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1.
Ann Hematol ; 2019 Nov 15.
Artigo em Inglês | MEDLINE | ID: mdl-31729544

RESUMO

The authors determined an error in the affiliation section; it was captured as Department of Hematology, Peking Union Hospital, CAMS & PUMC, Beijing 100,730, China. The correct affiliation should be Department of Hematology, Peking Union Medical College Hospital, Chinese Academy of Medical Science and Peking Union Medical College, Beijing, 100730, China.

2.
Mol Med Rep ; 20(6): 4953-4962, 2019 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-31702805

RESUMO

Inhibiting apoptosis of type II alveolar epithelial cells (AEC II) is an effective way to decrease hyperoxic acute lung injury (HALI); however, the specific underlying molecular mechanisms have not yet been fully elucidated. Although miRNA­21­5p has previously been reported to decrease H2O2­induced AEC II apoptosis by targeting PTEN in vitro, whether miR­21­5p can decrease HALI in vivo and the downstream molecular mechanisms remain unclear. In the present study, rats were endotracheally administered with an miR­21­5p­encoding (AAV­6­miR­21­5p) or a negative control adenovirus vector, and then a HALI model was established by exposure to hyperoxia. At 3 weeks following the administration of AAV­6­miR­21­5p, the severity of HALI was decreased, as evidenced by the improved outcome of the oxygenation index, respiratory index, wet/dry weight ratio and pathological scores of the HALI lungs. To further investigate the underlying mechanisms, AEC II cells were isolated from the lungs of the experimental rats and cultured. The expression levels of miR­21­5p and its target gene, PTEN, were detected, as well as the levels of phosphorylated and total AKT. In addition, the apoptosis rate of AEC II was detected by flow cytometry. The results demonstrated that AAV­6­miR­21­5p administration increased the miR­21­5p levels in primary AEC II cells, while it decreased the expression levels of PTEN. miR­21­5p overexpression also increased AKT phosphorylation in AEC II cells from the HALI lungs compared with that of the HALI alone group and the control virus group. The present study indicated that miR­21­5p ameliorated HALI in vivo, which may have resulted from the inhibition of PTEN/AKT­induced apoptosis of AEC II cells. These findings suggest that miR­21­5p and PTEN/AKT signaling might serve as potential targets for HALI treatment.

3.
J Environ Pathol Toxicol Oncol ; 38(2): 143-152, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31679277

RESUMO

The current study evaluated the cardioprotective activity of genistein in cases of doxorubicin-(Dox) induced cardiac toxicity and a probable mechanism underlying this protection, such as an antioxidant pathway in cardiac tissues. Animals used in this study were categorized into four groups. The first group was treated with sodium carboxymethylcellulose (0.3%; CMC-Na) solution. The second group received Dox (3.0 mg/kg, i.p.) on days 6, 12, 18, and 24. The third and fourth groups received Dox (3 mg/kg, i.p.) on days 6, 12, 18, and 24 and received protective doses of genistein (100 [group 3] and 200 [group 4] mg/kg/day, p.o.) for 30 days. Treatment with genistein significantly improved the altered cardiac function markers and oxidative stress markers. This was coupled with significant improvement in cardiac histopathological features. Genistein enhanced the Nrf2 and HO-1 expression, which showed protection against oxidative insult induced by Dox. Terminal deoxynucleotidyl transferase dUTP nick end labeling assay showed substantial inhibition of apoptosis by genistein in myocardia. The study showed that genistein has a strong reactive oxygen species scavenging property and potentially (P ≤ .001) decreases the lipid peroxidation as well as inhibits DNA damage in cardiac toxicity induced by Dox. In conclusion, the potential antioxidant effect of genistein may be because of its modulatory effect on Nrf2/HO-1 signalling pathway and by this means exhibits cardioprotective effects from Dox-induced oxidative injury.


