Comunicación asertiva, estado nutricional y desarrollo físico en adultos mayores / Assertive Communication; Nutritional Status and Physical Development in Aged Adults

Introducción: La asertividad es una herramienta comunicacional que puede contribuir de manera positiva en que los adultos mayores interpreten correctamente la necesidad e importancia de realizar acciones que permitan mantener un adecuado desarrollo físico y estado nutricional durante la tercera edad. Objetivo: Describir cómo la implementación de la comunicación asertiva puede ayudar a la incorporación de los adultos mayores al programa de actividades físicas del adulto mayor. Métodos: Se realizó una investigación básica, no experimental y descriptiva en una población de 157 adultos mayores, de los cuales 113 formaron parte de la muestra de investigación. Se aplicó la comunicación asertiva para lograr la incorporación de estos al programa de actividades físicas del adulto mayor. Resultados: El miedo al contagio con COVID-19 fue la principal causa referida para no participar en las actividades (17,70 por ciento). Predominaron los adultos mayores con nivel de conocimiento bajo sobre la importancia de las actividades físicas en los adultos mayores. Después de aplicar la comunicación asertiva se logró que el 64,60 por ciento de los ancianos se incorporaran al programa. Conclusiones: La asertividad, con sus técnicas y acciones, facilitó la incorporación de adultos mayores al programa de actividades físicas. Su aplicación se basó en la preparación y la capacidad de negociación con las personas de la tercera edad para poder lograr su incorporación a las actividades físicas del programa del adulto mayor(AU)

Introduction: Assertiveness is a communicational tool that can contribute positively to aged adults' correct interpretation of the need and importance of performing actions that allow them to maintain adequate physical development and nutritional status during older age. Objective: To describe how the implementation of assertive communication can help the incorporation of aged adults to the physical activity program for the elderly. Methods: A basic, nonexperimental and descriptive research was conducted with a population of 157 aged adults, of which 113 were part of the research sample. Assertive communication was applied to achieve their incorporation into the physical activity program for the elderly. Results: Fear of infection with COVID-19 was the main reported cause for not participating in the activities (17.70 percent). Aged adults with a low level of knowledge about the importance of physical activities for the elderly predominated. After applying assertive communication, 64.60 percent of the older adults could become part of the program. Conclusions: Assertiveness, with its techniques and actions, facilitated the incorporation of aged adults to the physical activities program. Its application was based on the preparation and the ability to negotiate with older adults in order to achieve their incorporation to the physical activities of the program for the elderly(AU)

Review: Unveiling the effect of beta-nerve growth factor on the reproductive function in llamas and cows.

The actions of the beta-nerve growth factor (ß-NGF) on the neuroendocrine and reproductive system have challenged classical views on the control of reproductive function. After endometrial absorption, ß-NGF triggers ovulation and promotes the development of functional corpora lutea in camelids. In this article, we review evidence showing that, in camelids, ß-NGF exerts its actions by acting in both the hypothalamus and the ovary. In the hypothalamus, ß-NGF may induce gonadotropin-releasing hormone (GnRH) release by interacting with neurons or glial cells expressing receptors for ß-NGF. The LH surge occurs under the influence of ovarian estradiol and requires the release of GnRH into the portal vessels to reach the pituitary gland. In the ovary, ß-NGF may be promoting the differentiation of follicular to luteal cells by modifying the steroidogenic profile of ovarian follicular cells in both camelids and ruminants. Although the mechanisms for these actions are largely undetermined, we aim to offer an update on the current understanding of the effects of ß-NGF controlling reproductive function in camelids and ruminants.

Palbociclib-Induced Cellular Senescence Is Modulated by the mTOR Complex 1 and Autophagy.

