A Comparative Study of Traditional Technique Guide versus Virtual Reality in Orthopedic Trauma Training.

Background: Medical and surgical education is an expansive field fraught with many challenges. Technology such as virtual reality could be a new venue that can offer a solution to improve surgical training.

Objective: The objective of this prospective, blinded study was to evaluate virtual reality as a training model for orthopedic surgery and surgical training at large.

More than a marker: potential pathogenic functions of MAP2.

Microtubule-associated protein 2 (MAP2) is the predominant cytoskeletal regulator within neuronal dendrites, abundant and specific enough to serve as a robust somatodendritic marker. It influences microtubule dynamics and microtubule/actin interactions to control neurite outgrowth and synaptic functions, similarly to the closely related MAP Tau. Though pathology of Tau has been well appreciated in the context of neurodegenerative disorders, the consequences of pathologically dysregulated MAP2 have been little explored, despite alterations in its immunoreactivity, expression, splicing and/or stability being observed in a variety of neurodegenerative and neuropsychiatric disorders including Huntington's disease, prion disease, schizophrenia, autism, major depression and bipolar disorder.

Schizophrenia-associated differential DNA methylation in brain is distributed across the genome and annotated to MAD1L1, a locus at which DNA methylation and transcription phenotypes share genetic variation with schizophrenia risk.

DNA methylation (DNAm), the addition of a methyl group to a cytosine in DNA, plays an important role in the regulation of gene expression. Single-nucleotide polymorphisms (SNPs) associated with schizophrenia (SZ) by genome-wide association studies (GWAS) often influence local DNAm levels. Thus, DNAm alterations, acting through effects on gene expression, represent one potential mechanism by which SZ-associated SNPs confer risk.

Virtual Reality Training in Unicompartmental Knee Arthroplasty: A Randomized, Blinded Trial.

Objective: The objective of this study was to evaluate the effectiveness of immersive virtual reality training in orthopedic surgery education in comparison to the standard technique guide for fixed-bearing medial unicompartmental knee arthroplasty DESIGN: Participants included 22 orthopedic surgery residents who were randomized to undergo fixed-bearing medial unicompartmental knee arthroplasty (UKA) surgical training with either an immersive virtual reality technology or by studying the traditional technique guide. Participants were randomized within their training year via block randomization. Participants then performed a medial UKA on a SawBone model using standard industry system surgical trays and equipment.

Density of small dendritic spines and microtubule-associated-protein-2 immunoreactivity in the primary auditory cortex of subjects with schizophrenia.

Previously, we demonstrated that dendritic spine density (DSD) in deep layer 3 of the primary auditory cortex (A1) is lower, due to having fewer small spines, in subjects with schizophrenia (SZ) than non-psychiatric control (NPC) subjects. We also previously demonstrated that microtubule-associated-protein-2 immunoreactivity (MAP2-IR) in A1 deep layer 3 is lower, and positively correlated with DSD, in SZ subjects. Here, we first sought to confirm these findings in an independent cohort of 25 SZ-NPC subject pairs (cohort 1).

DNA methylation in the human frontal cortex reveals a putative mechanism for age-by-disease interactions.

A consistent gene set undergoes age-associated expression changes in the human cerebral cortex, and our Age-by-Disease Model posits that these changes contribute to psychiatric diseases by "pushing" the expression of disease-associated genes in disease-promoting directions. DNA methylation (DNAm) is an attractive candidate mechanism for age-associated gene expression changes. We used the Illumina HumanMethylation450 array to characterize genome-wide DNAm in the postmortem orbital frontal cortex from 20 younger (<42 years) and 19 older (>60 years) subjects.

Wound complications after open reduction and internal fixation of tibial plateau fractures in the elderly: a multicentre study.

Purpose: The incidence of wound complications after open reduction with internal fixation (ORIF) of tibial plateau fractures in young patients has been reported to range from approximately 5 to 15%. Reports on wound complication rates in the elderly patients are limited. This study investigates the incidence of post-operative wound complications in elderly patients undergoing ORIF of their tibial plateau fractures.

