Abstract Introduction: Propofol is a widely used anesthetic and its dose is closely related to aging. Telomere length (TL) is a unique heritable trait, and emerging as a biomarker of aging, health and disease. Telomerase RNA component (TERC) plays an important role in maintaining TL. We proposed a hypothesis that propofol dose in general anesthesia can be predicted by measuring TL before operation, which greatly reduced the risk of anesthesia, especially the elderly. Methods: The association between the propofol dose in anesthesia induction and: TL in the DNA of peripheral blood leukocytes; body weight; sex; difference of the Bispectral Index (BIS) before and after anesthesia induction in patients was evaluated by multivariable linear regression analyses. The mutation at the 5’end or 3’end of TERC was detected. We recruited 100 patients of elective surgery. Results: We found that propofol dose in anesthesia induction was clearly correlated significantly with TL (r = 0.78, p < 0.001), body weight (r = 0.84, p = 0.004), sex (r = 0.83, p= 0.84, p = 0.004), sex (r = 0.83, p = 0.004), and difference of BIS before and after anesthesia induction (r = 0.85, p = 0.029). By comparing the absolute values of standardized regression coefficients (0.58, 0.21, 0.19, and 0.12) of the four variables, it can be seen that TL contributes the most to the propofol dose in anesthesia induction. However, the mutation at the 5’ end or 3’ end of TERC was not found. Conclusions: These findings provide preliminary evidence that the propofol dose in anesthesia induction was clearly correlated with genetically determined TL. TL may be a promising predictor of the propofol dose, which is beneficial to improve the safety of anesthesia and reduce perioperative complications.

SUMMARY: Gastrin plays a vital role in the development and progression of gastric cancer (GC). Its expression is up-regulated in GC tissues and several GC cell lines. Yet, the underlying mechanism remains to be investigated. Here, we aim to investigate the role and mechanism of gastrin in GC proliferation. Gastrin-overexpressing GC cell model was constructed using SGC7901 cells. Then the differentially expressed proteins were identified by iTRAQ analysis. Next, we use flow cytometry and immunofluorescence to study the effect of gastrin on the mitochondrial potential and mitochondria-derived ROS production. Finally, we studied the underlying mechanism of gastrin regulating mitochondrial function using Co-IP, mass spectrometry and immunofluorescence. Overexpression of gastrin promoted GC cell proliferation in vitro and in vivo. A total of 173 proteins were expressed differently between the controls and gastrin- overexpression cells and most of these proteins were involved in tumorigenesis and cell proliferation. Among them, Cox17, Cox5B and ATP5J that were all localized to the mitochondrial respiratory chain were down-regulated in gastrin-overexpression cells. Furthermore, gastrin overexpression led to mitochondrial potential decrease and mitochondria-derived ROS increase. Additionally, gastrin-induced ROS generation resulted in the inhibition of cell apoptosis via activating NF-kB, inhibiting Bax expression and promoting Bcl-2 expression. Finally, we found gastrin interacted with mitochondrial membrane protein Annexin A2 using Co-IP and mass spectrometry. Overexpr ession of gastrin inhibits GC cell apoptosis by inducing mitochondrial dysfunction through interacting with mitochondrial protein Annexin A2, then up-regulating ROS production to activate NF-kB and further leading to Bax/Bcl-2 ratio decrease.

RESUMEN: La gastrina juega un papel vital en el desarrollo y progresión del cáncer gástrico (CG). Su expresión está regulada al alza en tejidos de CG y en varias líneas celulares de CG. Sin embargo, el mecanismo subyacente aun no se ha investigado. El objetivo de este estudio fue investigar el papel y el mecanismo de la gastrina en la proliferación de CG. El modelo de células CG que sobre expresan gastrina se construyó usando células SGC7901. Luego, las proteínas expresadas diferencialmente se identificaron mediante análisis iTRAQ. A continuación, utilizamos la citometría de flujo y la inmunofluorescencia para estudiar el efecto de la gastrina en el potencial mitocondrial y la producción de ROS derivada de las mitocondrias. Finalmente, estudiamos el mecanismo subyacente de la gastrina que regula la función mitocondrial utilizando Co-IP, espectrometría de masas e inmunofluorescencia. La sobreexpresión de gastrina promovió la proliferación de células CG in vitro e in vivo. Un total de 173 proteínas se expresaron de manera diferente entre los controles y las células con sobreexpresión de gastrina y la mayoría de estas proteínas estaban implicadas en la tumorigenesis y la proliferación celular. Entre estas, Cox17, Cox5B y ATP5J, todas localizadas en la cadena respiratoria mitocondrial, estaban reguladas a la baja en las células con sobreexpresión de gastrina. Además, la sobreexpresión de gastrina provocó una disminución del potencial mitocondrial y un aumento de las ROS derivadas de las mitocondrias. Por otra parte, la generación de ROS inducida por gastrina resultó en la inhibición de la apoptosis celular mediante la activación de NF-kB, inhibiendo la expresión de Bax y promoviendo la expresión de Bcl-2. Finalmente, encontramos que la gastrina interactuaba con la proteína de membrana mitocondrial Anexina A2 usando Co-IP y espectrometría de masas. La sobreexpresión de gastrina inhibe la apoptosis de las células CG al inducir la disfunción mitocondrial a través de la interacción con la proteína mitocondrial Anexina A2, luego regula el aumento de la producción de ROS para activar NF-kB y conduce aún más a la disminución de la relación Bax/Bcl-2.