Assuntos
Cardiotônicos/farmacologia , Cardiotoxinas/toxicidade , Doxorrubicina/toxicidade , Genisteína/farmacologia , Heme Oxigenase-1/genética , Fator 2 Relacionado a NF-E2/genética , Estresse Oxidativo/efeitos dos fármacos , Animais , Cardiotoxicidade/etiologia , Heme Oxigenase-1/metabolismo , Masculino , Fator 2 Relacionado a NF-E2/metabolismo , Ratos , Ratos Wistar
5.
J Cell Physiol ; 2019 Oct 17.
Artigo em Inglês | MEDLINE | ID: mdl-31621909

RESUMO

It has been widely accepted that long-noncoding RNA (lncRNA) HOX transcript antisense intergenic RNA (HOTAIR) emerges as a crucial mediator in inflammation. Here, we first detected HOTAIR in lipopolysaccharide (LPS)-treated normal human liver cell line (L02) and hepatocellular carcinoma cell lines (C3A, HepG2, and SMMC-7721). Further, we explored the biological function of HOTAIR in LPS-induced hepatocytes (L02 and C3A) lesions and investigated the molecular mechanisms. Besides, we focused on inflammatory signaling crosstalk. The inflammatory insults were assayed by cell counting kit-8 (CCK-8), cell cycle and apoptosis analysis kit, and immunoblotting assay. HOTAIR level was examined by reverse-transcription polymerase chain reaction. To determine the effect of HOTAIR silence or overexpression in inflammation, we applied quantitative reverse-transcription polymerase chain reaction, immunoblotting assay, and enzyme-linked immuno sorbent assay. Regulator inhibitors of Janus kinase/signal transducer and activator of transcription (JAK2/STAT3; AG490) and nuclear factor κB (NF-κB; BAY-11-7082) were applied to treat cells. Our results suggested that LPS induced the overexpression of HOTAIR in L02, C3A, HepG2, and SMMC-7721 cells. LPS repressed viability, induced apoptosis, and facilitated the expression of interleukin (IL)-1ß, IL-6, and tumor necrosis factor (TNF)-α in L02 and C3A cells. IL-1ß, IL-6, and TNF-α were upregulated by HOTAIR overexpression while downregulated by HOTAIR knockdown in LPS-treated cells. We further observed that HOTAIR overexpression accelerated LPS-induced phosphorylation whereas HOTAIR silence blocked this progress. Inhibition of JAK/STAT and NF-κB contributed to the suppression of cytokines which was evoked by LPS. Collectively, our findings indicated that HOTAIR exerted a crucial role in cytokines expression by activating JAK/STAT and NF-κB.

6.
Nanoscale ; 11(36): 16860-16867, 2019 Sep 19.
Artigo em Inglês | MEDLINE | ID: mdl-31482914

RESUMO

Electrochemiluminescence (ECL) nanomaterials are usually deposited compactly on the surface of electrodes, which may cause poor mass transfer of reactants, thereby resulting in low ECL efficiency. In this work, we developed a novel kind of luminescent material denoted as C-Au-luminol nanospheres (C-Au-Lum NSs) by high dispersion of luminophores on porous carbon nanospheres (PCNSs). C-Au-Lum NSs were facilely prepared by the in situ reduction of chloroauric acid with the luminescent reagent luminol (Lum) on the nano-pores of PCNSs. Plenty of luminescent Au-Lum NPs were dispersedly concentrated inside the numerous pores and hollow interiors of PCNSs, effectively increasing the mass transfer of reagents and accelerating the electron transport inside the porous nanospheres. This greatly improved the availability of luminophores and endowed C-Au-Lum NSs with excellent ECL emission. After further integrating with enzymatic circulation and strand displacement, an ultrasensitive ECL biosensor was achieved for the ultrasensitive detection of an important tumor biomarker, mucin1. The logarithmically linear range from 0.1 pg mL-1 to 1 ng mL-1 with the detection limit of 47.6 fg mL-1 (S/N = 3) was achieved, demonstrating the superior performance of C-Au-Lum NSs. This work would provide new ideas for the construction of high-performance ECL sensing platforms for diverse applications.