Acute Exertional Compartment Syndrome with Rhabdomyolysis: Case Report and Review of Literature.

BACKGROUND Acute exertional compartment syndrome (AECS) is a rare cause of leg pain often associated with a delay in diagnosis and potentially leading to irreversible muscle and nerve damage. CASE REPORT We present the case of a previously healthy, high-level athlete who presented with the acute onset of unilateral anterior leg pain and foot drop the day after a strenuous workout. He was diagnosed with compartment syndrome and rhabdomyolysis.

DNA methylation age is not accelerated in brain or blood of subjects with schizophrenia.

Individuals with schizophrenia (SZ) exhibit multiple premature age-related phenotypes and die ~20years prematurely. The accelerated aging hypothesis of SZ has been advanced to explain these observations, it posits that SZ-associated factors accelerate the progressive biological changes associated with normal aging. Testing the hypothesis has been limited by the absence of robust, meaningful, and multi-tissue measures of biological age.

Popliteal Artery Entrapment or Chronic Exertional Compartment Syndrome?

Diagnosis of lower limb pain in an athlete can be a challenging task due to the variety of potential etiologies and ambiguity of presenting symptoms. Five of the most commonly encountered causes of limb pain in athletes are chronic exertional compartment syndrome (CECS), medial tibial stress syndrome (MTSS), tibial stress fractures, soleal sling syndrome, and popliteal artery entrapment syndrome (PAES). Of these, the least frequent but potentially most serious of the pathologies is PAES.

DNA methylation evidence against the accelerated aging hypothesis of schizophrenia.

The accelerated aging hypothesis of schizophrenia posits that physiological changes throughout the body that are associated with normal aging occur at an earlier age in individuals with schizophrenia. Testing this hypothesis has been limited by problems measuring biological age. Recently, a method using DNA methylation levels at 353 genomic sites to produce "DNA methylation age", an estimate of tissue biological age, was described and validated.

A novel mouse model of the aged brain: Over-expression of the L-type voltage-gated calcium channel Ca1.3.

The aged population is growing rapidly, which has sparked tremendous interest in elucidating mechanisms of aging in both the body and the brain. Animal models have become an indispensable tool in biomedical science, but because of the cost and extended timeframe associated with aging animals to appropriate time points, studies that rely on using aged animals are often not feasible. Somewhat surprisingly, there are relatively few animal models that have been specifically engineered to mimic physiological changes known to occur during "normal" aging.

Hypermethylation of BDNF and SST Genes in the Orbital Frontal Cortex of Older Individuals: A Putative Mechanism for Declining Gene Expression with Age.

Expression of brain-derived neurotrophic factor (BDNF) and somatostatin (SST) mRNAs in the brain decreases progressively and robustly with age, and lower BDNF and SST expression in the brain has been observed in many brain disorders. BDNF is known to regulate SST expression; however, the mechanisms underlying decreased expression of both genes are not understood. DNA methylation (DNAm) is an attractive candidate mechanism.

The age-by-disease interaction hypothesis of late-life depression.

The phenomenologic diagnosis of depression is successful in increasing diagnostic reliability, but it is a classification scheme without biologic bases. One subtype of depression for which evidence suggests a unique biologic basis is late-life depression (LLD), with first onset of symptoms after the age of 65. LLD is common and poses a significant burden on affected individuals, caretakers, and society.

Age-by-disease biological interactions: implications for late-life depression.

Onset of depressive symptoms after the age of 65, or late-life depression (LLD), is common and poses a significant burden on affected individuals, caretakers, and society. Evidence suggests a unique biological basis for LLD, but current hypotheses do not account for its pathophysiological complexity. Here we propose a novel etiological framework for LLD, the age-by-disease biological interaction hypothesis, based on the observations that the subset of genes that undergoes lifelong progressive changes in expression is restricted to a specific set of biological processes, and that a disproportionate number of these age-dependent genes have been previously and similarly implicated in neurodegenerative and neuropsychiatric disorders, including depression.

