Risk factor analysis and model construction for fish bone foreign body in children's pharynx.

OBJECTIVES: This study aimed to assess the risk factors for predicting the presence of fish bone foreign bodies and to develop a risk prediction model. METHODS: Data of 1405 children who underwent video-guided laryngoscope for suspected fish bone foreign body ingestion were retrospectively analyzed. Multi-factor logistic regression analyses were performed to analyze the risk factors for the presence of fish bone foreign body in patients, and a risk prediction model was established based on the results of the logistic regression analysis. RESULTS: The results of the statistical analysis showed the presence of an ulcerated surface increased the risk of having a fishbone foreign body in the pharynx by approximately 55.36-fold (95 % confidence interval (CI): 15.78-194.24), followed by a clear chief complaint site, which increased the risk of having a fishbone foreign body in the pharynx by approximately 7.963-fold (95 % CI: 4.820-13.15), and a tingling sensation, which increased the risk of having a fishbone foreign body by approximately 7-fold (95 % CI: 3.483, 14.233). A clinical prediction model (nomogram) was developed and its validation was performed using receiver operating characteristic (ROC) curve analysis, in which an area under the curve (AUC) value of 0.808 indicated that the model had a great prediction capability. CONCLUSION: The predictive capability of a logistic regression model for the detection of fish bone foreign bodies following ingestion is significant. Clinicians can concentrate on monitoring these risk factors and implementing appropriate interventions to reduce the risks of patients presenting with fish bone foreign bodies.

Storage, Disposal, and Use of Opioids Among Cancer Patients in Central China: A Multi-Center Cross-Sectional Study.

OBJECTIVE: Unsafe opioid-related practices can lead to abuse, diversion, and accidental overdoses. In this study, we aimed to describe the patterns and beliefs regarding the storage, disposal, and use of opioids among Chinese patients with cancer in their home settings, which remain unclear. METHODS: A multicenter cross-sectional survey was conducted in Hubei Province from October 2022 to June 2023. We collected information on the storage, disposal, and use of opioids among cancer pain inpatients in the oncology department. Logistic regression was used to estimate the factors associated with unsafe disposal and use of opioids. RESULTS: The survey included 221 patients with a median age of 62 years. Only 3.2% stored their opioids under lock and key, and 49.8% were unaware of proper disposal methods. Nearly one-fifth (19.5%) reported having received information on the safe storage (14.0%) and/or disposal (10.0%) of opioids. A total of 44.3% reported unsafe use by sharing (1.8%), losing (4.1%), or taking opioids at a higher dose than prescribed (42.5%). Patients who did not receive information on the safe disposal of opioids (OR = 4.57, P = .0423), had a history of alcohol use (OR = 1.91, P = .0399), and used opioids other than morphine (OR = 2.31, P = .0461) had higher odds of unsafe disposal practices. Individuals with an associate degree/bachelor's degree or above were less likely to dispose of (OR = 0.36, P = .0261) and use (OR = 0.31, P = .0127) opioids unsafely. CONCLUSION: A significant proportion of Chinese patients with cancer exhibit unsafe practices in the storage, disposal, and use of opioids. The study highlights an urgent need for implementing routine education programs and drug "take-back" initiatives to improve opioid-related practices.

[Subglottic cysts in infants: a report of 3 cases and literature review].

Subglottic cyst is a rare cause of laryngeal tinnitus in infants and young children, and only a few cases have been reported at home and abroad. In this paper, we report the clinical characteristics and treatment experience of three cases of subglottic cysts in Children's Hospital of Nanjing Medical University. All the 3 childrem were prematurechildren, with a history of tracheal intubation, and the main symptoms were coughing and wheezing.Electronic nasopharyngolaryngoscopy revealed spherical neoplasm under the glottis. Neck computed tomography （CT） showed a slightly hypodense shadow with poorly defined borders, and no significant enhancement was observed after enhancement. Under the self-retaining laryngoscope, the new organisms were clamped and nibbled, and the cyst wall was cauterized by low temperature plasma. There was no recurrence in postoperative follow-up.

Is a fish bone at a parallel angle in the throat more likely to fall out automatically？.

