Adjustment of the performance and stability of isostructural zeolitic tetrazolate-imidazolate frameworks.

Presented here are two isostructural SOD-type zeolitic tetrazolate-imidazolate frameworks (ZTIFs), Zn(etz)0.86(mim)1.14 (ZTIF-9, Hetz = 5-ethyltetrazole, Hmim = 2-methylimidazole) and Zn(vtz)0.63(mim)1.37 (ZTIF-10, Hvtz = 5-vinyltetrazole). The adjustment of the ligand ratios within these ZTIFs was realized through changing the substituent groups of tetrazole ligands. Remarkably, ZTIF-9 with a suitable ligand ratio perfectly balances gas uptake and stability, exhibiting 6-fold improvement of C2H2 uptake compared to the prototype ZIF-8 (Zn(mim)2).

Inhibitory effects of peripheral administration of exendin-4 on food intake are attenuated by lesions of the central nucleus of amygdala.

The long-acting glucagon-like peptide-1 receptor (GLP-1R) agonist exendin-4 suppresses food intake and decreases body weight. However, the mediating site(s) of action of the anorectic effects induced by peripheral administration of GLP-1R agonists are not well known. The present study investigated the effects of bilateral lesions of the central nucleus of the amygdala (CeA) on the suppression of chow and high-sucrose food intake by exendin-4 in rats. Adult male Sprague-Dawley rats with bilateral sham or electrolytic lesions (400 µA; 25 s) of the CeA were used for this experiment. No significant difference was found in the daily chow intake and high-sucrose food intake in rats with CeA lesion compared to sham-operated rats. Bilateral lesions of the CeA significantly attenuated the suppression of high-sucrose food intake by i.p. exendin-4, but not the suppression of chow intake. These results suggest that a mediating role of the CeA on the peripheral effects of exendin-4.

Homoeriodictyol protects human endothelial cells against oxidative insults through activation of Nrf2 and inhibition of mitochondrial dysfunction.

Excess intracellular reactive oxygen species (ROS) production is a significant causative factor of many diseases, exemplified by vascular diseases. Mitochondria are a major source of endogenous ROS, which simultaneously induce mitochondrial dysfunction. Nuclear factor-erythroid 2-related factor 2 (Nrf2) represents an important intracellular defense system that protects cells against oxidative insults caused by ROS. Therefore, molecules with the capacities of inducing Nrf2, and preventing mitochondrial dysfunction can inhibit cell apoptosis, and thus are potential drug candidates for the therapy of ROS-mediated vascular diseases. Homoeriodictyol (HE), previously isolated from Viscum articulatum Burm, has been found to be an Nrf2 inducer. In the present study, we investigated its protection on ROS-induced endothelial cell injury using a H2O2-induced human umbilical vein EA.hy926 cell oxidative insult model. Our results indicated that HE activated Nrf2 signaling pathway and protected cells against H2O2-induced cell damage. HE alleviated H2O2-induced loss of mitochondrial membrane potential (MMP), blocked the releases of cytochrome C and apoptosis inducing factor (AIF) from mitochondria, and thus inhibited mitochondria-mediated cell apoptosis. Furthermore, HE inhibited H2O2-induced changes of apoptosis-related proteins, such as Bcl-2, Bcl-xL, caspases -3, -9 and PARP. Further study demonstrated that the protection of HE against H2O2-induced endothelial cell damage was Nrf2-dependent. Collectively, our observations suggest that HE is capable of counteracting oxidative insults in endothelial cells, and has a potential to be a therapeutic agent against ROS-mediated vascular diseases.

Podoimbricatin A, a cytotoxic diterpenoid with an unprecedented 6/6/5/6-fused tetracyclic ring system from the twigs and leaves of Podocarpus imbricatus.

Podoimbricatin A (1), a diterpenoid possessing an unprecedented 6/6/5/6-fused tetracyclic ring system, and podoimbricatin B (2), a new abietane-type diterpenoid, together with four previously reported diterpenoids and a cyclic peptide were isolated from the twigs and leaves of Podocarpus imbricatus. Their structures were established on the basis of extensive spectroscopic analyses and the relative configuration of 1 was confirmed by single-crystal X-ray diffraction analysis. A plausible biogenetic pathway involving hetero-Diels-Alder cycloaddition as a key reaction is proposed for 1. Compounds 1, 5, and 7 showed inhibitory effects against the A549 and NCI-H292 cancer cell lines.

