Gut microbiota mediated the effects of high relative humidity on lupus in female MRL/lpr mice

Abstract Introduction The relationship between humidity and systemic lupus erythematosus (SLE) has yielded inconsistent results in prior research, while the effects of humidity on lupus in animal experiments and its underlying mechanism remain inadequately explored. Methods The present study aimed to investigate the impact of high humidity (80 ± 5%) on lupus using female and male MRL/lpr mice, with a particular focus on elucidating the role of gut microbiota in this process. To this end, fecal microbiota transplantation (FMT) was employed to transfer the gut microbiota of MRL/lpr mice under high humidity to blank MRL/lpr mice under normal humidity (50 ± 5%), allowing for an assessment of the effect of FMT on lupus. Results The study revealed that high humidity exacerbated lupus indices (serum anti-dsDNA, ANA, IL-6, and IFN- g, and renal pathology) in female MRL/lpr mice but had no significant effect on male MRL/lpr mice. The aggravation of lupus caused by high humidity may be attributed to the increased abundances of the Rikenella, Romboutsia, Turicibacter, and Escherichia-Shigella genera in female MRL/lpr mice. Furthermore, FMT also exacerbated lupus in female MRL/lpr mice but not in male MRL/lpr mice. Conclusion In summary, this study has demonstrated that high humidity exacerbated lupus by modulating gut microbiota in female MRL/lpr mice. The findings underscore the importance of considering environmental factors and gut microbiota in the development and progression of lupus, particularly among female patients.

O Pré-Condicionamento com Dexmedetomidina Atenua a Lesão de Isquemia/Reperfusão Miocárdica em Ratos, Suprimindo a Mitofagia Via Ativação do Receptor Α2-Adrenérgico / Dexmedetomidine Preconditioning Attenuates Myocardial Ischemia/Reperfusion Injury in Rats by Suppressing Mitophagy Via Activating Α2-Adrenergic Receptor

Resumo Fundamento A dexmedetomidina (DEX), um agonista específico do receptor α2-adrenérgico, é protetora contra lesão de isquemia/reperfusão miocárdica (I/R). No entanto, a associação entre a cardioproteção induzida pelo pré-condicionamento DEX e a supressão da mitofagia permanece pouco clara. Objetivo Portanto, nosso objetivo foi investigar se o pré-condicionamento com DEX alivia a I/R, suprimindo a mitofagia via ativação do receptor α2-adrenérgico. Método Sessenta corações de ratos isolados foram tratados com ou sem DEX antes de induzir isquemia e reperfusão; um antagonista do receptor α2-adrenérgico, a ioimbina (YOH), também foi administrado antes da isquemia, isoladamente ou com DEX. A frequência cardíaca (FC), pressão diastólica do ventrículo esquerdo (PDVE), pressão diastólica final do ventrículo esquerdo (PDFVE), taxa máxima e mínima de desenvolvimento da pressão ventricular esquerda (±dp/dtmax) e tamanho do infarto do miocárdio foram medidos. A ultraestrutura mitocondrial e as autofagossomas foram avaliadas por microscopia eletrônica de transmissão. O potencial de membrana mitocondrial e os níveis de espécies reativas de oxigênio (ROS) foram medidos usando os ensaios JC-1 e diacetato de diclorodi hidrofluoresceína, respectivamente. Os níveis de expressão das proteínas associadas à mitofagia Beclin1, relação LC3II/I, p62, PINK1 e Parkin foram detectados por western blotting. Resultados Em comparação com o grupo controle, no grupo isquemia/reperfusão, a FC, PDVE e ±dp/dtmax foram notavelmente diminuídas (p<0,05), enquanto os tamanhos da PDFVE e do infarto aumentaram significativamente (p<0,05). O pré-condicionamento com DEX melhorou significativamente a disfunção cardíaca, reduziu o tamanho do infarto do miocárdio, manteve a integridade estrutural mitocondrial, aumentou o potencial de membrana mitocondrial, inibiu a formação de autofagossomas e diminuiu a produção de ROS e a relação Beclin1, relação LC3II/I, expressão PINK1, Parkin e p62(p<0,05). Quando DEX e YOH foram combinados, o YOH cancelou o efeito da DEX, enquanto o uso de YOH sozinha não teve efeito. Conclusão Portanto, o pré-condicionamento DEX foi cardioprotetor contra I/R em ratos, suprimindo a mitofagia por meio da ativação do receptor α2-adrenérgico.