PURPOSE: To investigate the factors influencing the spontaneous expulsion of fish bone foreign bodies in the throat of children. METHODS: A retrospective cohort study was conducted between January 2018 and December 2021 of children hospitalized with fishbone foreign bodies in the throat, and subsequent electronic rhinolaryngoscopy to analyze the factors influencing the spontaneous expulsion of these foreign bodies. RESULTS: The effect of foreign body angle on the rate of dislodgement was found to be statistically significant. Parallel angle was more likely to dislodge relative to vertical (RR = 2.495, 95% CI 1.515-4.109, P = 0.000); inclined angle was more likely to dislodge relative to vertical (RR = 2.121, 95% CI 1.284-3.505, P = 0.003). For the three fish bone foreign body angles (vertical, inclined, and parallel), the percentage of dislodgement showed a linear trend (0.278, 0.600, and 0.723), indicating that the percentage of dislodgement appeared to increase with the increase of fish bone foreign body inclination angle (Ptrend = 0.000). CONCLUSION: There is a high rate of natural expulsion of fish bone foreign body from children's throat, and the rate of expulsion increases with the increase of the foreign body inclination angle.

Inhibition of the NF-κB pathway and ERK-mediated mitochondrial apoptotic pathway takes part in the mitigative effect of betulinic acid on inflammation and oxidative stress in cyclophosphamide-triggered renal damage of mice.

Betulinic acid (BA), an occurring pentacyclic triterpenoid, has various biological activities, such as anti-inflammation and antioxidation. Previous studies found that BA attenuated cyclophosphamide (CYP)-induced intestinal mucosal damage by inhibiting intestinal mucosal barrier dysfunctions and cell apoptosis. However, the effects and regulation mechanisms of BA on CYP-induced renal damage has not been reported in literature. Here, we found that BA pretreatment alleviated the elevation of serum urea level and inhibited the increase in serum neutrophil gelatinase-associated lipocalin level induced by CYP. Meanwhile, BA ameliorated renal tubular epithelial cell edema, and vacuolization of renal cortical tubular and renal glomerulus. Moreover, pretreatment with BA inhibited the mRNA expressions of pro-inflammatory cytokines interleukin-1ß (IL-1ß), IL-6, and tumor necrosis factor-α, and increased mRNA expressions of anti-inflammatory cytokines such as IL-10 and transforming growth factor-ß by inactivation nuclear factor kappa-B. Simultaneously, BA decreased the accumulation of reactive oxygen species and malondialdehyde, and lowered the levels of superoxide dismutase and glutathione, while increased the activity of glutathione peroxidase in CYP-induced kidney damage mice. Besides, BA reduced the phosphorylation of extracellular signal-regulated kinases (ERK), inhibited the ratio of Bcl-2/Bax and cell apoptosis in CYP-triggered kidney damage. Furthermore, BA and/or PD98059 (an inhibitor of ERK) regulated mitigation of CYP-elicited renal injury and deactivation of the ERK pathway and mitochondrial apoptotic pathway, indicating that the protective effect of BA on CYP-induced renal damage may be associated with the down-regulation of ERK-mediated mitochondrial apoptotic pathway. Thus, BA could be a candidate agent against chemotherapy drug-induced nephrotoxicity by reducing inflammation and oxidative stress through suppression of ERK-mediated mitochondrial apoptotic pathway.

Betulinic acid attenuates cognitive dysfunction, oxidative stress, and inflammation in a model of T-2 toxin-induced brain damage.

