Change in proportion of extraction and non-extraction in orthodontic patients.

The purpose of this study was to determine whether there has been an increase in the number of non-extraction cases over recent years and investigate the selection of treatment devices. Patients attending the Department of Orthodontics at Tokyo Dental College Chiba Hospital in whom orthodontic treatment was commenced between July 1989 and July 1990 (Group A) or between June 1998 and May 2003 (Group B) were included in the study. The orthodontic diagnostic records of the patients were examined. Patients requiring orthognathic surgery, those with congenital diseases or cleft palate, and those with an uncertain diagnostic record were excluded. The characteristics, initial age, and classification of malocclusion in the two groups were almost the same. The patients in both groups were further divided into two subgroups: one in which treatment was commenced in mixed dentition and another in which it was begun in permanent dentition. The final therapeutic strategy, that is to say, non-extraction or extraction, was investigated in all groups. The final observation date in the mixed dentition group in Group B was September 2011. No major differences were observed in pattern or type of malocclusion between the two groups. Group B, however, showed an increased rate of non-extraction treatment. A policy of non-extraction was pursued in a higher proportion of patients in whom treatment was commenced in mixed dentition than in those in which it was begun in permanent dentition.

Polysaccharide-hair cationic polypeptide nanogels: self-assembly and enzymatic polymerization of amylose primer-modified cholesteryl poly(L-lysine).

In this study, we prepared a new associating polymer, ChMaPLL, by the substitution of the poly(L-lysine) moiety with oligosaccharide amylose primer and cholesterol. ChMaPLL formed positively charged polypeptide nanogels (~50 nm) via self-assembly in water. The nanogels showed a secondary structural transition to an α-helix structure induced by poly(L-lysine) in response to an increase in pH. Oligosaccharides of the nanogels reacted with the phosphorylase a enzyme. Amylose-conjugated nanogels were obtained by enzymatic polymerization. The elongation of the saccharide chain shielded the positive charge of the nanogels. The multiresponsive polysaccharide-polypeptide hybrid nanogels might prove to be useful in the areas of biotechnology and biomedicine.

CAPS1 is involved in hippocampal synaptic plasticity and hippocampus-associated learning.

Calcium-dependent activator protein for secretion 1 (CAPS1) is a key molecule in vesicular exocytosis, probably in the priming step. However, CAPS1's role in synaptic plasticity and brain function is elusive. Herein, we showed that synaptic plasticity and learning behavior were impaired in forebrain and/or hippocampus-specific Caps1 conditional knockout (cKO) mice by means of molecular, physiological, and behavioral analyses. Neonatal Caps1 cKO mice showed a decrease in the number of docked vesicles in the hippocampal CA3 region, with no detectable changes in the distribution of other major exocytosis-related molecules. Additionally, long-term potentiation (LTP) was partially and severely impaired in the CA1 and CA3 regions, respectively. CA1 LTP was reinforced by repeated high-frequency stimuli, whereas CA3 LTP was completely abolished. Accordingly, hippocampus-associated learning was severely impaired in adeno-associated virus (AAV) infection-mediated postnatal Caps1 cKO mice. Collectively, our findings suggest that CAPS1 is a key protein involved in the cellular mechanisms underlying hippocampal synaptic release and plasticity, which is crucial for hippocampus-associated learning.

Excitation of prefrontal cortical neurons during conditioning enhances fear memory formation.

Animals can remember a situation associated with an aversive event. Contextual fear memory is initially encoded and consolidated in the hippocampus and gradually consolidated in multiple brain regions over time, including the medial prefrontal cortex (PFC). However, it is not fully understood how PFC neurons contribute to contextual fear memory formation during learning. In the present study, neuronal activity was increased in PFC neurons utilizing the pharmacogenetic hM3Dq-system in male mice. We show that fear expression and memory formation are enhanced by increasing neuronal activity in PFC during conditioning phase. Previous studies showed that the activation of hM3Dq receptor in a subset of amygdala neurons enhanced fear memory formation and biased which neurons are allocated to a memory trace, in which immediate early gene c-fos was preferentially expressed following memory retrieval in these pre-activated neurons. In this study, hM3Dq activation in PFC could not change the probability of c-fos expression in pre-activated neurons flowing memory retrieval. Instead, the number c-fos positive neurons following memory retrieval was significantly increased in the basolateral amygdala. Our results suggest that neuronal activity in PFC at the time of learning modulates fear memory formation and downstream cellular activity at an early phase.