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The etiological significance of neurological disorders in autism is debated, but it is clear that they complicate support provision and clinical management, and can have negative impact on outcomes. This systematic review and meta-analysis explored the full range of co-occurring neurological disorders in autism. We estimated the odds of having neurological complications compared to the general population and other neurodevelopmental conditions, as well as the overall prevalence of different neurological disorders. Seventy-nine articles were eligible for the systematic review, including 28 case-control studies, 43 prevalence studies, and 8 cohort studies. Findings were heterogeneous across studies. Overall, autistic individuals were significantly more likely than the general population to exhibit epilepsy, macrocephaly, hydrocephalus, cerebral palsy, migraine/headache, and congenital abnormalities of the nervous system, with prevalence estimates ranging from 1.1% (0%–3.3%; hydrocephalus) to 14.2% (11.3%–17.2%; epilepsy). Epilepsy was also more common in autism than in attention-deficit/hyperactivity disorder (odds ratio [95% confidence interval] = 4.06 [2.81–5.88]). Findings indicate that awareness of neurological disorders and neurological check-ups are indicated in autism to ensure adequate physical health care and support. Prospective studies of neurological disorders in children diagnosed with or at risk of autism might further enhance our understanding of causal pathways. Neurological disorders, such as epilepsy and cerebral palsy, have been reported to occur among individuals with autism beyond chance and may have an impact on daily living across the lifespan. Although there has been research investigating neurological disorders in autism, the findings are not always conclusive. Previous summaries of existing studies have not evaluated the full range of neurological disorders. This study aimed to comprehensively explore the neurological problems appearing in autism to provide updated information that is needed for better healthcare and support in this population. We looked at already published studies focusing on risk or frequency of neurological disorders in autism. Our results suggest that individuals with autism are more likely than the general population to have a range of neurological disorders, including epilepsy, macrocephaly, hydrocephalus, cerebral palsy, migraine/headache, and inborn abnormalities of the nervous system. In order to provide individualized healthcare and support of high quality to individuals diagnosed with autism, health care professionals and other support providers need to be attentive to neurological complications. To further improve our understanding about the link between autism and neurological disorders, future research should follow the neurological health of children who are diagnosed with or are at increased likelihood of autism. [ABSTRACT FROM AUTHOR]

The article focuses on the association between caffeine consumption, ADHD, and pediatric headaches. Topics include increased caffeine consumption and its potential role in self-medication for ADHD symptoms, caffeine withdrawal headache in children and adolescents, and the mechanisms of caffeine-associated headaches, including adenosine receptor up-regulation and interference with the circadian system.

Background: Nucleophosmin/nucleoplasmin family 1 (NPM1) has broad physiological functions, such as DNA replication, transcription, ribosome biogenesis, and centrosome replication. This study explored the clinicopathological importance of NPM1 as a prognostic marker for oral squamous cell carcinoma (OSCC). Methods: We collected specimens from 96 OSCC, 45 oral epithelial dysplasia (OED), and 29 normal oral mucosa (NOM). NPM1 expression was analyzed via immunohistochemistry. Correlations between NPM1and clinical parameters were analyzed using Student t test, chi‐squared test, and Kaplan‐Meier product‐limit method. Results: The NPM1 labeling indices (LIs) were significantly higher in OSCCs than in NOM and oral OED. Higher NPM1 expression was significantly correlated with larger tumor size, nodal metastasis, and advanced clinical stage. Multivariate analysis revealed that higher NPM1 LIs were an unfavorable independent factor for survival. Conclusions: Upregulated NPM1 is an independent biomarker of poor prognosis and NPM1 inhibitors may be promising in molecular targeted therapy against OSCC. [ABSTRACT FROM AUTHOR]