T-2 toxin is a mycotoxin that has harmful effects on the immune system and cognitive function. Betulinic acid (BA) is a plant-derived pentacyclic lupane-type triterpenoid which possesses a wide spectrum of bioactivities. The study was aimed to explore whether BA has a protective effect on cognitive impairment and oxidative stress caused by T-2 toxin. BA was suspended in 1% soluble starch by continuous intragastric administration for 14 days, then the brain damage in mice was induced by a single intraperitoneal injection of T-2 toxin (4 mg/kg). It was found that BA alleviated the reduction of discrimination index in T-2 toxin-treated mice, and enhanced dopamine (DA), 5-hydroxytryptamine (5-HT), and acetylcholine (ACH) levels of brain neurotransmitter. Meanwhile, BA pretreatment ameliorated oxidative stress through increase of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px), and glutathione (GSH) levels, and inhibition of the generation of reactive oxygen species (ROS) and malondialdehyde (MDA) in the brain of mice exposed to T-2 toxin. Moreover, BA reduced brain hemorrhage and ecchymosis, improved the mitochondrial morphology, enriched the number of organelles, and inhibited cell apoptosis in brain challenged with T-2 toxin. Furthermore, BA inhibited mRNA expression of pro-inflammatory cytokines such as interleukin-1ß (IL-1ß), IL-6, and tumor necrosis factor-α (TNF-α) as well as enhanced mRNA expression of anti-inflammatory cytokine such as IL-10 in the brain of T-2 toxin-triggered mice. Therefore, BA could improve the cognitive function, enhance the antioxidant capacity, and inhibit the secretion of proinflammatory cytokines in brain, thereby playing a preventive and protective role against brain damage caused by T-2 toxin.

Metabolomic and transcriptomic investigation of the mechanism involved in enantioselective toxicity of imazamox in Lemna minor.

Imazamox (IM) is a chiral pesticide that has been widely used in agriculture. Currently, few studies have investigated the toxicity mechanisms of imazamox to aquatic macrophyte from the enantiomer level. In this study, the enantioselective effects of IM on the toxicity and physiological and biochemical system of aquatic macrophyte Lemna minor were systematically investigated. Metabolomic and transcriptomic for Lemna minor were used to identify potential mechanisms of toxicity. 7 d EC50s for racemic-, R-, and S-IM were 0.036, 0.035, and 0.203 mg/L, respectively, showing enantioselective toxicity. In addition, IM caused Lemna minor lipid peroxidation and antioxidant damage, and inhibited the activities of the target enzymes. Metabolomic and transcriptomic data indicated that R-IM interferenced differentially expressed genes and metabolites of Lemna minor which were enriched in carbon fixation during photosynthesis, glutathione metabolic pathway, pentose phosphate pathway, zeatin biosynthesis, and porphyrin and chlorophyll metabolism. S-IM affected phenylalanine metabolism, phenylpropanoid biosynthesis, zeatin biosynthesis and secondary metabolite biosynthesis. Racemic-IM influenced carbon fixation during operation, glutathione metabolic pathway, zeatin biosynthesis and pentose phosphate pathway. The results provide new insights into the enantioselective toxicity mechanisms of IM to Lemna minor, and lay the foundation for conducting environmental risk assessments.

[Magnetic foreign body in bilateral nasal cavity in children:a case report].

In recent years, with the increase of magnetic toys, the intake of magnetic foreign bodies is an increasing problem in pediatric emergency.The strong suction of the magnetic foreign body can lead to necrosis, perforation, and infection of surrounding tissues.The site of magnetic foreign body injury is mainly the esophagus, intestines, stomach, a few in the pharynx, etc.This requires early assessment and appropriate intervention to avoid further harm.Because of its unique physical properties, magnetic foreign bodies in bilateral nasal cavity are rarely reported. Now we have a case of a bilateral magnetic foreign body in the nasal cavity.

Betulinic Acid Ameliorates the T-2 Toxin-Triggered Intestinal Impairment in Mice by Inhibiting Inflammation and Mucosal Barrier Dysfunction through the NF-κB Signaling Pathway.

