Endovascular Inferior Vena Cava Filters Placed in Duplicated Inferior Vena Cava Syndrome.

Duplicated inferior vena cava (D-IVC) is a relatively rare anatomical anomaly. Clinically, these anomalies are incidentally found on computed tomography (CT) or magnetic resonance imaging (MRI). Lack of pre-operative identification of this congenital malformation can lead to incomplete protection against thromboembolism or hemorrhage.

The 2023 Impact of Inflammatory Bowel Disease in Canada: Cancer and IBD.

Cancer is a major cause of morbidity and mortality among people with inflammatory bowel disease (IBD). Intestinal cancers may arise as a complication of IBD itself, while extra-intestinal cancers may arise due to some of the immunosuppressive therapies used to treat IBD. Colorectal cancer (CRC) and small bowel cancer risks remain elevated among persons with IBD as compared to age-and sex-matched members of the general population, and the lifetime risk of these cancers is strongly correlated to cumulative intestinal inflammatory burden.

Comparison of Osteopathic (DO) and Allopathic (MD) Candidates Matching Into Selected Surgical Subspecialties.

Context Medical students and graduates apply for post-graduate year-one positions every year through the Single Accreditation System (SAS) National Residency Match Program (NRMP). New opportunities have arisen for osteopathic graduates through the transition to a single match. There is a paucity of information evaluating the effects of this single match on osteopathic (DO) and allopathic (MD) candidates in relation to match rates in competitive surgical sub-specialties such as neurosurgery, thoracic surgery, vascular surgery, otolaryngology (ENT), plastic surgery, orthopedic surgery, and general surgery.

Social and emotional wellbeing among Indigenous Australian correctional officers.

The workplace challenges of correctional officers have been well documented. Yet little is known about how such stressors impact the wellbeing of correctional officers from minority cultural-subgroups. This study explored Indigenous Australian correctional officers' social and emotional wellbeing (SEWB) when managing workplace adversity.

Neurovascular unit pathology is observed very early in disease progression in the mutant SOD1 mouse model of amyotrophic lateral sclerosis.

Amyotrophic lateral sclerosis (ALS) is a debilitating neurodegenerative disease characterized by motor neuron degeneration that causes neuromuscular denervation, resulting in muscle weakness and atrophy. Work over the decades using ALS mouse models has revealed that while initial pathology may occur within motor neurons, disease pathology is cell non-autologous. Impairment of the blood-spinal cord barrier (BSCB) occurs before motor neuron frank degeneration; however, precisely when the early pathogenesis of the neurovascular units occurs is not fully understood.

Distance Learning in Surgical Education.

Background: Medical education has traditionally relied on in-person-based curriculums in medical school and residency . However, due to the COVID19 pandemic, medical schools and residency programs have been forced to rapidly transition to virtual platforms for learning. Surgical education poses a particular challenge, as virtual platforms cannot adequately replace hands-on learning of surgical skills.

Multi-omics analysis delineates the distinct functions of sub-cellular acetyl-CoA pools in Toxoplasma gondii.

Background: Acetyl-CoA is a key molecule in all organisms, implicated in several metabolic pathways as well as in transcriptional regulation and post-translational modification. The human pathogen Toxoplasma gondii possesses at least four enzymes which generate acetyl-CoA in the nucleo-cytosol (acetyl-CoA synthetase (ACS); ATP citrate lyase (ACL)), mitochondrion (branched-chain α-keto acid dehydrogenase-complex (BCKDH)) and apicoplast (pyruvate dehydrogenase complex (PDH)). Given the diverse functions of acetyl-CoA, we know very little about the role of sub-cellular acetyl-CoA pools in parasite physiology.

Adult Hippocampal Neurogenesis in Mammals (and Humans): The Death of a Central Dogma in Neuroscience and its Replacement by a New Dogma.

The review is a critical appraisal of the history and present status of the phenomenon of adult hippocampal neurogenesis (AHN) in the mammalian and human brain. Previous as well as most current studies of AHN have focused on highly inbred domestic mice and rats that are examined in rigorously controlled laboratory environments using psychology-based behavioral tests. However, this approach cannot reveal the adaptive significance of AHN, a key unresolved question in the field.