Abstract GnRH analogues were widely used for controlld ovary stimulation, but their effects on oocyte quality remain contradictory. This study aimed to explore the influence of GnRH analogues on oocyte quality in mice. A total of 120 mice were randomly assigned to four groups:(i)GnRH-a+PMSG group; (ii) GnRH-ant+PMSG group; (iii) PMSG group; (iv) Control group. Ovaries were collected for quantitative real-time polymerase chain reaction (qRT-PCR) to assess GDF9 and BMP15 mRNA expression, and protein expression were evaluated by western blotting. Moreover, embryo developmental progress in vitro and implantation rate in vivo were recorded. Compared with control group, both GDF9 mRNA and protein expressions were strengthened in PMSG group, but reduced in the presence of GnRH-a or GnRH-ant. The GnRH-a group exhibited decreased BMP15 mRNA expression compared to PMSG group, while the GnRH-ant group did not show the same pattern. BMP15 protein expression were not statisticlly different among the four groups. Notably, there was no statistically difference in the expression of these two factors between GnRH-a and GnRH-ant groups. The percentage of zygotes progressing to the 2-cell stage and percentage of 2-cell advancing to the blastocyst stage were similar in the PMSG group and control group. However, both the GnRH-a and GnRH-ant groups showed decreased embryos development rates compared to other two groups. The embryonic implantation rate in control group (53.3%) was higher than that in the GnRH-a and GnRH-ant groups (33.3% and 30.8%, P<0.05). The difference between the PMSG (45.0%) and GnRHa group was statistically significant (P value of 0.023), but not between the PMSG and GnRH-ant group (P value of 0.486). No statistical difference was confirmed between GnRH-a and GnRH-ant groups. Our findings shed light on the safety of GnRH analogues in ovary stimulation, and highlight the need for further research to establish optimal and effective controlled ovary stimulation protocol.

Abstract Introduction: Nutritional status can affect the treatment of hospitalized patients, and Malnutrition can even lead to death. However, the Nutritional status of patients with aplastic anemia (AA) is unclear. Objective: to assess the Nutritional status of aplastic anemia patients with body mass index (BMI) ≥ 24 kg/m2 (high BMI group) and BMI < 24 kg/m2 (low BMI group), and to compare the consistency between different Nutritional screening tools. Methods: patients with aplastic anemia hospitalized from January 2016 to December 2020 were collected. We used the combined index generated by Nutritional Risk Index (NRI), Prognostic Nutritional Index (PNI), Control Nutritional Status (CONUT) and Instant Nutritional Assessment (INA) to assess Nutritional status of patients with aplastic anemia. Kappa index was used to measure the consistency between different Nutritional screening tools. Receiver operating characteristic (ROC) curve was used to evaluate the diagnostic value of different Nutritional screening tools. Results: one hundred and ninety-five patients with aplastic anemia were enrolled. The overall prevalence of Malnutrition calculated by the combined index in patients with aplastic anemia was 51.3 %. The Malnutrition rates of patients in the low BMI group and high BMI group were 60.9 % and 38.8 %, respectively. The Malnutrition rates of very severe aplastic anemia (VSAA) patients, severe aplastic anemia (SAA) patients and ordinary patients were 76 %, 63.8 % and 45.1 %, respectively. Compared with the combined index, NRI had the highest consistency and area under the curve. Conclusions: the Nutritional status of patients with aplastic anemia was very poor; the more serious the disease, the worse the Nutritional status. Although the Malnutrition rate in the low-BMI group was higher than in the high BMI group, the Nutritional status of overweight or obese patients can not be ignored. NRI is the best tool for assessing the Nutritional status of patients with aplastic anemia.

