Journal of Neurobiology and Physiology

Previous studies reported the axis of brain and heart, brain and intestine. The reality of the problem is not well addressed on molecular basis. In other words, it is not enough to think or point out to possible existence of such a link. We need to develop some philosophical approaches to put theoretical frames. 
One of the previous studies showed that the exposure to brain traumatic injury through falling caused death after several days in ICU in hospital. It was surprising that the case of death was attributed to heart rather than traumatic brain injury. This was explained by increased expression of inducible nitric oxide synthase (iNOS) in cardiac tissue as a response to its over-expression in brain. It seems that brain can tolerate this high degree of iNOS expression, but heart cannot. This was thought to breakdown the molecular environment of the heart and led to death [1].

During an action observation (AO) and action execution, specific group of neural substrates are activated. They provide a neural mechanism for understanding the actions of others called as mirror neurons (MNs) [2]. They also carry out motor grounding, motion ersatz, language and emotion appreciation. Mirror neurons discharge not only throughout the self-experience of pain but also during the perception of other people’s pain [3]. Neuroimaging studies carried out in humans while experiencing, as well as witnessing pain demonstrates activity in their anterior cingulate cortex (ACC).

Different computational models and new devices are under development, aiming to better comprehend and alter brain function. Ternary computating offers new approach by considering a third physiological state of the neuronal membrane: the refractory period (-1), in addition to resting potential state (0) and the action potential. As implants and trustworthy maps of the brain become more sophisticated due to a revolution in material science, new therapies emerge, with potential to treat chronic and often hard to treat neurological issues.

Stroke is among the leading causes of disability and mortality in many countries of the world. The pathogenic mechanisms of ischemic stroke are very complex and have not been completely understood. The aim of this study was to estimate the amino acid (AA) pool in the brain hemisphere cortex of rats during Subtotal Cerebral Ischemia (SCI). The changes in the pool of AAs and their derivatives in the frontal cortex of the cerebral hemispheres after 2-hour bilateral filament occlusion were studied in 18 rats. The analyses of the levels of AAs and their derivatives were carried out in the supernatant of protein-free tissue homogenates by reversed-phase liquid chromatography using an Agilent 1100 chromatograph.

During vascular neurointervention procedures, the use of double antiaggregation therapy (mainly acetylsalicylic acid and clopidogrel) is required to minimize the risk of thromboembolic complications. Since clopidogrel is one of the most widely used agents in the perioperative management of patients undergoing neurointervention processes, knowing its mechanism of action and the factors that determine its activation and metabolism is of great importance to ensure the correct antiaggregation of these patients.

Intravascular large B-cell lymphoma (IVLBCL) is a rare and specific variant of diffuse large B-cell lymphoma (DLBCL) [1,2]. Epstein-Barr virus (EBV)-positive IVLBCL is particularly rare and highly aggressive. Up to present, only a few cases of EBV-positive IVLBCL have been reported in the literature. Here, we would like to further explore its clinicopathological and molecular features to ensure the awareness and accurate diagnosis of this entity.

Diabetes is a metabolic disease that compromises the integrity of multiple organs and systems including the nervous system. Not only does neurodegeneration occur in peripheral nerves of diabetic subjects but also in brain structures. Particularly, diabetes impairs olfactory functions which suggests the alteration of regions of the central nervous system related with olfaction, however, few studies have shed light on the mechanisms that cause these alterations.

Individuals with spinal cord injury (SCI) have a significantly increased risk for cognitive impairment that is associated with cerebrovascular remodeling and endothelial dysfunction. The sub-acute stage following high thoracic SCI is characterized by increased fibrosis and stiffness of cerebral arteries. However, a more prolonged duration after SCI exacerbates cerebrovascular injury by damaging endothelium. Endothelial dysfunction is associated with reduced expression of transient receptor potential cation channel 4 that mediates the production of nitric oxide and epoxyeicosatrienoic acids following shear stress and the response to carbachol and other endothelium-dependent vasodilators.

