Global prevalence and risk factors of emergence delirium in pediatric patients undergoing general anesthesia: A systemic review and meta-analysis.

PROBLEM: Emergence delirium (ED) in children post-general anesthesia has been persistently underestimated, impacting the well-being of children, nurses, and even parents. This study employs integrated analysis to establish a comprehensive understanding of ED, including its occurrence and related risk factors, emphasizing the imperative for enhanced awareness and comprehension among pediatric nursing care providers. ELIGIBILITY CRITERIA: A systematic review and meta-analysis were conducted using four electronic databases, namely PubMed, CINAHL via EBSCOhost, Embase via Elsevier, and ProQuest Dissertations and Theses. RESULTS: This meta-analysis included 16 studies involving 9598 children who underwent general anesthesia. The pooled prevalence of ED was 19.2% (95% confidence interval [CI] = 0.12 to 0.29), with younger patients exhibiting a higher prevalence of ED. ED research is scant in Africa and is mostly limited to the Asia Pacific region and Northern Europe. Neck and head surgery (odds ratio [OR] = 2.34, 95% CI = 1.29 to 4.27) were significantly associated with ED risk. CONCLUSIONS: ED should be monitored in children who receive general anesthesia. In this study, ED had a prevalence rate of 19.2%, and head and neck surgery were significantly associated with ED risk. Therefore, healthcare professionals should carefully manage and prevent ED in children undergoing general anesthesia. IMPLICATIONS: A comprehensive understanding of ED's prevalence and risk factors is crucial for enhancing nursing care. Adopting a family-centered care approach can empower parents with information to collaboratively care for their children, promoting a holistic approach to pediatric healthcare.

Curcumin and tetrahydrocurcumin induce cell death in Ara-C-resistant acute myeloid leukemia.

Most anticancer agents induce cancer cell death; however, multidrug-resistant cancers often lead to treatment failure. The effective use of curcumin as an anticancer agent has been demonstrated in clinical trials. Tetrahydrocurcumin, a major curcumin metabolite, exhibits pharmacological activities similar to those of curcumin. Curcumin induces cell death mainly through the apoptosis pathway, and tetrahydrocurcumin induces cell death mainly via an autophagy pathway in HL60 cells. Here, we investigated whether curcumin and tetrahydrocurcumin can induce apoptosis- and autophagy-mediated cell deaths in Ara-C-resistant cancer cells, respectively. The results demonstrated that curcumin and tetrahydrocurcumin induced cell death by apoptosis and autophagy, respectively, in Ara-C-resistant HL60 cells. Thus, curcumin and tetrahydrocurcumin have potential applications in the treatment of acute myeloid leukemia with Ara-C resistance.

Clinical Features and Genotypes of Patients with Hemoglobin H Disease in Taiwan.

BACKGROUND: The genetic background of patients with hemoglobin (Hb) H disease in Taiwan has been investigated; however, the clinical features and treatment outcomes were not reported. OBJECTIVE: To analyze the clinical features and genotypes of patients with HbH who reside in Taiwan. METHODS: We conducted a retrospective analysis of the clinical and molecular characteristics of 38 patients with HbH disease who were undergoing treatment at Kaohsiung Medical University Hospital, Taiwan. RESULTS: Initial Hb levels were lower and the numbers of patients requiring iron-chelation therapy were higher in the nondeletional HbH group than in the deletional HbH group (P <.05). Compared with the healthy population, the patients with HbH disease exhibited short body length, low body weight, and low body mass index (BMI). CONCLUSIONS: Patients with nondeletional HbH disease had lower Hb levels and a higher requirement for splenectomy and iron-chelation therapy than did those with deletional HbH disease. Also, growth status was compromised in patients with HbH disease.

Association between areca-stimulated vimentin expression and the progression of head and neck cancers.

BACKGROUND: Areca nut chewing is a common oral habit of Asians that is closely associated with the high incidence of head and neck carcinoma. The purpose of this study was to investigate the impacts of areca nut chewing on neoplastic process of head and neck carcinoma. METHODS: Head and neck carcinoma cells were treated with areca nut extract to perceive the phenotypic impacts. Tumor tissues were analyzed with immunohistochemistry (IHC) to understand the association between areca-associated molecular changes and clinical variables. RESULTS: Upon treatment with areca nut extract, carcinoma cells showed the increase of vimentin. The activation of extracellular signal-regulated kinase (ERK)/cyclooxygenase (COX)-2/prostaglandin (PGE)-2 cascade underlay the upregulation. These cells also exhibited the enhancement of migration and invasion. By knocking down COX-2 and vimentin expression, the increase of cell mobility was reversed. Tumor exhibiting extensive vimentin and/or COX-2 expression displayed a significantly worse disease-associated survival than contrast groups. CONCLUSION: Areca-modulated vimentin expression enhanced the progression of head and neck carcinoma.

