The neurocognitive basis of selfie-related behaviors in adolescents

Selfie-related behaviors which are accepted as only one of the results of social media addiction are known as selfie uploading, capturing selfie, sharing selfie, selfie posting and selfie editing and it also affects our daily life in every aspect. Neuro-behavioral studies which indicated the relationship between the behavior or addiction of heavy selfie takers and sharing them on social media and self-objectification, narcissism, and psychopathology have caused this current problem a syndrome feature such as a “Selfitis behaviors scale”. Screenagers-teenagers group constitutes a special risk group in selfie-related injuries and deaths owing to their high dynamic properties with especially in countries such as India where the adolescent population is high. Dangerous neurobehavioral acts related with problematic smartphone usage and selfie-related injuries are primarily associated with temporary distraction and the lack of self-awareness. Every behavior associated with many brain regions and it interacts each other in selfie-related behaviors. Through a multitude of afferent and efferent connections, prefrontal area is in mutual relationship with the other areas of cortex cerebri, namely thalamus, hypothalamus, basal ganglia, limbic system and cerebellum. We evaluated that the effects on adolescents of selfie-related behaviors with neurocognitive and behavioral perspective in this study.

Die neuromuskuläre Steuerung des Kaumechanismus und ihre Bedeutung für die Kieferorthopädie

ZusammenfassungDer Kaumechanismus gehört zu den kompliziertesten neuromuskulären Leistungen des menschlichen Organismus. Er setzt ein komplexes biologisches System mit einer optimalen multifaktoriellen Steuerung voraus. Dabei ist eine effektive afferente und efferente Innervation aller am Kaumechanismus beteiligten Strukturen sowie ihre optimale Koordination im Sinne eines neuromuskulären Regelkreises erforderlich. Der geregelte Ablauf der Kieferbewegungen wird durch neuronale Regelzyklen unter der Kontrolle des Cortex cerebri und subkortikaler Areale gesteuert. Dabei laufen alle Vorgänge der Steuerung in 3 Ebenen ab. In der lokalen Ebene registrieren Rezeptoren die lokale Situation, in der (sub)kortikalen Ebene werden Erregungen in Großhirnrinde und Basalganglien verarbeitet sowie die (extra)pyramidalen Bahnen formiert. Schließlich werden alle am Kauakt beteiligten Muskeln aktiviert. Fehlerhafte oder traumatische Okklusionskontakte, wie sie im Rahmen von Malokklusionen und bei erwachsenen Patienten im parodontal vorgeschädigten Gebiss auftreten, haben dabei das Potenzial, den neuromuskulären Regelkreis des stomatognathen Systems empfindlich zu verändern und Fehlregulationen auszulösen. Eine genaue Kenntnis der im Rahmen des Artikels besprochenen neuromuskulären Steuerung des Kaumechanismus ist daher für den Kieferorthopäden, der therapeutisch in dieses System eingreift, von großer Bedeutung.

Murine renal organic anion transporters mOAT1 and mOAT3 facilitate the transport of neuroactive tryptophan metabolites

Tryptophan metabolites such as kynurenate (KYNA), xanthurenate (XA), and quinolinate are considered to have an important impact on many physiological processes, especially brain function. Many of these metabolites are secreted with the urine. Because organic anion transporters (OATs) facilitate the renal secretion of weak organic acids, we investigated whether the secretion of bioactive tryptophan metabolites is mediated by OAT1 and OAT3, two prominent members of the OAT family. Immunohistochemical analyses of the mouse kidneys revealed the expression of OAT1 to be restricted to the proximal convoluted tubule (representing S1 and S2 segments), whereas OAT3 was detected in almost all parts of the nephron, including macula densa cells. In the mouse brain, OAT1 was found to be expressed in neurons of the cortex cerebri and hippocampus as well as in the ependymal cell layer of the choroid plexus. Six tryptophan metabolites, including the bioactive substances KYNA, XA, and the serotonin metabolite 5-hydroxyindol acetate inhibited [3H] p-aminohippurate (PAH) or 6-carboxyfluorescein (6-CF) uptake by 50–85%, demonstrating that these compounds interact with OAT1 as well as with OAT3. Half-maximal inhibition of mOAT1 occurred at 34 μM KYNA and 15 μM XA, and it occurred at 8 μM KYNA and 11.5 μM XA for mOAT3. Quinolinate showed a slight but significant inhibition of [3H]PAH uptake by mOAT1 and no alteration of 6-CF uptake by mOAT3. [14C]-Glutarate (GA) uptake was examined for both transporters and demonstrated differences in the transport rate for this substrate by a factor of 4. Trans-stimulation experiments with GA revealed that KYNA and XA are substrates for mOAT1. Our results support the idea that OAT1 and OAT3 are involved in the secretion of bioactive tryptophan metabolites from the body. Consequently, they are crucial for the regulation of central nervous system tryptophan metabolite concentration.