Deletion of the L-type calcium channel Ca(V) 1.3 but not Ca(V) 1.2 results in a diminished sAHP in mouse CA1 pyramidal neurons.

Trains of action potentials in CA1 pyramidal neurons are followed by a prolonged calcium-dependent postburst afterhyperpolarization (AHP) that serves to limit further firing to a sustained depolarizing input. A reduction in the AHP accompanies acquisition of several types of learning and increases in the AHP are correlated with age-related cognitive impairment. The AHP develops primarily as the result of activation of outward calcium-activated potassium currents; however, the precise source of calcium for activation of the AHP remains unclear.

Impaired long-term potentiation and enhanced neuronal excitability in the amygdala of Ca(V)1.3 knockout mice.

Previously, we demonstrated that mice in which the gene for the L-type voltage-gated calcium channel Ca(V)1.3 is deleted (Ca(V)1.3 knockout mice) exhibit an impaired ability to consolidate contextually-conditioned fear.

L-type voltage-gated calcium channels in conditioned fear: a genetic and pharmacological analysis.

Using pharmacological approaches, others have suggested that L-type voltage-gated calcium channels (L-VGCCs) mediate both consolidation and extinction of conditioned fear. In the absence of L-VGCC isoform-specific antagonists, we have begun to investigate the subtype-specific role of LVGCCs in consolidation and extinction of conditioned fear using a molecular genetics approach. Previously, we used this approach to demonstrate that the Ca(v)1.

Conditional forebrain deletion of the L-type calcium channel Ca V 1.2 disrupts remote spatial memories in mice.

To determine whether L-type voltage-gated calcium channels (L-VGCCs) are required for remote memory consolidation, we generated conditional knockout mice in which the L-VGCC isoform Ca(V)1.2 was postnatally deleted in the hippocampus and cortex. In the Morris water maze, both Ca(V)1.

The L-Type voltage-gated calcium channel Cav1.3 mediates consolidation, but not extinction, of contextually conditioned fear in mice.

Using pharmacological techniques, it has been demonstrated that both consolidation and extinction of Pavlovian fear conditioning are dependent to some extent upon L-type voltage-gated calcium channels (LVGCCs). Although these studies have successfully implicated LVGCCs in Pavlovian fear conditioning, they do not provide information about the specific LVGCC isoform involved. Both of the major LVGCC subtypes found in the brain (Cav1.

Hippocampal pyramidal cells in adult Fmr1 knockout mice exhibit an immature-appearing profile of dendritic spines.

Fragile X syndrome (FXS) is a common form of mental retardation caused by the absence of functional fragile X mental retardation protein (FMRP). FXS is associated with elevated density and length of dendritic spines, as well as an immature-appearing distribution profile of spine morphologies in the neocortex. Mice that lack FMRP (Fmr1 knockout mice) exhibit a similar phenotype in the neocortex, suggesting that FMRP is important for dendritic spine maturation and pruning.

Dendritic spine abnormalities in the occipital cortex of C57BL/6 Fmr1 knockout mice.

Fragile X syndrome (FXS) is the most common form of inherited mental retardation. Observed neuropathologies associated with FXS include abnormal length, morphology, and density of dendritic spines, reported in individuals with FXS and in Fmr1 knockout (KO) mice, an animal model of FXS. To date, however, these neuropathologies have been studied in Fmr1 KO mice bred in a FVB background (a strain with genetic mutations that complicate interpretation of results) and findings have been inconsistent.

Experience effects on brain development: possible contributions to psychopathology.

Researchers and clinicians are increasingly recognizing that psychological and psychiatric disorders are often developmentally progressive, and that diagnosis often represents a point along that progression that is defined largely by our abilities to detect symptoms. As a result, strategies that guide our searches for the root causes and etiologies of these disorders are beginning to change. This review describes interactions between genetics and experience that influence the development of psychopathologies.