Ginsenoside Rg1 ameliorates stress-exacerbated Parkinson's disease in mice by eliminating RTP801 and α-synuclein autophagic degradation obstacle.

Emerging evidence shows that psychological stress promotes the progression of Parkinson's disease (PD) and the onset of dyskinesia in non-PD individuals, highlighting a potential avenue for therapeutic intervention. We previously reported that chronic restraint-induced psychological stress precipitated the onset of parkinsonism in 10-month-old transgenic mice expressing mutant human α-synuclein (αSyn) (hαSyn A53T). We refer to these as chronic stress-genetic susceptibility (CSGS) PD model mice. In this study we investigated whether ginsenoside Rg1, a principal compound in ginseng notable for soothing the mind, could alleviate PD deterioration induced by psychological stress. Ten-month-old transgenic hαSyn A53T mice were subjected to 4 weeks' restraint stress to simulate chronic stress conditions that worsen PD, meanwhile the mice were treated with Rg1 (40 mg· kg-1 ·d-1, i.g.), and followed by functional magnetic resonance imaging (fMRI) and a variety of neurobehavioral tests. We showed that treatment with Rg1 significantly alleviated both motor and non-motor symptoms associated with PD. Functional MRI revealed that Rg1 treatment enhanced connectivity between brain regions implicated in PD, and in vivo multi-channel electrophysiological assay showed improvements in dyskinesia-related electrical activity. In addition, Rg1 treatment significantly attenuated the degeneration of dopaminergic neurons and reduced the pathological aggregation of αSyn in the striatum and SNc. We revealed that Rg1 treatment selectively reduced the level of the stress-sensitive protein RTP801 in SNc under chronic stress conditions, without impacting the acute stress response. HPLC-MS/MS analysis coupled with site-directed mutation showed that Rg1 promoted the ubiquitination and subsequent degradation of RTP801 at residues K188 and K218, a process mediated by the Parkin RING2 domain. Utilizing αSyn A53T+; RTP801-/- mice, we confirmed the critical role of RTP801 in stress-aggravated PD and its necessity for Rg1's protective effects. Moreover, Rg1 alleviated obstacles in αSyn autophagic degradation by ameliorating the RTP801-TXNIP-mediated deficiency of ATP13A2. Collectively, our results suggest that ginsenoside Rg1 holds promise as a therapeutic choice for treating PD-sensitive individuals who especially experience high levels of stress and self-imposed expectations.

A breakdown of metabolic reprogramming in microglia induced by CKLF1 exacerbates immune tolerance in ischemic stroke.

Ischemic stroke is characterized by the presence of reactive microglia. However, its precise involvement in stroke etiology is still unknown. We used metabolic profiling and showed that chemokine like factor 1 (CKLF1) causes acute microglial inflammation and metabolic reprogramming from oxidative phosphorylation to glycolysis, which was reliant on the AMP-activated protein kinase (AMPK)-mammalian target of rapamycin (mTOR)-hypoxia inducible factor 1α (HIF-1α) signaling pathway. Once activated, microglia enter a chronic tolerant state as a result of widespread energy metabolism abnormalities, which reduces immunological responses, including cytokine release and phagocytosis. Metabolically dysfunctional microglia were also found in mice using genome-wide RNA sequencing after chronic administration of CKLF1, and there was a decrease in the inflammatory response. Finally, we showed that the loss of CKLF1 reversed the defective immune response of microglia, as indicated by the maintenance its phagocytosis to neutrophils, thereby mitigating the long-term outcomes of ischemic stroke. Overall, CKLF1 plays a crucial role in the relationship between microglial metabolic status and immune function in stroke, which prepares a potential therapeutic strategy for ischemic stroke.

Silver-Rich Hybrid Framework Iodide Based on [Ag8I6]2+ Clusters Displays Low-Temperature Dual Emission and Luminescence Thermochromism.