Despite not dividing, senescent cells acquire the ability to synthesize and secrete a plethora of bioactive molecules, a feature known as the senescence-associated secretory phenotype (SASP). In addition, senescent cells often upregulate autophagy, a catalytic process that improves cell viability in stress-challenged cells. Notably, this "senescence-related autophagy" can provide free amino acids for the activation of mTORC1 and the synthesis of SASP components. However, little is known about the functional status of mTORC1 in models of senescence induced by CDK4/6 inhibitors (e.g., Palbociclib), or the effects that the inhibition of mTORC1 or the combined inhibition of mTORC1 and autophagy have on senescence and the SASP. Herein, we examined the effects of mTORC1 inhibition, with or without concomitant autophagy inhibition, on Palbociclib-driven senescent AGS and MCF-7 cells. We also assessed the pro-tumorigenic effects of conditioned media from Palbociclib-driven senescent cells with the inhibition of mTORC1, or with the combined inhibition of mTORC1 and autophagy. We found that Palbociclib-driven senescent cells display a partially reduced activity of mTORC1 accompanied by increased levels of autophagy. Interestingly, further mTORC1 inhibition exacerbated the senescent phenotype, a phenomenon that was reversed upon autophagy inhibition. Finally, the SASP varied upon inhibiting mTORC1, or upon the combined inhibition of mTORC1 and autophagy, generating diverse responses in cell proliferation, invasion, and migration of non-senescent tumorigenic cells. Overall, variations in the SASP of Palbociclib-driven senescent cells with the concomitant inhibition of mTORC1 seem to depend on autophagy.

Síndrome ansioso depresivo en pacientes con enfermedades reumáticas

Introducción: Las enfermedades reumáticas son conocidas por su carácter sistémico, afectando distintos órganos y sistemas de órganos. La afectación neuropsiquiátrica es frecuente y condiciona discapacidad adicional. El síndrome ansioso depresivo constituye una de las principales expresiones de afectación del sistema nervioso. Objetivo: Describir las características clínicas y epidemiológicas de presentación del síndrome ansioso depresivo en pacientes con enfermedades reumáticas. Métodos: Se realizó una investigación básica, con diseño no experimental, descriptivo, transversal y de campo. El universo estuvo constituido por 557 pacientes con diagnóstico de enfermedades reumáticas atendidos en el Hospital Clínica Metropolita de la ciudad de Riobamba durante el periodo enero 2020 - diciembre 2022. La muestra quedó constituida por un total de 229 pacientes. Resultados: Promedio de edad de 53,48 años, predominio de pacientes femeninas (72,49 %) y con comorbilidades asociadas (56,77 %). El hipotiroidismo (39,23 %), la hipertensión arterial (33,08 %) y la diabetes mellitus (21,54 %) fueron las comorbilidades más representadas. La artritis reumatoide (67,68 %) fue la enfermedad reumática que con mayor frecuencia fue identificada. El 42,36 % de los pacientes presentó manifestaciones de ansiedad y el 36,68 % manifestaciones clínicas compatibles con depresión. Conclusiones: Se identificaron porcentajes elevados de pacientes con enfermedades reumáticas y manifestaciones clínicas compatibles con ansiedad y depresión; en los pacientes con lupus eritematoso sistémico fue donde se identificó un mayor porcentaje de presentación de estas manifestaciones.

Introduction: Rheumatic diseases are known for their systemic nature, affecting different organs and organ systems. Neuropsychiatric involvement is frequent and conditions additional disability. Anxious-depressive syndrome is one of the main expressions of affectation of the nervous system. Objective: To describe the clinical and epidemiological characteristics of the presentation of the anxious-depressive syndrome in patients with rheumatic diseases. Methods: A basic investigation was carried out, with a non-experimental, descriptive, cross-sectional and field design. The universe consisted of 557 patients diagnosed with rheumatic diseases treated at the Hospital Clinica Metropolitana in the city of Riobamba during the period January 2020 - December 2022. The sample was made up of a total of 229 patients. Results: Average age of 53.48 years, predominance of female patients (72.49 %) and with associated comorbidities (56.77 %). Hypothyroidism (39.23%), arterial hypertension (33.08 %) and diabetes mellitus (21.54 %) were the most represented comorbidities. Rheumatoid arthritis (67.68 %) was the rheumatic disease that was most frequently identified. 42.36 % of the patients presented manifestations of anxiety and 36.68 % clinical manifestations compatible with depression. Conclusions: High percentages of patients with rheumatic diseases and clinical manifestations compatible with anxiety and depression were identified; a higher percentage of presentation of these manifestations was identified in patients with systemic lupus erythematosus.