Resumen Introducción: el estado nutricional puede afectar el tratamiento de los pacientes hospitalizados y la malnutrición puede incluso causar la muerte. Sin embargo, el estado nutricional de los pacientes con anemia aplásica (AA) no está claro. Objetivo: evaluar el estado nutricional de pacientes con anemia aplásica con índice de masa corporal (IMC) ≥ 24 kg/m2 (grupo de IMC mayor) e IMC < 24 kg/m2 (grupo de IMC inferior), y comparar la consistencia entre diferentes herramientas de cribado nutricional. Métodos: se recogieron datos de pacientes con anemia aplásica hospitalizados entre enero de 2016 y diciembre de 2020. El estado nutricional de los pacientes con anemia aplásica se evaluó utilizando un índice compuesto por el índice de riesgo nutricional (NRI), el índice de pronóstico nutricional (PNI), el índice de estado nutricional controlado (CONUT) y la evaluación nutricional instantánea (INA). El índice Kappa se utilizó para medir la coherencia entre los diferentes instrumentos de detección nutricional. Las curvas de características operativas de los sujetos (ROC) se utilizaron para evaluar el valor diagnóstico de las diferentes herramientas de detección nutricional. Resultados: un total de 195 pacientes con anemia aplásica fueron incluidos en el estudio. La prevalencia global de desnutrición calculada por el índice combinado en pacientes con anemia aplásica fue del 51,3 %. Las tasas de desnutrición de los pacientes en el grupo de bajo IMC y el grupo de alto IMC fueron 60,9 % y 38,8 %, respectivamente. Las tasas de desnutrición en pacientes con anemia aplásica muy grave (VSAA), anemia aplásica grave (SAA) y pacientes comunes fueron del 76 %, 63,8 % y 45,1 %, respectivamente. En comparación con el índice compuesto, NRI tiene la mayor consistencia y área bajo la curva. Conclusiones: el estado nutricional de los pacientes con anemia aplásica es muy deficiente; a mayor gravedad de la enfermedad, peor estado nutricional. Aunque la tasa de malnutrición en el grupo con bajo IMC es mayor que en el grupo con alto IMC, no se puede pasar por alto el estado nutricional de los pacientes con sobrepeso u obesidad. El NRI es la mejor herramienta para evaluar el estado nutricional de los pacientes con anemia aplásica.

Abstract Introduction: Noise-induced hearing loss is one of the most common forms of sensorineural hearing loss. Nevertheless, the mechanisms of noise-induced hearing loss are still not fully understood. Objective: To investigate the dynamics of inflammatory responses in the mammalian cochlea following noise trauma at two different times, once during the light cycle and once during the dark. Methods: We challenged C57BL/6J mice with moderate, continuous noise trauma at either 9 a.m. or 9 p.m. Auditory function, histological changes in hair cells, and modifications in gene expression levels of inflammatory mediators were assessed at specific time points. Shifts in auditory brainstem response thresholds were measured at 1, 3, 7 and 14 days after noise exposure to measure potential noise-induced hearing loss. Cochlear basilar-membrane immunofluorescent staining was performed at 3 and 14 days after noise exposure. The mRNA levels of several inflammatory mediators were measured via quantitative real-time polymerase chain reaction before (pre) and after (0, 3, 12, 24 and 72 h) noise exposure. Results: We found that all noise-exposed mice developed a temporary threshold shift and that there were no significant differences between daytime and nighttime noise exposures in terms of inducing hearing-threshold shifts. Similarly, we did not detect significant histological changes in hair cells between these two groups. However, we discovered an interesting phenomenon in that the peak mRNA levels of IL-1β, IL-6, CCL2 and TNF-α were higher in day noise-exposed mice compared to those in night noise-exposed mice, and these mRNA levels subsided more slowly in day noise-exposed mice. Conclusion: Overall, these observations suggest that the circadian timing of noise exposure has a significant effect on noise-induced inflammatory responses in the mouse cochlea and that a greater inflammatory response might occur after daytime exposure.

Abstract Background: In Alzheimer’s disease (AD), the neuroinflammatory response mediated by the activation of senescent microglia is closely related to energy dysmetabolism. However, the mechanism underlying the interaction between the energy metabolism of aging microglia and neuroinflammation remains unclear. Methods: We used biochemical methods, enzyme-linked immunosorbent assay (ELISA), immunofluorescence, and western blot to determine the effects and mechanism of CD38 knockdown on energy metabolism and neuroinflammation in Aβ1-40 injured BV2 cells. Using AD model mice, we detected CD38 enzyme activity, energy metabolism factors (ATP, NAD +, and NAD +/NADH), and neuroinflammatory factors (IL-1β, IL-6, and TNF-α) following the addition of CD38 inhibitor. Using a combination of biochemical analysis and behavioral testing, we analyzed the effects of the CD38 inhibitor on energy metabolism disorder, the neuroinflammatory response, and the cognition of AD mice. Results: Following Aβ1-40 injury, SA-β-Gal positive cells and senescence-related proteins P16 and P21 increased in BV2 cells, while energy-related molecules (ATP, NAD +, and NAD +/NADH) and mitochondrial function (mitochondrial ROS and MMP) decreased. Further studies showed that CD38 knockdown could improve Aβ1-40-induced BV2 cells energy dysmetabolism and reduce the levels of IL-1β, IL-6, and TNF-α. In vivo results showed an increase in senile plaque deposition and microglial activation in the hippocampus and cortex of 34-week-old APP/PS1 mice. Following treatment with the CD38 inhibitor, senile plaque deposition decreased, the number of Iba1 +BV2 cells increased, the energy metabolism disorder was improved, the proinflammatory cytokines were reduced, and the spatial learning ability was improved. Conclusions: Our results confirm that senescent microglia appeared in the brain of 34-week-old APP/PS1 mice, and that Aβ1-40 can induce senescence of BV2 cells. The expression of CD38 increases in senescent BV2 cells, resulting in energy metabolism disorder. Therefore, reducing CD38 expression can effectively improve energy metabolism disorder and reduce proinflammatory cytokines. Following intervention with the CD38 inhibitor in APP/PS1 mice, the energy metabolism disorder was improved in the hippocampus and cortex, the level of proinflammatory cytokines was reduced, and cognitive impairment was improved.