T-2 toxin, a trichothecene mycotoxin produced by Fusarium, is widely distributed in crops and animal feed and frequently induces intestinal damage. Betulinic acid (BA), a plant-derived pentacyclic lupane-type triterpene, possesses potential immunomodulatory, antioxidant and anti-inflammatory biological properties. The current study aimed to explore the protective effect and molecular mechanisms of BA on intestinal mucosal impairment provoked by acute exposure to T-2 toxin. Mice were intragastrically administered BA (0.25, 0.5, or 1 mg/kg) daily for 2 weeks and then injected intraperitoneally with T-2 toxin (4 mg/kg) once to induce an intestinal impairment. BA pretreatment inhibited the loss of antioxidant capacity in the intestine of T-2 toxin-treated mice by elevating the levels of CAT, GSH-PX and GSH and reducing the accumulation of MDA. In addition, BA pretreatment alleviated the T-2 toxin-triggered intestinal immune barrier dysregulation by increasing the SIgA level in the intestine at dosages of 0.5 and 1 mg/kg, increasing IgG and IgM levels in serum at dosages of 0.5 and 1 mg/kg and restoring the intestinal C3 and C4 levels at a dosage of 1 mg/kg. BA administration at a dosage of 1 mg/kg also improved the intestinal chemical barrier by decreasing the serum level of DAO. Moreover, BA pretreatment improved the intestinal physical barrier via boosting the expression of ZO-1 and Occludin mRNAs and restoring the morphology of intestinal villi that was altered by T-2 toxin. Furthermore, treatment with 1 mg/kg BA downregulated the expression of p-NF-κB and p-IκB-α proteins in the intestine, while all doses of BA suppressed the pro-inflammatory cytokines expression of IL-1ß, IL-6 and TNF-α mRNAs and increased the anti-inflammatory cytokine expression of IL-10 mRNA in the intestine of T-2 toxin-exposed mice. BA was proposed to exert a protective effect on intestinal mucosal disruption in T-2 toxin-stimulated mice by enhancing the intestinal antioxidant capacity, inhibiting the secretion of inflammatory cytokines and repairing intestinal mucosal barrier functions, which may be associated with BA-mediated inhibition of the NF-κB signaling pathway activation.

Relationship between enuresis and obstructive sleep apnea-hypopnea syndrome in children.

OBJECTIVE: We explored the relationship between enuresis and obstructive sleep apnea-hypopnea syndrome (OSAHS) in children and influencing factors of enuresis with OSAHS. METHODS: We recruited 196 children ≥5 years old from the otolaryngology outpatient department, who experienced snoring and underwent nasopharynx lateral radiography and in-laboratory polysomnography. We analyzed correlations between the apnea-hypopnea index (AHI) and lowest oxygen saturation (L-SaO2) with age, body mass index (BMI), tonsil size, and adenoidal-nasopharyngeal (A/N) ratio using the Pearson correlation test. Differences in severe OSAHS prevalence, age, AHI, L-SaO2, tonsil size, and A/N ratio between children with and without enuresis were assessed using the chi-square test and t-test. Risk factors of enuresis were analyzed using logistic regression. Follow-up was conducted to assess remission in children with enuresis after adenotonsillectomy. RESULTS: BMI, tonsil size, and A/N ratio were correlated with AHI and L-SaO2. Severe OSAHS prevalence, AHI, tonsil size, and A/N ratio were higher and L-SaO2 were lower in children with enuresis. Logistic regression showed that BMI, AHI, tonsil size, and sleep apnea were risk factors for enuresis. CONCLUSIONS: Our study findings showed that enuresis was associated with OSAHS in children. Adenotonsillectomy may improve the symptoms of enuresis.

Betulinic Acid Attenuates Oxidative Stress in the Thymus Induced by Acute Exposure to T-2 Toxin via Regulation of the MAPK/Nrf2 Signaling Pathway.

T-2 toxin, the most toxic of the trichothecenes, is widely found in grains and feeds, and its intake poses serious risks to the health of humans and animals. An important cytotoxicity mechanism of T-2 toxin is the production of excess free radicals, which in turn leads to oxidative stress. Betulinic acid (BA) has many biological activities, including antioxidant activity, which is a plant-derived pentacyclic triterpenoid. The protective effects and mechanisms of BA in blocking oxidative stress caused by acute exposure to T-2 toxin in the thymus of mice was studied. BA pretreatment reduced ROS production, decreased the MDA content, and increased the content of IgG in serum and the levels of SOD and GSH in the thymus. BA pretreatment also reduced the degree of congestion observed in histopathological tissue sections of the thymus induced by T-2 toxin. Besides, BA downregulated the phosphorylation of the p38, JNK, and ERK proteins, while it upregulated the expression of the Nrf2 and HO-1 proteins in thymus tissues. The results indicated that BA could protect the thymus against the oxidative damage challenged by T-2 toxin by activating Nrf2 and suppressing the MAPK signaling pathway.