Platelets and endothelial dysfunction in gestational diabetes mellitus.

The prevalence of gestational diabetes mellitus (GDM) has increased in recent years, along with the higher prevalence of obesity in women of reproductive age. GDM is a pathology associated with vascular dysfunction in the fetoplacental unit. GDM-associated endothelial dysfunction alters the transfer of nutrients to the foetus affecting newborns and pregnant women. Various mechanisms for this vascular dysfunction have been proposed, of which the most studied are metabolic alterations of the vascular endothelium. However, different cell types are involved in GDM-associated endothelial dysfunction, including platelets. Platelets are small, enucleated cell fragments that actively take part in blood haemostasis and thrombus formation. Thus, they play crucial roles in pathologies coursing with endothelial dysfunction, such as atherosclerosis, cardiovascular diseases, and diabetes mellitus. Nevertheless, platelet function in GDM is understudied. Several reports show a potential relationship between platelet volume and mass with GDM; however, platelet roles and signaling mechanisms in GDM-associated endothelial dysfunction are unclear. This review summarizes the reported findings and proposes a link among altered amount, volume, mass, reactivity, and function of platelets and placenta development, resulting in fetoplacental vascular dysfunction in GDM.

Polineuropatía por amiloidosis por transtiretina de inicio tardío. Caso clínico / Late-onset hereditary transthyretin amyloidosis with polyneuropathy. Report of one case

Hereditary transthyretin amyloidosis is a multisystemic autosomal dominant genetic disorder characterized by progressive distal sensory-motor polyneuropathy or restrictive cardiomyopathy, secondary to amyloid deposits. Its pathogenesis lies in the TTR gene mutation, and the Val50Met mutation is the most frequent. Patients have significant differences in the onset and severity of clinical presentation according to their country of origin. The diagnosis of this pathology is complex, even more in countries where it is not considered endemic. However, early suspicion and management are essential to improve survival and avoid unnecessary diagnostic and therapeutic strategies. We report a 69-year-old woman who presented a sensory-motor polyneuropathy, predominantly sensory, associated with distal neuropathic pain and bilateral vitritis. The history of her Italian father with polyneuropathy of unspecified etiology stood out. A vitreous biopsy identified amyloid substance deposits (congo red positive). These were also confirmed on a superficial peroneal nerve biopsy. During the etiological study of her polyneuropathy, an increased Kappa/Lambda index of 2.55 mg/L stood out. Therefore, light chain amyloidosis was suspected, and chemotherapy treatment was indicated without favorable response. After 10 years of progressive neurological and ophthalmological involvement, a genetic study confirmed the first case of late-onset hereditary transthyretin amyloidosis Val50Met with polyneuropathy in Chile.

A RUL Estimation System from Clustered Run-to-Failure Degradation Signals.

The prognostics and health management disciplines provide an efficient solution to improve a system's durability, taking advantage of its lifespan in functionality before a failure appears. Prognostics are performed to estimate the system or subsystem's remaining useful life (RUL). This estimation can be used as a supply in decision-making within maintenance plans and procedures. This work focuses on prognostics by developing a recurrent neural network and a forecasting method called Prophet to measure the performance quality in RUL estimation. We apply this approach to degradation signals, which do not need to be monotonical. Finally, we test our system using data from new generation telescopes in real-world applications.

Platelets, a Key Cell in Inflammation and Atherosclerosis Progression.

