Bioresorbable stent unloading during percutaneous coronary intervention:Early detection and management

In this letter,we comment on a recent case report by Sun et al in the World Journal of Cardiology.The report describes the successful management of a rare complication:The unloading or detachment of a bioresorbable stent(BRS)during percutaneous coronary intervention(PCI)in a male patient.The unloading of BRS was detected via angiography and intravascular ultrasound(IVUS)imaging of the left coronary artery and left anterior descending artery.Although this case is interesting,the authors’report lacked crucial details.Specifically,insufficient information about the type of BRS used,potential causes of BRS unloading,or whether optical coherence tomography(OCT)imaging for coronary arteries was performed before,during,or after PCI.The OCT imaging of coronary arteries before PCI can potentially prevent BRS unloading due to its higher resolution compared to IVUS.In addition,despite detecting myocardial bridging during the PCI,the authors did not provide any details regarding this variation.Here we discuss the various types of BRS,the importance of OCT in PCI,and the clinical relevance of myocardial bridging.

Tuberculosis-diabetes comorbidities: Mechanistic insights for clinical considerations and treatment challenges

Tuberculosis(TB)remains a leading cause of death among infectious diseases,particularly in poor countries.Viral infections,multidrug-resistant and ex-tensively drug-resistant TB strains,as well as the coexistence of chronic illnesses such as diabetes mellitus(DM)greatly aggravate TB morbidity and mortality.DM[particularly type 2 DM(T2DM)]and TB have converged making their control even more challenging.Two contemporary global epidemics,TB-DM behaves like a syndemic,a synergistic confluence of two highly prevalent diseases.T2DM is a risk factor for developing more severe forms of multi-drug resistant-TB and TB recurrence after preventive treatment.Since a bidirectional relationship exists between TB and DM,it is necessary to concurrently treat both,and promote recommendations for the joint management of both diseases.There are also some drug-drug interactions resulting in adverse treatment outcomes in TB-DM patients including treatment failure,and reinfection.In addition,autophagy may play a role in these comorbidities.Therefore,the TB-DM comorbidities present several health challenges,requiring a focus on multidisciplinary collaboration and integrated strategies,to effectively deal with this double burden.To effectively manage the comorbidity,further screening in affected countries,more suitable drugs,and better treatment strategies are required.

Suppression of hepatic steatosis in non-alcoholic steatohepatitis model by modified Xiaoyao San formula:Evidence,mechanisms and perspective

In this letter,we comment on a recent publication by Mei et al,in the World Journal of Hepatology,investigating the hepatoprotective effects of the modified Xiaoyao San(MXS)formula in a male rat model of non-alcoholic steatohepatitis(NASH).The authors found that MXS treatment mitigated hepatic steatosis and inflam-mation in the NASH model,as evidenced by the reduction in lipid droplets(LDs),fibrosis markers and lipogenic factors.Interestingly,these hepatoprotective effects were associated with androgen upregulation(based on metabolomics analysis of male steroid hormone metabolites),adenosine 5’-monophosphate-activated protein kinase(AMPK)activation,and restoration of phosphatase and tensin homolog(PTEN)expression.However,the authors did not clearly discuss the relationships between MXS-induced hepatic steatosis reduction in the NASH model,and androgen upregulation,AMPK activation,and restoration of PTEN expression.This editorial emphasizes the reported mechanisms and explains how they act or interact with each other to reduce hepatic steatosis and inflammation in the NASH model.As a perspective,we propose additional mechanisms(such as autophagy/lipophagy activation in hepatocytes)for the clearance of LDs and suppression of hepatic steatosis by MXS in the NASH model.A proper understanding of the mechanisms of MXS-induced reduction of hepatic steatosis might help in the treatment of NASH and related diseases.

Mechanistic insights into fasting-induced autophagy in the aging heart

Autophagy is a prosurvival mechanism for the clearance of accumulated abnormal proteins,damaged organelles,and excessive lipids within mammalian cells.A growing body of data indicates that autophagy is reduced in aging cells.This reduction leads to various diseases,such as myocardial hypertrophy,infarction,and atherosclerosis.Recent studies in animal models of an aging heart showed that fasting-induced autophagy improved cardiac function and longevity.This improvement is related to autophagic clearance of damaged cellular components via either bulk or selective autophagy(such as mitophagy).In this editorial,we summarize the mechanisms of autophagy in normal and aging hearts.In addition,the protective effect of fasting-induced autophagy in cardiac aging has been highlighted.