Abstract Background Dexmedetomidine (DEX), a specific α2-adrenergic receptor agonist, is protective against myocardial ischemia/reperfusion injury (MIRI). However, the association between DEX preconditioning-induced cardioprotection and mitophagy suppression remains unclear. Objective Hence, we aimed to investigate whether DEX preconditioning alleviates MIRI by suppressing mitophagy via α2-adrenergic receptor activation. Method Sixty isolated rat hearts were treated with or without DEX before inducing ischemia and reperfusion; an α2-adrenergic receptor antagonist, yohimbine (YOH), was also administered before ischemia, alone or with DEX. The heart rate (HR), left ventricular diastolic pressure (LVDP), left ventricular end-diastolic pressure (LVEDP), maximal and minimal rate of left ventricular pressure development (±dp/dtmax), and myocardial infarction size were measured. The mitochondrial ultrastructure and autophagosomes were assessed using transmission electron microscopy. Mitochondrial membrane potential and reactive oxygen species (ROS) levels were measured using JC-1 and dichloride hydrofluorescein diacetate assays, respectively. The expression levels of the mitophagy-associated proteins Beclin1, LC3II/I ratio, p62, PINK1, and Parkin were detected by western blotting. Results Compared with the control group, in the ischemia/reperfusion group, the HR, LVDP, and ±dp/dtmax were remarkably decreased (p< 0.05), whereas LVEDP and infarct sizes were significantly increased (p< 0.05). DEX preconditioning significantly improved cardiac dysfunction reduced myocardial infarction size, maintained mitochondrial structural integrity, increased mitochondrial membrane potential, inhibited autophagosomes formation, and decreased ROS production and Beclin1, LC3II/I ratio, PINK1, Parkin, and p62 expression(p< 0.05). When DEX and YOH were combined, YOH canceled the effect of DEX, whereas the use of YOH alone had no effect. Conclusion Therefore, DEX preconditioning was cardioprotective against MIRI in rats by suppressing mitophagy via α2-adrenergic receptor activation.

Diagnostic performance of cryobiopsy guided by radial-probe EBUS with a guide sheath for peripheral pulmonary lesions / Desempenho diagnóstico da criobiópsia guiada por EBUS radial com bainha guia para lesões pulmonares periféricas

ABSTRACT Objective: Transbronchial lung cryobiopsy (TBCB) has developed rapidly and has become one of the research hotspots of lung biopsy technology. The present study sought to evaluate the efficacy of TBCB guided by radial-probe EBUS (RP-EBUS) and a guide sheath (GS) without fluoroscopy for peripheral pulmonary lesions. Methods: In this retrospective study, McNemar's test was used in order to compare TBCB and transbronchial forceps biopsy (TBFB) in terms of diagnostic performance. A multivariate logistic regression model was designed to explore the association between predictive variables and the diagnostic yield of TBCB. Results: A total of 168 patients underwent GS-guided RP-EBUS. Of those, 157 had lesions that were visible and 11 had lesions that were not. Of those 157 patients, 24 were excluded because of missing data or an unclear final diagnosis. Therefore, 133 patients underwent RP-EBUS-GS-guided TBFB and TBCB. The pooled diagnostic yield of RP-EBUS-GS-guided TBCB without fluoroscopy was 71.5% (103/144). In 133 patients, the diagnostic yield of TBCB was significantly higher than that of TBFB (77.4% vs. 59.4%; p < 0.05). Multivariate analysis indicated that lesion size and site were independently associated with the diagnostic yield of TBCB (OR = 2.8, p = 0.03 and OR = 4.1, p = 0.01, respectively), although cryoprobe size was not. There was no significant difference between the 1.1-mm cryoprobe and the 1.9-mm cryoprobe in terms of diagnostic performance (78.4% vs. 76.8%; p > 0.05). Conclusions: GS-guided RP-EBUS is regarded as a practical option for guiding cryobiopsy, although it may not be able to replace fluoroscopy. Peripheral pulmonary lesions not located in the upper lobes or larger than 30 mm are significantly associated with a higher diagnostic yield of cryobiopsy.