Abstract Immature Litsea mollis fruits (ILMFs) are widely used as cold appetizers and seasonings in China. The free and bound volatile components of ILMFs from five distinct regions of China were determined by gas chromatography-mass spectrometry (GC-MS) combined with headspace solid phase microextraction (SPME) in the present work. The results reveal sixty six free-form volatiles and fifty two bound-form volatiles in ILMFs and terpene hydrocarbons and oxygenated terpenes are the dominate components. In addition, sixty-seven volatile compounds are found in Litsea mollis fruit for the first time. The free α-pinene, eucalyptol, linalool, α,β-citral, geraniol and citronellal, and bound β-myrcene, α-citral, geraniol, citronellal and eugenol are the major odor contributors of ILMFs. Multivariate statistical analysis indicates that the free and bound volatiles profiles of ILMFs of Fujian and Guangxi in southern China are similar and those of Yunnan and Sichuan in southwestern China are similar. The odor profiles of all of the ILMFs are floral, fruity and herbaceous.

Abstract Ginger is traditionally used as a sexual enhancer in folk medicine. Despite extensive studies on the effect of ginger on reproduction, the molecular mechanism of ginger prevention effect on ethanol-induced reproductive disorder is not fully understood. Twenty-four adult male ratswereallocated into control, ethanol (4 g/kg of body weight (BW)/day), ginger (250 mg/kg of BW/day) and ginger-ethanol group. Ginger and ethanol were administrated by gavage for 28 days. Testicular concentration of testosterone, TNF-α, and antioxidant enzymes activity and serum concentration of gonadotropins hormone and testosterone were measured. The gene expression of Nrf2 and NF-κB which regulate oxidative damage and inflammation, respectively, and StAR, P450scc and 17βHSD which are involved in testosterone synthesis were detected. Ethanol significantly decreased gonadotropin hormones, oxidative markers, expression of genes involved in testosterone synthesis and Nrf2, and in reverse significantly increased TNF-α, MDA and gene expression of NF-κB compared to control (p<0.05). While ginger could significantly improve all of the above factors compared to the ethanol group (p<0.05). These results were also supported by histological findings. It can be concluded that ginger prevents the ethanol-induced reproductive dysfunction by improving the gonadotropins, oxidative damage and inflammation and the genes involved in testosterone synthesis.

Resumo Introdução e objetivos Os mecanismos de neurotoxicidade dos anestésicos locais são complexos. A apoptose e a autofagia são mecanismos altamente organizados que mantêm a homeostase celular durante o estresse. Estudos revelam que a ativação da autofagia atua como mecanismo de proteção in vitro. Não está claro se a autofagia também desempenha essa função in vivo. O objetivo deste estudo foi analisar o papel da autofagia na neurotoxicidade induzida por anestésico local e esclarecer o mecanismo dessa neurotoxicidade utilizando um modelo de injeção intratecal em ratos. Métodos Dezoito ratos Sprague‐Dawley machos adultos saudáveis foram divididos aleatoriamente em três grupos. Antes de receber a injeção intratecal de bupivacaína a 1%, cada rato recebeu injeção intraperitoneal de veículo ou rapamicina (1 mg.kg‐1) uma vez ao dia durante 3 dias. As alterações patológicas foram examinadas por coloração com Hematoxilina e Eosina (HE). A apoptose foi analisada por coloração com o método dUTP Nick‐End Labeling (TUNEL) mediado por TdT. A expressão de caspase‐3, Beclin1 e LC3 foram examinadas por coloração Imunohistoquímica (IHQ). A expressão de Beclin1 e LC3 e a razão LC3‐II/LC3‐I foram detectadas por análise de western blot. Resultados Após a injeção intratecal de bupivacaína, ocorreu lesão patológica nos neurônios da medula espinhal e os níveis de apoptose e caspase‐3 aumentaram. A ativação da autofagia causada pela rapamicina mitigou de forma expressiva as alterações patológicas e diminuiu os níveis de apoptose e caspase‐3, aumentando a expressão de LC3 e Beclin1 e a razão LC3‐II/LC3‐I. Conclusões O aumento da autofagia diminui a apoptose dependente da caspase‐3 e melhora a sobrevivência neuronal in vivo. A ativação da autofagia pode ser uma estratégia terapêutica potencial para a neurotoxicidade induzida por anestésicos locais.