Ferulic Acid Attenuates Hypoxia/Reoxygenation Injury by Suppressing Mitophagy Through the PINK1/Parkin Signaling Pathway in H9c2 Cells.

Ferulic acid protects against cardiac injury by scavenging free radicals. However, the role of mitophagy in ferulic acid-induced cardioprotection remains obscure. In the present study, H9c2 cells were exposed to hypoxia/reoxygenation and ferulic acid treatment during hypoxia. We illustrated the impact of ferulic acid on oxidative damage in H9c2 cells. Our results showed that ferulic acid significantly attenuated apoptosis induced by hypoxia/reoxygenation injury and reduced mitochondrial dysfunction, evidenced by a decline in the overproduction of reactive oxygen species and ATP depletion and recovery of the membrane potential. We also found that mitophagy, a selective form of autophagy, was excessively activated in H9c2 cells subjected to hypoxia/reoxygenation. Ferulic acid reduced the binding of mitochondria to lysosomes, down-regulated the PINK1/Parkin pathway, and was accompanied by increased p62 and decreased LC3-II/LC3-I levels. Ferulic acid also antagonistically reduced the activation of mitophagy by rapamycin. These findings suggest that ferulic acid may protect H9c2 cells against ischemia/reperfusion injury by suppressing PINK1/Parkin-dependent mitophagy. Accordingly, our findings may provide a potential target and powerful reference for ferulic acid in clinical prevention and treatment of hypoxia/reoxygenation injury.

Biocompatible Self-Healing Coating Based on Schiff Base for Promoting Adhesion of Coral Cells.

Layer-by-layer self-assembly (LBL) technique is a very efficient and convenient method to modify the substrate surface. In this study, we report a self-repairing surface coating that can promote cell adhesion, especially for enhancing the adhesion of coral cells on the basal surface. The results confirmed that the modified chitosan-dialdehyde starch film based on Schiff base has good biocompatibility for common mammalian cells, such as normal human dermal fibroblasts (NHDFs) and relatively special cells (coral cells). The cytotoxicity test indicated that the optical density values of the experimental group films at 490 nm were higher than those of the control group in this study. In addition, the self-repairing coating modified by phase transition lysozyme can maintain its adhesion ability underwater for a period of time. Therefore, they have great application on substrates requiring underwater adhesion. Our results confirmed that the modified chitosan-dialdehyde starch self-healing films could provide a biocompatible coating material to promote the adhesion of normal human epidermal fibroblasts or coral cells.

γ-Oryzanol suppresses cell apoptosis by inhibiting reactive oxygen species-mediated mitochondrial signaling pathway in H2O2-stimulated L02 cells.

γ-Oryzanol, a mixture of ferulic acid esters of plant sterols and triterpene alcohols existed in rice bran oil, can ameliorate lipid metabolism and enhance antioxidant activity. In this study, we used hydrogen peroxide (H2O2)-induced injury in human hepatic L02 cells to investigate the mechanisms involved in the hepatoprotective activity of γ-oryzanol. The injuries produced by H2O2 in L02 cells include increased levels of malondialdehyde (MDA) and intracellular reactive oxygen species (ROS), decreased activities of superoxide dismutase (SOD) and catalase (CAT), loss of mitochondrial membrane potential (MMP), increased protein expressions of caspase-9 and caspase-3, and induced apoptosis. Pretreatment with γ-oryzanol enhanced the ROS scavenging activity of endogenous antioxidant enzymes and decreased lipid peroxidation in H2O2 treated cells. Moreover, pretreatment with γ-oryzanol inhibited H2O2-induced apoptosis by restoring MMP, upregulating the expression ratio of Bcl-2/Bax, and inhibiting the activation of caspase-9 and caspase-3. These findings show that γ-oryzanol can prevent H2O2-induced apoptosis by suppressing intracellular accumulation of ROS and impeding ROS-activated mitochondrial apoptotic pathway.