The sympathetic nervous system regulates skeletal muscle motor innervation and acetylcholine receptor stability.

Aim: Symptoms of autonomic failure are frequently the presentation of advanced age and neurodegenerative diseases that impair adaptation to common physiologic stressors. The aim of this work was to examine the interaction between the sympathetic and motor nervous system, the involvement of the sympathetic nervous system (SNS) in neuromuscular junction (NMJ) presynaptic motor function, the stability of postsynaptic molecular organization, and the skeletal muscle composition and function.

Methods: Since muscle weakness is a symptom of diseases characterized by autonomic dysfunction, we studied the impact of regional sympathetic ablation on muscle motor innervation by using transcriptome analysis, retrograde tracing of the sympathetic outflow to the skeletal muscle, confocal and electron microscopy, NMJ transmission by electrophysiological methods, protein analysis, and state of the art microsurgical techniques, in C57BL6, MuRF1KO and Thy-1 mice.

The Aftermath of the Fukushima Daiichi Accident: a Perspective from the British Embassy in Tokyo.

The British Embassy in Tokyo was at the heart of providing information in the immediate aftermath of the Fukushima Daiichi accident. Richard Oppenheim, who was present at the time, and Keith Franklin, who joined the Embassy shortly afterwards, give their perspectives on communicating information on radiation to the public and what lessons can be learned. Richard Oppenheim was head of the Climate Change and Energy team at the British Embassy in Tokyo from 2011 to 2015 and part of the Embassy team responding to the crisis.

Metabolic Needs and Capabilities of Toxoplasma gondii through Combined Computational and Experimental Analysis.

Toxoplasma gondii is a human pathogen prevalent worldwide that poses a challenging and unmet need for novel treatment of toxoplasmosis. Using a semi-automated reconstruction algorithm, we reconstructed a genome-scale metabolic model, ToxoNet1. The reconstruction process and flux-balance analysis of the model offer a systematic overview of the metabolic capabilities of this parasite.

BCKDH: the missing link in apicomplexan mitochondrial metabolism is required for full virulence of Toxoplasma gondii and Plasmodium berghei.

While the apicomplexan parasites Plasmodium falciparum and Toxoplasma gondii are thought to primarily depend on glycolysis for ATP synthesis, recent studies have shown that they can fully catabolize glucose in a canonical TCA cycle. However, these parasites lack a mitochondrial isoform of pyruvate dehydrogenase and the identity of the enzyme that catalyses the conversion of pyruvate to acetyl-CoA remains enigmatic. Here we demonstrate that the mitochondrial branched chain ketoacid dehydrogenase (BCKDH) complex is the missing link, functionally replacing mitochondrial PDH in both T.

Characterization of early pathogenesis in the SOD1(G93A) mouse model of ALS: part II, results and discussion.

Pathological events are well characterized in amyotrophic lateral sclerosis (ALS) mouse models, but review of the literature fails to identify a specific initiating event that precipitates disease pathology. There is now growing consensus in the field that axon and synapses are first cellular sites of degeneration, but controversy exists over whether axon and synapse loss is initiated autonomously at those sites or by pathology in the cell body, in nonneuronal cells or even in nonmotoneurons (MNs). Previous studies have identified pathological events in the mutant superoxide dismutase 1 (SOD1) models involving spinal cord, peripheral axons, neuromuscular junctions (NMJs), or muscle; however, few studies have systematically examined pathogenesis at multiple sites in the same study.

Characterization of early pathogenesis in the SOD1(G93A) mouse model of ALS: part I, background and methods.

Charcot first described amyotrophic lateral sclerosis (ALS) in 1869; however, its causes remain largely unknown and effective, long-term treatment strategies are not available. The first mouse model of ALS was developed after the identification of mutations in the superoxide dismutase 1 (SOD1) gene in 1993, and accordingly most of our knowledge of the etiology and pathogenesis of the disease comes from studies carried out using this animal model. Although numerous preclinical trials have been conducted in the mutant SOD1 mouse models, the results have been disappointing because they did not positively translate to clinical trials.