Cluster-based framework metal iodides have diverse structures and excellent luminescence properties, and show promising applications in sensing and solid-state lighting. However, the design and synthesis of these materials remain great challenges because excess I- ions introduced into the synthesis systems decrease the condensation degree of M-I units. In this work, a new strategy is developed to control the condensation behavior of Ag-I units, and a new silver-rich cluster-based framework iodide [DabcoAg8I6(SPh)2]n (1) (Dabco = 1,4-diazabicyclo [2.2.2] octane) has been synthesized under solvothermal conditions in the presence of silver thiophenolate (AgSPh)n. Compound 1 features a three-dimensional (3-D) cluster-based framework with a pillared layer structure composed of cationic [Ag8I6]2+ clusters bridged by SPh- and Dabco, and displays low-temperature dual emission and luminescence thermochromism.

Regulatory T cells in ischemic stroke.

Recent evidence shows that when ischemic stroke (IS) occurs, the BBB would be destructed, thereby promoting the immune cells to migrate into the brain, suggesting that the immune responses can play a vital role in the pathology of IS. As an essential subpopulation of immunosuppressive T cells, regulatory T (Treg) cells are involved in maintaining immune homeostasis and suppressing immune responses in the pathophysiological conditions of IS. During the past decades, the regulatory role of Treg cells has attracted the interest of numerous researchers. However, whether they are beneficial or detrimental to the outcomes of IS remains controversial. Moreover, Treg cells exert distinctive effects in the different stages of IS. Therefore, it is urgent to elucidate how Treg cells modulate the immune responses induced by IS. In this review, we describe how Treg cells fluctuate and play a role in the regulation of immune responses after IS in both experimental animals and humans, and summarize their biological functions and mechanisms in both CNS and periphery. We also discuss how Treg cells participate in poststroke inflammation and immunodepression and the potential of Treg cells as a novel therapeutic approach.

Characteristics of immune function of full-term infants with different feeding patterns at the age of 3 months: a prospective cohort study. / ä¸åŒå–‚å »æ–¹å¼çš„è¶³æœˆå„¿3æœˆé¾„æ—¶å ç–«åŠŸèƒ½ç‰¹ç‚¹åˆ†æžçš„å‰çž»æ€§é˜Ÿåˆ—ç ”ç©¶.

OBJECTIVES: To explore the characteristics of immune function of healthy full-term infants at the age of 3 months, and to analyze the relationship of immune function with feeding pattern and sex. METHODS: A total of 84 healthy full-term infants born in four hospitals in Beijing and Hohhot, China were prospectively recruited. Their feeding patterns remained unchanged within 4 months after birth. They were divided into a breast-feeding group and a milk powder feeding group according to their feeding patterns. At the age of 3 months after birth, peripheral venous blood samples of the two groups were collected to evaluate cellular immunity and humoral immunity and perform routine blood test. The laboratory indices were compared between infants with different feeding patterns and sexes. RESULTS: Compared with the milk powder feeding group, the breast-feeding group had significantly lower proportion of T cell second signal receptor CD28, immunoglobulin M, and proportion and absolute count of neutrophils (P<0.05) and significantly higher expression and proportion of HLA-DR, a surface activation marker of CD8+ T cells, and proportion of lymphocytes (P<0.05). The male infants had a significantly lower white blood cell count and a significantly higher proportion of eosinophils compared with the female infants (P<0.05). CONCLUSIONS: Sex has no significant effect on the proportion of lymphocyte subsets in 3-month-old full-term infants, but feeding patterns are associated with the proportion of CD28+ T cells (lymphocyte functional subset) and HLA-DR+ T cells (lymphocyte activation subset), suggesting that feeding patterns have a certain effect on the development of immune function in 3-month-old full-term infants.

Prevalence and risk factors associated with the comprehensive needs of cancer patients in China.

