351 research outputs found

    Halitosis: new insight into a millennial old problem

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    Comment on Halitosis: could it be more than mere bad breath? [Intern Emerg Med. 2011

    Rethinking clinical decision-making to improve clinical reasoning

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    : Improving clinical reasoning techniques is the right way to facilitate decision-making from prognostic, diagnostic, and therapeutic points of view. However, the process to do that is to fill knowledge gaps by studying and growing experience and knowing some cognitive aspects to raise the awareness of thinking mechanisms to avoid cognitive errors through correct educational training. This article examines clinical approaches and educational gaps in training medical students and young doctors. The authors explore the core elements of clinical reasoning, including metacognition, reasoning errors and cognitive biases, reasoning strategies, and ways to improve decision-making. The article addresses the dual-process theory of thought and the new Default Mode Network (DMN) theory. The reader may consider the article a first-level guide to deepen how to think and not what to think, knowing that this synthesis results from years of study and reasoning in clinical practice and educational settings

    A methodological look at the controversy about the influence of salt intake on cardiovascular risk.

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    Comment on: Reduced dietary salt for the prevention of cardiovascular disease. [Cochrane Database Syst Rev. 2011] Reduced dietary salt for the prevention of cardiovascular disease: a meta-analysis of randomized controlled trials (Cochrane review). [Am J Hypertens. 2011

    Left ventricular diastolic filling alterations in subjects with mitral valve prolapse: a Doppler echocardiographic study

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    To assess left ventricular diastolic filling in mitral valve prolapse (MVP), we studied 22 patients with idiopathic MVP and 22 healthy controls matched for sex, age, body surface area and heart rate. A two-dimensional, M-mode and Doppler echocardiographic examination was performed to exclude any cardiac abnormalities. The two groups had similar diastolic and systolic left ventricular volumes, left ventricle mass and ejection fraction. Doppler measurements of mitral inflow were: E and A areas (the components of the total flow velocity-time integral in the early passive period of ventricular filling, E; and the late active period of atrial emptying, A), the peak E and A velocities (cm.s-1), acceleration and deceleration half-times (ms) of early diastolic rapid inflow, acceleration time of early diastolic flow (AT), total diastolic filling time (DFT) (ms), and the deceleration of early diastolic flow (cm.s-2). From these measurements were calculate: peak A/E ratio (A/E), E area/A area, the early filling fraction, the atrial filling fraction, AT/DFT ratio. All the Doppler measurements reported are the average of three cardiac cycles selected at end expiration. The mean peak A velocity, A/E velocity ratio, deceleration half time and atrial filling fraction were each significantly higher for subjects presenting a MVP (60 +/- 12 cm.s-1 vs 49 +/- 14, P < 0.008; 98 +/- 13% vs 64 +/- 12%, P < 0.0001; 120 +/- 36 ms vs 92 +/- 11, P < 0.002; 0.45 +/- 0.14 vs 0.36 +/- 0.08, P < 0.02

    Rapid left ventricular filling in untreated hypertensive subjects with or without left ventricular hypertrophy

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    In this study, independent contribution of age, HR, BMI, casual and ambulatory blood pressure, LVM and LVEF in evaluating diastolic filling have been investigated in 34 never-treated hypertensive patients and in 15 healthy normotensive subjects. All the subjects were free from coronary artery disease, valvular disease, heart failure, renal disease and psychiatric problems. All the hypertensive subjects (never treated) were subgrouped according to presence or absence of LVH. The PFR decreased significantly and tPFR increased significantly in hypertensive patients in comparison with normotensive subjects and they did not change in the presence vs absence of LVH. The PFR was inversely correlated with BMI, age, 24-h mean SBP and with 24-h DBP. In multiple regression analysis, PFR decreased with BMI, age, 24-h mean SBP and DBP but not with LVMI. These results suggest that BMI, age and 24-h mean blood pressure were the major determinants of PFR abnormalities in hypertensive patients

    Role of multidrug-resistant pathogens in health-care-associated pneumonia.

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    Comment on: Rethinking the concepts of community-acquired and health-care-associated pneumonia. [Lancet Infect Dis. 2010

    COVID-19, Cation Dysmetabolism, Sialic Acid, CD147, ACE2, Viroporins, Hepcidin and Ferroptosis: A Possible Unifying Hypothesis

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    Background: iron and calcium dysmetabolism, with hyperferritinemia, hypoferremia, hypocalcemia and anemia have been documented in the majority of COVID-19 patients at later/worse stages. Furthermore, complementary to ACE2, both sialic acid (SA) molecules and CD147 proved relevant host receptors for SARS-CoV-2 entry, which explains the viral attack to multiple types of cells, including erythrocytes, endothelium and neural tissue. Several authors advocated that cell ferroptosis may be the core and final cell degenerative mechanism. Methods: a literature research was performed in several scientific search engines, such as PubMed Central, Cochrane Library, Chemical Abstract Service. More than 500 articles were retrieved until mid-December 2021, to highlight the available evidence about the investigated issues. Results: based on COVID-19 literature data, we have highlighted a few pathophysiological mechanisms, associated with virus-based cation dysmetabolism, multi-organ attack, mitochondria degeneration and ferroptosis. Our suggested elucidated pathological sequence is: a) spike protein subunit S1 docking with sialylated membrane glycoproteins/receptors (ACE2, CD147), and S2 subunit fusion with the lipid layer; b) cell membrane morpho-functional changes due to the consequent electro-chemical variations and viroporin action, which induce an altered ion channel function and intracellular cation accumulation; c) additional intracellular iron concentration due to a deregulated hepcidin-ferroportin axis, with higher hepcidin levels. Viral invasion may also affect erythrocytes/erythroid precursors, endothelial cells and macrophages, through SA and CD147 receptors, with relative hemoglobin and iron/calcium dysmetabolism. AB0 blood group, hemochromatosis, or environmental elements may represent possible factors which affect individual susceptibility to COVID-19. &nbsp;&nbsp;&nbsp; Conclusions: our literature analysis confirms the combined role of SA molecules, ACE2, CD147, viroporins and hepcidin in determining the cation dysmetabolism and final ferroptosis in the cells infected by SARS-CoV-2. The altered ion channels and electrochemical gradients of the cell membrane have a pivotal role in the virus entry and cell dysmetabolism, with subsequent multi-organ immune-inflammatory degeneration and erythrocyte/hemoglobin alterations
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