Cancer, potentially the second leading cause of mortality globally, poses a significant health challenge. The conventional treatment for solid tumors typically involves surgical intervention, followed by chemotherapy, radiotherapy, and targeted therapies. However, cancer recurrence and metastasis remain major issues. Anesthesia is essential for ensuring patient comfort and safety during surgery. Despite its crucial role in surgery, the precise effect of anesthesia on cancer patients' outcomes has not been clearly understood. This comprehensive review aims to elucidate perioperative anesthesia strategies for cancer patients and their potential effects on prognosis. Given the complexity of cancer treatments, understanding the relationship between anesthesia and cancer outcomes is crucial. By examining potential implications of anesthesia strategies for cancer prognosis, this review may help better understand treatment efficacy and risk factors for cancer recurrence and metastasis. Ultimately, a detailed analysis of anesthesia practices in cancer surgery may provide insights to refine existing anesthesia protocols and reduce risk factors for poor patient outcomes.

Inflammation plays a crucial role in the initiation and progression of sepsis and induces alterations in brain neurotransmission, thereby contributing to the development of sepsis-associated encephalopathy (SAE). Parvalbumin (PV) interneurons are pivotal contributors to cognitive processes and have been implicated in various central nervous system dysfunctions, including SAE. Oxytocin, known for its ability to augment the firing rate of gamma-aminobutyric acid (GABA)-ergic interneurons and directly stimulate inhibitory interneurons to enhance the tonic inhibition of pyramidal neurons, has prompted an investigation into its potential therapeutic effects on cognitive dysfunction in SAE. In the current study, we administered intranasal oxytocin to SAE mice induced by lipopolysaccharide. Behavioral assessments, including open field, Y-maze, and fear conditioning, were used to evaluate cognitive performance. Golgi staining revealed hippocampal synaptic deterioration, local field potential recordings showed weakened gamma oscillations, and immunofluorescence staining demonstrated decreased PV expression in the cornu ammonis 1 (CA1) region of the hippocampus following lipopolysaccharide treatment, all of which were alleviated by oxytocin administration. Furthermore, immunofluorescence staining of PV co-localization with vesicular glutamate transporter 1 or vesicular GABA transporter indicated a balanced excitation/inhibition effect of neurotransmitters on PV interneurons after oxytocin administration in the SAE mice, leading to an improved cognitive function. In conclusion, oxytocin treatment improved cognitive function by increasing the number of PV⁺ neurons in the hippocampal CA1 region, restoring the balance of excitatory/inhibitory synaptic transmission on PV interneurons, and enhancing hippocampal CA1 local field potential gamma oscillations. These findings suggest a potential mechanism underlying the beneficial effects of oxytocin in SAE.

The prevalence of stunting in Indonesian children under five years of age is approximately 20%. Chronic maternal malnutrition contributes to the risk of stunting by affecting global DNA methylation. In the present study, we aimed to evaluate the levels of 5-methyl-cytosine (5mC) as a surrogate marker of global DNA methylation in buccal swabs and its potential association with the risk of stunting and cognitive performance. The levels of 5mC were measured using an enzyme-linked immunosorbent assay. The Wechsler Preschool and Primary Scale of Intelligence (WPPSI) was used to measure cognitive function. Buccal swab DNA samples and anthropometric data were collected from a total of 231 children aged zero to five years. In this cross-sectional cohort, the prevalence of stunting was 37% in 138 children aged zero to two years and 30% in 93 children aged over two years. The univariable analysis revealed that the levels of 5mC in buccal swab DNA were significantly lower in severely stunted children (median, 2.84; interquartile range [IQR], 2.39-4.62) and children aged less than two years (median, 2.81; IQR, 2.53-4.62) than those in normal children (median, 3.75; IQR, 2.80-4.74; P-value, 0.028) and children aged over four years (median, 4.01; IQR, 3.39-4.87; P-value < 0.001), respectively. We also found that the average cognitive scores tended to be low in boys and stunted children, although the differences were not statistically significant. Furthermore, the levels of 5mC found in buccal swab and mouthwash DNA were not associated with cognitive scores.

Most papillary thyroid carcinoma (PTC) patients have a good prognosis. However, lymph node metastasis (LNM), the most common manifestation of disease progression, is frequently associated with a poor prognosis. Nevertheless, few studies have focused on the underlying mechanisms of LNM. In the current study, we aimed to investigate the potential role of exosomal circRNAs that contribute to LNM in PTC. We identified 9000 differentially expressed exosomal circRNAs in PTC patients with LNM, including 684 upregulated and 2193 downregulated circRNAs. Functional enrichment analysis revealed that these differentially expressed circRNAs were primarily involved in a variety of molecular and signaling pathways correlated with PTC progression and LNM. Through bioinformatics analysis, we identified 14 circRNA-miRNA-mRNA networks related to LNM-associated signaling pathways in PTC. Moreover, both circTACC2-miR-7-EGFR and circBIRC6-miR-24-3p-BCL2L11 axes were verified for their potential involvement in PTC with LNM. Additionally, we identified four upregulated circRNA-related hub genes and eight hub genes correlated with downregulated circRNAs, some of which were validated as being potentially involved in LNM in PTC. Collectively, our findings provide a novel framework for an in-depth investigation of the function of dysregulated exosomal circRNAs and their potential as biomarkers in PTC patients with LNM.

