Increased Improvement in Speech-Language Skills After Transcranial Photobiomodulation Plus Speech-Language Therapy, Compared to Speech-Language Therapy Alone: Case Report with Aphasia.

Objective: This is a case report showing that transcranial photobiomodulation (tPBM) combined with traditional, speech-language therapy improved and accelerated the results from speech-language therapy, in a stroke person with aphasia (PWA). Background: tPBM is a safe, noninvasive technique using red and near-infrared light to improve the metabolism of cells. tPBM helps by promoting neuromodulation, while decreasing neuroinflammation and promoting vasodilation. Several studies have shown that tPBM can help individuals with stroke or traumatic brain injury achieve significant cognitive improvements. Methods: A 38-year-old female, who sustained an ischemic stroke on the left side of the brain, received two, 5-month series of treatments. The first series of treatments included traditional speech-language therapy, for the first 5 months poststroke. The second series of treatments included tPBM in combination with speech-language therapy, for the next 5 months. The tPBM treatments included application of red (630 and 660 nm) and near-infrared (850 nm) wavelengths of photons applied to left hemisphere scalp areas. The major cortical language areas were subjacent to the scalp placements along the line of the Sylvian fissure. At each session, first a light-emitting diode (LED) cluster head with red (630 and 660 nm) and near-infrared (850 nm) wavelengths, with an irradiance (power density) of 200 mW/cm2, a beam size of 4.9 cm2, and a fluence (energy density) of 12 J/cm2 per minute, was applied to the left side of the scalp/brain, along the Sylvian fissure for 60 sec at each at the following eight, language network target areas: frontal pole, prefrontal cortex, and inferior frontal gyrus (Broca's area); supramarginal gyrus and angular gyrus in the parietal lobe; inferior motor/sensory cortex (mouth area); and posterior superior temporal gyrus (Wernicke's area) and superior temporal sulcus in the temporal lobe, for a total of 8 min. Second, for the next 20 min (1200 sec), simultaneous with speech-language therapy, an LED PBM helmet was applied to the scalp/head. This helmet contained 256 separate LED lights, near-infrared (810 nm) wavelength, 60 mW power per LED light, total power, 15 W; energy, 72 Joules; fluence, 28.8 J/cm2; and irradiance, 24 mW/cm2. Results and conclusions: During the initial, 5-month treatment series with traditional speech-language therapy only, there was little to no improvement in dysarthria and expressive language. During the second, 5-month treatment series, however, with tPBM applied first, to the left hemisphere only, and second, to both hemispheres during each session plus simultaneous speech-language therapy, there was marked improvement in the dysarthria and expressive language. After the first 5-month series, this PWA had utilized a slow rate of speech with a production of ∼25 to 30 words-per-minute during conversations and spontaneous speech. Utterance length was only 4-6 words with simple, grammatical structure. After the second, 5-month series of treatment combining tPBM plus speech-language therapy, the rate of speech increased to 80+ words-per-minute and utterance length was increased to 9-10 words, with more complex grammatical structure.

New Ecuadorian records of the eyeless banjo catfish Micromyzon akamai (Siluriformes: Aspredinidae) expand the species range and reveal intraspecific morphological variation.

Two specimens of Micromyzon akamai, an eyeless and miniaturized species previously known only from the deep channels of the eastern Amazon basin in Brazil, are reported from the Curaray River, a tributary of the Napo River in Ecuador. The new specimens are the first records of Micromyzon in the headwaters of the Amazon River and the first records of M. akamai outside Brazil. External morphological characters and a phylogenetic analysis of cytochrome c oxidase I (coI) gene support the identification of the new specimens as M. akamai. Nevertheless, the new specimens also indicate that some features previously hypothesized to be apomorphic for M. akamai are intraspecifically variable.

Epicatechin Reduces Spatial Memory Deficit Caused by Amyloid-ß25⁻35 Toxicity Modifying the Heat Shock Proteins in the CA1 Region in the Hippocampus of Rats.

Alzheimer's disease (AD) is a neurodegenerative disorder characterized by dementia and the aggregation of the amyloid beta peptide (Aß). Aß25-35 is the most neurotoxic sequence, whose mechanism is associated with the neuronal death in the Cornu Ammonis 1 (CA1) region of the hippocampus (Hp) and cognitive damage. Likewise, there are mechanisms of neuronal survival regulated by heat shock proteins (HSPs). Studies indicate that pharmacological treatment with flavonoids reduces the prevalence of AD, particularly epicatechin (EC), which shows better antioxidant activity. The aim of this work was to evaluate the effect of EC on neurotoxicity that causes Aß25-35 at the level of spatial memory as well as the relationship with immunoreactivity of HSPs in the CA1 region of the Hp of rats. Our results show that EC treatment reduces the deterioration of spatial memory induced by the Aß25-35, in addition to reducing oxidative stress and inflammation in the Hp of the animals treated with EC + Aß25-35. Likewise, the immunoreactivity to HSP-60, -70, and -90 is lower in the EC + Aß25-35 group compared to the Aß25-35 group, which coincides with a decrease of dead neurons in the CA1 region of the Hp. Our results suggest that EC reduces the neurotoxicity induced by Aß25-35, as well as the HSP-60, -70, and -90 immunoreactivity and neuronal death in the CA1 region of the Hp of rats injected with Aß25-35, which favors an improvement in the function of spatial memory.