Abstract Background and objectives The mechanisms by which local anesthetics cause neurotoxicity are very complicated. Apoptosis and autophagy are highly coordinated mechanisms that maintain cellular homeostasis against stress. Studies have shown that autophagy activation serves as a protective mechanism in vitro. However, whether it also plays the same role in vivo is unclear. The aim of this study was to explore the role of autophagy in local anesthetic-induced neurotoxicity and to elucidate the mechanism of neurotoxicity in an intrathecally injected rat model. Methods Eighteen healthy adult male Sprague-Dawley rats were randomly divided into three groups. Before receiving an intrathecal injection of 1% bupivacaine, each rat received an intraperitoneal injection of vehicle or rapamycin (1 mg.kg-1) once a day for 3 days. The pathological changes were examined by Haematoxylin and Eosin (HE) staining. Apoptosis was analysed by TdT-mediated dUTP Nick-End Labelling (TUNEL) staining. Caspase-3, Beclin1 and LC3 expression was examined by Immunohistochemical (IHC) staining. Beclin1 and LC3 expression and the LC3-II/LC3-I ratio were detected by western blot analysis. Results After bupivacaine was injected intrathecally, pathological damage occurred in spinal cord neurons, and the levels of apoptosis and caspase-3 increased. Enhancement of autophagy with rapamycin markedly alleviated the pathological changes and decreased the levels of apoptosis and caspase-3 while increasing the expression of LC3 and Beclin1 and the ratio of LC3-II to LC3-I. Conclusions Enhancement of autophagy decreases caspase-3-dependent apoptosis and improves neuronal survivalin vivo. Activation of autophagy may be a potential therapeutic strategy for local anaesthetic-induced neurotoxicity.

Abstract This study optimized using a headspace solid-phase microextraction (HS-SPME) method for extracting volatile aroma compounds, terpenoids in particular, from Litsea mollis Hemsl. immature fruit (LMIF). Gas chromatography-mass spectrometry was used to separate and identify volatile terpenoids in LMIF. The types of SPME fiber coating, salt addition, and desorption time were optimized by single factor-experiments to determine the range of extraction temperature. Built on insights from the single factor-experiments, the response surface methodology was further used to optimize the extraction temperature, extraction time, and equilibrium time of HS-SPME. The results showed that the optimal HS-SPME conditions for extracting volatile terpenoids from LMIF were: 50/30 μm of DVB/CAR/PDMS SPME fiber, 2.0 g of added sodium chloride, desorption at a temperature of 250 °C for 3 min, extraction and equilibrium temperature of 46 °C, extraction time of 36 min, and equilibrium time of 20 min. Under the above conditions, the predicted value of extraction was 66.92, while the experimental value was 65.78. The prediction value matched well with the experimental value with good repeatability. The designed model was proven to be valid, which can be applied for future extraction of aroma compounds from IMIF.

SUMMARY: This study aimed to examine the differences in bone microarchitecture between different regions of the atlas in 28 dry atlas specimens using micro-CT, in order to explain the mechanism of the predilection sites of atlas fractures from the morphological point of view. A total of 28 dry specimens of intact adult atlas were randomly selected, scanned by micro-CT, and divided into a region from the anterior arch midpoint (AAM) to the lateral masses (LM), a LM region, and a region from the LM to the posterior arch midpoint (PAM). Trabecular thickness, separation, number, connectivity, and structure model index were measured for each of the three regions using the built-in software of the CT scanner. Trabecular thickness was all measured to be 0.11 ± 0.00 mm for AAM to LM, LM, and LM to PAM. Trabecular separation: AAM to LM > LM to PAM > LM. Trabecular number: LM > LM to PAM > AAM to LM. Connectivity: LM > LM to PAM > AAM to LM. Structure model index: LM > LM to PAM > AAM to LM. A lower trabecular number and connectivity and higher trabecular separation were seen in the anterior and posterior arches of the atlas, in which higher fracture rates were reported. By contrast, a higher trabecular number and connectivity and lower trabecular separation were seen in the lateral masses, in which lower fracture rates were reported.

RESUMEN: Este estudio tuvo como objetivo examinar las diferencias en la microarquitectura ósea entre diferentes regiones del atlas en 28 muestras de atlas secas utilizando micro-CT, con el fin de informar el área de mayor frecuencia en las fracturas de atlas, desde el punto de vista morfológico. Se seleccionaron al azar un total de 28 muestras secas de atlas adultos intactas las que se escanearon por micro-CT y se dividieron en una región desde el punto medio del arco anterior (MAA) hasta las masas laterales (ML), una región ML y una región desde el ML hasta el punto medio del arco posterior (MAP). Se midió el grosor trabecular, la separación, el número, la conectividad y el índice del modelo de estructura para cada una de las tres regiones utilizando el software incorporado del escáner CT. El grosor trabecular se midió en 0,11 ± 0,00 mm para MAA a ML, ML y ML a MAP. Separación trabecular: MAA a ML> ML a MAP> ML. Número trabecular: ML> ML a MAP> MAA a ML. Conectividad: ML> ML a MAP> MAA a ML. Índice del modelo de estructura: ML> ML a MAP> MAA a ML. Se observó un menor número de estructuras trabeculares y conectividad y una mayor separación trabecular en los arcos anterior y posterior del atlas, en los que se informaron tasas de fracturas más altas. Por el contrario, se observó un mayor número de estructuras trabeculares y conectividad, y una menor separación trabecular en las masas laterales, en las que se observó un número menor de fracturas.