Platelets play important roles in thrombosis-dependent obstructive cardiovascular diseases. In addition, it has now become evident that platelets also participate in the earliest stages of atherosclerosis, including the genesis of the atherosclerotic lesion. Moreover, while the link between platelet activity and hemostasis has been well established, the role of platelets as modulators of inflammation has only recently been recognized. Thus, through their secretory activities, platelets can chemically attract a diverse repertoire of cells to inflammatory foci. Although monocytes and lymphocytes act as key cells in the progression of an inflammatory event and play a central role in plaque formation and progression, there is also evidence that platelets can traverse the endothelium, and therefore be a direct mediator in the progression of atherosclerotic plaque. This review provides an overview of platelet interactions and regulation in atherosclerosis.

[Late-onset hereditary transthyretin amyloidosis with polyneuropathy. Report of one case]. / Polineuropatía por amiloidosis por transtiretina de inicio tardío. Caso clínico.

Hereditary transthyretin amyloidosis is a multisystemic autosomal dominant genetic disorder characterized by progressive distal sensory-motor polyneuropathy or restrictive cardiomyopathy, secondary to amyloid deposits. Its pathogenesis lies in the TTR gene mutation, and the Val50Met mutation is the most frequent. Patients have significant differences in the onset and severity of clinical presentation according to their country of origin. The diagnosis of this pathology is complex, even more in countries where it is not considered endemic. However, early suspicion and management are essential to improve survival and avoid unnecessary diagnostic and therapeutic strategies. We report a 69-year-old woman who presented a sensory-motor polyneuropathy, predominantly sensory, associated with distal neuropathic pain and bilateral vitritis. The history of her Italian father with polyneuropathy of unspecified etiology stood out. A vitreous biopsy identified amyloid substance deposits (congo red positive). These were also confirmed on a superficial peroneal nerve biopsy. During the etiological study of her polyneuropathy, an increased Kappa/Lambda index of 2.55 mg/L stood out. Therefore, light chain amyloidosis was suspected, and chemotherapy treatment was indicated without favorable response. After 10 years of progressive neurological and ophthalmological involvement, a genetic study confirmed the first case of late-onset hereditary transthyretin amyloidosis Val50Met with polyneuropathy in Chile.

Seminal plasma nerve growth factor signaling on the reproductive physiology of female llamas.

The ovulation mechanism is one of the fascinating physiological processes in reproductive biology in mammals. From the reproductive point of view, the species have been classified as spontaneous or induced ovulators. Although the release of GnRH followed by the preovulatory LH surge is shared between both types of ovulation, the stimulus to initiate GnRH release varies between both categories. In spontaneous ovulators, ovulation depends on the systemic concentration of ovarian steroids, however, in induced ovulators, different stimuli such as copulation, environmental, and social cues can facilitate or induce ovulation regardless of the increases in systemic estradiol concentration. In this review, we document evidence that a male-derived protein is the main factor responsible for inducing ovulation and also modulating the ovarian function in the domestic South American camelid, the llama. The neurotrophin beta-Nerve Growth Factor (ß-NGF) is the principal factor present in the semen of llamas responsible for inducing ovulation in this species. After the intrauterine deposit of semen during mating, ß-NGF is absorbed through the endometrium to reach the circulatory system, where it reaches the hypothalamus and stimulates GnRH release. The potential site of action of this neurotrophin at the brain has not been elucidated, however, hypotheses are raised that the factor may cross the blood-brain barrier and stimulate upstream neuronal networks that lead to the stimulation of GnRH-secreting neurons. It is possible that ß-NGF could be sensed at the median eminence without crossing the blood-brain barrier. Finally, it has been observed that this factor is not only a powerful stimulator of ovulation but also has a luteotrophic effect, resulting in the development of a corpus luteum capable of secreting more progesterone when compared to other ovulation-stimulating analogues.