Areca nut extract upregulates vimentin by activating PI3K/AKT signaling in oral carcinoma.

BACKGROUND: Areca nut is a group I carcinogen. Areca nut extract (ANE) is known to activate signaling pathways in oral epithelial cells. Activation of the serine/threonine protein kinase AKT/pKB (AKT) signaling pathway is known to be important during the neoplastic process. Vimentin is a mesenchymal intermediate filament and a regulator of tumor progression. This study investigated the impact of ANE on PI3K/AKT activation during vimentin expression. MATERIALS AND METHODS: Oral carcinoma cells were treated with ANE to explore the signaling changes underlying vimentin expression. Oral carcinoma tissues were subjected to immunohistochemical analysis to study the implications that vimentin expression has on patient survival. RESULTS: After ANE treatment, the OECM-1 and Fadu cells developed a fibroblastoid morphology and there was an increase in vimentin expression. The treatment also induced the phosphorylation of AKT and glycogen synthase kinase 3ß in OECM-1 cells. Blockage of phosphatidylinositol 3-kinase (PI3K)/AKT signaling attenuated vimentin expression when it was induced by ANE. However, it did not affect ANE-mediated extracellular signal-regulated kinase (ERK) activation or cyclooxygenase 2 (COX-2) upregulation. Oral carcinoma tissue samples were found to have significantly higher levels of vimentin and pAKT expression than their controls. Tumors exhibiting no vimentin expression and weak AKT phosphorylation were found to be associated with better survival than groups with high levels of expression. CONCLUSION: Our results imply that PI3K/AKT activation and vimentin expression are important pathogenic cascades in areca-associated oral carcinogenesis.

Areca nut extract treatment down-regulates involucrin in normal human oral keratinocyte through P13K/AKT activation.

Areca (betel) is an important etiological factor linked to the high prevalence of oral carcinoma and other oral diseases in South Asians. Involucrin is a key component of the cornified envelop and a differentiation marker of keratinocyte. In this study, we found that 5 microg/ml non-toxic areca nut extract (ANE) treatment resulted in the 0.5-fold down-regulation of involucrin and disruption in involucrin distribution in normal human oral keratinocyte (NHOK). Progressive down-regulation of involucrin during oral carcinogenesis was noted. Activation of AKT by 1.7-fold and up-regulation of COX-2 by 2-fold were elicited following ANE treatment in NHOK. Treatment with PI3K/AKT blockers reverted the down-regulation of involucrin. ANE also down-regulated involucrin by 0.6-fold and disturbed both cornified envelope and cell aggregation in calcium-induced differentiated NHOK. However, such phenomena seemed to be independent from the ANE-associated COX-2 activation. The ANE-associated down-regulation of involucrin through AKT pathway could underlie the areca-associated epithelial pathogenesis.

Ripe areca nut extract induces G1 phase arrests and senescence-associated phenotypes in normal human oral keratinocyte.

Around 200-600 million Asians chew areca (also called betel), which contains a mixture of areca nut and other ingredients. Epidemiological evidences indicated that areca use is tightly linked to oral carcinogenesis. This study investigated the effects of ripe areca nut extract (ANE) on cultured normal human oral keratinocyte (NHOK). Acute subtoxic ANE treatment inhibited DNA synthesis and induced cell cycle arrest at G1 phase in early passage (< 4th passage) cells. This was accompanied by a slight increase in the sub-G1 cellular fraction. O6-Methylguanine-DNA methyltransferase (MGMT), Hsp27 and p38MAPK was upregulated. p16 and p21 were remarkably upregulated early and declined afterwards. In contrast, the increase of dephosphorylated Rb seemed to be secondary to the episodes of p16 and p21 upregulation. To simulate the chronic areca exposure in vivo, constant ANE treatment in serial NHOK culture was performed. It resulted in a significant decrease in the population doubling, increase in senescence-associated beta-galactosidase (SA-beta-Gal) and decrease in cell proliferation in NHOK of late passages (> or = 4th passage). Induction of senescence-associated phenotypes, G2/M accumulation and genomic instability following long-term ANE treatment were also observed in a low-grade oral carcinoma cell. ANE-treated NHOK also had a higher nuclear factor-kappaB (NF-kappaB) fraction and a lower cytosolic IkappaBalpha level relative to the control in late passages. Moreover, electrophoretic mobility shift assay (EMSA) indicated that ANE treatment shifted the NF-kappaB complex from high mobility position to lower mobility position in late-passaged NHOK. ANE treatment also upregulated IL-6 and cyclooxygenase-2 (COX-2) mRNA expressions in late-passaged NHOK. In summary, our findings suggest that ANE induces the cell cycle arrest at G1/S phase and the occurrence of senescence-associated phenotypes of NHOK. The upregulation of p38MAPK, p16, p21, NF-kappaB, IL-6 and COX-2 are likely to participate in the control of these impacts.