SUMMARY: This study aimed to investigate the sagittal spinal-pelvic morphological changes, as well as the relationship between pelvic anatomical changes and the spinal-pelvic plane in patients with adolescent idiopathic scoliosis (AIS), in order to provide guidelines for orthopedic surgery in AIS. X-ray data were collected for retrospective analysis from 30 patients diagnosed as AIS in the Departments of Radiology at the Second Affiliated Hospital of Inner Mongolia Medical University and the Inner Mongolia International Mongolian Medical Hospital from April 2014 to November 2018, along with 30 normal adolescents as control. Pelvic parameters, including pelvic incidence (PI), pelvic tilt (PT), and sacral slope (SS), a spinal parameter, lumbar lordosis (LL), and anatomical parameters, including sacral width (SW) and femoral head- sacrum distance (FH-S), were measured. The spinal-pelvic parameters were compared between AIS patients and normal controls and also between male and female AIS patients. Pearson correlation was performed to analyze correlation between spinal-pelvic parameters and between spinal-pelvic parameters and anatomical parameters in both AIS patients and normal controls. PT was significantly lower in AIS patients than in normal controls (P < 0.05), whereas no significant difference was found in the other spinal-pelvic parameters, i. e. , LL, PI, and SS. There was a significant difference in PT between sexes in AIS patients. SS was significantly correlated with LL in EIA patients (P < 0.05, r > 0.5). SS was significantly correlated with LL and PI, and PT with LL, PI, and SS in normal controls (all P < 0.05), and there was no significant correlation between the other sagittal spinal-pelvic parameters (P > 0.05). FH-S was significantly correlated with LL, PI, SS, and PT in AIS patients (all P < 0.05). AIS affects some of the sagittal spinalpelvic parameters and anatomical parameters. In AIS, there is a significant correlation between the spinal-pelvic parameters, and the anatomical parameter is significantly correlated with multiple spinal-pelvic parameters.

RESUMEN: Este estudio tuvo como objetivo investigar los cambios morfológicos sagitales de la columna vertebral-pélvica, así como la relación entre los cambios anatómicos pélvicos y el plano espinal-pélvico en pacientes con escoliosis idiopática adolescente (EIA), con el fin de proporcionar pautas para la cirugía ortopédica en AIS. Se obtuvieron los datos de rayos X para el análisis retrospectivo de 30 pacientes diagnosticados como EIA en los Departamentos de Radiología del hospital Second Affiliated Hospital of Inner Mongolia Medical University y el hospital Inner Mongolia International Mongolian Medical Hospital, desde abril de 2014 hasta noviembre del 2018, junto con 30 adolescentes normales como control. Se midieron los parámetros pélvicos, que incluyeron incidencia pélvica (IP), inclinación pélvica (P) y pendiente sacra (PS), un parámetro espinal, lordosis lumbar (LL) y parámetros anatómicos, que incluyeron el ancho sacro (AS) y la distancia del sacro cabeza femoral (FH-S). Los parámetros espinalpélvicos se compararon entre los pacientes con EIA y los controles normales, como también entre pacientes con EIA masculinos y femeninos. La correlación de Pearson se realizó para analizar la correlación entre los parámetros espinal-pélvicos y entre los parámetros espinal-pélvicos y los parámetros anatómicos tanto en pacientes con EIA como en controles normales. PT fue significativamente menor en pacientes con EIA que en los controles normales (P <0,05), mientras que no se encontraron diferencias significativas en los otros parámetros espinal-pélvicos, i. mi. , LL, PI y SS. Hubo una diferencia significativa en PT en pacientes de ambos sexos con EIA. SS se correlacionó significativamente con LL en pacientes con EIA (P <0,05, r> 0,5). SS se correlacionó significativamente con LL y PI, y PT con LL, PI y SS en controles normales (todos P <0,05), y no hubo correlación significativa entre los otros parámetros sagitales de la columna vertebral-pélvica (P> 0,05) FH-S se correlacionó significativamente con LL, PI, SS y PT en pacientes con EIA (todos P <0,05). EIA afecta algunos de los parámetros sagitales de la columna vertebral-pélvica y los parámetros anatómicos. En EIA, existe una correlación significativa entre los parámetros espinal-pélvicos, y el parámetro anatómico se correlaciona significativamente con múltiples parámetros espinales-pélvicos.

Abstract Aflatoxin is a carcinogenic secondary metabolite produced mainly by Aspergillus flavus and Aspergillus parasiticus, which can seriously endanger the health of humans and animals. Oxidative stress is a common defense response, and it is known that reactive oxygen species (ROS) can induce the synthesis of a series of secondary metabolites, including aflatoxin. By using mutants lacking the afap 1 gene, the role of afap 1 gene in oxidative stress and aflatoxin synthesis was assessed. The growth of the mutant strains was significantly inhibited by the increase in the concentration of H2O2, inhibition was complete at 40mmol/l. However, in the quantitative analysis by HPLC, the concentration of AFB1 increased with the increased H 2O 2 until 10mmol/l. Following an analysis based on the information provided by the NCBI BLAST analysis, it was assumed that Afap1, a basic leucine zipper (bZIP) transcription factor, was associated with the oxidative stress in this fungus. Treatment with 5mmol/l H 2O 2 completely inhibited the growth of the mutant strains in afap 1 but did not affect the growth of the CA14PTs strain (non-mutant strain). In addition, the concentration of AFB 1 in the mutant strains was approximately V of that observed in the CA14PTs strain. These results suggested that Afap1 plays a key role in the regulation of oxidative stress and aflatoxin production in A. flavus. ©2018 Published by Elsevier España, S.L.U. on behalf of Asociación Argentina de Microbiología. This is an open access article under the CC BY-NC-ND license (https://creativecommons.org/ licenses/by-nc-nd/4.0/).

