Global trends in research of mitophagy in liver diseases over past two decades: A bibliometric analysis.

Increasing evidence indicated that mitophagy might play a crucial role in the occurrence and progression of liver diseases. In order to enhance our understanding of the intricate relationship between mitophagy and liver diseases, a comprehensive bibliometric analysis of the existing literature in this field was conducted. This analysis aimed to identify key trends, potential areas of future research, and forecast the development of this specific field. We systematically searched the Web of Science Core Collection (WoSCC) for publications related to mitophagy in liver diseases from 2000 to 2022. We conducted the bibliometric analysis and data visualization through VOSviewer and CiteSpace. The analysis of publication growth revealed a substantial increase in articles published in this field over the past years, indicating mitophagy's growing interest and significance in liver diseases. China and USA emerged as the leading contributors in the number of papers, with 294 and 194 independent papers, respectively. Exploring the mechanism of mitophagy in the initiation and procession of liver diseases was the main content of studies in this field, and Parkin-independent mediated mitophagy has attracted much attention recently. "Lipid metabolism," "cell death," "liver fibrosis" and "oxidative stress" were the primary keywords clusters. Additionally, "nlrp3 inflammasome", "toxicity" and "nonalcoholic steatohepatitis" were emerging research hotspots in this area and have the potential to continue to be focal areas of investigation in the future. This study represents the first systematic bibliometric analysis of research on mitophagy in liver diseases conducted over the past 20 years. By providing an overview of the existing literature and identifying current research trends, this analysis sheds light on the critical areas of investigation and paves the way for future studies in this field.

A Novel Nomogram for Predicting Risk Factors and Outcomes in Bloodstream Infections Caused by Klebsiella pneumoniae.

Background: Our study aimed to explore the risk factors in bloodstream infections Klebsiella pneumoniae (BSI-KP) patients and establish nomograms to predict the probability of BSI-CRKP and the prognosis of BSI-KP. Methods: A total of 252 BSI-KP patients were enrolled from a tertiary teaching hospital between January 1, 2015, and May 31, 2020. Risk factors associated with BSI-CRKP and factors associated with the 30-day mortality were identified using LASSO analysis, univariate and multivariate analysis. Results: There were 121 (48.0%) patients with carbapenem-resistant K. pneumoniae (CRKP) and 131 (52.0%) patients with carbapenem-susceptible K. pneumoniae (CSKP). The multivariate logistic regression analysis demonstrated that gastric tube indwelling before BSI (OR=2.442, P=0.043) and more types of antibiotics use before BSI (OR=1.305, P=0.009) were independent risk factors for BSI-CRKP. And previous transplantations, prior ICU stay, gastric tube indwelling before BSI, more types of antibiotics use before BSI, lower Hb and cholinesterase were associated with CRKP-BSI. The C-index of models indicated its good accuracy (C-index 0.816, 95% CI 0.763-0.868). In patients with BSI-CRKP, further logistic regression analysis revealed urinary catheterization (OR=0.298, P=0.017) was found to be an independent risk factor for 30-day mortality, while ceftazidime/avibactam use (OR=8.438, P=0.003) was an independent favorable prognostic factor. The nomogram predicated CRKP, ICU hospitalization, more types of antibiotics use, tigecycline, PLT, urinary catheterization were associated with 30-day mortality in patients with BSI-KP. The discriminative ability of the predictive model, as assessed by C-index, was 0.813 (95% CI: 0.780-0.867). Conclusion: Previous transplantations, prior ICU stay, gastric tube indwelling before BSI, more types of antibiotics use before BSI, lower Hb and cholinesterase represent significant risk factors for the development of BSI-CRKP. Our nomogram predicated thrombocytopenia was a sign for poor prognosis. Tigecycline resulted in higher mortality for patients with BSI-KP. Rational use of nomograms may help clinicians make better Clinical decisions when treating BSI-KP patients.

A Meta-Analysis of Prognostic Factors in Patients with Posterior Circulation Stroke after Mechanical Thrombectomy.

BACKGROUND: Posterior circulation stroke is characterized by poor prognosis because its optimal thrombolysis "time window" is always missed. After mechanical thrombectomy (MT), the recanalization rate of posterior circulation obstruction is significantly increased, but prognosis remains poor. To best manage patients, prognostic factors are needed to inform MT triaging after posterior circulation stroke. METHODS: A systematic literature search was done for the period through April 2020. Studies included those with posterior circulation stroke cases that underwent MT. The primary outcome measure in this study was the modified Rankin Scale on day 90. RESULTS: No outcome differences were found in gender, atrial fibrillation, smoking, and coronary artery disease (OR = 1.07, 95% CI: 0.90-1.28; OR = 1.02, 95% CI: 0.82-1.26; OR = 1.26, 95% CI: 0.94-1.68; and OR = 0.84, 95% CI: 0.58-1.22, respectively). Hypertension, diabetes mellitus, and previous stroke correlated with poorer prognosis (OR = 0.61, 95% CI: 0.48-0.77; OR = 0.60, 95% CI: 0.50-0.73; and OR = 0.74, 95% CI: 0.55-0.99, respectively). However, hyperlipidemia correlated with better prognosis (OR = 1.28, 95% CI: 1.04-1.58). CONCLUSION: Our analysis indicates that hypertension, diabetes mellitus, or previous stroke correlate with poorer outcomes. Intriguingly, hyperlipidemia correlates with better prognosis. These factors may help inform triage decisions when considering MT for posterior circulation stroke patients. However, large, multicenter, randomized controlled trials are needed to validate these observations.