Myocardial fibrosis is a major pathogenic factor contributing to cardiac remodeling and heart failure. Recent research has indicated that microRNAs play a crucial role in the progression of cardiac fibrosis. Bone morphogenetic protein and activin membrane-bound inhibitor (BAMBI) have been shown to alleviate myocardial fibrosis by inhibiting the transforming growth factor β1 (TGF-β1) signaling pathway. Therefore, the current study aimed to elucidate the post-transcriptional regulation of BAMBI by miR-19a-3p and its role in TGF-β1-induced cardiac fibroblast activation. We found that transverse aortic constriction induced both myocardial interstitial and perivascular collagen deposition. Quantitative reverse transcription-PCR (qRT-PCR) analysis showed that the expression level of miR-19a-3p was increased in the myocardial tissues of cardiac fibrosis, and TGF-β1 induced an upregulation in miR-19a-3p expression in cardiac fibroblasts. The dual-luciferase reporter assay and qRT-PCR verified that miR-19a-3p directly bound to the 3′ untranslated regions of BAMBI mRNA, thereby reducing BAMBI expression and diminishing its ability to inhibit the TGF-β1 signaling pathway. Furthermore, overexpression of miR-19a-3p mimic increased the activation of TGF-β1/SMAD2/3 pathway signaling, promoting cardiac fibroblast activation. However, this activation was blocked by BAMBI overexpression. These findings imply that miR-19a-3p enhances the activation of TGF-β1/SMAD2/3 by inhibiting BAMBI, further boosting the activation of cardiac fibroblasts and contributing to myocardial fibrosis.

Although p21-activated kinase 2 (PAK2) is an essential serine/threonine protein kinase, its role in the progression of lung squamous cell carcinoma (LUSC) has yet to be fully understood. We analyzed PAK2 mRNA levels, DNA copy numbers, and protein levels by quantitative reverse transcription-PCR and immunohistochemical staining in both human LUSC tissues and adjacent normal tissues. Then, we performed colony formation assays, cell counting kit-8 assays, Matrigel invasion assays, wound healing assays, and xenograft models in nude mice to investigate the functions of PAK2 in LUSC progression. We demonstrated that PAK2 mRNA levels, DNA copy numbers, and protein levels were upregulated in human LUSC tissues, compared with adjacent normal tissues. Additionally, higher PAK2 expression was associated with poorer prognosis in LUSC patients. In the in vitro study, we found that PAK2 promoted cell growth, migration, invasion, epithelial-mesenchymal transition, and cell morphology regulation in LUSC cells. Mechanistically, PAK2 promoted tumor cell proliferation, migration, and invasion by regulating actin dynamics through the LIMK1/cofilin signaling pathway. Our findings indicate that the PAK2/LIMK1/cofilin signaling pathway may serve as a potential clinical marker and therapeutic target for LUSC.

Meiotic resumption in mammalian oocytes involves nuclear and organelle structural changes, notably the chromatin configuration transition from a non-surrounding nucleolus (NSN) to surrounding nucleolus (SN) in germinal vesicle oocytes. In the current study, we found that nuclear speckles (NSs), a subnuclear structure mainly composed of serine-arginine (SR) proteins, changed from a diffuse spotted distribution in mouse NSN oocytes to an aggregated pattern in SN oocytes. We also found that the SR protein-specific kinase 1 (SRPK1), an enzyme that phosphorylates SR proteins, co-localized with NSs at the SN stage, and that NSN oocytes failed to transition to SN oocytes after the inhibition of SRPK1 activity. Furthermore, the typical structure of the chromatin ring around the nucleolus in SN oocytes collapsed after treatment with an SRPK1 inhibitor. Mechanistically, phosphorylated SR proteins were found to be related to chromatin as shown by a salt extraction experiment, and in situ DNase I assay showed that the accessibility of chromatin was enhanced in SN oocytes when SRPK1 was inhibited, accompanied by a decreased repressive modification on histone and the abnormal recurrence of a transcriptional signal. In conclusion, our results indicated that SRPK1-regulated phosphorylation of SR proteins was involved in the NSN-SN transition and played an important role in maintaining the condensed nucleus of SN oocytes via interacting with chromatin.