BACKGROUND: The incidence and mortality rates of cancer have been increasing in developing countries, particularly in Asia. Therefore to provide optimal comprehensive care to the cancer patients, the care plan must focus on the comprehensive needs of cancer patients. The purpose of this study was to investigate the comprehensive needs of cancer patients, and explore the associated factors. METHODS: In a cross-sectional questionnaire study, a total of 200 cancer patient-caregiver dyads were selected and interviewed in Mainland China by convenient sampling method. Patients' comprehensive needs were assessed with Comprehensive Needs Assessment Tool in cancer for Patients (CNAT), including seven domains (Information, Psychological Problems, Health Care Staffs, Physical Symptoms, Hospital Facilities and Services, Social/Religious/Spiritual Support and Practical Support). Both cancer patients and caregivers completed the sociodemographic survey. The mean differences in domain scores for different characteristics groups were compared by one-way ANOVA or non-parametric analyses, and influencing factors defined with multivariate regression analysis. RESULTS: The cancer patients' need for Health Care Staffs (78.35 ± 13.08) was the highest among the seven domains, followed by the need for Information (71.18 ± 17.39) and the need for Hospital Facilities and Services (52.65 ± 13.35). The lowest score was the need for Physical Symptoms (35.12 ± 16.68). Patients who were female, with low family monthly income, at their own expense, and with highly educated caregivers had higher score of CNAT. Also sociodemographic characteristics were associated with each domain need of cancer patients. CONCLUSION: This study shows that cancer patients experience high levels of needs for health-care staff and information, and the different needs are closely related to their sociological characteristics. The provision of health care can be adapted to meet the different needs of cancer patients of different epidemiological characteristics at different times during the course of treatment.

Roles of HDAC2 and HDAC8 in Cardiac Remodeling in Renovascular Hypertensive Rats and the Effects of Valproic Acid Sodium.

Recent studies indicate that histone deacetylases (HDACs) activity is associated with the development and progression of cardiac hypertrophy. In this study, we investigated the effects of a HDACs inhibitor, valproic acid sodium (VPA), on cardiac remodeling and the differential expression of HDACs in left ventricles (LVs) of renovascular hypertensive rats. Renovascular hypertension was induced in rats by the two-kidney two-clip (2K2C) method. Cardiac remodeling, heart function and the differential expression of HDACs were examined at different weeks after 2K2C operation. The effects of VPA on cardiac remodeling, the expressions of HDACs, transforming growth factor-beta 1 (TGF-ß1) and connective tissue growth factor (CTGF) in LV were investigated. The expressions of atrial natriuretic factor, ß-myosin heavy chain, HDAC2 and HDAC8 increased in LV of 2K2C rats at 4, 8, 12 weeks after operation. Cardiac dysfunction, cardiac hypertrophy and fibrosis were markedly attenuated by VPA treatment in 2K2C rats. Further studies revealed that VPA inhibited the expressions of HDAC2, HDAC8, TGF-ß1 and CTGF in LV of 2K2C rats. In summary, these data indicate that HDAC2 and HDAC8 play a key role in cardiac remodeling in renovascular hypertensive rats and that VPA attenuates hypertension and cardiac remodeling. The effect of VPA is possibly exerted via decreasing HDAC2, HDAC8, TGF-ß1 and CTGF expressions in LV of 2K2C rats.

Microarray Expression Profile of Circular RNAs in Heart Tissue of Mice with Myocardial Infarction-Induced Heart Failure.

BACKGROUND/AIMS: Myocardial infarction (MI) is a serious complication of atherosclerosis associated with increasing mortality attributable to heart failure. This study is aimed to assess the global changes in and characteristics of the transcriptome of circular RNAs (circRNAs) in heart tissue during MI induced heart failure (HF). METHODS: Using a post-myocardial infarction (MI) model of HF in mice, we applied microarray assay to examine the transcriptome of circRNAs deregulated in the heart during HF. We confirmed the changes in circRNAs by quantitative PCR. RESULTS: We revealed and confirmed a number of circRNAs that were deregulated during HF, which suggests a potential role of circRNAs in HF. CONCLUSIONS: The distinct expression patterns of circulatory circRNAs during HF indicate that circRNAs may actively respond to stress and thus serve as biomarkers of HF diagnosis and treatment.

Evaluating a physiologically based pharmacokinetic model for predicting the pharmacokinetics of midazolam in Chinese after oral administration.

