RESUMEN
Aging often associates with a chronic low-grade inflammatory status that can be consequent to the activation of Toll-like receptors (TLRs) and the downstream NLR family pyrin domain containing 3 (NLRP3) inflammasome and causes a chronic secretion of pro-inflammatory cytokines. Since exercise has known anti-inflammatory effects, we investigated the effect of Nordic walking training on inflammasome activation and downstream effectors in elderly women. A population of elderly women was divided into EXP (n = 29) that completed 12 weeks of the moderate-intensity aerobic training program and CTRL (n = 29), performing no activity. Blood samples were taken before and after the first (T1-pre and T1-post, respectively) and last (T2-pre and T2-post, respectively) exercise unit. Inflammasome activation status was assessed by whole blood NLRP3 and TLR4 expression by RT-qPCR. Serum levels of IL-1ß, IL-6, TNFα, and IL-18 cytokines were assayed by multiplex fluorescent beads-based immunoassays or ELISA. NLRP3 and TLR4 levels were reduced 2 folds between T1-pre and T2-pre and induced at T2-post, compared to T2-pre, by 2.6- and 2.9-fold, respectively. A single exercise bout elicited a 1. 38-, 1. 5-, and 1.36-fold rise of IL-1ß, TNFα, and IL-6 concentration, respectively, although not significant, at the beginning of the training (T1-pre vs. T1-post), a 1.4-fold decrease for IL-1ß and TNFα at the end of the training (T1-pre vs. T2-pre), and a 2-, 1.8- and 1.26-fold increase after the last exercise session (T2-pre vs. T2-post) for the three cytokines. When stratifying the population based on BMI in normal weight (NW) and overweight (OW), NLRP3 and TLR4 expression was affected only in NW. As for inflammatory cytokines, IL-1ß was modulated in NW at the beginning of the training, whereas in OW at the end of the training; for TNFα, this time-dependent modulation was significant only in OW. Applied aerobic training affected the resting expression of inflammasome constituents (NLRP3 and TLR4) and levels of downstream effectors (IL-1ß, TNFα, and IL-6). However, at the end of the program, participants acquire an acute inflammatory response to exercise that was absent at baseline. Future studies would have to define the molecular mechanisms associated with, and how to potentiate, the exercise-associated inflammatory response.
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Background: COVID-19 pandemic has exacerbated the problem of physical inactivity and weight gain. Consequently, new strategies to counteract weight gain are being sought. Because of their accessibility, interval training and cold therapy are the most popular such strategies. We here aimed to examine the effect of 6 units of high-intensity interval training (HIIT), applied alone or in combination with 10 sessions of whole-body cryotherapy (WBC; 3 min at -110 ∘C per session) on incretins, myokines, and adipokines levels. Materials and methods: The study involved 65 subjects (body mass index of approximately 30 kgâ¢m-2). The subjects were randomly divided into training group (TR; n = 27) and training supported by WBC group (TR-WBC; n = 38). Blood samples were collected before, immediately following, and 4 weeks after the intervention. Results: Fibroblast growth factor 21 (FGF21) levels significantly increased (p = 0.03) and adiponectin levels increased in the TR group (p = 0.05) compared with those recorded in TR-WBC group 24 h after the end of experimental protocol. Beneficial changes in the lipid profile (p = 0.07), a significant drop in visfatin levels (p < 0.05), and the improvement in ß-cell function (HOMA-B; p = 0.02) were also observed in the TR group in the same time point of study. While TR-WBC did not induce similar changes, it ameliorated blood glucose levels (p = 0.03). Changes induced by both interventions were only sustained for 4 weeks after treatment. Conclusion: Collectively, HIIT, alone and in combination with WBC, positively affects metabolic indicators, albeit, most likely, different mechanisms drive the beneficial effects of different treatments.