RESUMO Objetivo: A criobiópsia transbrônquica (CBTB) desenvolveu-se rapidamente e tornou-se um dos focos de pesquisa de tecnologia de biópsia pulmonar. O presente estudo buscou avaliar a eficácia da CBTB guiada por EBUS radial com bainha guia sem fluoroscopia no diagnóstico de lesões pulmonares periféricas. Métodos: Neste estudo retrospectivo, o teste de McNemar foi usado para comparar a CBTB e a biópsia transbrônquica com pinça (BTB) quanto ao desempenho diagnóstico. Um modelo de regressão logística multivariada foi criado para explorar a relação entre variáveis preditivas e o rendimento diagnóstico da CBTB. Resultados: Um total de 168 pacientes foram submetidos a EBUS radial com bainha guia. Destes, 157 apresentavam lesões que puderam ser visualizadas e 11 apresentavam lesões que não puderam ser visualizadas. Dos 157 pacientes, 24 foram excluídos em virtude de dados incompletos ou diagnóstico final incerto. Portanto, 133 pacientes foram submetidos a BTB e CBTB guiadas por EBUS radial com bainha guia. O rendimento diagnóstico combinado da CBTB guiada por EBUS radial com bainha guia foi de 71,5%. O rendimento diagnóstico da CBTB foi significativamente maior que o da BTB (77,4% vs. 59,4%; p < 0,05). A análise multivariada indicou que o tamanho e o local da lesão apresentaram relação independente com o rendimento diagnóstico da CBTB (OR = 2,8, p = 0,03 e OR = 4,1, p = 0,01, respectivamente); o tamanho da criossonda, por sua vez, não apresentou relação com o rendimento diagnóstico da CBTB. Não houve diferença significativa entre a criossonda de 1,1 mm e a de 1,9 mm no que tange ao desempenho diagnóstico (78,4% vs. 76,8%; p > 0,05). Conclusões: EBUS radial com bainha guia é uma opção prática para guiar a criobiópsia, embora talvez não possa substituir a fluoroscopia. Lesões pulmonares periféricas que não estejam nos lobos superiores ou que tenham mais de 30 mm apresentam relação significativa com maior rendimento diagnóstico da criobiópsia.

Variation of plantaris muscle: a case report with clinical significance / Variación del músculo plantar: reporte de un caso con significado clínico

SUMMARY: The plantaris muscle is located between the soleus and gastrocnemius muscles, within the posterior calf group. Due to degeneration and its loss of plantar-flexion function, the muscle is vestigial in human beings, but it retains clinical significance. Few cases of variation in the plantaris muscle have been reported, and this, therefore, appears to be rare. Nonetheless, absence of this muscle was identified via the dissection of a left lower limb (male), which also indicated the absence of an attachment in the usual position. The present report, which addresses such variation, may provide both inspiration and reference points for the clinical treatment of so-called "tennis leg", and for the use of plantaris muscle for the purposes of clinical, autologous graft repair.

RESUMEN: El músculo plantar se ubica entre los músculos sóleo y gastrocnemio, dentro del grupo posterior de la pierna. Debido a la degeneración y la pérdida de la función de flexión plantar, el músculo es un vestigio en los seres humanos, pero conserva su importancia clínica. Se han informado pocos casos de variación en el músculo plantar y, por lo tanto, esto parece ser raro. No obstante, se observó la ausencia de este músculo durante la disección de un miembro inferior izquierdo (masculino). El presente informe, que aborda dicha variación, puede proporcionar puntos de referencia para el tratamiento clínico de la llamada "pierna de tenista" y para el uso del músculo plantar con fines de reparación clínica con injerto autólogo.

O Pré-Condicionamento com Dexmedetomidina Reduz a Lesão de Isquemia-Reperfusão do Miocárdio em Ratos, Inibindo a Via PERK / Dexmedetomidine Preconditioning Reduces Myocardial Ischemia-Reperfusion Injury in Rats by Inhibiting the PERK Pathway