AIM: To evaluate the SimCYP simulator ethnicity-specific population model for predicting the pharmacokinetics of midazolam, a typical CYP3A4/5 substrate, in Chinese after oral administration. METHODS: The physiologically based pharmacokinetic (PBPK) model for midazolam was developed using a SimCYP population-based simulator incorporating Chinese population demographic, physiological and enzyme data. A clinical trial was conducted in 40 Chinese subjects (the half was females) receiving a single oral dose of 15 mg midazolam. The subjects were separated into 4 groups based on age (20-50, 51-65, 66-75, and above 76 years), and the pharmacokinetics profiles of each age- and gender-group were determined, and the results were used to verify the PBPK model. RESULTS: Following oral administration, the simulated profiles of midazolam plasma concentrations over time in virtual Chinese were in good agreement with the observed profiles, as were AUC and Cmax. Moreover, for subjects of varying ages (20-80 years), the ratios of predicted to observed clearances were between 0.86 and 1.12. CONCLUSION: The SimCYP PBPK model accurately predicted the pharmacokinetics of midazolam in Chinese from youth to old age. This study may provide novel insight into the prediction of CYP3A4/5-mediated pharmacokinetics in the Chinese population relative to Caucasians and other ethnic groups, which can support the rational design of bridging clinical trials.

[Chemical constituents from aerial part of Aconitum brachypodum].

OBJECTIVE: To study the chemical constituents from the aerial part of Aconitum brachypodum. METHODS: The constituents were isolated and purified by silica gel, activated alumina and Sephadex LH-20 column chromatography. their structures were elucidated on the basis of spectral data and physiochemical evidence. RESULTS: Eleven compounds were isolated from 80% ethanol extract and identified as secokaraconitine (1), brachyaconitines A (2), C (3), talatisamine (4), hypaconitine (5), songrine (6), bullatine A (7), 7-carbony sitosterone (8), lupeol (9), ß-sitosterol (10) and daucosterol (11). CONCLUSION: All compounds are isolated from the aerial part of Aconitum brachypodum for the first time.

CRISPR/Cas13a-based genome editing for establishing the detection method of H9N2 subtype avian influenza virus.

Avian influenza virus (AIV) subtype H9N2 has significantly threatened the poultry business in recent years by having become the predominant subtype in flocks of chickens, ducks, and pigeons. In addition, the public health aspects of H9N2 AIV pose a significant threat to humans. Early and rapid diagnosis of H9N2 AIV is therefore of great importance. In this study, a new method for the detection of H9N2 AIV based on fluorescence intensity was successfully established using CRISPR/Cas13a technology. The Cas13a protein was first expressed in a prokaryotic system and purified using nickel ion affinity chromatography, resulting in a high-purity Cas13a protein. The best RPA (recombinase polymerase amplification) primer pairs and crRNA were designed and screened, successfully constructing the detection of H9N2 AIV based on CRISPR/Cas13a technology. Optimal concentration of Cas13a and crRNA was determined to optimize the constructed assay. The sensitivity of the optimized detection system is excellent, with a minimum detection limit of 10° copies/µL and didn't react with other avian susceptible viruses, with excellent specificity. The detection method provides the basis for the field detection of the H9N2 AIV.

[Chemical constituents of Aconitum brachypodum from Dong-Chuan area].

Aconitum brachypodum is traditionally known to be toxic chinese medicie, but its chemical constituents is not enough studied to date. To further elucidate the chemical constituents of A. brachypodum, 80% ethanol extract of A. brachypodum collected from Dong-Chuan area was investigated, which led to isolation of seventeen compounds. By spectroscopic methods, their structures were determined as hypaconitine (1), mesaconitine (2), talatisamine (3), neoline (4), fuziline (5), aconine (6), bullatine A (7), lepeine (8), songrine (9), isocorydine (10), beta-sitosterol (11), daucosterol (12), stearic acid (13), triacontanol (14), palmitic acid (15), benzoic acid (16), and inosine (17), respectively. All compounds except for compounds 1 and 7 were isolated from A. brachypodum for the first time.

miR-124 is upregulated in diabetic mice and inhibits proliferation and promotes apoptosis of high-glucose-induced ß-cells by targeting EZH2.