Resumen La aflatoxina es un metabolito secundario cancerígeno producido principalmente por Aspergillus flavus y Aspergillus parasiticus, que pone en riesgo grave a la salud de los humanos y los animales. El estrés oxidativo es una respuesta de defensa común, y es sabido que las especies reactivas de oxígeno (ROS) pueden inducir la síntesis de una serie de metabolitos secundarios, incluida la aflatoxina. Empleando mutantes carentes del gen afap1 se evaluó el papel de Afap1 en el estrés oxidativo y la síntesis de aflatoxinas. El crecimiento de las cepas mutadas se vio significativamente inhibido con el aumento de la concentración de H 2O 2, la inhibición fue completa a 40mmol/l. Sin embargo, en el análisis cuantitativo por HPLC, la concentración de la aflatoxina AFBi aumentó con el aumento de la concentración de H 2O 2 hasta 10mmol/l. Tras un análisis apoyado en la información provista por la herramienta NCBI BLAST, se supuso que Afap1, un factor de transcripción de la cremallera de leucina básica (bZIP), estaba asociado con el estrés oxidativo en este hongo. El tratamiento con 5mmol/l de H 2O 2 inhibió completamente el crecimiento de las cepas mutantes en afap1, pero no afectó el crecimiento de la cepa CA14PTs (cepa no mutada). Además, la concentración de AFB 1 en las cepas mutadas fue de aproximadamente 1/4 de la observada en CA14PTs. Estos resultados sugieren que Afap1 juega un papel clave en la regulación del estrés oxidativo y la producción de aflatoxinas en A. flavus.

Objetivo: Buscamos testar os efeitos de diferentes doses de pioglitazona (PIO) sobre a expressão glomerular de podocalixina e sobre a excreção de podocalixina em células do sedimento urinário, além de explorar o potencial mecanismo de proteção renal. Materiais e métodos: O diabetes tipo 1 foi induzido em 36 ratos Sprague-Dawley machos com estreptozotocina (65 mg/kg). Os animais foram tratados apenas com o veículo, ou com 10, 20, 30 mg/kg/d de PIO por 8 semanas. Oito ratos foram colocados no grupo controle. Resultados: Na oitava semana, os ratos foram sacrificados para se observar a lesão renal em microscopia eletrônica. A produção de podocalixina glomerular, incluindo mRNA e proteína, foi determinada por RT-PCR e imuno-histoquímica, respectivamente. Os níveis urinários de albumina e podocalixina nas células do sedimento urinário e o índice de lesão renal estavam todos significativamente aumentados, enquanto a expressão glomerular da proteína podocalixina e do mRNA estava significativamente diminuída em ratos diabéticos comparados com o controle normal. A análise dos efeitos dose-dependentes revelou que o efeito protetor da PIO melhorou as mudanças fisiopatológicas e atingiu um pico na dose de 20 mg/kg/dia. Conclusão: A PIO pode melhorar a injúria renal de forma dose-dependente e este papel pode estar associado com a prevenção da excreção de podocalixina nas células do sedimento urinário e com a preservação da expressão glomerular de podocalixina.

Objective: We sought to test the effect of different dosages of pioglitazone (PIO) on the glomerular expression of podocalyxin and urinary sediment podocalyxin excretion and to explore the potential renoprotective mechanism. Materials and methods: Type 1 diabetes induced with streptozotocin (65 mg/kg) in 36 male Sprague-Dawley rats were randomly allocated to be treated with vehicle or 10, 20, 30 mg/kg/d PIO respectively for 8 weeks. Eight rats were enrolled in the normal control group. Results: At 8th week, rats were sacrificed for the observation of kidney injury through electron microscope. Glomerular podocalyxin production including mRNA and protein were determined by RT-PCR and immunohistochemistry respectively. Levels of urinary albumin excretion and urinary sediment podocalyxin, kidney injury index were all significantly increased, whereas expression of glomerular podocalyxin protein and mRNA were decreased significantly in diabetic rats compared to normal control. Dosages-dependent analysis revealed that protective effect of PIO ameliorated the physiopathological changes and reached a peak at dosage of 20 mg/kg/d. Conclusion: PIO could alleviate diabetic kidney injury in a dose-dependent pattern and the role may be associated with restraining urinary sediment podocalyxin excretion and preserving the glomerular podocalyxin expression.