Anti-inflammatory effect and potential mechanism of betulinic acid on λ-carrageenan-induced paw edema in mice.

λ-Carrageenan (Carr), a seaweed polysaccharide, is used as a proinflammatory agent in research. Betulinic acid (BA), a naturally occurring pentacyclic triterpenoid, exerts immunomodulatory, antioxidant, anti-inflammatory, antitumor, anti-malarial and anti-HIV effects. The aim of this study was to investigate whether BA exerts anti-inflammatory effect against Carr-induced paw edema in mice, and how BA could mediate the expression of inflammation-associated MAPK-COX-2-PGE2 signal pathway. BA pretreatment significantly reduced the inflammatory response to Carr-induced paw edema, especially at 4 h after injection. BA reduced the serum levels of pro-inflammatory cytokines, such as IL-1α, IL-1ß, IL-5, IL-6, GM-CSF, KC, MCP-1 and PGE2 in Carr-treated mice, and increased those of anti-inflammatory cytokines, such as IL-12. It also increased SOD, CAT and GSH-Px activities, and GSH content, and reduced MDA content in the liver of Carr-treated mice. Besides, BA reduced neutrophil infiltration in the basal and subcutaneous layers of the paw of Carr-treated mice, decreased the expression of COX-2 protein, and reduced the phosphorylation of JNK, p38 and ERK1/2. These results indicated that the protective effect of BA on Carr-induced paw edema might be due to its alleviation of inflammatory response and inhibition of oxidative stress, possibly by inhibiting MAPK-COX-2-PGE2 signaling pathway activation.

Human Parainfluenza Virus Type 3 Matrix Protein Reduces Viral RNA Synthesis of HPIV3 by Regulating Inclusion Body Formation.

Human parainfluenza virus type 3 is one of the main causes of lower respiratory illness in newborns and infants. The role of the matrix protein (M) in viral budding is extensively studied, but the effect of M on viral replication remains to be determined. Using an HPIV3 minigenome assay, we found that M reduced HPIV3 mingenome-encoded reporter activity even though it had an unspecific effect on the expression of cellular genes. Furthermore, the inhibition effect of M on viral RNA synthesis was proven to be independent of its virus-like particles (VLPs)' release ability. A VLP's defective mutant (ML302A) decreased the expression of minigenome reporter as wild type M did. Using an immunofluorescence assay, we found that M weakened the formation of inclusion bodies (IBs), although it did not co-localize with the IBs. Moreover, using another mutant, ML305A , which is defective in M-nucleoprotein (N) interaction, we found that ML305A had no effect on reporter activity and IB formation as the wild type of M did. Taken together, we conclude that M reduces the replication of HPIV3 and IB formation by M-N interaction.

An alanine residue in human parainfluenza virus type 3 phosphoprotein is critical for restricting excessive N0-P interaction and maintaining N solubility.

The phosphoprotein (P) of human parainfluenza virus type 3 (HPIV3) plays a pivotal role in viral RNA synthesis, which interacts with the nucleoprotein (N) to form a soluble N0-P complex (N0, free of RNAs) to prevent the nonspecific RNA binding and illegitimate aggregation of N. Functional regions within P have been studied intensively. However, the precise site (s) within P directly involved in N0-P interaction still remains unclear. In this study, using a series of deleted and truncated mutants of P of HPIV3, we demonstrate that amino-terminal 40 amino acids (aa) of P restrict and regulate N0-P interaction. Furthermore, using in vivo HPIV3 minigenome replicon assay, we identify a critical P mutant (PA28P) located in amino-terminal 40 aa, which fails to support RNA synthesis of HPIV3 minigenome replicon. Although PA28P maintains an enhanced N-P interaction, it is unable to form N0-P complex and keep N soluble, thus, resulting in aggregation and functional abolishment of N-P complex. Moreover, we found that recombinant HPIV3 with mutation of A28P in P failed to be rescued. Taken together, we identified a residue within the extreme amino-terminus of P, which plays a critical role in restricting the excessively N-P interaction and keeping a functional N0-P complex formation.