BACKGROUND: Diabetes is a chronic metabolic disease, and a variety of miRNA are involved in the occurrence and development of diabetes. In clinical studies, miR-124 is highly expressed in the serum of patients with diabetes and in pancreatic islet ß-cells. However, few reports exist concerning the role and mechanism of action of miR-124 in diabetes. AIM: To investigate the expression of miR-124 in diabetic mice and the potential mechanism of action in islet ß-cells. METHODS: The expression levels of miR-124 and enhancer of zeste homolog 2 (EZH2) in pancreatic tissues of diabetic mice were detected. The targeted relationship between miR-124 and EZH2 was predicted by Targetscan software and verified by a double luciferase reporter assay. Mouse islet ß-cells Min6 were grown in a high glucose (HG) medium to mimic a diabetes model. The insulin secretion, proliferation, cell cycle and apoptosis of HG-induced Min6 cells were detected after interference of miR-124a and/or EZH2. RESULTS: The expression of miR-124 was upregulated and EZH2 was downregulated in the pancreatic tissue of diabetic mice compared with control mice, and the expression of miR-124 was negatively correlated with that of EZH2. miR-124 was highly expressed in HG-induced Min6 cells. Inhibition of miR-124 promoted insulin secretion and cell proliferation, induced the transition from the G0/G1 phase to the S phase of the cell cycle, and inhibited cell apoptosis in HG-induced Min6 cells. EZH2 was one of the targets of miR-124. Co-transfection of miR-124 inhibitor and siRNA-EZH2 could reverse the effects of the miR-124 inhibitor in HG-induced Min6 cells. CONCLUSION: miR-124 is highly expressed in diabetic mice and HG-induced Min6 cells and regulates insulin secretion, proliferation and apoptosis of islet ß-cells by targeting EZH2.

The efficacy of tolvaptan for heart failure in chronic kidney disease: A protocol for systematic review and meta-analysis.

BACKGROUND: Approximately half of people with heart failure have chronic kidney disease (CKD). Tolvaptan is reported to be effective in treating heart failure. However, the safety and efficacy of its use in patients with CKD is uncertain. In this study, we conducted a protocol for systematic review and meta-analysis to investigate the efficacy and safety of tolvaptan on patients with heart failure and CKD. METHODS: This study protocol has been registered in the PROSPERO and the registration number is CRD42022368148. The consent of this protocol report is based on the Preferred Reporting Items for Systematic Review and Meta-Analysis Protocols (PRISMA-P) 2015 statement guidelines. We will include randomized controlled trials related to tolvaptan in patients with heart failure and CKD. Two research members will electronically and independently search 4 English databases (EMBASE, PubMed, National Guideline Clearinghouse, and Cochrane Central Register of Controlled Trials) and 4 Chinese databases (Chinese Biomedical Literature Database, Chinese National Knowledge Infrastructure, Wanfang Database, and VIP Database) from their inception to November 2022. The risk of bias in each included study will be assessed utilizing the Cochrane Collaboration's risk of bias tool. All statistical analyses will be conducted using the software program Review Manager version 5.3. RESULTS: The results of this systematic review will be published in a peer-reviewed journal. CONCLUSION: This review can provide convincing evidence to help clinicians make decisions when dealing with heart failure and CKD.

Pharmacokinetics and safety of calcium L-threonate in healthy volunteers after single and multiple oral administrations.

AIM: To evaluate the pharmacokinetics of L-threonate after single or multiple oral administrations and its safety profile in healthy Chinese volunteers. METHODS: This was an open-label, single- and multiple-dose study. The subjects were assigned to receive a single dose, 675, 2025, or 4050 mg, of calcium L-threonate (n=12) or repeated doses of 2025 mg twice daily for 4 d (n=12). Serial plasma and urine samples were analyzed with HPLC-MS/MS. Pharmacokinetic parameters of L-threonate were calculated using non-compartmental analysis with WinNonlin software. RESULTS: In the single dose group, C(max) reached at 2.0 h and the mean t(1/2) was approximately 2.5 h. Area under curve (AUC) and C(max) increased with dose escalation, but dose proportionality was not observed over the range of 675 to 4050 mg. AUC and C(max) in the fasted subjects were lower compared with those in the non-fasted subjects. Cumulative urinary excretion of L-threonate over 24 h represented 5.9% of the administered dose with a mean Cl/r of 0.8 L/h. In the multiple-dose study, no accumulation appeared upon repeated doses of 2025 mg twice daily for 4 d. There were no serious adverse events that occurred during this study. CONCLUSION: Calcium L-threonate was well tolerated in healthy Chinese subjects, with no pattern of dose-related adverse events. Plasma exposure increased with dose escalation, but linear pharmacokinetics were not observed over the studied doses. L-threonate was absorbed rapidly, and its absorption was enhanced by food intake. No systemic accumulation appeared after repeated administrations.