Natural isothiocyanates of the genus Capparis as potential agonists of apoptosis and antitumor agents:Mechanisms and implications

In this editorial,we comment on a recent publication,which highlights the important findings from the study,including the antitumor and anti-inflammatory effects of isothiocyanates,their underlying mechanisms,and implications.Additionally,a related perspective is discussed.

Ethanol-induced hepatic autophagy: Friend or foe?

Excessive alcohol intake may induce hepatic apoptosis, steatosis, fibrosis, cirrhosis and even cancer. Ethanolinduced activation of general or selective autophagy as mitophagy or lipophagy in hepatocytes is generally considered a prosurvival mechanism. On the other side of the coin, upregulation of autophagy in nonhepatocytes as stellate cells may stimulate fibrogenesis and subsequently induce detrimental effects on the liver. The autophagic response of other non-hepatocytes as macrophages and endothelial cells is unknown yet and needs to be investigated as these cells play important roles in ethanol-induced hepatic steatosis and damage. Selective pharmacological stimulation of autophagy in hepatocytes may be of therapeutic importance in alcoholic liver disease.

Parkin in cancer:Mitophagy-related/unrelated tasks

Dysfunctional mitochondria may produce excessive reactive oxygen species, thus inducing DNA damage, which may be oncogenic if not repaired. As a major role of the PINK1-Parkin pathway involves selective autophagic clearance of damaged mitochondria via a process termed mitophagy, Parkin-mediated mitophagy may be a tumorsuppressive mechanism. As an alternative mechanism for tumor inhibition beyond mitophagy, Parkin has been reported to have other oncosuppressive functions such as DNA repair, negative regulation of cell proliferation and stimulation of p53 tumor suppressor function. The authors recently reported that acute ethanol-induced mitophagy in hepatocytes was associated with Parkin mitochondrial translocation and colocalization with accumulated 8-OHd G(a marker of DNA damage and mutagenicity). This finding suggests:(1) the possibility of Parkin-mediated repair of damaged mitochondrial DNA in hepatocytes of ethanol-treated rats(ETRs) as an oncosuppressive mechanism; and(2) potential induction of cytoprotective mitophagy in ETR hepatocytes if mitochondrial damage is too severe to be repaired. Below is a summary of the various roles Parkin plays in tumor suppression, which may or may not be related to mitophagy. A proper understanding of the various tasks performed by Parkin in tumorigenesis may help in cancer therapy by allowing the PINK1-Parkin pathway to be targeted.

Surgically Important Relationships of Recurrent and Nonrecurrent Laryngeal Nerves to the Coexisting Variant Vessels

The retroesophageal right subclavian artery may be associated with multiple neurovascular variations, which may impact various cervicothoracic surgeries. During the dissection of 27 cadavers, the authors detected a retroesophageal right subclavian artery in old man arising from distal aortic arch, crossed ventrally by left recurrent laryngeal nerve and dorsally by thoracic duct. On the right side, the aberrant subclavian artery was associated with nonrecurrent laryngeal nerve crossing a large tortuous inferior thyroid artery at multiple intersection points. Importantly, the nonrecurrent laryngeal nerve gave rise to extra laryngeal branch passing over Zuckerkandl’s tubercle of thyroid gland before its termination into the larynx. The relationships of the aberrant subclavian artery in the present case to thoracic duct, recurrent and nonrecurrent laryngeal nerves may have clinical relevance to various operations such as thyroidectomy, esophagectomy and surgical correction of the aberrant vessel. Therefore, these relationships should be well known by surgeons for prevention of iatrogenic damage of essential neurovascular structures during various surgeries.

Anomalous muscles in carpal tunnel associated with neurovascular variations: Case report and brief review

Anomalous muscles in carpal tunnel (CT) may cause carpal tunnel syndrome (CTS), and may be also associated with neurovascular abnormalities, altering the diagnosis and surgical interventions for CTS. The authors report a case of bilateral Gantzer’s muscles (GMs) inserted into the tendons of flexor digitorum profundus within the CTs in an old male cadaver. The left GM was associated with enlarged lumbrical muscles in the CT and bifid median nerve (MN) communicating with ulnar nerve in the hand. The right GM was associated with perforation of MN branches in the hand by superficial palmar arch. This unreported coexistence of anomalous GMs and the associated neurovascular variations may have clinical relevance to etiology, diagnosis and treatment of CTS.