7.
Nature ; 573(7774): 398-402, 2019 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-31501569

RESUMO

Hindered ethers are of high value for various applications; however, they remain an underexplored area of chemical space because they are difficult to synthesize via conventional reactions1,2. Such motifs are highly coveted in medicinal chemistry, because extensive substitution about the ether bond prevents unwanted metabolic processes that can lead to rapid degradation in vivo. Here we report a simple route towards the synthesis of hindered ethers, in which electrochemical oxidation is used to liberate high-energy carbocations from simple carboxylic acids. These reactive carbocation intermediates, which are generated with low electrochemical potentials, capture an alcohol donor under non-acidic conditions; this enables the formation of a range of ethers (more than 80 have been prepared here) that would otherwise be difficult to access. The carbocations can also be intercepted by simple nucleophiles, leading to the formation of hindered alcohols and even alkyl fluorides. This method was evaluated for its ability to circumvent the synthetic bottlenecks encountered in the preparation of 12 chemical scaffolds, leading to higher yields of the required products, in addition to substantial reductions in the number of steps and the amount of labour required to prepare them. The use of molecular probes and the results of kinetic studies support the proposed mechanism and the role of additives under the conditions examined. The reaction manifold that we report here demonstrates the power of electrochemistry to access highly reactive intermediates under mild conditions and, in turn, the substantial improvements in efficiency that can be achieved with these otherwise-inaccessible intermediates.

8.
Med Sci Monit ; 25: 6539-6546, 2019 Aug 31.
Artigo em Inglês | MEDLINE | ID: mdl-31472071

RESUMO

BACKGROUND Long non-coding RNAs (lncRNAs) have been shown to play an important regulatory role in many tumors. This study was designed to investigate the expression of lncRNA ENST00000429227.1 in hepatocellular carcinoma (HCC) and to determine whether the expression of lncRNA ENST00000429227.1 affects the prognosis of HCC. MATERIAL AND METHODS lncRNA ENST00000429227.1 showing differences in expression between M1 and M2 was screened by microarray expression measurements. Quantitative real-time PCR (qRT-PCR) was used to detect the expression of lncRNA ENST00000429227.1 in 161 HCC patients. The chi-square test was used to evaluate the relationship between the expression of ENST00000429227.1 and clinicopathological parameters. A survival curve was drawn and analyzed by Kaplan-Meier method. Cox regression was used for univariate and multivariate analysis to determine whether lncRNA ENST00000429227.1 is an independent factor of the occurrence and prognosis of HCC. RESULTS A total of 3703 differentially expressed lncRNAs were obtained, of which 1777 were upregulated and 1926 were downregulated, with multiple change >1.5. The expression of lncRNA ENST00000429227.1 was upregulated in M2 cells. The expression of lncRNA ENST00000429227.1 in HCC tissues was higher than that in adjacent normal tissues (p<0.05), which was correlated with pathological parameters such as surgical margin (p=0.042), AFP (p=0.022) and Barcelona Clinic Liver Cancer (BCLC) stage (p=0.008). Survival analysis showed that high expression of lncRNA ENST00000429227.1 was associated with a decrease in overall survival (OS) rate of HCC patients. Cox regression analysis showed that high expression of ENST00000429227.1 may be an independent risk factor affecting the prognosis of HCC patients. CONCLUSIONS The results suggest that upregulation of ENST00000429227.1 is associated with poor prognosis of HCC patients, and may be a new biomarker for the diagnosis of HCC.