Influenza Virus Vaccination Elicits Poorly Adapted B Cell Responses in Elderly Individuals.

Influenza is a leading cause of death in the elderly, and the vaccine protects only a fraction of this population. A key aspect of antibody-mediated anti-influenza virus immunity is adaptation to antigenically distinct epitopes on emerging strains. We examined factors contributing to reduced influenza vaccine efficacy in the elderly and uncovered a dramatic reduction in the accumulation of de novo immunoglobulin gene somatic mutations upon vaccination. This reduction is associated with a significant decrease in the capacity of antibodies to target the viral glycoprotein, hemagglutinin (HA), and critical protective epitopes surrounding the HA receptor-binding domain. Immune escape by antigenic drift, in which viruses generate mutations in key antigenic epitopes, becomes highly exaggerated. Because of this reduced adaptability, most B cells activated in the elderly cohort target highly conserved but less potent epitopes. Given these findings, vaccines driving immunoglobulin gene somatic hypermutation should be a priority to protect elderly individuals.

Spec-seq unveils transcriptional subpopulations of antibody-secreting cells following influenza vaccination.

Vaccines are among the most effective public health tools for combating certain infectious diseases such as influenza. The role of the humoral immune system in vaccine-induced protection is widely appreciated; however, our understanding of how antibody specificities relate to B cell function remains limited due to the complexity of polyclonal antibody responses. To address this, we developed the Spec-seq framework, which allows for simultaneous monoclonal antibody (mAb) characterization and transcriptional profiling from the same single cell. Here, we present the first application of the Spec-seq framework, which we applied to human plasmablasts after influenza vaccination in order to characterize transcriptional differences governed by B cell receptor (BCR) isotype and vaccine reactivity. Our analysis did not find evidence of long-term transcriptional specialization between plasmablasts of different isotypes. However, we did find enhanced transcriptional similarity between clonally related B cells, as well as distinct transcriptional signatures ascribed by BCR vaccine recognition. These data suggest IgG and IgA vaccine-positive plasmablasts are largely similar, whereas IgA vaccine-negative cells appear to be transcriptionally distinct from conventional, terminally differentiated, antigen-induced peripheral blood plasmablasts.

Influenza Infection in Humans Induces Broadly Cross-Reactive and Protective Neuraminidase-Reactive Antibodies.

Antibodies to the hemagglutinin (HA) and neuraminidase (NA) glycoproteins are the major mediators of protection against influenza virus infection. Here, we report that current influenza vaccines poorly display key NA epitopes and rarely induce NA-reactive B cells. Conversely, influenza virus infection induces NA-reactive B cells at a frequency that approaches (H1N1) or exceeds (H3N2) that of HA-reactive B cells. NA-reactive antibodies display broad binding activity spanning the entire history of influenza A virus circulation in humans, including the original pandemic strains of both H1N1 and H3N2 subtypes. The antibodies robustly inhibit the enzymatic activity of NA, including oseltamivir-resistant variants, and provide robust prophylactic protection, including against avian H5N1 viruses, in vivo. When used therapeutically, NA-reactive antibodies protected mice from lethal influenza virus challenge even 48 hr post infection. These findings strongly suggest that influenza vaccines should be optimized to improve targeting of NA for durable and broad protection against divergent influenza strains.

Low CD21 expression defines a population of recent germinal center graduates primed for plasma cell differentiation.

In this study, we report that antigen-specific CD19+CD27+CD21lo (CD21lo) B cells are transiently induced 14 to 28 days after immunization, at the time germinal centers (GCs) peak. Although clonally related to memory B cells and plasmablasts, CD21lo cells form distinct clades within phylogenetic trees based on accumulated variable gene mutations, supporting exit from active GCs. CD21lo cells express a transcriptional program, suggesting that they are primed for plasma cell differentiation and are refractory to GC differentiation, although they do not spontaneously secrete antibody. In addition, CD21lo cells differentially express multiple cell surface markers and have elevated intracellular levels of Blimp-1 and T-bet protein compared with memory B cells. Together, these data support a model in which CD21lo cells are recent GC graduates that represent a distinct population from CD27+ classical memory cells, are refractory to GC reentry, and are predisposed to differentiate into long-lived plasma cells.

Alzheimer's disease and metabolic syndrome: A link from oxidative stress and inflammation to neurodegeneration.