OBJECTIVE: To identify factors driving the rapid increase in caesarean section in China between 1988 and 2008. METHODS: Data from four national cross-sectional surveys (1993, 1998, 2003 and 2008) and modified Poisson regression were used to determine whether changes in household income, access to health insurance or women's education accounted for the rise in caesarean sections in urban and rural areas. FINDINGS: In 2008, 64.1% of urban women and 11.3% of women in the poorest rural region reported giving birth by caesarean section. A fast rise was occurring in all socioeconomic groups. Between 1993 and 2008, the risk of caesarean section had increased more than threefold in urban areas (relative risk, RR: 3.63; 95% confidence interval, CI: 2.61-5.04) and more than 15-fold in rural areas (RR: 15.46; 95% CI: 10.46-22.86). After adjustment for improvements in income, education and access to health insurance over the study period, the RR dropped minimally in urban areas (RR: 3.07; 95% CI: 2.32-4.07), which suggests that these factors do not explain the rise; in rural areas, the adjusted RR dropped to 7.18 (95% CI: 4.82-10.69), which shows that socioeconomic change is only partly responsible for the rise. Socioeconomic region of residence was a more important driver of the caesarean section rate than individual socioeconomic status. CONCLUSION: The large variation in caesarean section rate by socioeconomic region - independent of individual income, health insurance or education - suggests that structural factors related to service supply have influenced the increasing rate more than a woman's ability to pay.

OBJETIVO: Identificar los factores que propiciaron un rápido incremento de las cesáreas en China entre 1988 y 2008. MÉTODOS: Se utilizaron datos procedentes de cuatro encuestas transversales (1993, 1998, 2003 y 2008), así como la regresión de Poisson modificada para determinar si los cambios en los ingresos familiares, el acceso al seguro sanitario o la educación de las mujeres contribuyeron al aumento de las cesáreas en áreas urbanas y rurales. RESULTADOS: En 2008 se informó de que el 64,1% de las mujeres residentes en áreas urbanas y el 11,3% de las mujeres residentes en áreas rurales dieron a luz mediante cesárea. Se produjo un rápido incremento en todos los grupos socioeconómicos. Entre 1993 y 2008, el riesgo de dar a luz mediante cesárea aumentó más de tres veces en áreas urbanas (riesgo relativo, RR: 3,63; 95% intervalo de confianza, IC: 2,61-5,04) y más de 15 veces en áreas rurales (RR: 15,46; 95% IC: 10,46-22,86). Después del ajuste de las mejoras en los ingresos, educación y acceso al seguro sanitario durante el periodo de estudio, el RR registró una reducción mínima en las áreas urbanas (RR: 3,07; 95% IC: 2,32-4,07), lo que sugiere que estos factores no explican el aumento; en áreas rurales el RR ajustado se redujo hasta 7,18 (95% IC: 4,82-10,69), lo que demuestra que el cambio socioeconómico solo es parcialmente responsable del aumento. La región socioeconómica de residencia fue un impulsor más importante que el estatus socioeconómico individual para el aumento de la tasa de cesárea. CONCLUSIÓN: La gran variación en la tasa de cesárea por región socioeconómica, independientemente de los ingresos individuales, del seguro sanitario o de la educación, sugiere que los factores estructurales relacionados con el suministro de servicios han influido más en el aumento de dicha tasa que la solvencia de las mujeres.

OBJECTIF: Identifier les facteurs de l'augmentation rapide du nombre de césariennes en Chine entre 1988 et 2008. MÉTHODES: Les données de quatre enquêtes nationales transversales (1993, 1998, 2003 et 2008) et une régression modifiée de Poisson ont été utilisées pour déterminer si des changements dans le revenu des ménages, dans l'accès à l'assurance maladie ou dans l'éducation des femmes expliquaient la hausse du nombre de césariennes dans les zones urbaines et rurales. RÉSULTATS: En 2008, 64,1% des citadines et 11,3% des femmes des régions rurales les plus pauvres ont déclaré avoir donné naissance par césarienne. Une hausse accélérée s'est produite dans tous les groupes socioéconomiques. Entre 1993 et 2008, le risque de césarienne a plus que triplé dans les zones urbaines (risque relatif, RR: 3,63, intervalle de confiance de 95%, IC: 2,61-5,04) et a été multiplié par 15 dans les zones rurales (RR: 15,46, IC de 95%: 10,46-22,86). Après ajustement pour améliorations de revenu, d'éducation et d'accès à l'assurance maladie au cours de la période d'étude, le RR a peu chuté dans les zones urbaines (RR: 3,07, IC de 95%: 2,32-4,07), ce qui suggère que ces facteurs n'expliquent pas l'augmentation. Dans les zones rurales, le RR ajusté a chuté à 7,18 (IC de 95%: 4,82-10,69), ce qui montre que l'évolution socioéconomique n'est que partiellement responsable de la hausse. La région socioéconomique de résidence a plus influencé le taux de césarienne que le statut socioéconomique individuel. CONCLUSION: La grande variation du taux de césarienne par région socioéconomique, indépendamment du revenu individuel, de l'assurance maladie ou de l'éducation, suggère que des facteurs structurels liés à la fourniture de services ont influencé la hausse du taux, plus que la capacité de paiement de la femme.