9.
Zhonghua Wei Zhong Bing Ji Jiu Yi Xue ; 31(8): 978-982, 2019 Aug.
Artigo em Chinês | MEDLINE | ID: mdl-31537223

RESUMO

OBJECTIVE: To investigate the effect of overexpression of microRNA-21-5p (miR-21-5p) on early apoptosis of type II alveolar epithelial cells (AEC II) in rats with hyperoxic acute lung injury (HALI). METHODS: The Sprague-Dawley (SD) rats were randomly divided into four groups: control group (CON group), hyperoxia group (H group), overexpression group (OE group) and empty vector group (EV group), with 20 rats in each group. HALI animal model was made by inhaling high concentration oxygen (oxygen concentration ≥ 90%); CON group was arranged to inhale room air. The miR-21-5p adeno-associated virus-6 (AAV-6) overexpression vectors or empty vectors were dripped into the lungs of OE group and EV group through tracheal tube, respectively. The hyperoxia model was prepared after 3 weeks of feeding. At 0, 24, 48 and 60 hours after making model, 5 rats were selected to detect lung injury parameters: oxygenation index (OI), respiratory index (RI), wet/dry ratio (W/D), pathological injury score of lung tissue; real-time quantitative polymerase chain reaction (RT-qPCR) was used to detect the expression of miR-21-5p in AEC II, and flow cytometry was used to detect the early apoptotic rate of AEC II. RESULTS: (1) The lung injury parameters: in H group, the OI gradually decreased with time, but the RI, lung W/D ratio and pathological score increased gradually with time, the difference between CON group was statistically significant at 24 hours [OI (mmHg, 1 mmHg = 0.133 kPa): 336.04±5.79 vs. 400.22±19.70, RI: 0.20±0.02 vs. 0.10±0.06, lung W/D ratio: 5.04±0.09 vs. 4.85±0.09, lung tissue pathological score: 0.13±0.01 vs. 0.07±0.01, all P < 0.05]. It indicated that HALI model could be successfully established by inhaling high concentration oxygen continuously. (2) The expression of miR-21-5p: the miR-21-5p was gradually increased in H, OE and EV groups, and the expression of miR-21-5p was significantly higher than that in CON group at 24, 48 and 60 hours. Compared with H group, the expression of miR-21-5p was significantly increased further in OE group at 0, 24, 48 and 60 hours (2-ΔΔCt: 3.75±0.11 vs. 0.98±0.14, 3.98±0.12 vs. 1.18±0.13, 4.28±0.18 vs. 1.49±0.06, 4.66±0.12 vs. 1.80±0.12, all P < 0.05). (3) The early apoptosis of AEC II: the early apoptosis rate gradually increased with time in H, OE and EV groups, and the early apoptosis of AEC II was significantly higher than that in CON group at 24, 48 and 60 hours. Compared with H group, the early apoptosis rate was significantly decreased in OE group at 24, 48 and 60 hours [(1.22±0.63)% vs. (2.84±0.59)%, (5.76±0.18)% vs. (13.10±2.01)%, (29.48±0.48)% vs. (49.04±1.36)%, all P < 0.05]. (4) There was no significant difference in the expression of miR-21-5p and the early apoptosis of AEC II cells between EV group and H group at each time point. CONCLUSIONS: Overexpression of miR-21-5p could inhibit the early apoptosis of AECII in rats with HALI.


Assuntos
Lesão Pulmonar Aguda , Hiperóxia , MicroRNAs/metabolismo , Células Epiteliais Alveolares , Animais , Apoptose , Pulmão , Distribuição Aleatória , Ratos , Ratos Sprague-Dawley
10.
Exp Cell Res ; 384(1): 111618, 2019 Nov 01.
Artigo em Inglês | MEDLINE | ID: mdl-31505167