Alzheimer's disease (AD) is the most common cause of dementia and one of the most important causes of morbidity and mortality among the aging population. AD diagnosis is made post-mortem, and the two pathologic hallmarks, particularly evident in the end stages of the illness, are amyloid plaques and neurofibrillary tangles. Currently, there is no curative treatment for AD. Additionally, there is a strong relation between oxidative stress, metabolic syndrome, and AD. The high levels of circulating lipids and glucose imbalances amplify lipid peroxidation that gradually diminishes the antioxidant systems, causing high levels of oxidative metabolism that affects cell structure, leading to neuronal damage. Accumulating evidence suggests that AD is closely related to a dysfunction of both insulin signaling and glucose metabolism in the brain, leading to an insulin-resistant brain state. Four drugs are currently used for this pathology: Three FDA-approved cholinesterase inhibitors and one NMDA receptor antagonist. However, wide varieties of antioxidants are promissory to delay or prevent the symptoms of AD and may help in treating the disease. Therefore, therapeutic efforts to achieve attenuation of oxidative stress could be beneficial in AD treatment, attenuating Aß-induced neurotoxicity and improve neurological outcomes in AD. The term inflammaging characterizes a widely accepted paradigm that aging is accompanied by a low-grade chronic up-regulation of certain pro-inflammatory responses in the absence of overt infection, and is a highly significant risk factor for both morbidity and mortality in the elderly.

Análisis de la resiliencia en personas divorciadas, según su nivel educativo e ingresos económicos / Analysis of resilience in divorced people according to their educational and income levels

Resumen El propósito de esta investigación fue identificar los niveles de resiliencia en personas divorciadas de acuerdo con el nivel educativo y los ingresos económicos. Para Gómez (2010), las situaciones adversas se afrontan mejor con adecuados niveles de resiliencia. El estudio contó con 139 parti cipantes divorciados, hombres (44,6 %), y mujeres (55,4 %); con estudios básicos (48,2 %), con estudios universitarios (51,8 %), con ingresos económicos inferiores a $1.800.000 (60,4 %), y superiores a $1.800.000 (39,6 %). Se utilizó una metodología cuantitativa, con diseño transversal, se corrieron Análisis de Varianza (ANOVA) con el fin de responder a las preguntas de investiga ción. Las personas con educación superior mostraron mayores niveles de resiliencia en compe tencia social y apoyo social, así mismo, los que tenían mayores ingresos económicos mostraron mayor fortaleza y confianza en sí mismos, competencia social, apoyo familiar y estructura; a su vez, se encontró un efecto de interacción entre el nivel de ingresos económicos y el nivel educativo en fortaleza y confianza en sí mismos. Para futuras investigaciones se sugiere profundizar en estos resultados a nivel cualitativo.

Abstract The purpose of this research was to identify levels of resilience in divorced people according to their education and income levels. For Gomez (2010), adverse situations are best dealt with ad equate levels of resilience. The study involved 139 divorced participants: divorced men (44.6 %) and women (55.4 %); with basic education (48.2 %), college educated (51.8 %), with an income of less than COP $1.8 million (60.4 %) and with an income higher than COP $1.8 million (39.6 %). The methodology was quantitative with a cross design and ANOVAS were run in order to answer the research questions. People with college education showed higher levels of resilience in social competence and social support. Furthermore, those with higher income showed greater strength and self-confidence, social competence, family support and structure. In addition, an effect was found between the interaction of levels of income and education level, and the in strength and self-confidence. For future research, it is suggested to deepen these results on qualitative level.

Aminoguanidine treatment ameliorates inflammatory responses and memory impairment induced by amyloid-beta 25-35 injection in rats.

Alzheimer disease (AD) is a neurodegenerative disorder caused by accumulation of the amyloid-beta peptide (Aß) in neuritic plaques. Its neurotoxic mechanisms are associated with inflammatory responses and nitrosative stress generation that promote expression of inducible nitric oxide synthase (iNOS) and increased nitric oxide causing neuronal death and memory impairment. Studies suggest that treatment with anti-inflammatory and anti-oxidant agents decreases the risk of developing AD. Aminoguanidine (AG) is an iNOS inhibitor with anti-inflammatory and anti-oxidant effects. In this study, we evaluated the effects of systemic administration of AG (100 mg/kg/day for 4 days) on spatial memory and inflammatory responses induced by an injection of Aß(25-35) [100 µM] into the temporal cortex (TCx) of rats. A significant improvement of spatial memory was evident in the Aß(25-35)-treated group at day 30 post-injection subjected to AG treatment; this effect was correlated with decreases in reactive gliosis, IL-1ß, TNF-α, and nitrite levels, as well as a reduction in neurodegeneration in the TCx and hippocampus (Hp). These results suggest that AG treatment inhibited glia activation and cytokine release, which may help to counteract neurodegenerative events induced by the toxicity of Aß.