[Analysis of mitochondrial DNA gene tRNALeu(UUR) A3243G mutation in diabetic pedigrees].

OBJECTIVE: To investigate the clinical characteristics and the prevalence of mitochondrial gene A3243G mutation in diabetic pedigrees. METHODS: Nineteen suspected mitochondrial DNA diabetic family members from three families were recruited. The gene fragment was amplified by PCR, and mutation was detected by direct sequencing. RESULTS: In three pedigrees, the three probands and their mothers were found carrying the most common nt3243A>G mutation. Most of diabetic patients in these families were deaf and diabetes was developed at early age, characterized by impaired beta cell function and low body mass index (BMI). CONCLUSION: The mitochondrial gene A3243G mutation may cause diabetes mellitus and deaf.

[Relationship between brainstem auditory evoked potential and serum neuron-specific enolase in neonates with asphyxia].

OBJECTIVE: To study the correlation between brainstem auditory evoked potential (BAEP) and serum neuron-specific enolase (NSE) in neonates with asphyxia and explore the role of NSE in the evaluation of hearing impairment following asphyxia. METHODS: Fifty-two term neonates with asphyxia, including 38 cases of simple asphyxia (mild: 23 cases; severe: 15 cases) and 14 cases of asphyxia complicated by hypoxic-ischemic encephalopathy (HIE), were enrolled. In the double-blind trial, BAEP and NSE were simultaneously detected 7 days after birth. The patients who did not pass BAEP test received another BAEP and NSE examinations 3 months after birth. Thirty healthy term neonates served as normal control group. RESULTS: Of the 52 neonates with asphyxia, 50.0% and 21.2% of patients failed the initial and the second BAEP tests, respectively. The detection rates of BAEP anomalies in the simple severe asphyxia group in the initial and the second tests (63.3% and 26.3%, respectively) were significantly higher than those in the simple mild asphyxia group (36.9% and 5.9%, respectively)(P<0.05). The neonates with asphyxia complicated by HIE showed a higher detection rate of BAEP anomalies in the second test compared with the asphyxiated neonates without HIE (31.3% vs 16.7%; P<0.05). Mean serum NSE levels in asphyxiated neonates were significantly higher than those in normal controls (<0.01). There were significant differences in serum NSE levels between the neonates with mild and severe asphyxia (26.70+/-2.34 microg/L vs 17.18+/-3.16 microg/L; P<0.01). The asphyxiated neonates with HIE had serum NSE levels similar to the simple severely asphyxiated neonates. Serum NSE levels in patients who failed the initial BAEP test were significantly higher than those who passed the test (25.69+/-4.12 microg/L vs 17.15+/-3.09 microg/L; <0.01). Serum NSE levels had a positive correlation with wave V reaction threshold detected in the BAFP test (<0.05). CONCLUSIONS: The serum level of NSE is closely correlated with BAEP, and it may be useful to the evaluation of the hearing impairment and the outcome in neonates with asphyxia.

[Auditory capability evaluation for children after cochlear implantation using meaningful auditory integration scale].

OBJECTIVE: To analyze the auditory capability of preschool children before and after cochlear implantation using meaningful auditory integration scale (MAIS) questionnaire. METHODS: Eighty-two prelingually deaf patients participated in this study. They received a cochlear implant at the age of 3 to 6 years and 11 months. The audiologists who were trained for the research used the MAIS questionnaire. Audiologists asked for the parents' answers and recorded all the information about the device using (Q1,2) and the patient's spontaneous auditory behavioural responses including spontaneous alerting to sound Q3 approximately 6 and deriving meaning from sound (Q7 approximately 10). The evaluation was performed before operation and 1 , 3, 6 months, 1, 1.5, 2 years after switch-on. RESULTS: The scores of question 1a and 1b were not significantly different among the different periods after switch-on. The scores of question 2 to 10 were significantly different among the different periods after switch-on. CONCLUSIONS: Considerable variability across subjects' auditory ability after cochlear implantation was noted. Most of the patients showed no consistent response to sound in everyday life before implantation. After cochlear implantation, a significant increase in auditory capability occurred. The children demonstrated faster development of device using relative to spontaneous alerting to sound and deriving meaning from sound.