RESUMO

End binding protein 1 (EB1) is a key regulator of microtubule dynamics that orchestrates hierarchical interaction networks at microtubule plus ends to control proper cell division. EB1 activity is known to be regulated by serine/threonine phosphorylation; however, how tyrosine phosphorylation affects EB1 activity remains poorly understood. In this study, we mapped the tyrosine phosphorylation pattern of EB1 in synchronized cells and identified two tyrosine phosphorylation sites (Y217 and Y247) in mitotic cells. Using phospho-deficient (Y/F) and phospho-mimic (Y/D) mutants, we revealed that Y247, but not Y217, is critical for astral microtubule stability. The Y247D mutant contributed to increased spindle angle, indicative of defects in spindle orientation. Time-lapse microscopy revealed that the Y247D mutant significantly delayed mitotic progression by increasing the duration times of prometaphase and metaphase. Structural analysis suggests that Y247 mutants lead to instability of the hydrophobic cavity in the EB homology (EBH) domain, thereby affecting its interactions with p150glued, a protein essential for Gαi/LGN/NuMA complex capture. These findings uncover a crucial role for EB1 phosphorylation in the regulation of mitotic spindle orientation and cell division.

11.
Plast Reconstr Surg ; 2019 Aug 27.
Artigo em Inglês | MEDLINE | ID: mdl-31464980

RESUMO

BACKGROUND: Surgical delay can improve flap viability, leading to vasodilation, neovascularization, and vessel reorganization. Experiments suggest similar positive effect of botulinum toxin A (BTX-A) on pedicled flaps' viability. However, whether it may convert the choke anastomoses into the true anastomoses and how to identify the optimal timing for flap transfer remains unclear. METHODS: One hundred and fifty-four Sprague-Dawley rats were divided into a control group, three saline injection groups, and three BTX-A injection groups defined by time of injection (2, 3, 4 weeks before flap harvest). A pedicled flap of 11×3 cm was marked on the unilateral dorsum of rat. Before flap harvest, the flap donors were assessed by the infrared thermal imaging, postmortem arteriography, immunohistochemical staining of CD 31 and ELISA. Flap survival areas percentage was measured on postoperative day 7. RESULTS: In the control group and saline groups, the infrared thermography showed three independent white hotspots interspaced by red zones over flaps, whereas it presented a continuous white band in the BTX-A groups. There was a significant increase in the flap survival area, flap surface temperatures, the numbers of identifiable vessels in the choke zones, microvascular density and vascular endothelial growth factor concentration in the BTX-A groups. CONCLUSIONS: BTX-A can convert the choke anastomoses into the true anastomoses and its preconditioning effect cannot increase over time; it is appropriate to choose the timing point when the infrared thermal images show a continuous white band existing over flaps for flap transfer.

12.
J Clin Invest ; 130: 3786-3791, 2019 Aug 12.
Artigo em Inglês | MEDLINE | ID: mdl-31403469

RESUMO

Nutrient excess, a major driver of obesity, diminishes hypothalamic responses to exogenously administered leptin, a critical hormone of energy balance. Here, we aimed to identify a physiological signal that arises from excess caloric intake and negatively controls hypothalamic leptin action. We found that deficiency of the gastric inhibitory polypeptide receptor (Gipr) for the gut-derived incretin hormone GIP protected against diet-induced neural leptin resistance. Furthermore, a centrally administered antibody that neutralizes GIPR had remarkable antiobesity effects in diet-induced obese mice, including reduced body weight and adiposity, and a decreased hypothalamic level of SOCS3, an inhibitor of leptin actions. In contrast, centrally administered GIP diminished hypothalamic sensitivity to leptin and increased hypothalamic levels of Socs3. Finally, we show that GIP increased the active form of the small GTPase Rap1 in the brain and that its activation was required for the central actions of GIP. Altogether, our results identify GIPR/Rap1 signaling in the brain as a molecular pathway linking overnutrition to the control of neural leptin actions.