Thyroid metastasis from chondrosarcoma.

For chondrosarcoma, metastasis to the thyroid gland is extremely rare. The diagnosis and treatment of thyroid metastasis from chondrosarcoma are discussed here.We found a case of thyroid malignancy occurring after treatment of chondrosarcoma. We reviewed patient characteristics, histological presentations on initial chondrosarcoma and thyroid metastasis, treatments, times of recurrence and death. In addition, we searched Embase, PubMed, and ISI Web of Science databases (1996-2018) for articles published in the English language using the key words "chondrosarcoma" and "thyroid" and we reviewed almost all the reports about thyroid metastasis from chondrosarcoma.Only 5 cases of chondrosarcoma metastases in the thyroid gland have been reported in the literature. We found that most patients are adults, with compression signs or pain, most of whom have poor prognoses. The main examinations are ultrasound, CT and fine needle aspiration biopsy, and primary treatment is surgery.These rare cases of chondrosarcoma presenting as a metastasis in the thyroid gland highlight the importance of close communication between radiologists, histopathologists, and clinicians to ensure that such exceptional cases are not missed.

A potentially common peptide target in secreted heat shock protein-90α for hypoxia-inducible factor-1α-positive tumors.

Deregulated accumulation of hypoxia-inducible factor-1α (HIF-1α) is a hallmark of many solid tumors. Directly targeting HIF-1α for therapeutics is challenging. Our finding that HIF-1α regulates secretion of heat shock protein-90α (Hsp90α) for cell migration raises the exciting possibility that targeting the secreted Hsp90α from HIF-1α-positive tumors has a better clinical outlook. Using the HIF-1α-positive and metastatic breast cancer cells MDA-MB-231, we show that down-regulation of the deregulated HIF-1α blocks Hsp90α secretion and invasion of the cells. Reintroducing an active, but not an inactive, HIF-1α into endogenous HIF-1α-depleted cells rescues both Hsp90α secretion and invasion. Inhibition of Hsp90α secretion, neutralization of secreted Hsp90α action, or removal of the cell surface LRP-1 receptor for secreted Hsp90α reduces the tumor cell invasion in vitro and lung colonization and tumor formation in nude mice. Furthermore, we localized the tumor-promoting effect to a 115-amino acid region in secreted Hsp90α called F-5. Supplementation with F-5 is sufficient to bypass the blockade of HIF-1α depletion and resumes invasion by the tumor cells under serum-free conditions. Because normal cells do not secrete Hsp90α in the absence of stress, drugs that target F-5 should be more effective and less toxic in treatment of HIF-1α-positive tumors in humans.

TbetaRI/Alk5-independent TbetaRII signaling to ERK1/2 in human skin cells according to distinct levels of TbetaRII expression.

TGFß binding to the TGFß receptor (TßR) activates R-Smad-dependent pathways, such as Smad2/3, and R-Smad-independent pathways, such as ERK1/2. The mechanism of the TGFß-TßRII-TßRI-Smad2/3 pathway is established; however, it is not known how TGFß activates ERK1/2. We show here that although TGFß equally activated Smad2/3 in all cells, it selectively activated ERK1/2 in dermal cells and inhibited ERK1/2 in epidermal cells. These opposite effects correlated with the distinct expression levels of TßRII, which are 7- to 18-fold higher in dermal cells than in epidermal cells. Reduction of TßRII expression in dermal cells abolished TGFß-stimulated ERK1/2 activation. Upregulation of TßRII expression in epidermal cells to a similar level as that in dermal cells switched TGFß-induced ERK1/2 inhibition to ERK1/2 activation. More intriguingly, in contrast to the equal importance of TßRII in mediating TGFß signaling to both Smad2/3 and ERK1/2, knockdown of TßRI/Alk5 blocked activation of only Smad2/3, not ERK1/2, in dermal cells. Similarly, expression of the constitutively activated TßRI-TD kinase activated only Smad2/3 and not ERK1/2 in epidermal cells. This study provides an explanation for why TGFß selectively activates ERK1/2 in certain cell types and direct evidence for TßRI-independent TßRII signaling to a R-Smad-independent pathway.