Functional genomics of Plasmodium falciparum using metabolic modelling and analysis.

Plasmodium falciparum is an obligate intracellular parasite and the leading cause of severe malaria responsible for tremendous morbidity and mortality particularly in sub-Saharan Africa. Successful completion of the P. falciparum genome sequencing project in 2002 provided a comprehensive foundation for functional genomic studies on this pathogen in the following decade.

Nicotinamide mononucleotide adenylyltransferase 2 (Nmnat2) regulates axon integrity in the mouse embryo.

Using transposon-mediated gene-trap mutagenesis, we have generated a novel mouse mutant termed Blad (Bloated Bladder). Homozygous mutant mice die perinatally showing a greatly distended bladder, underdeveloped diaphragm and a reduction in total skeletal muscle mass. Wild type and heterozygote mice appear normal.

Drp1-mediated mitochondrial dynamics and survival of developing chick motoneurons during the period of normal programmed cell death.

Mitochondrial morphology is dynamically remodeled by fusion and fission in neurons, and this process is implicated in nervous system development and pathology. However, the mechanism by which mitochondrial dynamics influence neuronal development is less clear. In this study, we found that the length of mitochondria is progressively reduced during normal development of chick embryo motoneurons (MNs), a process partly controlled by a fission-promoting protein, dynamin-related protein 1 (Drp1).

Motoneuron programmed cell death in response to proBDNF.

Motoneurons (MN) as well as most neuronal populations undergo a temporally and spatially specific period of programmed cell death (PCD). Several factors have been considered to regulate the survival of MNs during this period, including availability of muscle-derived trophic support and activity. The possibility that target-derived factors may also negatively regulate MN survival has been considered, but not pursued.

Evidence for the spontaneous production but massive programmed cell death of new neurons in the subcallosal zone of the postnatal mouse brain.

In the last 10 years, many studies have reported that neural stem/progenitor cells spontaneously produce new neurons in a subset of adult brain regions, including the hippocampus, olfactory bulb (OB), cerebral cortex, substantia nigra, hypothalamus, white matter and amygdala in several mammalian species. Although adult neurogenesis in the hippocampus and OB has been clearly documented, its occurrence in other brain regions is controversial. In the present study, we identified a marked accumulation of new neurons in the subcallosal zone (SCZ) of Bax-knockout mice in which programmed cell death (PCD) of adult-generated hippocampal and OB neurons has been shown to be completely prevented.

Motor neuron trophic factors: therapeutic use in ALS?

The modest effects of neurotrophic factor (NTF) treatment on lifespan in both animal models and clinical studies of Amyotropic Lateral Sclerosis (ALS) may result from any one or combination of the four following explanations: 1.) NTFs block cell death in some physiological contexts but not in ALS; 2.) NTFs do not rescue motoneurons (MNs) from death in any physiological context; 3.

Increased intramuscular nerve branching and inhibition of programmed cell death of chick embryo motoneurons by immunoglobulins from patients with motoneuron disease.

Massive programmed cell death (PCD) of developing chick embryo motoneurons (MNs) occurs in a well defined temporal and spatial sequence between embryonic day (E) 6 and E10. We have found that, when administered in ovo, either circulating immunoglobulins G (IgGs) or cerebrospinal fluid from patients with MN disease can rescue a significant number of chick embryo MNs from normally occurring PCD. An increase of branching of intramuscular nerves was also observed that may account for the rescuing effects of pathologic IgGs.

Acetylcholine negatively regulates development of the neuromuscular junction through distinct cellular mechanisms.

Emerging evidence suggests that the neurotransmitter acetylcholine (ACh) negatively regulates the development of the neuromuscular junction, but it is not clear if ACh exerts its effects exclusively through muscle ACh receptors (AChRs). Here, we used genetic methods to remove AChRs selectively from muscle. Similar to the effects of blocking ACh biosynthesis, eliminating postsynaptic AChRs increased motor axon branching and expanded innervation territory, suggesting that ACh negatively regulates synaptic growth through postsynaptic AChRs.