13.
BMC Psychiatry ; 19(1): 242, 2019 Aug 05.
Artigo em Inglês | MEDLINE | ID: mdl-31382945

RESUMO

BACKGROUND: To date no study has compared more specifically the psychotropic medication treatment patterns for patients with schizophrenia living in community between rural and urban areas. This study examined the rural-urban differences of the use of psychotropic drugs among community-dwelling individuals with schizophrenia in China. METHOD: Data on 993 community-dwelling patients with schizophrenia (n = 479 in rural area and n = 514 urban area) were collected by interviews during 2013-2014, and 2015-2016 according to the diagnosis of DSM-IV or ICD-10. Data on patients' socio-demographic and clinical characteristics, prescriptions of psychotropic drugs were collected using a standardized protocol and data acquisition procedure. RESULTS: Multivariate analyses revealed that in comparison with the rural counterparts, the patients from the urban area were significantly more frequently prescribed antipsychotic polypharmacy, clozapine, and benzodiazepines, but the patients from the rural area had more frequently prescribed anticholinergics. CONCLUSIONS: Substantial variations in psychotropic medication treatment patterns for patients with schizophrenia living in community were found between rural and urban areas in China. Common use of antipsychotic polypharmacy, clozapine and benzodiazepines in urban area, and anticholinergics in rural area need to be further addressed.

14.
Med Sci Monit ; 25: 6221-6229, 2019 Aug 19.
Artigo em Inglês | MEDLINE | ID: mdl-31423008

RESUMO

BACKGROUND Increasing evidence suggests that long non-coding RNA (lncRNA) is closely related to the development of cancer. The present study investigated the potential predictive value of lncRNA GMDS divergent transcript (GMDS-DT) in the prognosis of patients with hepatocellular carcinoma (HCC) after hepatectomy. MATERIAL AND METHODS GMDS-DT was acquired by microarray data in 3 pairs of M1 and M2 macrophage duplicate samples. Real-time polymerase chain reaction (PCR) was performed to evaluate expression levels of GMDS-DT in liver cancer relative to normal tissue of 198 patients. The significance of GMDS-DT in prognosis after hepatectomy was examined via Kaplan-Meier test and Cox regression analysis. RESULTS The expression of GMDS-DT in liver cancer tissue was significantly lower than that in adjacent normal liver tissue (P<0.001), and was significantly associated with drinking history and metastasis (both P<0.05). The Kaplan-Meier test suggested that patients with lower expression levels of GMDS-DT in liver cancer tissue had significantly shorter disease-free survival and overall survival times after hepatectomy (P=0.028 and P=0.003, respectively). Cox regression analysis further indicated that GMDS-DT was an independent risk factor for disease-free survival and overall survival times of patients after hepatectomy (P=0.015 and P=0.001, respectively). CONCLUSIONS LncRNA GMDS-DT might be a potential biomarker for the prognosis of patients with liver cancer after hepatectomy.

15.
J Neuroimmunol ; 335: 577004, 2019 Oct 15.
Artigo em Inglês | MEDLINE | ID: mdl-31446341

RESUMO

BACKGROUND: Some previous studies already explored associations of interleukin-6 (IL-6) and interleukin-10 (IL-10) polymorphisms with ischemic stroke (IS). However, the results were conflicting. In this meta-analysis, we aimed to better analyze the relationship between IL-6/IL-10 polymorphisms and IS in a larger pooled population. METHODS: We performed a systematic search of PubMed, Web of Science, Embase and CNKI. We calculated pooled odds ratios (ORs) and 95% confidence intervals (CIs) to estimate associations between IL-6/IL-10 polymorphisms and IS. RESULTS: Totally 37 studies were included for analyses. A significant association with IS was observed for IL-10 rs1800896 polymorphism in AA versus GG + GA (recessive model, p = .001, OR = 1.42, 95%CI 1.15-1.75) in overall population. Further subgroup analyses showed that IL-6 rs1800795 was significantly associated with IS in Asians in GG versus GC + CC (dominant model, p = .0005, OR = 0.74, 95%CI 0.62-0.88), CC versus GG + GC (recessive model, p = .003, OR = 1.61, 95%CI 1.17-2.21) and G versus C (allele model, p = .01, OR = 0.74, 95%CI 0.58-0.93), whereas IL-10 rs1800896 polymorphism was significantly associated with cerebral infarction (CI) in GG versus GA + AA (dominant model, p = .02, OR = 2.04, 95%CI 1.14-3.64), GA versus GG + AA (overdominant model, p = .03, OR = 0.50, 95%CI 0.27-0.93) and G versus A (allele model, p = .01, OR = 1.92, 95%CI 1.16-3.17). CONCLUSIONS: Our findings indicated that IL-6 rs1800795 polymorphism was significantly associated with individual susceptibility to IS in Asians, but not in Caucasians. In addition, IL-10 rs1800896 polymorphism was also significantly associated with individual susceptibility to IS, especially for CI.