Seminal plasma nerve growth factor signaling on the reproductive physiology of female llamas

The ovulation mechanism is one of the fascinating physiological processes in reproductive biology in mammals. From the reproductive point of view, the species have been classified as spontaneous or induced ovulators. Although the release of GnRH followed by the preovulatory LH surge is shared between both types of ovulation, the stimulus to initiate GnRH release varies between both categories. In spontaneous ovulators, ovulation depends on the systemic concentration of ovarian steroids, however, in induced ovulators, different stimuli such as copulation, environmental, and social cues can facilitate or induce ovulation regardless of the increases in systemic estradiol concentration. In this review, we document evidence that a male-derived protein is the main factor responsible for inducing ovulation and also modulating the ovarian function in the domestic South American camelid, the llama. The neurotrophin beta-Nerve Growth Factor (β-NGF) is the principal factor present in the semen of llamas responsible for inducing ovulation in this species. After the intrauterine deposit of semen during mating, β-NGF is absorbed through the endometrium to reach the circulatory system, where it reaches the hypothalamus and stimulates GnRH release. The potential site of action of this neurotrophin at the brain has not been elucidated, however, hypotheses are raised that the factor may cross the blood-brain barrier and stimulate upstream neuronal networks that lead to the stimulation of GnRH-secreting neurons. It is possible that β-NGF could be sensed at the median eminence without crossing the blood-brain barrier. Finally, it has been observed that this factor is not only a powerful stimulator of ovulation but also has a luteotrophic effect, resulting in the development of a corpus luteum capable of secreting more progesterone when compared to other ovulation-stimulating analogues.(AU)

La pandemia COVID-19 inductor de tecnoestrés en docentes de la educación ecuatoriana de segundo nivel / The COVID-19 pandemic inducer of technostress in teachers of the Ecuadorian education of second level

Casi dos años después de que se impuso la adecuación del trabajo docente a la modalidad remota, la política pública educativa no visualiza en su discurso actual la atención al tecnoestrés docente como prioridad y no existen acciones concretas encaminadas en ese sentido. Se realizó un estudio cuantitativo, observacional, descriptivo y correlacional en tres colegios fiscales, a fin de obtener información sobre la prevalencia de tecnoestrés en docentes y aportar evidencia empírica acerca de las diferencias entre ambos sexos, en cuanto a algunos factores asociados a este. Los resultados tecnoestrés en los y las docentes participantes, independientemente a la edad, sexo y años de experiencias y correlacionado con la sobre carga tecnológica, la intensidad de trabajo diario, tecno-invasión y las consecuencias socioemocionales al trabajar fuera el horario laboral, en contexto COVID-19 y, como consecuencias impacto negativo en su bienestar psicológicos; los datos aportados sugieren implicancias interesantes del uso de las TICs que se extienden más allá de lo educativo y lo tecnológico, alcanzando además los campos: social, salud ocupacional y psicológico. Por lo que se recomienda seguir realizando investicaciones acerca de este fenómeno durante y post COVID-19(AU)

Almost two years after the adaptation of teaching work to the remote modality was imposed, the educational public policy does not visualize in its current discourse the attention to teaching techno-stress as a priority and there are no concrete actions directed in that direction. A quantitative, observational, descriptive and correlational study was carried out in three public schools, in order to obtain information on the prevalence of technostress in teachers and provide empirical evidence about the differences between the sexes, in terms of some factors associated with it. The results of techno-stress in the participating teachers, regardless of age, sex and years of experience and correlated with technological overload, intensity of daily work, techno-invasion and the socio-emotional consequences of working outside working hours, in context COVID-19 and, as consequences, a negative impact on their psychological well-being; the data provided suggest interesting implications of the use of ICTs that extend beyond education and technology, also reaching the fields: social, occupational health and psychological. Therefore, it is recommended to continue conducting research on this phenomenon during and after COVID-19(AU)

Efecto de extractos de frutas y hortalizas en la incorporación de glucosa en células musculares in vitro / Effect of fruit and vegetable extracts on the incorporation of glucose in muscle cells "in vitro"

