Transcranial near-infrared light in treatment of neurodegenerative diseases.

Light is a natural agent consisting of a range of visible and invisible electromagnetic spectrum travels in waves. Near-infrared (NIR) light refers to wavelengths from 800 to 2,500 nm. It is an invisible spectrum to naked eyes and can penetrate through soft and hard tissues into deep structures of the human body at specific wavelengths. NIR light may carry different energy levels depending on the intensity of emitted light and therapeutic spectrum (wavelength). Stimulation with NIR light can activate intracellular cascades of biochemical reactions with local short- and long-term positive effects. These properties of NIR light are employed in photobiomodulation (PBM) therapy, have been linked to treating several brain pathologies, and are attracting more scientific attention in biomedicine. Transcranial brain stimulations with NIR light PBM in recent animal and human studies revealed a positive impact of treatment on the progression and improvement of neurodegenerative processes, management of brain energy metabolism, and regulation of chronic brain inflammation associated with various conditions, including traumatic brain injury. This scientific overview incorporates the most recent cellular and functional findings in PBM with NIR light in treating neurodegenerative diseases, presents the discussion of the proposed mechanisms of action, and describes the benefits of this treatment in neuroprotection, cell preservation/detoxification, anti-inflammatory properties, and regulation of brain energy metabolism. This review will also discuss the novel aspects and pathophysiological role of the glymphatic and brain lymphatics system in treating neurodegenerative diseases with NIR light stimulations. Scientific evidence presented in this overview will support a combined effort in the scientific community to increase attention to the understudied NIR light area of research as a natural agent in the treatment of neurodegenerative diseases to promote more research and raise awareness of PBM in the treatment of brain disorders.

Demographics of Astrocytoma in Central Texas: The Interaction Between Race, Histology, and Primary Tumor Site.

Introduction The epidemiological factors surrounding astrocytoma and gliomas have been studied with little avail. Even limited conclusions have not been reached in spite of significant past research efforts. Ionizing radiation is currently one of the only factors consistently associated with glioma formation. Studies in an attempt to link environmental and occupational exposures with brain neoplasms have continued to produce inconsistent results. This study aims to explore the distribution and epidemiology of astrocytomas within a Central Texas patient population in order to elucidate any possible differences in epidemiologic and prognostic factors based on race, histology, and primary tumor site. Methods Eight hundred forty-five clinical cases with the diagnosis of astrocytoma were retrospectively obtained from the tumor registry of the Scott & White Integrated Healthcare System from 1976 to 2014. We investigated the effects of gender, race, tumor histology, tumor site, treatment methods, and mortality of this cohort of patients in Central Texas. Results Prevalence data echoes that of the national epidemiology in that among our sample, White individuals had the highest prevalence (n=666, 78.8%), followed by Hispanics (n=94, 11.1%) and Black individuals (n=78, 9.2%). White patients had higher rates of parietal lobe (6.6% vs. 0.6%, p<0.01), brain overlapping (6.8% vs. 0.0%, p<0.01), and brainstem (5.9% vs. 1.7%, p=0.02) tumors. Black patients had higher rates of tumors located in brain (not otherwise specified) (35.9% vs. 15.7%, p<0.01) and cerebellum (33.3% vs. 5.6%, p<0.01). Hispanic patients had higher rates of tumor located in the temporal lobe (31.9% vs. 22.8%, p<0.05) and brain (not otherwise specified) (28.7% vs. 16.1%, p<0.01). Hispanics had the largest proportion of deaths (72.3% vs. 38.0%, p<0.01) when compared to the remainder of the sample, followed by White individuals (39.6% vs. 49.7%, p=0.02) and Black individuals (21.8% vs. 43.8%, p<0.01). Conclusions Discrepancies in mortality rates amongst various racial groups may be due to a number of factors. Primary tumor site and histology seem to indeed play a role in mortality and may present variably between ethnic groups. Mortality is also influenced by race, genetic predisposition, environmental and occupational exposure, and access to healthcare.

Cinnamaldehyde suppresses NLRP3 derived IL-1ß via activating succinate/HIF-1 in rheumatoid arthritis rats.

Cinnamaldehyde (CA) is an essential component of cinnamon (Cinnamomum cassia Presland), which is often used as a flavoring condiment in beverages, pastries, perfumes, etc. Cinnamon is also used as herbal medicine in China and Southeast Asia to treat rheumatoid arthritis. However, the molecular mechanism is unclear. In this study, we aim to investigate its anti-inflammatory effects against Rheumatoid arthritis (RA) using activated macrophages (Raw246.7) in vitro and adjuvant arthritis rats (AA) in vivo. The results demonstrated that CA significantly reduced synovial inflammation in AA rats, possibly due to suppression of the expressions of pro-inflammatory cytokines, especially the IL-1ß. Further investigation found that CA also suppressed the activity of HIF-1α by inhibiting the accumulation of succinate in cytoplasm. As we know, the reduction of HIF-1α nucleation slows down IL-1ß production, because HIF-1α activates the expression of NLRP3, which is involved in the assembly of inflammasome and processing of IL-1ß. In addition, CA also inhibited the expression of the succinate receptor GPR91, which in turn inhibited the activation of HIF-1α. In conclusions, our results suggested that CA might be a potential therapeutic compound to relieve rheumatoid arthritis progress by suppressing IL-1ß through modulating succinate/HIF-1α axis and inhibition of NLRP3.

The changing epidemiology of liver diseases in the Asia-Pacific region.