16.
Artigo em Inglês | MEDLINE | ID: mdl-31436374

RESUMO

Electrospinning technology has been widely used in the past few decades to prepare nanofibrous scaffolds that mimic extracellular matrices. However, traditional two-dimensional (2D) electrospun nanofibrous mats still have some inherent disadvantages for bone tissue engineering, such as limited cell infiltration and lack of three-dimensional (3D) structure. The development of 3D electrospun scaffolds with larger pore sizes and porosity provides new perspectives for electrospinning-based tissue engineering scaffolds. However, there are still some challenges and areas for improvement. In this review, the applications of 3D electrospun nanofibrous scaffolds in the field of bone tissue engineering from its fabrication methods to bio-functionalization are summarized, with the aim of providing new insights into the design of electrospinning-based bone tissue engineering scaffolds.

17.
Br J Clin Pharmacol ; 85(11): 2614-2622, 2019 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-31418902

RESUMO

AIMS: The aim of this study was to improve medication reconciliation and reduce the occurrence of duplicate prescriptions by pharmacists and physicians within 72 hours of hospital admission using an intelligent prescription system combined with the National Health Insurance PharmaCloud system to integrate the database with the medical institution computerized physician order entry (CPOE) system. METHODS: This 2-year intervention study was implemented in the geriatric ward of a hospital in Taiwan. We developed an integrated CPOE system linked with the PharmaCloud database and established an electronic platform for coordinated communication with all healthcare professionals. Patients provided written informed consent to access their PharmaCloud records. We compared the intervention effectiveness within 72 hours of admission for improvement in pharmacist medication reconciliation, increased at-home medications documentation and decreased costs from duplicated at-home prescriptions. RESULTS: The medication reconciliation rate within 72 hours of admission increased from 44.0% preintervention to 86.8% postintervention (relative risk = 1.97, 95% confidence interval [CI]: 1.69-2.31; P < .001). The monthly average of patients who brought and took home medications documented in the CPOE system during hospitalization increased by 7.54 (95% CI 5.58-20.49, P = .22). The monthly average of home medications documented increased by 102.52 (95% CI 38.44-166.60; P = .01). Savings on the monthly average prescription expenditures of at-home medication increased by US$ 2,795.52 (95% CI US$1310.41-4280.63; P < .01). CONCLUSION: Integrating medication data from PharmaCloud to the hospital's medical chart system improved pharmacist medication reconciliation, which decreased duplicated medications and reduced in-hospital medication costs.

18.
Ann Hematol ; 98(10): 2283-2291, 2019 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-31396670

RESUMO

Paroxysmal nocturnal hemoglobinuria (PNH) is an acquired hemolytic disease with thrombosis as a major complication. The mechanism of thrombosis and related risk factors in PNH patients are still not well characterized. We retrospectively enrolled 99 patients with newly diagnosed PNH at our institute from 2011 to 2016. According to binary logistic regression model analysis, we first identified four baseline clinical risk factors which may be associated with incidence of thrombosis in the PNH cohort, including PNH clone sizes (fluorescent aerolysin of neutrophil) ≤ 80 (OR 1.056, 95%CI 1.016-1.097, P = 0.005), hemoglobin ≤ 75 g/L (OR 4.202, 95%CI 0.984-17.954, P = 0.053), platelet > 100 × 109/L (OR 6.547, 95%CI 1.490-28.767, P = 0.013) and rs495828 = G (OR 5.243, 95%CI 1.314-20.916, P = 0.019). These independent risk factors were combined together to develop a risk model to evaluate thrombosis risk (AUC = 0.756, 95%CI 0.607-0.905, P < 0.001). Our risk model revealed a higher cumulative incidence of thrombosis and an earlier thrombosis events in PNH patients with high risk (risk score ≥ 23) compared with those with low risk (risk score < 23, P < 0.001 and P = 0.043, respectively). Although with some limitations, we set up a prediction model for thrombosis risk in patients with PNH for the first time, but it needed to be verified in a prospective study with larger patients and longer follow-up time in the future.