Resumo Fundamento A cardiopatia isquêmica atraiu muito atenção devido às altas taxas de mortalidade, custos do tratamento e a crescente morbidade na população jovem. Estratégias de reperfusão reduziram a mortalidade. Porém, a reperfusão pode levar à morte do cardiomiócito e subsequente dano irreversível ao miocárdio. No momento, não há um tratamento eficiente e direcionado para a lesão de isquemia-reperfusão (I/R). Objetivos Avaliar se a dexmedetomidina (DEX) tem efeito protetivo na I/R do miocárdio e explorar os possíveis mecanismos por trás dela. Métodos Corações de ratos foram perfundidos com o sistema de perfusão de Langendorff e aleatoriamente distribuídos em cinco grupos: grupo controle, perfundido com solução de Krebs-Henseleit (K-H) por 205 minutos sem isquemia; e quatro grupos de teste que foram submetidos a 40 minutos de isquemia global e 120 minutos de reperfusão. O Grupo DEX, o grupo ioimbina (IO) e o grupo DEX + IO foram perfundidos com DEX (10 nM), IO (1 μM) ou a combinação de DEX e IO antes da reperfusão, respectivamente. A hemodinâmica cardíaca, o tamanho do infarto do miocárdio e a histologia do miocárdio foram avaliados. A expressão da proteína-78 regulada pela glicose (GRP78), a proteína quinase do retículo endoplasmático (PERK), a PERK fosforilada, o fator de iniciação eucariótico 2α (eIF2α), eIF2α fosforilado, o fator de transcrição 4 (TCF-4) e a proteína homóloga à proteína ligadora do acentuador CCAAT (CHOP) foram avaliados. P< 0,05 foi considerado para indicar a diferença estatisticamente significativa. Resultados O pré-condicionamento com DEX melhorou a função cardíaca nos corações com I/R, reduziu o infarto do miocárdio, a apoptose do miocárdio e a expressão de GRP78, p-PERK, eIF2α, p-eIF2α, TCF-4 e CHOP. Conclusões O pré-tratamento com DEX reduziu a lesão de I/R no miocárdio ao suprimir a apoptose, o que foi induzido pela via PERK.

Abstract Background Ischemic heart disease has attracted much attention due to its high mortality rates, treatment costs and the increasing morbidity in the young population. Strategies for reperfusion have reduced mortality. However, reperfusion can lead to cardiomyocyte death and subsequent irreversible myocardial damage. At present, the timely and targeted treatment of ischemia-reperfusion (I/R) injury is often lacking. Objectives To evaluate if dexmedetomidine (DEX) has a protective effect in myocardiual I/R and explore the possible mechanism behind it. Methods Rat hearts were perfused with a Langendorff perfusion system, and randomly assigned to five groups: control group, perfused with Krebs-Henseleit (K-H) solution for 205 minutes without ischemia; and four test groups that underwent 40 minutes of global ischemia and 120 min of reperfusion. The DEX group, the yohimbine (YOH) group and the DEX + YOH group were perfused with DEX (10 nM), YOH (1 μM) or the combination of DEX and YOH prior to reperfusion, respectively. Cardiac hemodynamics, myocardial infarct size, and myocardial histology were evaluated. The expression of glucose-related protein 78 (GRP78), protein kinase R-like ER kinase (PERK), phosphorylated PERK, eukaryotic initiation factor 2α (eIF2α), phosphorylated eIF2α, activating transcription factor 4 (ATF4), and CCAAT/enhancer-binding protein homologous protein (CHOP) were assessed. P<0.05 was considered to indicate a statistically significant difference. Results DEX preconditioning improved the cardiac function of I/R hearts, reduced myocardial infarction, myocardial apoptosis, and the expression of GRP78, p-PERK, eIF2α, p-eIF2α, ATF4 and CHOP. Conclusions DEX pretreatment reduced myocardial I/R injury by suppressing apoptosis, which was induced by the PERK pathway.

Resveratrol inhibits TNF-α-induced inflammation to protect against renal ischemia/reperfusion injury in diabetic rats

Abstract Purpose To examine effects of resveratrol on renal ischemia/ reperfusion injury (I/R) in a streptozotocin (STZ)-induced diabetic rat model. Methods Twenty-four male Sprague Dawley rats were treated with STZ injection for the development of diabetes, and divided into the following groups: Sham group, I/R group and Resveratrol group (n=8). Resveratrol (RSV) was administered at a dose of 10 mg.kg-1.d-1 fourteen days prior to suffering from I/R. Renal function, histology, SOD, MDA, TUNEL assay and expression of TNF-α, IL-1β, NF-κB-P65, COX-2 and Caspase3, Bcl2 and Bax were analyzed. Results Administration of RSV significantly reduced the serum levels of renal dysfunction and injury markers, including creatinine, blood urea nitrogen and MDA; in the other hand, it significantly increased the serum levels of SOD. The protective effect of RSV was also reflected on histologic evaluation. RSV reduced the number of apoptotic cells as determined by TUNEL assay. RSV significantly reduced the protein expression of TNF-α, IL-1β, NF-κB-P65, COX-2 and Caspase3, and Bax. Meanwhile, RSV significantly increased the protein expression of Bcl2. Conclusion RSV attenuated I/R-induced renal injury in diabetic rats through the modulation of oxidative stress and TNF-α-stimulated inflammation.