Skeletal muscle appears to play a central role in the development of insulin resistance (IR) and consequently the metabolic syndrome due to high-fat diets, obesity, and aging. Recent evidence suggests that some bioactive compounds present in natural products can affect blood glucose, possibly due to interactions between the compounds and glucose transporters. As an objective, to evaluate the effect of the extract of the green bean (PV, Phaseolus vulgaris) and apple of small fruit of thinning (Malus domestica, MAF and MIT extracts) on the incorporation of glucose in C2C12 muscle cells. For this, the cytotoxic effect of the extracts on the cells was determined by detecting formazan. Subsequently, glucose incorporation was determined using a fluorescent glucose analog in cells treated with the extracts. Finally, the effect of the extracts on IL-6 and TNFα production was evaluated by ELISA. Results: PV and MAF decreased 50% of viability at 1000µg / mL while MIT only decreased 10% at that concentration. PV had no significant effect on glucose incorporation and the MAF and MIT extract extracts significantly increased glucose incorporation at 100 µg / mL (13500 and 18000 URF respectively). PV increases the secretion of IL-6 and TNF-α, MAF and MIT only increase the expression of IL-6. Conclusion: These results make it possible to establish natural extracts derived from thinning small fruit apple can be used as a possible treatment for pathologies with high blood glucose levels.

Unilateral Ureteral Obstruction for 28 Days in Rats Is Not Associated with Changes in Cardiac Function or Alterations in Mitochondrial Function.

Our work evaluated cardiac function and mitochondrial bioenergetics parameters in hearts from male Wistar rats subjected to the UUO model during 28 days of progression. We measured markers of kidney damage and inflammation in plasma and renal fibrosis by histological analysis and Western blot. Cardiac function was evaluated by echocardiography and proteins involved in cardiac damage by Western blot. Oxygen consumption and transmembrane potential were monitored in cardiac mitochondria using high-resolution respirometry. We also determined the activity of ATP synthase and antioxidant enzymes such as glutathione peroxidase, glutathione reductase, and catalase. Our results show that, although renal dysfunction is established in animals subjected to ureteral obstruction, cardiac function is maintained along with mitochondrial function and antioxidant enzymes activity after 28 days of injury evolution. Our results suggest that renocardiac syndrome might develop but belatedly in obstruction-induced renal damage, opening the opportunity for treatment to prevent this condition.

mTOR Activity and Autophagy in Senescent Cells, a Complex Partnership.

Cellular senescence is a form of proliferative arrest triggered in response to a wide variety of stimuli and characterized by unique changes in cell morphology and function. Although unable to divide, senescent cells remain metabolically active and acquire the ability to produce and secrete bioactive molecules, some of which have recognized pro-inflammatory and/or pro-tumorigenic actions. As expected, this "senescence-associated secretory phenotype (SASP)" accounts for most of the non-cell-autonomous effects of senescent cells, which can be beneficial or detrimental for tissue homeostasis, depending on the context. It is now evident that many features linked to cellular senescence, including the SASP, reflect complex changes in the activities of mTOR and other metabolic pathways. Indeed, the available evidence indicates that mTOR-dependent signaling is required for the maintenance or implementation of different aspects of cellular senescence. Thus, depending on the cell type and biological context, inhibiting mTOR in cells undergoing senescence can reverse senescence, induce quiescence or cell death, or exacerbate some features of senescent cells while inhibiting others. Interestingly, autophagy-a highly regulated catabolic process-is also commonly upregulated in senescent cells. As mTOR activation leads to repression of autophagy in non-senescent cells (mTOR as an upstream regulator of autophagy), the upregulation of autophagy observed in senescent cells must take place in an mTOR-independent manner. Notably, there is evidence that autophagy provides free amino acids that feed the mTOR complex 1 (mTORC1), which in turn is required to initiate the synthesis of SASP components. Therefore, mTOR activation can follow the induction of autophagy in senescent cells (mTOR as a downstream effector of autophagy). These functional connections suggest the existence of autophagy regulatory pathways in senescent cells that differ from those activated in non-senescence contexts. We envision that untangling these functional connections will be key for the generation of combinatorial anti-cancer therapies involving pro-senescence drugs, mTOR inhibitors, and/or autophagy inhibitors.

Gestational diabesity and foetoplacental vascular dysfunction.

