Introduction: The high morbidity and mortality by hypertensive cardiopathy demand the construction and validation of tools to stratify the risk of developing this condition.
Objective: To design and validate an index, based on risk factors, that permits to predict the development of hypertensive cardiopathy in patients with a diagnosis of essential arterial hypertension.
Methods: A prospective cohort study was done in hypertensive patients assisted at the specialized arterial hypertension physicians’ office of the “Carlos Manuel de Céspedes” Specialty Policlinic attached to the General University Hospital, Bayamo Municipality, Granma Province, Cuba from January 1st, 2010 to December 31, 2016. Internal and external validity and the internal consistency of the index were determined.
Results: The index sensitivity was of 97, 20 (IC: 93, 93-94.09) and specificity of 65, 38 (IC: 76, 25-76, 20). Both the index discriminative capacity (area under the ROC curve= 0,944; interval of confidence: 0.932-0.956; p<0.0005) and calibration (p=0.751) were adequate.
Conclusions: The present study proposes an index to predict the risk of developing hypertensive cardiopathy, with adequate discriminative capacity and calibration (external validity). The index can be used as a tool of clinical and epidemiological surveillance since it permits to identify subjects with greater probability of developing the condition and to stratify the risk.
Patients with chronic kidney disease are at increased risk of thromboembolic complications and are therefore often managed with anticoagulation therapy [1]. While these patients are traditionally treated with Vitamin K antagonists (VKAs), the Non-Vitamin K antagonist oral anticoagulants (NOACs), such as rivaroxaban and apixaban are being used with increasing frequency. Relatively new to the anticoagulant treatment arsenal, both compounds are direct Factor Xa inhibitors and represent an alternative to traditional VKA treatments, such as warfarin. However, because these compounds are at least partially renally eliminated, achieving safe and effective anticoagulation in this vulnerable population has proven to be a challenge [2,3]. With limited published data, there is often uncertainty surrounding which of the NOACs can be safely used.
Background: Patients with myocardial infarction (MI) often experience anxiety, depression and poor quality of life (QoL) compared with a normative population. Mood disturbances and QoL have been extensively investigated, but only a few studies have examined the long-term effects of MI on these complex phenomena.
Aims: To examine the levels and associated predictors of anxiety, depression, and QoL in patients 2 years after MI.
Methods: This was a single center, observational study of patients with MI (n=377, 22% women, median age 66 years). Two years after MI (2012-2014), the patients were asked to answer the Hospital Anxiety and Depression Scale (HADS) and EuroQol 5-dimension (EQ-5D-3L) questionnaires.
Results: Most patients experienced neither anxiety (87%, 95% confidence interval [CI]: 83-90%) nor depression (94%, 95% CI: 92-97%) 2 years post-MI. Elderly patients experienced more depression than younger patients (p=0.003) and women had higher anxiety levels than men (p=0.009).
Most patients had “no problems” with any of the EQ-5D-3L dimensions (72-98%), but 48% (95% CI: 43%-53%) self-reported at least “some problems” with pain/discomfort. In a multiple logistic regression model (EQ-5D-3L) higher age (p<0.001) and female sex (p<0.001) were associated with more pain/discomfort. Female sex (p=0.047) and prior MI (p=0.038) were associated with anxiety/depression. History of heart failure was associated with worse mobility (p=0.005) and problems with usual activities (p=0.006). The median total health status of the patients (EQ-VAS) was 78 (95% CI: 75-80)
Victor Tsirkin*, Alexander Nozdrachev, Elena Sizova, Tatyana Polezhaeva, Svetlana Khlybova, Marina Morozova, Andrew Trukhin, Julia Korotaeva and Grigory Khodyrev
The results of the 20 years studies of the presence in blood serum and other body fluids of endogenous modulators of adrenergic and M-cholinergic impact as a component of humoral link of autonomic nervous system. The article is devoted to the endogenous sensitizer of beta-adrenergic receptor (ESBAR) - water-soluble low molecular weight substances, analogs of which are histidine, tryptophan, tyrosine, mildronat and preductal. It is shown, that separate dilutions of human serum and animal (as a source of ESBAR) and analogs of ESBAR ways to enhance the effectiveness of activation of beta-adrenoceptors (AR) of smooth muscle (uterus, coronary and renal arteries, trachea, stomach), myocardium, erythrocytes and platelets (respectively influenced of histidine and tryptophan). It is reported that content of ESBAR in human serum (according to the titers of its dilution) depends on the sex and the presence of somatic diseases, and at women are also on the stage of reproduction and obstetric complications It is discussed possible mechanisms of ESBAR action, its physiological role, including as a component of beta-adrenoceptor inhibitory mechanism for myometrium, as well as the prospect of the use of analogs of ESBAR, including for the prevention of preterm labor, and for the treatment of bronchial asthma, coronary heart disease, hypertension and heart failure.