Neuroprotective effects of an Nrf2 agonist on high glucose-induced damage in HT22 cells

BACKGROUND: Oxidative stress is the hallmark of diabetic encephalopathy, which may be caused by hyperglycaemic toxicity. We aimed to discover pharmacologic targets to restore redox homeostasis. We identified the transcription factor Nrf2 as such a target. METHODS: HT22 cells were cultured in 25 or 50 mM D-glucose with various concentrations of sulforaphane (SFN) (from 1.25 to 5.0 µM). Cell viability was tested with the Cell Counting Kit-8 assay. Reactive oxygen species (ROS) production was detected with an inverted fluorescence microscope using the dichlorodihydrofluorescein-diacetate fluorescent probe. The expression of NF-E2-related factor 2 (Nrf2), haem oxygenase-1 (HO-1) and nuclear factor-κB (NF-κB) at the mRNA and protein levels was detected by reverse transcription quantitative polymerase chain reaction and western blotting. RESULT: We found that a high glucose concentration (50 mM) increased the generation of ROS, downregulated the expression of Nrf2/HO-1 and upregulated the expression of NF-κB. Moreover, HT22 cell viability significantly decreased after culture in high-glucose medium for 24, 48 and 72 h, whereas the activation of the Nrf2/HO-1 pathway using a pharmacological Nrf2 activator abrogated this high-glucose-induced toxicity. CONCLUSION: This study suggests that the activation of the Nrf2-ARE signalling pathway might be a therapeutic target for the treatment of diabetic encephalopathy.

Association of dietary nutrients with blood lipids and blood pressure in 18 countries: a cross-sectional analysis from the PURE study

BACKGROUND: The relation between dietary nutrients and cardiovascular disease risk markers in many regions worldwide is unknown. In this study, we investigated the effect of dietary nutrients on blood lipids and blood pressure, two of the most important risk factors for cardiovascular disease, in low-income, middle-income, and high-income countries.METHODS: We studied 125 287 participants from 18 countries in North America, South America, Europe, Africa, and Asia in the Prospective Urban Rural Epidemiology (PURE) study. Habitual food intake was measured with validated food frequency questionnaires. We assessed the associations between nutrients (total fats, saturated fatty acids, monounsaturated fatty acids, polyunsaturated fatty acids, carbohydrates, protein, and dietary cholesterol) and cardiovascular disease risk markers using multilevel modelling. The effect of isocaloric replacement of saturated fatty acids with other fats and carbohydrates was determined overall and by levels of intakes by use of nutrient density models. We did simulation modelling in which we assumed that the effects of saturated fatty acids on cardiovascular disease events was solely related to their association through an individual risk marker, and then compared these simulated risk marker-based estimates with directly observed associations of saturated fatty acids with cardiovascular disease events.

The value of preoperative magnetic resonance imaging in predicting postoperative recovery in patients with cervical spondylosis myelopathy: a meta-analysis

This meta-analysis was designed to elucidate whether preoperative signal intensity changes could predict the surgical outcomes of patients with cervical spondylosis myelopathy on the basis of T1-weighted and T2-weighted magnetic resonance imaging images. We searched the Medline database and the Cochrane Central Register of Controlled Trials for this purpose and 10 studies meeting our inclusion criteria were identified. In total, 650 cervical spondylosis myelopathy patients with (+) or without (-) intramedullary signal changes on their T2-weighted images were examined. Weighted mean differences and 95g% confidence intervals were used to summarize the data. Patients with focal and faint border changes in the intramedullary signal on T2 magnetic resonance imaging had similar Japanese Orthopaedic Association recovery ratios as those with no signal changes on the magnetic resonance imaging images of the spinal cord did. The surgical outcomes were poorer in the patients with both T2 intramedullary signal changes, especially when the signal changes were multisegmental and had a well-defined border and T1 intramedullary signal changes compared with those without intramedullary signal changes. Preoperative magnetic resonance imaging including T1 and T2 imaging can thus be used to predict postoperative recovery in cervical spondylosis myelopathy patients.