Gestational diabetes mellitus (GDM) shows a deficiency in the metabolism of D-glucose and other nutrients, thereby negatively affecting the foetoplacental vascular endothelium. Maternal hyperglycaemia and hyperinsulinemia play an important role in the aetiology of GDM. A combination of these and other factors predisposes women to developing GDM with pre-pregnancy normal weight, viz. classic GDM. However, women with GDM and prepregnancy obesity (gestational diabesity, GDty) or overweight (GDMow) show a different metabolic status than women with classic GDM. GDty and GDMow are associated with altered l-arginine/nitric oxide and insulin/adenosine axis signalling in the human foetoplacental microvascular and macrovascular endothelium. These alterations differ from those observed in classic GDM. Here, we have reviewed the consequences of GDty and GDMow in the modulation of foetoplacental endothelial cell function, highlighting studies describing the modulation of intracellular pH homeostasis and the potential implications of NO generation and adenosine signalling in GDty-associated foetal vascular insulin resistance. Moreover, with an increase in the rate of obesity in women of childbearing age worldwide, the prevalence of GDty is expected to increase in the next decades. Therefore, we emphasize that women with GDty and GDMow should be characterized with a different metabolic state from that of women with classic GDM to develop a more specific therapeutic approach for protecting the mother and foetus.

Progressive Reduction in Mitochondrial Mass Is Triggered by Alterations in Mitochondrial Biogenesis and Dynamics in Chronic Kidney Disease Induced by 5/6 Nephrectomy.

The five-sixth nephrectomy (5/6Nx) model is widely used to study the mechanisms involved in chronic kidney disease (CKD) progression. Mitochondrial impairment is a critical mechanism that favors CKD progression. However, until now, there are no temporal studies of the change in mitochondrial biogenesis and dynamics that allow determining the role of these processes in mitochondrial impairment and renal damage progression in the 5/6Nx model. In this work, we determined the changes in mitochondrial biogenesis and dynamics markers in remnant renal mass from days 2 to 28 after 5/6Nx. Our results show a progressive reduction in mitochondrial biogenesis triggered by reducing two principal regulators of mitochondrial protein expression, the peroxisome proliferator-activated receptor-gamma coactivator 1-alpha and the peroxisome proliferator-activated receptor alpha. Furthermore, the reduction in mitochondrial biogenesis proteins strongly correlates with the increase in renal damage markers. Additionally, we found a slow and gradual change in mitochondrial dynamics from fusion to fission, favoring mitochondrial fragmentation at later stages after 5/6Nx. Together, our results suggest that 5/6Nx induces the progressive reduction in mitochondrial mass over time via the decrease in mitochondrial biogenesis factors and a slow shift from mitochondrial fission to fusion; both mechanisms favor CKD progression in the remnant renal mass.

Endothelial transmigration of platelets depends on soluble factors released by activated endothelial cells and monocytes.

Cardiovascular diseases (CVDs) remain leading causes of death worldwide. While platelet-mediated thrombus formation following the rupture of an atherosclerotic plaque is one of the key pathophysiologic events in CVDs, the role of platelets in previous or more advanced stages of atherosclerosis is less known. Interestingly, the presence of platelets has been observed at the core of the atherosclerotic plaque.In order to study the conditions necessary for platelets to migrate toward an atherosclerotic lesion, we designed an in vitro co-culture model. Platelets were co-cultured with monocytes in Transwell inserts covered with a confluent endothelium and the number of migrating platelets and/or monocytes was determined under different conditions. Platelets were also exposed to media conditioned obtained from co-cultures prior to migration assays.Here we show that coculturing platelets and monocytes increased platelet transmigration, with a considerable number of transmigrated platelets found not associated to monocytes. Interestingly, conditioned media from platelet-monocyte co-cultures also increased platelet transmigration and aggregation, suggesting the existence of soluble factors secreted by monocytes that enhance the migratory and pro-aggregating capabilities of platelets.We conclude that platelets have the machinery to migrate through an activated endothelium, a response that requires the interaction with secreted factors produce in the context of the interaction with monocytes under atherogenic conditions.