This Review presents current epidemiological trends of the most common liver diseases in Asia-Pacific countries. Hepatitis B virus (HBV) remains the primary cause of cirrhosis; despite declining prevalence in most Asian nations, this virus still poses a severe threat in some territories and regions. Mortality resulting from HBV infection is declining as a result of preventive measures and antiviral treatments. The epidemiological transition of hepatitis C virus (HCV) infection has varied in the region in the past few decades, but the medical burden of infection and the prevalence of its related cancers are increasing. The lack of licensed HCV vaccines highlights the need for novel treatment strategies. The prevalence of nonalcoholic fatty liver disease (NAFLD) has risen in the past decade, mostly owing to increasingly urbanized lifestyles and dietary changes. Alternative herbal medicine and dietary supplements are major causes of drug-induced liver injury (DILI) in some countries. Complications arising from these chronic liver diseases, including cirrhosis and liver cancer, are therefore emerging threats in the Asia-Pacific region. Key strategies to control these liver diseases include monitoring of at-risk populations, implementation of national guidelines and increasing public and physician awareness, in concert with improving access to health care.

Ocimum flavone Orientin as a countermeasure for thrombocytopenia.

Thrombocytopenia or chronic depletion of platelets in blood, could create life-threatening conditions in patients who receive aggressive systemic radiation and chemotherapy. Currently there are no approved agents for the rapid treatment of thrombocytopenia. In the present study, we demonstrate that administration of Orientin, a glycosidic flavonoid or dietary administration of Orientin containing Tulsi (Holy Basil) leaves, results in a significant increase in circulating platelets in a clinically relevant mouse model. No noticeable effects were observed on red blood cells, white blood cells or other hematologic parameters in treated animals indicating that Orientin specificity enhances platelet formation. The gene expression and immunophenotyping of bone marrow revealed that Orientin stimulates megakaryopoiesis specific transcriptional program. A significant increase in colony formation in bone marrow cells from Orientin pretreated mice further complemented the effect of Orientin on progenitor cells. The ex-vivo differentiation of irradiated human peripheral blood CD34+ stem cells demonstrated stimulatory effects of Orientin on megakaryocyte erythrocyte progenitors (MEP). The results show that Orientin, a non-toxic readily available natural product can counter platelet imbalances. Thrombocytopenia also develop as a consequence of multiple hematologic malignancies and side effects of treatments. Dietary supplementation of Orientin containing phytochemicals could be effective as countermeasures and viable therapeutics.

Catalpol protects synaptic proteins from beta-amyloid induced neuron injury and improves cognitive functions in aged rats.

Synapse loss is one of the common factors contributing to cognitive disorders, such as Alzheimer's disease (AD), which is manifested by the impairment of basic cognitive functions including memory processing, perception, problem solving, and language. The current therapies for patients with cognitive disorders are mainly palliative; thus, regimens preventing and/or delaying dementia progression are urgently needed. In this study, we evaluated the effects of catalpol, isolated from traditional Chinese medicine Rehmannia glutinosa, on synaptic plasticity in aged rat models. We found that catalpol markedly improved the cognitive function of aged male Sprague-Dawley rats and simultaneously increased the expression of synaptic proteins (dynamin 1, PSD-95, and synaptophysin) in the cerebral cortex and hippocampus, respectively. In beta-amyloid (Aß) injured primary rat's cortical neuron, catalpol did not increase the viability of neuron but extended the length of microtubule-associated protein 2 (MAP-2) positive neurites and reversed the suppressive effects on expression of synaptic proteins induced by Aß. Additionally, the effects of catalpol on stimulating the growth of MAP-2 positive neurites and the expression of synaptic proteins were diminished by a PKC inhibitor, bisindolylmaleimide I, suggesting that PKC may be implicated in catalpol's function of preventing the neurodegeneration induced by Aß. Altogether, our study indicates that catalpol could be a potential disease-modifying drug for cognitive disorders such as AD.

Hyperbaric oxygen therapy of spinal cord injury.

Spinal cord injury (SCI) is a complex disease process that involves both primary and secondary mechanisms of injury and can leave patients with devastating functional impairment as well as psychological debilitation. While no curative treatment is available for spinal cord injury, current therapeutic approaches focus on reducing the secondary injury that follows SCI. Hyperbaric oxygen (HBO) therapy has shown promising neuroprotective effects in several experimental studies, but the limited number of clinical reports have shown mixed findings. This review will provide an overview of the potential mechanisms by which HBO therapy may exert neuroprotection, provide a summary of the clinical application of HBO therapy in patients with SCI, and discuss avenues for future studies.

Traumatic Brain Injury pathophysiology and treatments: early, intermediate, and late phases post-injury.

Traumatic Brain Injury (TBI) affects a large proportion and extensive array of individuals in the population. While precise pathological mechanisms are lacking, the growing base of knowledge concerning TBI has put increased emphasis on its understanding and treatment. Most treatments of TBI are aimed at ameliorating secondary insults arising from the injury; these insults can be characterized with respect to time post-injury, including early, intermediate, and late pathological changes. Early pathological responses are due to energy depletion and cell death secondary to excitotoxicity, the intermediate phase is characterized by neuroinflammation and the late stage by increased susceptibility to seizures and epilepsy. Current treatments of TBI have been tailored to these distinct pathological stages with some overlap. Many prophylactic, pharmacologic, and surgical treatments are used post-TBI to halt the progression of these pathologic reactions. In the present review, we discuss the mechanisms of the pathological hallmarks of TBI and both current and novel treatments which target the respective pathways.