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Adipoquinas/metabolismo , Crioterapia , Citocinas/metabolismo , Glucosa/metabolismo , Entrenamiento de Intervalos de Alta Intensidad , Homeostasis , Obesidad/fisiopatología , Sobrepeso/fisiopatología , Humanos , Obesidad/metabolismo , Sobrepeso/metabolismoRESUMEN
The COVID-19 pandemic and subsequent self-isolation exacerbated the problem of insufficient amounts of physical activity and its consequences. At the same time, this revealed the advantage of vitamin D. Thus, there was a need to verify the effects of those forms of training that can be performed independently. In this study, we examined the effects of Nordic walking (NW) and high intensity interval training (HIIT) with regard to the impact of the metabolite vitamin D. We assigned 32 overweight adults (age = 61 ± 12 years) to one of two training groups: NW = 18 and HIIT = 14. Body composition assessment and blood sample collection were conducted before starting the training programs and a day after their completion. NW training induced a significant decrease in myostatin (p = 0.05) concentration; however, the range was dependent on the baseline concentrations of vitamin D metabolites. This drop was accompanied by a significant negative correlation with the decorin concentration. Unexpectedly, NW caused a decrement in both forms of osteocalcin: undercarboxylated (Glu-OC) and carboxylated-type (Gla-OC). The scope of Glu-OC changes was dependent on a baseline concentration of 25(OH)D2 (r = -0.60, p = 0.01). In contrast, the HIIT protocol did not induce any changes. Overall results revealed that NW diminished the myostatin concentration and that this effect is more pronounced among adults with a sufficient concentration of vitamin D metabolites.
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COVID-19 , Entrenamiento de Intervalos de Alta Intensidad , Miostatina/sangre , Caminata Nórdica , Sobrepeso , SARS-CoV-2/metabolismo , Vitamina D/sangre , Anciano , COVID-19/sangre , COVID-19/fisiopatología , Femenino , Humanos , Masculino , Persona de Mediana Edad , Sobrepeso/sangre , Sobrepeso/fisiopatologíaRESUMEN
Although schizophrenia and anorexia nervosa are seemingly very distinct psychiatric disorders, their symptoms are connected by various types of relationships. The present article reviews the literature and recapitulates the views of various authors on the links between these two disorders. Symptoms of anorexia may 1) precede the onset of psychosis; 2) evolve in its active phase or more rarely manifest in remission; and, conversely, 3) psychotic symptoms may occur transiently in the course of anorexia nervosa. When anorexia precedes the manifestation of psychosis, symptoms of anorexia can be treated as a component of the prodromal phase of schizophrenia. Another possibility of co-existence of a psychosis (e.g., schizophrenia) with anorexia is when the eating disorder syndrome manifests at the same time as the full-blown psychotic syndrome. In such cases, when the symptoms of the two disorders occur simultaneously, it is often difficult to say whether the patient is suffering from schizophrenia, in the course of which anorexia has arisen secondary to psychotic symptoms or whether he/she is suffering from anorexia during which he/she has developed psychotic symptoms, usually thematically associated with eating. Studies published so far, mainly case reports, point to the complex nature of the interrelationships between schizophrenia and anorexia nervosa. Further research is needed to conclusively explain the relationships between psychotic disorders and anorexia nervosa, which would allow physicians to use more effective methods of treatment in this group of patients.
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Anorexia Nerviosa/diagnóstico , Anorexia Nerviosa/epidemiología , Esquizofrenia/diagnóstico , Esquizofrenia/epidemiología , Anorexia Nerviosa/psicología , Imagen Corporal , Comorbilidad , Humanos , Escalas de Valoración Psiquiátrica , Factores de Riesgo , Psicología del Esquizofrénico , AutoimagenRESUMEN
Several lines of evidence suggest that up-regulation of immune response and alterations of kynurenine pathway function are involved in pathogenesis of schizophrenia. Correlations among clinical status (using PANNS, SANS and SAPS scales) and blood levels of kynurenic acid (KYNA), 3-hydroxykynurenine (3-HK) and levels of selected immunoactive molecules, soluble interleukin-2 receptor (sIL-2R), interferon-α (IFN-α) and IL-4 were analyzed in 51 chronic schizophrenia patients during acute relapse, after four weeks of therapy and at remission. KYNA levels were significantly lower in comparison with controls (N=45) throughout the study, whereas 3-HK did not differ from controls at admission and during therapy, but increased at remission. The KYNA/3-HK ratio and IL-4 levels, but not sIL-2R and IFN-α levels, were consistently decreased in schizophrenia patients at all analyzed time points. KYNA level and KYNA/3-HK ratio measured at admission correlated negatively with the duration of illness, whereas 3-HK level correlated negatively with the improvement of SANS score at discharge. sIL-2R level before treatment was positively linked with number of relapses. In the subgroup of patients with poor response to pharmacotherapy, treated with clozapine later on, initial KYNA level and the ratio KYNA/3-HK correlated negatively with number of relapses. Positive association of sIL-2R level with number of relapses was also evident in this subgroup. Furthermore, among these patients, starting IFN-α level was negatively linked with the improvement of total PANSS score at discharge. Presented here data support the concept of disturbed kynurenine pathway function in schizophrenia and suggest that assessment of KYNA and 3-HK levels during acute relapse might be useful in prediction of response to antipsychotic therapy. Deficit of peripheral KYNA and higher 3-HK levels could be associated with more severe symptoms of schizophrenia. Further studies with larger samples size are needed to validate our results.