[Application of neuroendoscope in the treatment of skull base chordoma].

OBJECTIVE: To further explore the application, approach, indication and prognosis of neuroendoscope treatment for skull base chordoma. METHODS: A total of 101 patients of skull base chordoma were admitted at our hospital from May 2000 to April 2010. There were 59 males and 42 females. Their major clinical manifestations included headache, cranial nerve damage and dyspnea. They were classified according to the patterns of tumor growth: Type I (n = 13): tumor location at a single component of skull base, i. e. clivus or sphenoid sinus with intact cranial dura; Type II (n = 56): tumor involving more than two components of skull e. g clivus, sphenoid and nasal/oral cavity, etc. But there was no intracranial invasion; Type III (n = 32) : tumor extending widely and intradurally forming compression of brain stems and multiple cranial nerves. Based on the types of chordoma, different endoscopic approaches were employed, viz. transnasal, transoral, trans-subtemporal fossa and plus microsurgical craniotomy for staging in some complex cases. RESULTS: Among all patients, total resection was achieved (n = 19), subtotal (n = 58) and partial (n = 24). In partial resection cases, 16 cases were considered to be subtotal due to a second-stage operation. Most cases had conspicuous clinical improvements. Self-care recovery within one week post-operation accounted for 58.4%, two weeks 30.7%, one month 6.9% and more than one month 1.9%. Postoperative complications occurred in 13 cases (12.8%) and included CSF leakage (n = 4) cranial nerve palsy (n = 5), hemorrhagic nasal wounds (n = 3) and delayed intracranial hemorrhage (n = 1). All of these were cured or improved after an appropriate treatment. A follow-up of 6 - 60 months was conducted in 56 cases. CONCLUSION: Early detection and early treatment are crucial for achieving a better outcome in chordoma. Neuroendoscopic treatment plays an important role in managing those complicated cases. Precise endoscopic techniques plus different surgical approaches and staging procedures are required to improve the post-operative quality of life for patients.

Human Serum-derived Extracellular Vesicles Protect A549 from PM 2.5-induced Cell Apoptosis.

OBJECTIVE: Epidemiological studies reveal that exposure to fine particulate matter (aerodynamic diameter ≤ 2.5 µm, PM 2.5) increases the morbidity and mortality of respiratory diseases. Emerging evidence suggests that human circulating extracellular vesicles (EVs) may offer protective effects against injury caused by particulate matter. Currently, however, whether EVs attenuate PM 2.5-induced A549 cell apoptosis is unknown. METHODS: EVs were isolated from the serum of healthy subjects, quantified via nanoparticle tracking analysis, and qualified by the marker protein CD63. PM 2.5-exposed (50 µg/mL) A549 cells were pre-treated with 10 µg/mL EVs for 24 h. Cell viability, cell apoptosis, and AKT activation were assessed via Cell Counting Kit-8, flow cytometry, and Western blot, respectively. A rescue experiment was also performed using MK2206, an AKT inhibitor. RESULTS: PM 2.5 exposure caused a 100% increase in cell apoptosis. EVs treatment reduced cell apoptosis by 10%, promoted cell survival, and inhibited the PM 2.5-induced upregulation of Bax/Bcl2 and cleaved caspase 3/caspase 3 in PM 2.5-exposed A549 cells. Moreover, EVs treatment reversed PM 2.5-induced reductions in p-AKT Thr308 and p-AKT Ser473. AKT inhibition attenuated the anti-apoptotic effect of EVs treatment on PM 2.5-exposed A549 cells. CONCLUSIONS: EVs treatment promotes cell survival and attenuates PM 2.5-induced cell apoptosis via AKT phosphorylation. Human serum-derived EVs may be an efficacious novel therapeutic strategy in PM 2.5-induced lung injury.

Delivery room resuscitation and short-term outcomes of extremely preterm and extremely low birth weight infants: a multicenter survey in North China.