Oxymatrine ameliorates renal ischemia-reperfusion injury from oxidative stress through Nrf2/HO-1 pathway

PURPOSE: To investigate if oxymatrine pretreatment could ameliorate renal I/R injury induced in rats and explore the possible role of oxymatrine in Nrf2/HO-1 pathway. METHODS: Unilaterally nephrectomized rats were insulted by I/R in their left kidney. Twenty four rats were randomly divided into three groups: sham group, I/R + saline-treated group, I/R + OMT-treated group. Oxymatrine or vehicle solution was administered intraperitoneally injected 60 min before renal ischemia, respectively. Renal function, histology, makers of oxidative stress, cell apoptosis and Nrf2/HO-1 expressions were assessed. RESULTS: Oxymatrine pretreatment exhibited an improved renal functional recovery, alleviated histological injury and oxidative stress, inhibiting tubular apoptosis, and accompanied by upregulated the expression of Nrf2/HO-1 proteins. CONCLUSION: Oxymatrine may attenuate renal ischemia/reperfusion injury, and this renoprotective effect may be through activating the Nrf2/HO-1 pathway. .

Ozone oxidative preconditioning protects the rat kidney from reperfusion injury via modulation of the TLR4-NF-κB pathway

PURPOSE: To investigate the protective effects of ozone oxidative preconditioning (OzoneOP) were associated with the modulation of TLR4-NF-κB pathway. METHODS: Thirty six rats were subjected to 45 min of renal ischemia, with or without treatment with OzoneOP (1 mg/kg). Blood samples were collected for the detection of blood urea nitrogen and creatinine levels. Histologic examinations were evaluated and immunohistochemistry was also performed for localization of TLR4 and NF-κB. The expression of TNF-α, IL-1β, IL-6, ICAM-1 and MCP-1 were studied by Real-time PCR. Western blot was performed to detect the expression of TLR4 and NF-κB. RESULTS: The results indicated that blood urea nitrogen and creatinine levels increased significantly in I/R group. Rats treated with OzoneOP showed obviously less renal damage. Immunohistochemistry showed that TLR4 were ameliorated by OzoneOP. Realtime PCR showed that OzoneOP could significantly inhibit the increased mRNA levels of TNF-α, IL-1β, IL-6, ICAM-1 and MCP-1 induced by I/R. Western blot indicated that the expression of TLR4 and NF-κB were upregulated in I/R group, but OzoneOP could inhibit this increase. CONCLUSION: These findings indicated that OzoneOP had potent anti-inflammatory properties by the modulation of the TLR4-NF-κB pathway in renal ischemia/reperfusion injury. .

Acute hyperglycemia prevents dexmedetomidine-induced preconditioning against renal ischemia-reperfusion injury

PURPOSE: To investigate the effects of acute hyperglycemia on dexmedetomidine-induced preconditioning against renal ischemia-reperfusion injury. METHODS: Sprague-Dawley rats were randomly arranged to the normoglycemic (NG) or hyperglycemic group (HG), with each group further divided into sham (no I/R injury), I/R (ischemia-reperfusion) and dex (given by dexmedetomidine) groups. Acute hyperglycemia was induced by intraperitoneal injection (i.p.) of 25% glucose (3 g/kg) 45 min before ischemia. Dexmedetomidine (50 μg/kg, i.p.) was administrated 30 min before induction of ischemia. Renal function, histology, apoptosis, expression of Bax, Bcl-2 and phosphorylated AKT (p-AKT) were detected. RESULTS: I/R insult significantly increased the serum levels of blood urea nitrogen and creatinine, apoptotic tubular epithelial cells, expression of Bax and p-AKT, but decreased Bcl-2 expression. All these changes were further enhanced by hyperglycemia (p<0.05). In hyperglycemic condition, there was no statistically difference between the I/R group and Dex group in all the aforementioned detection indexes (p>0.05). CONCLUSION: Acute hyperglycemia attenuates dexmedetomidine-induced preconditioning against renal ischemia-reperfusion injury in non-diabetic rats. .

