59 research outputs found

    EGFR and COX-2 protein expression in non-small cell lung cancer and the correlation with clinical features

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    <p>Abstract</p> <p>Background</p> <p>To evaluate the expression of EGFR and COX-2 and their correlation with prognosis in NSCLC</p> <p>Methods</p> <p>The paraffin embedded tumor samples of 50 NSCLC patients receiving radical resection were analyzed immunohistochemically for EGFR and COX-2 expression and their prognostic values were explored.</p> <p>Results</p> <p>The positive rate of EGFR protein in NSCLC tumor cells was 46%, which was significantly higher than its expression in normal lung (p = 0.0234) and paracancerous tissues (p = 0.020). EGFR expression was significantly higher in nodal positive than in nodal negative patients (p = 0.04). The mean survival time for EGFR positive patients (31 months) was significantly lower than that for patients with EGFR negative expression (48 months) (p = 0.008,). In patients receiving post-operation thoracic irradiation, the mean survival time for EGFR positive patients was significantly lower than that for patients without EGFR positive expression (25 vs. 48 months, P = 0.004). The positive rate of COX-2 protein expression in NSCLC tumor cells was 90%, which was significantly higher than that in normal tissue(p = 0.00) and paracancerous tissue (p = 0.00). There was no correlation between COX-2 expression and patient survival, and no correlation between COX-2 and EGFR protein expression (P = 0.555).</p> <p>Conclusions</p> <p>COX-2 and EGFR are over-expressed in NSCLC. EGFR is an independent prognostic factor and a predictive factor for radiotherapy response in NSCLC.</p

    Modeling habitat suitability for Yunnan Snub-nosed monkeys in Laojun Mountain National Park

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    We provide new information on Yunnan snub-nosed monkey (Rhinopithecus bieti) behavioral ecology, contributing to future conservation efforts within the Laojun Mountain National Park. Habitat evaluation procedures are used to quantify the value of land as a habitat for a species. We analyzed environmental variables hypothesized to influence habitat suitability for Yunnan snub-nosed monkeys, and mapped the distribution of suitable habitats across the study area and adjacent areas. Spatial analysis with GPS data was conducted to investigate home-range change of these monkeys. Predictor variables were generated using ArcMap and R programming language. We prepared 34 environmental variables at 30-m spatial resolution. Maxent was used to analyze environmental variables that contributed to suitability. Using satellite remote sensing and GIS, we modeled the distribution of suitable habitat for Yunnan snub-nosed monkeys in the Jinsichang area of the Laojun Mountains in China. This study did not describe the frequency or intensity of habitat use. Habitat suitability was affected by several variables, the most influential, as determined by permutation importance, being mean diurnal temperature range (31.6%), precipitation during the wettest quarter of the year (30.4%), average annual precipitation (17%), normalized difference vegetation index (5%), wetness (4.6%), and aspect (4.5%). This habitat suitability model provides information about the current distribution of Yunnan snub-nosed monkeys, which is important for appropriate implementation of conservation actions

    Low-dose dobutamine cardiovascular magnetic resonance segmental strain study of early phase of intramyocardial hemorrhage rats

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    BACKGROUND: This study investigates the segmental myocardial strain of the early phase of intramyocardial hemorrhage (IMH) caused by reperfused myocardial infarction (MI) in rats by low-dose dobutamine (LDD) cardiovascular magnetic resonance (CMR) feature-tracking. METHODS: Nine sham rats and nine rats with 60-min myocardial ischemia followed by 48-h reperfusion were investigated using CMR, including T2*-mapping sequence and fast imaging with steady-state precession (FISP)-cine sequence. Another FISP-cine sequence was acquired after 2 min of dobutamine injection; the MI, IMH, and Non-MI (NMI) areas were identified. The values of peak radial strains (PRS) and peak circumferential strains (PCS) of the MI, IMH and NMI segments were acquired. The efficiency of PRS and PCS (EPRS and EPCS, respectively) were calculated on the basis of the time of every single heartbeat. RESULTS: The PRS, PCS, EPRS, and EPCS of the sham group increased after LDD injection. However, the PRS, PCS, EPRS, and EPCS of the IMH segment did not increase. Moreover, the PRS and PCS of the MI and NMI segments did not increase, but the EPRS and EPCS of these segments increased. The PRS, PCS, EPRS, and EPCS of the IMH segment were lower than those of the MI and NMI segments before and after LDD injection, but without a significant difference between MI segment and NMI segment before and after LDD injection. CONCLUSIONS: LDD could help assess dysfunctions in segments with IMH, especially using the efficiency of strain. IMH was a crucial factor that decreased segmental movement and reserved function

    Myocardial infarction size as an independent predictor of intramyocardial haemorrhage in acute reperfused myocardial ischaemic rats