BACKGROUND: Delivery room resuscitation assists preterm infants, especially extremely preterm infants (EPI) and extremely low birth weight infants (ELBWI), in breathing support, while it potentially exerts a negative impact on the lungs and outcomes of preterm infants. This study aimed to assess delivery room resuscitation and discharge outcomes of EPI and ELBWI in China. METHODS: The clinical data of EPI (gestational age [GA] <28 weeks) and ELBWI (birth weight [BW] <1000 g), admitted within 72 h of birth in 33 neonatal intensive care units from five provinces and cities in North China between 2017 and 2018, were analyzed. The primary outcomes were delivery room resuscitation and risk factors for delivery room intubation (DRI). The secondary outcomes were survival rates, incidence of bronchopulmonary dysplasia (BPD), and risk factors for BPD. RESULTS: A cohort of 952 preterm infants were enrolled. The incidence of DRI, chest compressions, and administration of epinephrine was 55.9% (532/952), 12.5% (119/952), and 7.0% (67/952), respectively. Multivariate analysis revealed that the risk factors for DRI were GA <28 weeks (odds ratio [OR], 3.147; 95% confidence interval [CI], 2.082-4.755), BW <1000 g (OR, 2.240; 95% CI, 1.606-3.125), and antepartum infection (OR, 1.429; 95% CI, 1.044-1.956). The survival rate was 65.9% (627/952) and was dependent on GA. The rate of BPD was 29.3% (181/627). Multivariate analysis showed that the risk factors for BPD were male (OR, 1.603; 95% CI, 1.061-2.424), DRI (OR, 2.094; 95% CI, 1.328-3.303), respiratory distress syndrome exposed to ≥2 doses of pulmonary surfactants (PS; OR, 2.700; 95% CI, 1.679-4.343), and mechanical ventilation ≥7 days (OR, 4.358; 95% CI, 2.777-6.837). However, a larger BW (OR, 0.998; 95% CI, 0.996-0.999), antenatal steroid (OR, 0.577; 95% CI, 0.379-0.880), and PS use in the delivery room (OR, 0.273; 95% CI, 0.160-0.467) were preventive factors for BPD (all P < 0.05). CONCLUSION: Improving delivery room resuscitation and management of respiratory complications are imperative during early management of the health of EPI and ELBWI.

Ethyl 4-(furan-2-yl)-6-methyl-2-oxo-1,2,3,4-tetra-hydro-pyrimidine-5-carboxyl-ate.

The asymmetric unit of the title compound, C(12)H(14)N(2)O(4), contains two independent mol-ecules. In one independent mol-ecule, the furanyl fragment is rotationally disordered between two orientations in a 0.625 (6):0.375 (6) ratio. In the crystal, inter-molecular pyrimidine-pyrimidinone N-H⋯O hydrogen bonds link the mol-ecules into centrosymmetric tetra-mers, which are further associated into ribbons extending in [010] via weak inter-molecular pyrimidine-carboxyl N-H⋯O hydrogen bonds.

Effect of bone marrow stromal cell-conditioned medium on the glutamate uptake of peroxide-injured astrocytes.

We aimed to investigate the effect of bone marrow stromal cell-conditioned medium (BCM) on glutamate uptake of peroxide (H(2)O(2))-injured astrocytes. Bone marrow stromal cells (BMSC) were isolated from rat bone marrow. Confluent BMSC cultures were incubated with serum-free Dulbecco's Modified Eagle's Medium to create the BCM. Astrocytes were isolated from 1-day-old rats. H(2)O(2)-injured astrocytes were cultured in BCM (experimental group) or serum-free medium (control group). The labeled glutamate ((3)H-L-glutamate) uptake by H(2)O(2)-injured astrocytes with or without BCM was compared after 1 and 3 days. We found that astrocytes cultured in BCM exhibited increased glutamate uptake compared to those cultured in serum-free medium following H(2)O(2)-induced injury (p<0.01) and concluded that BCM increased the glutamate uptake capability of H(2)O(2)-injured rat astrocytes. The therapeutic benefits associated with BMSC transplantation following brain injury might be partly due to increased glutamate uptake by astrocytes.