It was investigated contractility and adrenoreactivity of intact myocardium strips of right ventricular in experiment with 60 rats. They were assessed by the force of induce contraction and its changes under the influence of adrenaline (10-9 or 10-5 g / ml). Found that these indicators do not depend on the phases of the estrous cycle and the presence of pregnancy. Histidine (10-10-10-4 g / ml) did not increase the response to adrenalin (10-9 g / ml), but increased the force of the contractions in rats in progesterone dominance (trend) and pregnancy (statistically significant). Against the background of propranolol (10-8 g / mL) or atenolol (10-8, 10-6 g / mL), adrenaline (10-5 g / mL) instead of increasing the force of contraction reduced it (probably due to activation of beta3-, alpha1 - and alpha1 a2- adrenergic receptors), and histidine (10-4 g / mL) prevented this reduction, but does not restore full ability of adrenaline to exert a positive inotropic effect. On the background of nicergoline (10-8 g / mL or nicergoline and propranolol (10-8 g / mL), adrenaline (10-5 g / mL) did not alter the force of contraction, and histidine (10-4 g/mL) restore ability of adrenaline to exert a positive inotropic effect but only in the experiments with nicergoline. Concluded that histidine increases the efficiency of the activation of all three (beta1-, beta2- and beta3-) populations of myocardial beta-adrenoceptoprs, including at lower by adrenergic blockers. Therefore, histidine proposed as an antagonist of beta-adrenergic blockers and as resensitizator of these receptors.
Core Tip: In the experiments with strips of the right ventricle of 40 nonpregnant and 20 pregnant rats histidine (10-10-10-4 g /mL) did not increase the response to adrenaline (10-9 g / ml), but increased the force of contractions in pregnant rats. On the background of propranolol (10-8 g / mL) or atenolol (10-8, 10-6 g / mL), adrenaline (10-5g/mL) showed a negative inotropic effect, and histidine (10-4 g / mL) prevented it, but does not restore the ability of adrenaline to show positive inotropic effect,. i.e histidine exhibits the properties of the antagonist of beta-blockers and of resensitizator of beta-adrenoceptors
Post cardiac surgery stroke is a devastating complication with an incidence as high as 50%1. The association between intra-operative mean arterial blood pressure (MAP- better called linear blood pressure) during cardiopulmonary bypass (CPB) and the development of postoperative stroke-as diagnosed by neuroimaging- and of cognitive dysfunction (POCD) is controversial. This is due to differences in the study populations, stroke assessment tools, operation and conduction of MAPs, variations in neurocognitive testing and duration of follow up. As a result there is a gap in the knowledge on an ideal MAP as a preventive measure of post CPB stroke and POCD.
Background: Human papillomavirus (HPV) infection causes cervical cancer (CC), a common malignancy among Kenyan women. New CC screening methods rely on oncogenic HPV (“high-risk”, or HR-HPV) detection, but most have not been evaluated in swabs from Kenyan women.
Methods: HPV typing was performed on 155 cervical swabs from Kenyan women using the Roche Linear Array® (LA) and careHPV™ (careHPV) assays. Detection of 14 oncogenic HPV types in careHPV assay was compared to LA results.