Dopamine is used often in the NICU to increase cardiac output and blood pressure in neonates that are acutely ill. Dopamine is a catecholamine and as a short plasma half-life of approximately two minutes. It is interesting that the effect on the neonate is dosed dependent. In low doses (<2mcg/kg/min) vasodilation occurs as specific dopamine receptors are stimulated. In a moderate dose (2-10mcg/kg/min) there is additional stimulation of beta 1-adrenergic receptors which can result in improved cardiac contractility. If a higher dose is used (>10mcg/kg/min) alpha-adrenergic receptors become involved and there is an increase in vasoconstriction and peripheral resistance. This dose dependency pathophysiology only increases the complex interactions which make it difficult to predict neonatal effects.

The human brain is a complex network of billions of neurons accompanied by astrocytes and microglia among others [1]. Neurons communicate via specialized sites of cell-cell contacts called synapses, where information is transmitted via the presynaptic release of neurotransmitter from synaptic vesicles (SVs) [2]. Through the integration of information transmitted via large networks of neurons, complex tasks, such as learning, memory and various behaviors, are regulated. Hence synapses are very important functional units, operating largely autonomously, with the capacity to not only mediate neurotransmission but also undergo stable changes in synaptic strength whilst maintaining their own integrity.

In neurological diseases like diabetic neuropathy, Alzheimer’s disease, and schizophrenia, the expression of some genes such as caspase-3 and -9 and Bcl2 increases. Oxidative stress is one of the causes of Parkinson’s disease, multiple sclerosis, spongiform encephalopathy, Huntington’s disease, and amyotrophic lateral sclerosis. Silibinin, the powerful antioxidant without any side effects, can be used in treating of neurological diseases.

Computational Fluid Dynamics (CFD) is a well-established and accepted tool for simulation and prediction of complex physical phenomena e.g., in combustion, aerodynamics or blood circulation. Recently CFD has entered the medical field due to the readily available high computational power of current graphics processing units, GPUs. Efficient numerical codes, commercial or open source, are available now. Thus, a wide range of medical themes is available for CFD almost in real-time in the medical environment now. The available methods are on the point of reaching a usability status ready for everyday clinical use as a potential medical decision support system, provided adherence to the appropriate patient data protection rules and proper certification as a medical device.

This case study focuses on the clinical course of a patient who underwent decompressive surgery for an acute on chronic cervical spinal cord injury and developed white cord syndrome, a reperfusion injury, as a result of the decompression. This case study is the eighth recorded case of white cord syndrome reported globally at the time of writing this case report. Clinical pearls and some basic science explaining the mechanism of injury are presented along with best practices for the management of patients with this type of new onset neurological deterioration. Finally, the authors offer a call to action for further research in ensuring the best possible outcomes for patients.

Unusual presentations of disease states that have been well characterized over the years is key to ensuring the safety of patients and decreasing the overall mortality and morbidity. Patients often present with variations on classical conditions and it is key that providers be able to recognize these variations. This case study presents a 70-year-old female with a complex past medical history with variation of the classical Hakim-Adams triad of Normal Pressure Hydrocephalus. In this case, the patient’s symptoms included an increasingly depressed mood with some suicidal ideation, a potentially difficult to parse out gait disturbance, and urinary incontinence that had to be elucidated through conscious efforts. The patient was ultimately referred to neurosurgery for ventricular-peritoneal shunt placement. This case study includes a differential diagnosis with rationale for the different potential diagnoses, an in-depth look at the pathophysiology of Normal Pressure Hydrocephalus, the major treatment strategies, and highlights some clinical pearls for trainees and practicing providers.

Adrenarche, the post-natal onset of adrenal production of DHEA (dehydroepiandrosterone) and its sulfate (DHEA-S) marks the 5-8 transition and the onset of middle childhood. However, the role of DHEA and/or DHEA-S in the cognitive, emotional and physical changes of the so-called 5-8 transition are not well-understood. Recent findings from the U.S. NIH Normal Brain and Development Study clearly demonstrate a role for DHEA in the development of the dorsolateral prefrontal cortex, associated with executive function, and the right temporal parietal junction, associated with mentalization. In addition, results from the Australian Childhood to Adolescence Transition study implicate DHEA in increased anxiety during middle childhood through increased connectivity of the amygdala with the anterior cingulate cortex and insula, a circuit that underlies both bodily perception and emotion. At the cellular level, DHEA acts on the sigma-1 receptor to promote both glutamatergic transmission and the production of BDNF (brain derived neurotrophic factor), which in turn promotes activity-dependent synaptic plasticity.