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    BACKGROUND: In previous studies, haemorrhage occurred only with large infarct sizes, and studies found a moderate correlation between the extent of necrosis and haemorrhage, but the extent of infarction size in these studies was limited. This study aimed to find the correlations between intramyocardial haemorrhage (IMH), myocardial infarction (MI), and myocardial oedema (ME) from small to large sizes of MI in a 7.0-T MR scanner. METHODS: Different sizes of myocardial infarction were induced by occluding different sections of the proximal left anterior descending coronary artery (1-3 mm under the left auricle). T2*-mapping, T2-mapping and late gadolinium enhancement (LGE) sequences were performed on a 7.0 T MR system at Days 2 and 7. T2*- and T2-maps were calculated using custom-made software. All areas were expressed as a percentage of the entire myocardial tissue of the left ventricle. The rats were divided into two groups based on the T2* results and pathological findings; MI with IMH was referred to as the + IMH group, while MI without IMH was referred to as the -IMH group. RESULTS: The final experimental sample consisted of 25 rats in the + IMH group and 10 rats in the -IMH group. For the + IMH group on Day 2, there was a significant positive correlation between IMH size and MI size (r = 0.677, P \u3c 0.01) and a positive correlation between IMH size and ME size (r = 0.552, P \u3c 0.01). On Day 7, there was a significant positive correlation between IMH size and MI size (r = 0.711, P \u3c 0.01), while no correlation was found between IMH size and ME size (r = 0.429, P = 0.097). The MI sizes of the + IMH group were larger than those of the -IMH group (P \u3c 0.01). CONCLUSIONS: Infarction size prior to reperfusion is a critical factor in determining IMH size in rats

    Prognosis for patients with apical hypertrophic cardiomyopathy: A multicenter cohort study based on propensity score matching

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    Background: Apical hypertrophic cardiomyopathy (AHCM) is a subtype of HCM, and few studies on the prognosis in AHCM are available.Aims: This study aimed to explore the clinical prognosis for AHCM and non-AHCM patients through clinical data based on propensity score matching (PSM) in a large cohort of Chinese HCM patients.Methods: The cohort study included 2268 HCM patients, 226 AHCM and 2042 non-AHCM patients from 13 tertiary hospitals, who were treated between 1996 and 2021. Fifteen demographic and clinical variables of 226 AHCM patients and 2042 non-AHCM patients were matched using 1:2 PSM. A Cox proportional hazard regression model was constructed to assess the effect of AHCM on mortality.Results: During a median follow-up of 5.1 (2.4–8.4) years, 353 (15.6%) of the 2268 HCM patients died, of whom 205 died due to cardiovascular mortality/cardiac transplantation and 94 experienced sudden cardiac death (SCD). In the matched cohort, the ACHM patients had lower rates of all-cause mortality (P = 0.003), cardiovascular mortality/cardiac transplantation (P = 0.03), and SCD (P = 0.02) than the non-AHCM patients. Furthermore, the Cox proportional hazard regression model showed that AHCM was an independent prognostic predictor of all-cause HCM mortality (P = 0.004) and a univariable prognostic predictor of cardiovascular mortality/cardiac transplantation (P = 0.03) and for SCD (P = 0.03). However, AHCM was not significant in multivariable Cox regression models in relation to cardiovascular mortality/cardiac transplantation and SCD.Conclusion: AHCM had a favorable prognosis both before and after matching, with lower all-cause mortality, cardiovascular mortality/cardiac transplantation, and SCD than non-AHCM

    Specifically Progressive Deficits of Brain Functional Marker in Amnestic Type Mild Cognitive Impairment

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    Background: Deficits of the default mode network (DMN) have been demonstrated in subjects with amnestic type mild cognitive impairment (aMCI) who have a high risk of developing Alzheimer’s disease (AD). However, no longitudinal study of this network has been reported in aMCI. Identifying links between development of DMN and aMCI progression would be of considerable value in understanding brain changes underpinning aMCI and determining risk of conversion to AD. Methodology/Principal Findings: Resting-state fMRI was acquired in aMCI subjects (n = 26) and controls (n = 18) at baseline and after approximately 20 months follow up. Independent component analysis was used to isolate the DMN in each participant. Differences in DMN between aMCI and controls were examined at baseline, and subsequent changes between baseline and follow-up were also assessed in the groups. Posterior cingulate cortex/precuneus (PCC/PCu) hyper-functional connectivity was observed at baseline in aMCI subjects, while a substantial decrement of these connections was evident at follow-up in aMCI subjects, compared to matched controls. Specifically, PCC/PCu dysfunction was positively related to the impairments of episodic memory from baseline to follow up in aMCI group. Conclusions/Significance: The patterns of longitudinal deficits of DMN may assist investigators to identify and monitor the development of aMCI

    Global, regional, and national under-5 mortality, adult mortality, age-specific mortality, and life expectancy, 1970–2016: a systematic analysis for the Global Burden of Disease Study 2016