Sleep disorders are known to increase the risk of hypertension, yet few studies have investigated the relation between sleep disorders and morning blood pressure (BP). This study aimed to determine, whether the morning BP is associated with sleep quality and sleep-disordered breathing. A total of 144 hypertensive patients were included in this cross-sectional study. Each subject underwent anthropometric measurements, biochemical testing, 24-h ambulatory BP monitoring, and polysomnography (PSG). Sleep quality and sleep-disordered breathing were determined by PSG parameters of sleep architecture and sleep respiratory. There were no significant differences between subjects with and without morning hypertension in the parameters of sleep architecture and sleep respiratory. In multiple regression analysis, morning BP was independently associated with night-time BP and morning BP surge, but not with the parameters of sleep architecture and sleep respiratory. Further analysis showed that both night-time BP and morning BP surge were independently associated with the sleep respiratory parameters. In conclusion, sleep-disordered breathing might indirectly affect the morning BP by elevated night-time BP, yet neither poor sleep quality nor sleep-disordered breathing was major determinants of elevated morning BP in hypertensive patients. [ABSTRACT FROM AUTHOR]

A reprogrammable transgenic mouse strain, called Col1a1 4F2A‐Oct4‐GFP, was bred for the present study. Because the somatic cells of this mouse strain contain only two copies of each Yamanaka factor, these animals are inefficient at producing induced pluripotent stem cells (iPSCs; approx. 0.005%) under traditional culture conditions. With an optimized culture condition, the iPSC production rate of mouse embryonic fibroblasts (MEFs) of Col1a1 4F2A‐Oct4‐GFP mice (MEFCol1a14F2A‐Oct4‐GFP) was increased to approximately 8%. Further, promotion of cell proliferation by serum supplementation did not enhance iPSC production. Inhibition of transforming growth factor β (TGF‐β) in the serum by SB431542 neither affected the growth rate of MEFCol1a14F2A‐Oct4‐GFP nor promoted iPSC production. However, the use of the gamma‐irradiated STO‐NEO‐LIF (γSNL) cells to serve as feeders for iPSC production resulted in a 5‐fold higher rate of iPSC production than the use of γMEFICR feeders. Interestingly, the use of SB431542 with the γMEFICR‐adopted system could eliminate this difference. RT‐PCR‐based comparative analysis further demonstrated that TGF‐β expression was 10‐fold higher in γMEFICR than in γSNL cells. Consistent with previous reports, mesenchymal to epithelial transition was found to participate in the initial steps of reprogramming in the specific context of MEFCol1a14F2A‐Oct4‐GFP. Moreover, we found that the initial seeding density is one of the pivotal factors for determining a high efficiency of iPSC generation. The iPSCs efficiently generated from our MEFCol1a14F2A‐Oct4‐GFP resembled mouse embryonic stem cells (mESCs) in aspects of teratoma formation and germline transmission. Depending on the culture conditions, our Col1a1 4F2A‐Oct4‐GFP mouse system can generate bona fide iPSCs with variable efficiencies, which can serve as a tool for interrogating the route taken by cells during somatic reprogramming. [ABSTRACT FROM AUTHOR]

The aim of the present study was to investigate the pharmacokinetic effect of silibinin on methadone in rats. Twenty‐four male Sprague–Dawley rats were randomly divided into 4 groups: control group, single dose of 100 mg/kg group, multiple doses of 100 mg/kg group, and multiple doses of 30 mg/kg group. A single dose of 6 mg/kg methadone was administrated to rats orally without or with silibinin. Plasma samples were collected via tail vein at different time points and concentrations of methadone and its metabolite, 2‐ethylidene‐1,5‐dimethyl‐3,3‐diphenylpyrrolidine (EDDP), were determined by ultra performance liquid chromatography–tandem mass spectrometry (UPLC–MS/MS). Compared with the control group (without silibinin), both 30 and 100 mg/kg silibinin significantly increased the Cmax of methadone, but only 100 mg/kg silibinin significantly increased the AUC(0‐t) of methadone and decreased its clearance. Pharmacokinetics parameters of EDDP were not altered by 30 mg/kg silibinin; its Tmax was decreased by 100 mg/kg silibinin and the Cmax was increased by single dose of 100 mg/kg silibinin. It is concluded that silibinin significantly altered the pharmacokinetics of methadone in rats by increasing the exposure of methadone. Further investigations in human should be conducted. Therapeutic drug monitoring of methadone in individuals undergoing methadone maintenance therapy is recommended when silibinin is concomitant. [ABSTRACT FROM AUTHOR]