Impaired speech input and output processing abilities in children with cleft palate speech disorder.

BACKGROUND: Cleft lip and palate is one of the most common oral and maxillofacial deformities associated with a variety of functional disorders. Cleft palate speech disorder (CPSD) occurs the most frequently and manifests a series of characteristic speech features, which are called cleft speech characteristics. Some scholars believe that children with CPSD and poor speech outcomes may also have weaknesses in speech input processing ability, but evidence is still lacking so far. AIMS: (1) To explore whether children with CPSD and speech output disorders also have defects in speech input processing abilities; (2) to explore the correlation between speech input and output processing abilities. METHODS & PROCEDURES: Children in the experimental group were enrolled from Beijing Stomatological Hospital, Capital Medical University, and healthy volunteers were recruited as controls. Then three tasks containing real and pseudo words were performed sequentially. Reaction time, accuracy and other indicators in three tasks were collected and then analysed. OUTCOMES & RESULTS: The indicators in the experimental group were significantly lower than those in the control group. There was a strong correlation between speech input and output processing tasks. The performance of both groups when processing pseudo words in the three tasks was worse than that when dealing with real words. CONCLUSIONS & IMPLICATIONS: Compared with normal controls, children with CPSD have deficits in both speech input and output processing, and there is a strong correlation between speech input and output speech processing abilities. In addition, the pseudo words task was more challenging than the real word task for both groups. WHAT THIS PAPER ADDS: What is already known on the subject Children with cleft lip and palate often have speech sound disorders known as cleft palate speech disorder (CPSD). CPSD is characterised by consonant errors called cleft speech characteristics, which can persist even after surgery. Some studies suggest that poor speech outcomes in children with CPSD may be associated with deficits in processing speech input. However, this has not been validated in mainland China. What this paper adds to existing knowledge The results of our study indicate that children with CPSD exhibit poorer performance in three tasks assessing speech input and output abilities compared to healthy controls, suggesting their deficits in both speech input and output processing. Furthermore, a significant correlation was observed between speech input and output processing abilities. Additionally, both groups demonstrated greater difficulty in processing pseudo words compared to real words, as evidenced by their worse performance in dealing with pseudo words. What are the potential or actual clinical implications of this work? The pseudo word tasks designed and implemented in our study can be employed in future research and assessment of speech input and output abilities in Chinese Mandarin children with CPSD. Additionally, our findings revealed the significance of considering both speech output processing abilities and potential existence of speech input processing ability for speech and language therapists when evaluating and developing treatment options for children with CPSD as these abilities are also important for the development of literacy development.

Articulation-Function-Associated Cortical Developmental Changes in Patients with Cleft Lip and Palate.

Cleft lip and palate (CLP) is one of the most common craniofacial malformations. Overall, 40-80% of CLP patients have varying degrees of articulation problems after palatoplasty. Previous studies revealed abnormal articulation-related brain function in CLP patients. However, the association between articulation disorders and cortical structure development in CLP patients remains unclear. Twenty-six CLP adolescents (aged 5-14 years; mean 8.88 years; female/male 8/18), twenty-three CLP adults (aged 18-35 years; mean 23.35 years; female/male 6/17), thirty-seven healthy adolescents (aged 5-16 years; mean 9.89 years; female/male 5/16), and twenty-two healthy adults (aged 19-37 years; mean 24.41 years; female/male 19/37) took part in the experiment. The current study aims to investigate developmental changes in cortical structures in CLP patients with articulation disorders using both structural and functional magnetic resonance imaging (MRI). Our results reveal the distinct distribution of abnormal cortical structures in adolescent and adult CLP patients. We also found that the developmental pattern of cortical structures in CLP patients differed from the pattern in healthy controls (delayed cortical development in the left lingual gyrus (t = 4.02, cluster-wise p < 0.05), inferior temporal cortex (z = -4.36, cluster-wise p < 0.05) and right precentral cortex (t = 4.19, cluster-wise p < 0.05)). Mediation analysis identified the cortical thickness of the left pericalcarine cortex as the mediator between age and articulation function (partial mediation effect (a*b = -0.48), 95% confident interval (-0.75, -0.26)). In conclusion, our results demonstrate an abnormal developmental pattern of cortical structures in CLP patients, which is directly related to their articulation disorders.

BET bromodomain inhibitor JQ1 promotes immunogenic cell death in tongue squamous cell carcinoma.

Drug resistance substantially limits the curative capability of chemotherapy in head and neck cancers such as oral squamous cell carcinoma. Immunosuppression is considered a potential cause of drug resistance. A key discovery in the past decade is that chemotherapeutics can alter tumor cell immunogenicity via inducing release of damage-associated molecular patterns (DAMPs), including ecto-calreticulin (ecto-CALR), high mobility group box 1 (HMGB1) and ATP, causing tumor cells to die in a manner known as bona fide immunogenic apoptosis or immunogenic cell death (ICD). Intriguingly, JQ1 was found in this study to exhibit therapeutic potential in tongue squamous cell carcinoma (TSCC) by inducing ICD. JQ1 induced significant release of calreticulin (CALR), HMGB1 and ATP from Cal27 and SCC7 cells in vitro. Immature dendritic cells (Im-DCs) cocultured with JQ1-pretreated Cal27 cells exhibited significant upregulation of mature markers on their surface and an increase in the secretion of cytokines. In vivo experiments demonstrated that JQ1-pretreated dying SCC7 cells protected immunocompetent mice from rechallenge of SCC7 cells. Intravenous injection of JQ1 efficiently reduced tumor growth and increased tumor-infiltration of CD3+/CD8+ T cells in C3H mice.