Intracellular cyclic nucleotides (cyclic adenosine monophosphate and cyclic guanosine monophosphate) and downstream cellular signal transduction are regulated by phosphodiesterases (PDEs). The neuroplasticity, neurotransmitter pathways, and neuroinflammation-controlling functions of PDEs were demonstrated in numerous in vitro and animal model studies. We comprehensively reviewed the literature regarding the expression of PDEs in various brain regions.Subsequently, articles regarding schizophrenia and PDEs were examined. The pathophysiological mechanisms of schizophrenia and PDEs in preclinical and clinical investigations are briefly reviewed. Particularly for those who do not respond to conventional antipsychotics, specific PDE inhibitors may offer innovative therapeutic alternatives. Although the connection between schizophrenia and PDEs is intriguing, additional research is required. Comprehending the brain’s PDE isoforms, their therapeutic potential, and any adverse effects of inhibiting them is essential for progress in this field.

Intracellular cyclic nucleotides (cyclic adenosine monophosphate and cyclic guanosine monophosphate) and downstream cellular signal transduction are regulated by phosphodiesterases (PDEs). The neuroplasticity, neurotransmitter pathways, and neuroinflammation-controlling functions of PDEs were demonstrated in numerous in vitro and animal model studies. We comprehensively reviewed the literature regarding the expression of PDEs in various brain regions.Subsequently, articles regarding schizophrenia and PDEs were examined. The pathophysiological mechanisms of schizophrenia and PDEs in preclinical and clinical investigations are briefly reviewed. Particularly for those who do not respond to conventional antipsychotics, specific PDE inhibitors may offer innovative therapeutic alternatives. Although the connection between schizophrenia and PDEs is intriguing, additional research is required. Comprehending the brain’s PDE isoforms, their therapeutic potential, and any adverse effects of inhibiting them is essential for progress in this field.

Intracellular cyclic nucleotides (cyclic adenosine monophosphate and cyclic guanosine monophosphate) and downstream cellular signal transduction are regulated by phosphodiesterases (PDEs). The neuroplasticity, neurotransmitter pathways, and neuroinflammation-controlling functions of PDEs were demonstrated in numerous in vitro and animal model studies. We comprehensively reviewed the literature regarding the expression of PDEs in various brain regions.Subsequently, articles regarding schizophrenia and PDEs were examined. The pathophysiological mechanisms of schizophrenia and PDEs in preclinical and clinical investigations are briefly reviewed. Particularly for those who do not respond to conventional antipsychotics, specific PDE inhibitors may offer innovative therapeutic alternatives. Although the connection between schizophrenia and PDEs is intriguing, additional research is required. Comprehending the brain’s PDE isoforms, their therapeutic potential, and any adverse effects of inhibiting them is essential for progress in this field.

Intracellular cyclic nucleotides (cyclic adenosine monophosphate and cyclic guanosine monophosphate) and downstream cellular signal transduction are regulated by phosphodiesterases (PDEs). The neuroplasticity, neurotransmitter pathways, and neuroinflammation-controlling functions of PDEs were demonstrated in numerous in vitro and animal model studies. We comprehensively reviewed the literature regarding the expression of PDEs in various brain regions.Subsequently, articles regarding schizophrenia and PDEs were examined. The pathophysiological mechanisms of schizophrenia and PDEs in preclinical and clinical investigations are briefly reviewed. Particularly for those who do not respond to conventional antipsychotics, specific PDE inhibitors may offer innovative therapeutic alternatives. Although the connection between schizophrenia and PDEs is intriguing, additional research is required. Comprehending the brain’s PDE isoforms, their therapeutic potential, and any adverse effects of inhibiting them is essential for progress in this field.

OBJECTIVE: To investigate the resistance to sliding (RS) in self-ligating and conventional ligation bracket systems at 5 different second-order bracket angulations by using low-stiffness alignment wires in a 3-bracket experimental model and to verify the performance of the main RS components in both systems when these wires are used. METHODS: Interactive self-ligating brackets with closed and open slides were used for the self-ligating (SL) and conventional ligation (CL) groups, respectively; elastomeric ligatures (1 mm inner diameter) were used in the latter system. The alignment wire used was 0.014 inch heat-activated NiTi (austenitic finish temperature set at 36degrees C by the manufacturer). A custom-made testing machine was used to measure frictional resistance. Tests were repeated 5 times at every angulation simulated. All data were analyzed statistically. RESULTS: The RS increased significantly with increasing angulation in both SL and CL groups (p < 0.0001). However, the RS values were significantly higher at every angulation (p < 0.0001) in the CL group. CONCLUSIONS: Despite the relevance of the binding phenomenon, ligation forces predominantly affect the RS when low-stiffness alignment wires are used.
Elastomers ; Friction ; Ligation ; Models, Theoretical ; Polymers