The term “tandem spinal stenosis (TSS)” has been used to describe combined cervical and lumbar canal stenosis. We identified in our large series of cases that approximately 58% of cases with cervical canal stenosis were considered to be TSS, and 15% needed surgery for concurrent lumbar spinal canal stenosis (LCS) [1]. The simultaneous presence of thoracic canal stenosis and LCS is also frequently observed at a clinical site. As was discussed in the previous article, “Surgical outcomes of the thoracic ossification of ligamentum flavum: a retrospective analysis of 61 cases”, primary thoracic spinal stenosis is rare, and the thoracic ossification of ligamentum flavum (T-OLF) coincides with spinal spondylosis deformans, leading to a high incidence of tandem T-OLF and other stenosis lesions in the cervical (38%) or lumbar area (75%), sometimes with the ossification of ligaments [2]. The author outlined the clinical and radiological features of T-OLF, especially focusing on this high incidence of combined spinal stenosis, and comparing the clinical outcomes among surgical methods in the present article.

Humans are within the rare 5% of mammal species that have paternal investment [1]. The quantity and quality of paternal investment is facultative on environmental and social context [1-3]. Because paternal investment is facultative in nature, father presence is not necessarily critical for survival [4-6]. However, the presence and involvement of the father can provide socio-competitive advantages, and indicate valuable information about the safety and predictability of the environment that can have many downstream effects on development and health [7,8]. The safety and predictability of the environment is particularly critical in early childhood during the calibration of the hypothalamic-pituitary-adrenal axis (HPA-axis) and can shape sensitivity to stressors as children age, as discussed below [9-13].

Parkinson’s disease is a multifaceted illness that requires interdisciplinary approach to be fully addressed. The etiology of the disease is not completely understood, but genetic and environmental cues play important roles. Histological hallmarks of the disease are the accumulation of alpha-synuclein aggregates, mitochondrial changes and loss of dopaminergic neurons in the substantia nigra. The dopaminergic shortage leads to many motor and non-motor symptoms that affect patient quality of life. Current treatments are symptomatic only, for none can stop disease progression or cure it. Among them are intense physical exercise, dopaminergic drug intake, deep brain stimulation and the use of medical cannabis.

Rathke cleft cysts (RCC) are the embryological remnants of the pars intermedia within the Rathke’s pouch, and they represent the benign end of a spectrum of lesions originating from this region. RCCs are commonly small asymptomatic lesion; however, they often attain large size and exert mass effect on surrounding vital neurovascular structures, and hence become symptomatic. RCCs are the target of transsphenoidal surgery when symptomatic; however, surgical management of RCC is challenging, because aggressive resection may carry a high risk of complications - commonly diabetes insipidus (DI), due to the embryological proximity to the neurohypophysis – whereas sub-optimal resection may result in higher rates of cyst recurrence. In this commentary, we highlight nuances in diagnosis, and our philosophy to optimize surgical treatment of RCCs.

Although essential metal ions are required in the body, neurotoxicity occurs when exposed to a concentration of metal that the body cannot accommodate. In the case of non-essential metals which are important in industry, these elements have the property of causing neurotoxicity even at small concentrations. When such neurotoxicity progresses chronically, it can contribute to various neurodegenerative disorders, such as Alzheimer’s disease and Parkinson’s disease. Therefore, research on the relationships between neurotoxicity and metal metabolism are being actively conducted, and some recent research has suggested that the mechanisms of metal-induced neurotoxicity critically involve endoplasmic reticulum (ER) stress and mitochondrial dysfunction. Hence, this mini-review is to summarize some examples of such evidence and raise new questions in attempting to address metal-induced neurotoxicity with ER stress and mitochondria dysfunctions, two important topics for the effects of metals in neurodegenerative diseases.