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Interferón-alfa/sangre , Interleucina-4/sangre , Ácido Quinurénico/sangre , Quinurenina/análogos & derivados , Receptores de Interleucina-2/sangre , Esquizofrenia/sangre , Adulto , Antipsicóticos/uso terapéutico , Clozapina/uso terapéutico , Femenino , Humanos , Quinurenina/sangre , Masculino , Escalas de Valoración Psiquiátrica , Recurrencia , Estudios Retrospectivos , Esquizofrenia/tratamiento farmacológico , Transducción de Señal/efectos de los fármacos , Transducción de Señal/fisiología , Estadísticas no Paramétricas , Factores de Tiempo , Regulación hacia Arriba/fisiología , Adulto JovenRESUMEN
BACKGROUND: Processing speed turns out to be the central area of research on cognition in schizophrenia. So far the relationship between this dimension and the IQ level of patients and their healthy siblings has not been investigated. AIM: To investigate the differences in cognitive speed in patients with schizophrenia and their healthy siblings, and to determine whether cognitive speed as a covariate affects differences in IQ and cognitive profiles between groups. METHODS: Forty-seven inpatients diagnosed with schizophrenia according to DSM-IV (SCH) and their 36 healthy siblings (HSB) were tested with cognitive speed tasks according to Bartzokis et al. method and Wechsler Intelligence Scale. Additional control for the possible impact of antipsychotic drugs and selected demographic variables on the cognitive performance was taken into account. RESULTS: The siblings scored significantly higher in the cognitive speed task (p < 0.01) than patients, the WAIS-R cognitive test profiles were also significantly different in two ways: between groups, and between single test results in each of the assessed groups. The interaction effect: ANOVA, F(10, 770) = 2.798, p = 0.002. Similarly, the Performance and Full Scale IQs were significantly different, at p < 0.01. After controlling for cognitive speed, all significant differences no longer exist: e.g. Full Scale IQ, p = 0.459. CONCLUSIONS: Significant differences in cognitive speed between patients and their healthy siblings generate the differences in the cognitive profile assessed with Wechsler Intelligence Scale. Some problems of cognitive speed diagnosis and further research on the cognitive schizophrenia endophenotype were discussed.
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Disfunción Cognitiva/fisiopatología , Inteligencia/fisiología , Esquizofrenia/fisiopatología , Hermanos , Adulto , Disfunción Cognitiva/etiología , Femenino , Humanos , Masculino , Esquizofrenia/complicaciones , Adulto JovenRESUMEN
Kynurenic acid (KYNA) is a neuroactive metabolite of tryptophan formed in the brain and in the periphery, known to block ionotropic glutamate receptors and α7 nicotinic receptors, and to act as a ligand of G protein-coupled GPR35 receptors and human aryl hydrocarbon (AHR) receptors. KYNA seems to modulate a number of mechanisms involved in the pathogenesis of schizophrenia including dopaminergic transmission in mesolimbic and mesocortical areas or glutamatemediated neurotransmission. The kynurenine hypothesis of schizophrenia links the occurrence of positive and negative symptoms of schizophrenia and cognitive impairments characteristic for the disease with the disturbances of kynurenine pathway function. Available data suggest that antipsychotic drugs may restore balance among kynurenine pathway metabolites, and that co-administration of glycine with antipsychotics may reduce extrapyramidal symptoms in patients suffering from schizophrenia. Central level of KYNA may increase in the course of inflammation, which is consistent with the inflammatory hypothesis of schizophrenia. Alterations of immune response and disturbed functioning of kynurenine pathway may lead to disproportion between neuroprotective and neurotoxic mechanisms in the brain. Currently, intense research efforts are focused on the role of kynurenine pathway metabolites in pathogenesis of schizophrenia, their association with the response to antipsychotic treatment, and search for novel medications modulating the function of kynurenine pathway.