Neurologic symptoms that develop unconsciously and are incompatible with known pathophysiologic mechanisms or anatomic pathways belong to Conversion Disorder (CD). CD diagnosis is based on the clinical history and the exclusion of physical disorders causing significant distress or social and occupational impairment. In a subgroup of CD, called functional weakness (FW), symptoms affecting limbs may be persistent, thus causing a permanent or transient loss of limb function. Physiotherapy, pharmacotherapy, hypnotherapy and repetitive transcranial magnetic stimulation (rTMS) have been proposed as treatment strategies for FW-CD. Herein, we report a 30 year-old male, presenting with lower limb functional paraparesis, having obtained positive, objectively, and stable effects from a prolonged r-TMS protocol associated to a multidisciplinary approach, including psychological and sexuological counseling, and monitored by gait analysis. We postulate that our rTMS protocol, combined with a multidisciplinary approach may be the proper treatment strategy to improve FW-CD.
Brain* ; Conversion Disorder ; Counseling ; Diagnosis ; Drug Therapy ; Extremities ; Gait ; Humans ; Hypnosis ; Lower Extremity ; Male ; Neurologic Manifestations ; Paraparesis* ; Transcranial Magnetic Stimulation

No abstract available.
Dystonia*

Background: Ferric carboxymaltose (FCM) is a parenteral, dextran-free iron formulation designed to overcome the limitations of existing iron preparations. The main aim of this study was to retrospectively examine results obtained from a long period of FCM therapy in hemodialysis patients who have been previously treated with ferric gluconate (FX).Markers of iron metabolism, erythropoietin (EPO) doses, and effects on anemic status have been analysed. Methods: The study was performed with a follow up period of 4 years, when patients were treated before with FX and then switched to FCM. A total of 25 patients were included in the study. Results: FCM increased transferrin saturation (TSAT) levels by 11.9% (P < 0.001) with respect to FX. Events of TSAT less than 20% were reduced during FCM. The monthly dose of EPO was reduced in the FCM period (-6,404.1 international unit [IU]; 95% confidence interval, -10,643.5 IU; -2,164.6 IU; P = 0.003), as well as the erythropoietin resistance index (P = 0.004). During the period with FCM, ferritin levels were higher than during FX (P < 0.001), while transferrin was reduced (P = 0.001). Conclusion During FCM treatment, minor doses of EPO were administered if compared to those delivered during FX therapy. Stable and on target levels of hemoglobin were maintained with better control of anemia through high levels of ferritin and TSAT.

Objective: To identify the available evidence on the effects of rapid maxillary expansion (RME) with three-dimensional imaging and provide meta-analytic data from studies assessing the outcomes using computed tomography. Methods: Eleven electronic databases were searched, and prospective case series were selected. Two authors screened all titles and abstracts and assessed full texts of the remaining articles. Seventeen case series were included in the quantitative synthesis. Seven outcomes were investigated: nasal cavity width, maxillary basal bone width, alveolar buccal crest width, alveolar palatal crest width, inter-molar crown width, inter-molar root apex width, and buccopalatal molar inclination. The outcomes were investigated at two-time points: postexpansion (2–6 weeks) and post-retention (4–8 months). Mean differences and 95% confidence intervals were used to summarize and combine the data. Results: All the investigated outcomes showed significant differences postexpansion (maxillary basal bone width, +2.46 mm; nasal cavity width, +1.95 mm; alveolar buccal crest width, +3.90 mm; alveolar palatal crest width, +3.09 mm; intermolar crown width, +5.69 mm; inter-molar root apex width, +2.85 mm; and dental tipping, +3.75°) and post-retention (maxillary basal bone width, +2.21 mm; nasal cavity width, +1.55 mm; alveolar buccal crest width, +3.57 mm; alveolar palatal crest width, +3.32 mm; inter-molar crown width, +5.43 mm; inter-molar root apex width, +4.75 mm; and dental tipping, 2.22°) compared to pre-expansion. Conclusions After RME, skeletal expansion of the nasomaxillary complex was greater in most caudal structures. Maxillary basal bone showed 10% post-retention relapse. During retention period, uprighting of maxillary molars occurred.