Results: Compared to LA, sensitivity and specificity of careHPV assay was 53.0% and 80.9%, respectively. The sensitivity and specificity of careHPV in swabs from women with cervical dysplasia was 74.1% and 65.2%, respectively. The sensitivity and specificity of careHPV in swabs from HIV-infected women was 55.9% and of 96.4%, respectively. Overall agreements of careHPV assay with LA was substantial.
Conclusion: The results for careHPV assay are promising for oncogenic HPV detection in Kenyan women. The low sensitivity of careHPV for detection of HR-HPV could limit it’s benefit as a screening tool. Thus, a full clinical validation study is highly desirable before the careHPV assay can be accepted for cervical cancer screening.
Rubella remains an important pathogen worldwide, with many cases of congenital rubella syndrome per year. Rubella vaccination is included in the vaccination program of many countries. WHO has set goals for the elimination of measles and rubella and prevention of congenital rubella syndrome by 2020. Worldwide, the rubella vaccine is highly effective and safe, and as a result, endemic rubella transmission has been halted in the Americas since 2009. Incomplete rubella vaccination programs result in continuous disease transmission, as evidenced by major recent outbreaks in some countries around the world. In this review, we present the rubella control, elimination and eradication policies and a brief review of the rubella laboratory diagnosis.
Ephedra, an ancient herb, is applied to treat common cold and influenza for such a long time in China. Pseudoephedrine is a main active ingredient from Ephedra which is used for relieving nasal congestion clinically. We previously reported that pseudoephedrine showed a potent anti-inflammatory effect other than sympathomimetic effects. In the present study, we aimed to investigate whether pseudoephedrine could protect mice from the H1N1 virus infection. The mice were infected with a 20% LD50 influenza A virus (IAV) suspension via intranasal administration to establish a virus infection model. Further, the mice were orally administered pseudoephedrine or oseltamivir for 4 days from one day after infection. Our results showed that pseudoephedrine improved lung pathological damage during the IVA infection period, and it dramatically increased the survival rate and attenuated loss of body weight compared with the virus-infected control group. In addition, pseudoephedrine inhibited the cytokine storms and mRNAs expression of the TLR7 signaling pathway. Surprisingly, pseudoephedrine showed an inhibitory effect on the replication of IAV. These results give clear evidence that pseudoephedrine is a potential anti-influenza drug by blunting cytokine storms and inhibition of replication of IAV, and following these results, we speculate that it should be tested in the novel coronavirus pneumonia (COVID-19, a severe epidemic in China currently) in which the cytokine storms play a key role to damage bronchi and lung in the early stage.
The Hypothesis born on a simple clinical data noted by some Chinese Reserchers during the starting point of epidemic began in the dicember of the 2019, for the novel member of human coronavirus, officially named as SARS‐CoV‐2 (severe acute respiratory syndrome coronavirus 2) by International Committee on Taxonomy of Viruses (ICTV) is a new strain of RNA viruses that has not been previously identified in humans [1]. Sars-COV and SARS CoV-2 have some clinical differences. First: The Sars, severe acute respiratory sindrome induce a respiratory disease in immunocompetent hosts, although can cause severe infections in infant, young children and elderly individuals; Sars-CoV-2 induce a middle infection into the young children but the mortality is more high in to the adult population. We made a macthing with balst p of these sequences, Sars COV-2, taken on GENEBANK with H1N1 neuraminidase and the not structural protein NS1 and NS2 an interferon antagonist that may also stimulate proinflammatory cytokines in infected cells We can speculate that the mutation is occurred on accessories protein making a different virulence action between the two species Sars Cov and Sars Cov-2, same action we have founded in the H1N1 viral pandemic of the 2019.
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Elisabeth H Wiig
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BS, PharmD., MBA, CPHIMS, FHIMSS, Adjunct Professor, Global Healthcare Management, MCPHS University, Chief Strategy Offi cer, MedicaSoft, Senior Advisor, National Health IT (NHIT) Collaborative for Underserved, New York HIMSS, National Liaison, Health 2.0 Boston, Past Chair, Chair Innovation, USA
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