A percepção das mães sobre a obesidade em escolares: pesquisa e o impacto de uma intervenção educativa / Mothers' perception of obesity in schoolchildren: a survey and the impact of an educational intervention

OBJETIVOS: Investigar o conhecimento das mães a respeito do problema de peso dos filhos e avaliar o impacto de uma intervenção educativa na conscientização das mães sobre a obesidade dos filhos. MÉTODOS: Doze escolas primárias foram escolhidas aleatoriamente na cidade de Teerã, Irã. As crianças obesas foram selecionadas, e 300 mães participaram do estudo. Um questionário foi preenchido pelas mães, que a seguir foram divididas aleatoriamente em dois grupos. Um grupo recebeu instrução sobre obesidade, enquanto o outro grupo não recebeu nenhuma intervenção. Depois de 2 meses, o mesmo questionário foi preenchido pelos dois grupos. Foi realizada regressão logística múltipla. RESULTADOS: O conhecimento preexistente da mãe sobre obesidade, sua escolaridade e ocupação, assim como a renda familiar, tiveram efeitos significativos na exatidão das mães em identificar a obesidade nos filhos. A intervenção educativa melhorou significativamente a capacidade das mães em identificar a obesidade dos filhos, quando comparadas às que não receberam intervenção (OR = 15,23; IC95 por cento 5,95-38,96). CONCLUSÕES: No Irã, a maioria das mães não possui conhecimento geral sobre qual deve ser o peso saudável para uma criança, portanto foi incapaz de reconhecer que seus filhos estavam obesos. Intervenções educacionais poderiam reduzir a proporção de tal engano e posteriormente modificar o cuidado parental.

OBJECTIVES: To investigate mothers’ awareness of their children’s weight problem, and to evaluate the impact of an educational intervention on improving mothers’ recognition of obesity in their children. METHODS: Twelve primary schools from Tehran, Iran, were randomly chosen. Obese children were selected, and 300 mothers participated in the study. A questionnaire was completed by the mothers, who were then randomly divided into two groups. One group received education on obesity, whereas the other group did not receive any intervention. After 2 months, the same questionnaire was completed by both groups. A multiple logistic regression was performed. RESULTS: Mother's pre-existing knowledge on obesity, their education and occupation, as well as family income, had significant effects on mothers’ accuracy in identifying obesity in their children. The educational intervention significantly improved mothers’ ability to identify obesity in their children compared with those without any intervention (OR = 15.23; 95 percentCI 5.95-38.96). CONCLUSIONS: In Iran, a large proportion of mothers do not have general knowledge on healthy body weight for children, thus failing to recognize that their children are obese. Educational interventions could reduce the rate of such mistake and subsequently alter parental care.

Construction of a recombinant adenovirus co-expressing truncated human prostate-specific membrane antigen and mouse 4-1BBL genes and its effect on dendritic cells

Our aim was to construct a recombinant adenovirus co-expressing truncated human prostate-specific membrane antigen (tPSMA) and mouse 4-1BBL genes and to determine its effect on dendritic cells (DCs) generated from bone marrow suspensions harvested from C57BL/6 mice for which the effect of 4-1BBL on DCs is not clear, especially during DCs processing tumor-associated antigen. Replication deficient adenovirus AdMaxTM Expression System was used to construct recombinant adenovirus Ad-tPSMA-internal ribosome entry site-mouse 4-1BBL (Ad-tPSMA-IRES-m4-1BBL) and Ad-enhanced green fluorescent protein. Day 7 proliferating DC aggregates generated from C57BL/6 mice were collected as immature DCs and further mature DCs were obtained by lipopolysaccharide activated immature DCs. After DCs were exposed to the recombinant adenovirus with 250 multiplicity of infection, the expression of tPSMA and m4-1BBL proteins were detected by Western blot, and the apoptosis and phenotype of DCs were analyzed by flow cytometry. Cytokines (IL-6 and IL-12) in the supernatant were detected by enzyme-linked immunosorbent assay (ELISA). Proliferation of T cells was detected by allogeneic mixed lymphocyte reactions. The tPSMA and m4-1BBL proteins were expressed correctly. The apoptosis rate of DCs transfected with Ad-tPSMA-IRES-m4-1BBL was 14.6 percent, lower than that of control DCs. The expression of co-stimulatory molecules [CD80 (81.6 ± 5.4 percent) and CD86 (80.13 ± 2.81 percent)] up-regulated in Ad-tPSMA-IRES-m4-1BBL-pulsed DCs, and the level of IL-6 (3960.2 ± 50.54 pg/mL) and IL-12 (249.57 ± 12.51 pg/mL) production in Ad-tPSMA-IRES-m4-1BBL-transduced DCs were significantly higher (P < 0.05) than those in control DCs. Ad-tPSMA-IRES-m4-1BBL induced higher T-cell proliferation (OD450 = 0.614 ± 0.018), indicating that this recombinant adenovirus can effectively enhance the activity of DCs.