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    BACKGROUND: Detailed assessments of mortality patterns, particularly age-specific mortality, represent a crucial input that enables health systems to target interventions to specific populations. Understanding how all-cause mortality has changed with respect to development status can identify exemplars for best practice. To accomplish this, the Global Burden of Diseases, Injuries, and Risk Factors Study 2016 (GBD 2016) estimated age-specific and sex-specific all-cause mortality between 1970 and 2016 for 195 countries and territories and at the subnational level for the five countries with a population greater than 200 million in 2016. METHODS: We have evaluated how well civil registration systems captured deaths using a set of demographic methods called death distribution methods for adults and from consideration of survey and census data for children younger than 5 years. We generated an overall assessment of completeness of registration of deaths by dividing registered deaths in each location-year by our estimate of all-age deaths generated from our overall estimation process. For 163 locations, including subnational units in countries with a population greater than 200 million with complete vital registration (VR) systems, our estimates were largely driven by the observed data, with corrections for small fluctuations in numbers and estimation for recent years where there were lags in data reporting (lags were variable by location, generally between 1 year and 6 years). For other locations, we took advantage of different data sources available to measure under-5 mortality rates (U5MR) using complete birth histories, summary birth histories, and incomplete VR with adjustments; we measured adult mortality rate (the probability of death in individuals aged 15-60 years) using adjusted incomplete VR, sibling histories, and household death recall. We used the U5MR and adult mortality rate, together with crude death rate due to HIV in the GBD model life table system, to estimate age-specific and sex-specific death rates for each location-year. Using various international databases, we identified fatal discontinuities, which we defined as increases in the death rate of more than one death per million, resulting from conflict and terrorism, natural disasters, major transport or technological accidents, and a subset of epidemic infectious diseases; these were added to estimates in the relevant years. In 47 countries with an identified peak adult prevalence for HIV/AIDS of more than 0·5% and where VR systems were less than 65% complete, we informed our estimates of age-sex-specific mortality using the Estimation and Projection Package (EPP)-Spectrum model fitted to national HIV/AIDS prevalence surveys and antenatal clinic serosurveillance systems. We estimated stillbirths, early neonatal, late neonatal, and childhood mortality using both survey and VR data in spatiotemporal Gaussian process regression models. We estimated abridged life tables for all location-years using age-specific death rates. We grouped locations into development quintiles based on the Socio-demographic Index (SDI) and analysed mortality trends by quintile. Using spline regression, we estimated the expected mortality rate for each age-sex group as a function of SDI. We identified countries with higher life expectancy than expected by comparing observed life expectancy to anticipated life expectancy on the basis of development status alone. FINDINGS: Completeness in the registration of deaths increased from 28% in 1970 to a peak of 45% in 2013; completeness was lower after 2013 because of lags in reporting. Total deaths in children younger than 5 years decreased from 1970 to 2016, and slower decreases occurred at ages 5-24 years. By contrast, numbers of adult deaths increased in each 5-year age bracket above the age of 25 years. The distribution of annualised rates of change in age-specific mortality rate differed over the period 2000 to 2016 compared with earlier decades: increasing annualised rates of change were less frequent, although rising annualised rates of change still occurred in some locations, particularly for adolescent and younger adult age groups. Rates of stillbirths and under-5 mortality both decreased globally from 1970. Evidence for global convergence of death rates was mixed; although the absolute difference between age-standardised death rates narrowed between countries at the lowest and highest levels of SDI, the ratio of these death rates-a measure of relative inequality-increased slightly. There was a strong shift between 1970 and 2016 toward higher life expectancy, most noticeably at higher levels of SDI. Among countries with populations greater than 1 million in 2016, life expectancy at birth was highest for women in Japan, at 86·9 years (95% UI 86·7-87·2), and for men in Singapore, at 81·3 years (78·8-83·7) in 2016. Male life expectancy was generally lower than female life expectancy between 1970 and 2016, an

    (&amp;#956;-3,5,9,11-Tetraoxo-4,10-diazatetracyclo[5.5.2.02,6.08,12]tetradec-13-ene-4,10-diido-&amp;#954;2N:N&amp;#8242;)bis[(2,2&amp;#8242;-bipyridine-&amp;#954;2N,N&amp;#8242;)silver(I)] dihydrate

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    In the title complex, [Ag2(C12H8N2O4)(C10H8N2)2]&amp;#183;2H2O, the AgI ion is three-coordinated by two N atoms from a chelating 2,2&amp;#8242;-bipyridine ligand and one N atom from an imide ligand in a Y-shaped fashion. The imide ligand and the complex lie on a twofold rotation axis. The ligand bridges two AgI ions, forming a dinuclear complex. In the crystal, O&amp;#8212;H...O hydrogen bonds link the lattice water molecules and the complex molecules into a ribbon-like structure along [001]. &amp;#960;&amp;#8211;&amp;#960; interactions are observed between the pyridine rings [centroid&amp;#8211;centroid distance = 3.8289&amp;#8197;(14)&amp;#8197;&amp;#197;]

    Poly[[μ 2

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