Assuntos
Hemoglobinúria Paroxística , Modelos Biológicos , Trombose , Adolescente , Adulto , Idoso , Feminino , Seguimentos , Hemoglobinúria Paroxística/sangue , Hemoglobinúria Paroxística/complicações , Hemoglobinúria Paroxística/epidemiologia , Humanos , Incidência , Masculino , Pessoa de Meia-Idade , Valor Preditivo dos Testes , Estudos Retrospectivos , Fatores de Risco , Trombose/sangue , Trombose/epidemiologia , Trombose/etiologia
19.
Transplant Proc ; 51(6): 2116-2123, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31303407

RESUMO

Besides being used in the therapy of type 2 diabetes, exenatide reduces cerebral ischemia-reperfusion (I/R) injury. We evaluated the potential effects of exenatide on inhibition of apoptosis in kidney grafts donated after cardiac death and on reduction of I/R injury after kidney transplantation (KTx) in a rat model. We used a rat syngeneic KTx model with kidney grafts obtained after cardiac death, and apoptosis was detected in the graft before KTx. Graft function, rat survival, morphologic examination, and activation of inflammatory molecules were analyzed after KTx. By the end of the cold storage, exenatide pretreatment donors had significantly reduced caspase pathway activation, terminal deoxynucleotidyl transferase dUTP nick-end labeling--positive cells, release of mitochondrial porin proteins into the cytosol, and expression of cleaved caspase-3 and poly (ADP-ribose) polymerase in kidney grafts. Exenatide pretreatment improved renal function survival rate with lower scores of acute tubular necrosis, infiltrating macrophages, and interstitial fibrosis as well as reduced messenger RNA expression of inflammatory mediators (tumor necrosis factor α, interleukin-6, interleukin-1ß, and intercellular adhesion molecule-1) after KTx. Our study showed that exenatide reduced I/R injury in kidneys donated after cardiac death in a rat transplantation model and improved recipient survival and graft function.

20.
Biosens Bioelectron ; 141: 111479, 2019 Sep 15.
Artigo em Inglês | MEDLINE | ID: mdl-31260903

RESUMO

While glucose monitoring technology is widely available, the continued prevalence of diabetes around the world coupled with its debilitating effects continues to grow. The significant limitations which exist in the current technology, instils the need for materials capable of non-invasive glucose detection. In this study a unique non-enzymatic electrochemical glucose sensor was developed, utilising a gold honeycomb-like framework upon which sharp Co3O4 needles are anchored. This composite nanomaterial demonstrates excellent sensing performance in glucose concentrations ranging between 20 µM and 4 mM, exceeding the range required for non-invasive glucose sensing. In conjunction with this high sensitivity (2.014 mA mM-1·cm-2), the material possesses excellent selectivity towards glucose for commonly interfering physiological species such as uric acid and ascorbic acid. Glucose detection in synthetic saliva was then performed showing excellent capability in the low concentration range (20 µM-1 mM) for non-invasive sensing performance. Further tests showed good selectivity of the sensor in physiological contaminants commonly found in saliva such as cortisol and dopamine. This development provides excellent scope to create next-generation non-invasive diabetes monitoring platforms, with excellent performance when detecting low glucose concentrations in complex solutions such as saliva.

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