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Antipsicóticos/uso terapéutico , Encéfalo/metabolismo , Ácido Quinurénico/farmacología , Esquizofrenia/etiología , Factores de Transcripción con Motivo Hélice-Asa-Hélice Básico/agonistas , Encéfalo/efectos de los fármacos , Humanos , Ácido Quinurénico/metabolismo , Antagonistas Nicotínicos/farmacología , Receptores de Hidrocarburo de Aril/agonistas , Receptores Ionotrópicos de Glutamato/antagonistas & inhibidores , Receptores Nicotínicos , Esquizofrenia/tratamiento farmacológico , Esquizofrenia/metabolismoRESUMEN
UNLABELLED: Violence against women has many various short- and long-term effects. Although violence by an intimate partner has been widely documented, still little is known about its long-term somatic consequences for the victim. THE AIM: of the study was to examine the prevalence of intimate partner violence (IPV) among patients seeing a general practitioner as well as to determine relationships between IPV and somatic complaints other than direct somatic consequences (such as injuries), including somatic diseases and healthcare services use. MATERIALS AND METHODS: The study sample comprised 151 women seeing a family doctor consecutively. The participants were administered a structured interview questionnaire developed for the purpose of this study. RESULTS: The prevalence of IPV for the total sample of primary health care female patients was 35.1% during 12 months preceding the examination. Compared to patients with no violence history, those experiencing IPV reported significantly more physical complaints and symptoms, particularly about cardiovascular, nervous, digestive and genitourinary systems. They were also at a higher risk of developing numerous diseases, with the greatest risk of peptic ulcer (OR, 6.62), and ischaemic heart disease (OR, 5.98). IPV victims were also more likely to seek help of a family doctor and the following specialists: neurologist (OR, 3.88), cardiologist (OR, 4.01), gastroenterologist (OR, 4.51), psychiatrist (OR, 2.43), endocrinologist (OR, 1.6), and pulmonologist (OR, 1.2). They were also more likely to use emergency department (OR, 3.23) and require hospitalization (OR, 3.61). CONCLUSIONS: It is recommended that the medical interview should include questions referring to violence, especially in case of patients reporting various symptoms about different systems and organs that have no medical explanation, or symptoms with intensity greater than it should be given the patients' actual physical state.
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Violencia de Pareja/estadística & datos numéricos , Trastornos Somatomorfos/etiología , Femenino , Humanos , Isquemia Miocárdica/epidemiología , Isquemia Miocárdica/etiología , Úlcera Péptica/epidemiología , Úlcera Péptica/etiología , Polonia , Prevalencia , Atención Primaria de Salud , Trastornos Somatomorfos/epidemiología , Encuestas y CuestionariosRESUMEN
The mechanism of action of antipsychotic drugs is mainly associated with changes in dopaminergic system. The application of antipsychotic agents simultaneously produces changes in concentrations of metabolites (e.g. kynurenic acid - KYNA, 3-hydroxykynurenine - 3-OHKYN, kynurenine - KYN) of the kynurenine pathway, the pathway engaged in glutamatergic transmission. The increase in KYNA levels in certain areas of the central nervous system results in inhibition of glutamatergic transmission. Pharmacologically induced elevation of KYNA levels produces effects similar to those observed after administering ketamine or phencyclidine (the noncompetitive NMDA receptor antagonist), concerning increased activity of mesolimbic dopamine neurons, as well as reduction in dopamine release from the prefrontal cortex. Recent research results confirm the predictive value of changes in concentrations of kynurenine pathway metabolites for assessment of effectiveness of antipsychotic treatment. Significant relationships were found 1) in schizophrenia between the reduction of psychopathological symptoms and variations in 3-OHKYN levels as well as changes in KYNA/3-OHKYN and KYN/KYNA ratios, 2) in mania between varying tryptophan concentrations and the reduction in manic symptoms achieved with antipsychotic treatment. The research as well presented the possibilities of kynurenine pathway modifications, raising high hopes for their future application as target points for the action of novel antipsychotic agents.