue scaffolds fabricated using these nanomaterials is provided, including the unique physicochemical properties and mechanisms that induce cell adhesion, growth, and differentiation into specific tissues. In addition, in vitro and in vivo cytotoxic effects and biodegradation behavior of these nanomaterials are presented. We also discuss challenges and gaps that still exist and need to be addressed in future research before clinical translation of these promising nanomaterials can be realized in a safe, efficacious, and economical manner.

Background: Pericardial fat (PF) is highly associated with cardiovascular disease but the effectiveness of surgical resection of PF is still unknown for myocardial mitochondrial structure and function in acute myocardial infarction (AMI) with obesity. The aim of this study was to demonstrate the difference in myocardial mitochondrial structure and function between obese AMI with additionally resected PF and those without resected PF. Methods: Obese rats with 12-week high fat diet (45 kcal% fat, n = 21) were randomly assigned into 3 groups: obese control, obese AMI and obese AMI with additionally resected PF. One week after developing AMI and additional resection of PF, echocardiogram, myocardial mitochondrial histomorphology, oxidative phosphorylation system (OXPHOS), anti-oxidative enzyme and sarcoplasmic reticulum Ca 2+ ATPase 2 (SERCA2) in the non-infarcted area were assessed between these groups. Results: There was significant improvement of systolic function in AMI with PF resection compared with the AMI group in the echocardiogram. Even though the electron microscopic morphology for the mitochondria seems to be similar between the AMI with PF resection and AMI groups, there was an improved expression of PGC-1α and responsive OXPHOS including NDUFB3, NDUFB5 and SDHB are associated with the ATP levels in the AMI with PF resection compared with those in the AMI group. In addition, the expression levels of antioxidant enzymes (MnSOD) and SERCA2 were improved in the AMI with PF resection compared with those in the AMI group. Conclusion Surgical resection of PF might ameliorate myocardial mitochondria dysfunction in obese AMI.

Background and Objectives: Identifying patients with high bleeding risk (HBR) is important when making decisions for antiplatelet therapy strategy. This study evaluated the impact of ticagrelor monotherapy after 3-month dual antiplatelet therapy (DAPT) according to HBR in acute coronary syndrome (ACS) patients treated with drug eluting stents (DESs). Methods: In this post-hoc analysis of the TICO trial, HBR was defined by 2 approaches: meeting Academic Research Consortium for HBR (ARC-HBR) criteria or Predicting Bleeding Complications in Patients Undergoing Stent Implantation and Subsequent DAPT (PRECISEDAPT) score ≥25. The primary outcome was a 3–12 months net adverse clinical event (composite of major bleeding and adverse cardiac and cerebrovascular events). Results: Of the 2,980 patients without adverse events during the first 3 months after DES implantation, 453 (15.2%) were HBR by ARC-HBR criteria and 504 (16.9%) were HBR by PRECISE-DAPT score. The primary outcome rate was higher in HBR versus non-HBR patients (by ARC-HBR criteria: hazard ratio [HR], 2.87; 95% confidence interval [CI], 1.76– 4.69; p<0.001; by PRECISE-DAPT score: HR, 3.09; 95% CI, 1.92–4.98; p<0.001). Ticagrelor monotherapy after 3-month DAPT was associated with lower primary outcome rate than ticagrelor-based 12-month DAPT regardless of HBR by ARC-HBR criteria, with similar magnitudes of therapy effect for HBR and non-HBR patients (p-interaction=0.400). Results were consistent by PRECISE-DAPT score (p-interaction=0.178). Conclusions In ACS patients treated with DESs, ticagrelor monotherapy after 3-month DAPT was associated with lower rate of adverse clinical outcomes regardless of HBR, with similar magnitudes of therapy effect between HBR and non-HBR.Trial Registration: ClinicalTrials.gov Identifier: NCT02494895