"TENSIVE TARGET ORGAN DAMAGE/MONITORING PREHYPERTENSION SYNDROME", ALIAS CUGINI'S SYNDROME, AS NARRATED BY THE AUTHOR

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Magnetic phase diagram of the austenitic Mn-rich Ni-Mn-(In,Sn) Heusler alloys

Heusler compounds have been intensively studied owing to the important technological advancements that they provide in the field of shape memory, thermomagnetic energy conversion and spintronics. Many of their intriguing properties are ultimately governed by their magnetic states and understanding and possibly tuning them is evidently of utmost importance. In this work we examine the \alloys alloys with Density Functional Theory simulations and $^{55}$Mn Nuclear Magnetic Resonance and combine these two methods to carefully describe their ground state magnetic order. In addition, we compare the results obtained with the conventional generalized gradient approximation with the ones of strongly constrained and appropriately normed (SCAN) semilocal functionals for exchange and correlation. Experimental results eventually allow to discriminate between two different scenarios identified by ab initio simulations

Diagnosing silent cardiac dysautonomia via ambulatory blood pressure monitoring: early diagnosis shown by the lack of heart rate circadian rhythm in type 1 diabetes mellitus

Introduction. Diabetes mellitus (DM) can be complicated by an involvement of Neurovegetative System (NVS), conventionally and non-invasively diagnosed by the means of Ewing's test and Heart Rate Variability (HRV) analysis. It is well known that the NVS is physiologically responsible, via biological clocks, for the regulation of Circadian Rhythms (CR) characterizing the majority of biological functions. Therefore, this study is aimed at investigating the CR of Heart Rate (HR) and Blood Pressure (BP) in DM, postulating that the diagnosis of Silent Cardiac Dysautonomia (SCD) could be facilitated by detecting anomalous rhythmometric changes, including the worse one, i.e., the lose of a CR. Materials and Methods. The study has been performed on 30 clinically healthy subjects (CHS), 10 patients with DM1 and 30 patients with DM2, who underwent an ambulatory BP monitoring (ABPM) collecting data equidistantly every 30 minutes, under standardized conditions of lifestyle. The group specific monitored values of systolic (S), diastolic (D) BP, as well as HR have been analyzed via: 1. a conventional analysis of their intradiem variability; 2. a chronobiometric analysis (Cosinor method) of their CR. Results. The conventional analysis disclosed that in CHS, DM1 and DM2, both the HR and BP show an intradiem variability that is significant (p<0.001). The chronobiological analysis showed that in CHS and DM2, both the HR and BP show a significant CR (p<0.001), viceversa in DM1 HR is characterized by a non significant CR (p=0.124), notwithstanding that the SBP and DBP maintain a significant CR (p<0.001). Conclusions. The disappearance of HR CR in DM1 reveals the involvement of neurovegetative biological clock that selectively controls the HR CR, as it is demonstrated by the pathophysiological finding of an internal desynchronization between the HR and BP CR. The selective lose of HR CR in DM1 leads to conclude that the ABPM, along with its Cosinor analysis, might be a practical, repeatable, low cost, low risk technique for diagnosing the SCD, at least in DM1. Clin Ter 2010; 161(1):e1-e1

“TENSIVE TARGET ORGAN DAMAGE/MONITORING PREHYPERTENSION SYNDROME”, ALIAS CUGINI’S SYNDROME, AS NARRATED BY THE AUTHOR

This is the tale in first person of how I discovered the &ldquo;Tensive target organ damage/Monitoring prehypertension syndrome&rdquo;, which received an acknowledgement of paternity with the nosographic eponym of &ldquo;Cugini&rsquo;s syndrome&rdquo;. The presentation is made with the intention of showing how the <em>research methodology </em>and <em>clinical reasoning</em> can act as an<em> epistemological guide</em>, primarily in detecting and, secondarily in defining such a syndromic picture. I will narrate, in an anecdotal way, the history of this syndrome that has origin in 1980 when I received the invitation to approach, as Visiting Professor, the Chronobiology Laboratories of Minnesota University, directly from their legendary Chief, Prof. Franz Halberg, the Founder of the discipline &ldquo;Chronobiology&rdquo;. As an invited participant to an international project of research named: &ldquo;International Womb-to-Tomb Chronome Initiative&rdquo;, devoted to standardize the time-qualified reference limits of blood pressure from neonatal to old age, I could use the first available equipments (Pressurometers) for executing the Ambulatory Blood Pressure Monitoring. Accordingly, I started to collect the ABPM of a large sample size of clinically healthy subjects. Collection continued going back and forth between Italy and USA. In this activity of recruitment for creating a database of true normotensives and true hypertensives, I had the chance to meet some <em>office normotensives</em> who inexplicably showed <em>initial signs of hypertensive retinopathy</em>, a sign of &ldquo;Target Organ Damage&rdquo; (TOD), while, unexpectedly, were showing <em>no supranormal BP values</em> at the ABPM. In order to explain the retinal TOD, I suspected that they were true non-hypertensives but not true normotensives (presumably normotensives <em>alias</em> putative normotensives). Therefore, I compared the Daily Mean Level of their 24-h systolic (S) and diastolic (D) BP values [DML(SBP/DBP)] with the analogous estimate of the true normotensives. With surprise I could see that the retinopathic putative normotensives, despite the lack of surpranormal at the ABPM, had their DML(SBP/DBP) significantly increased, just in between true normotension and true hypertension. It was the year 1997, when I called this intermediate BP regimen: &ldquo;ABPM-diagnosable prehypertension&rdquo;, <em>alias</em> &ldquo;monitoring prehypertension&rdquo;, <em>alias</em> &ldquo;pressurometric prehypertension&rdquo;, <em>alias</em> &ldquo;masked prehypertension&rdquo;, and described the &ldquo;Minimal-change hypertensive retinopathy/monitoring prehypertension syn- drome&rdquo;. The association of a minimal tensive TOD with a monitoring prehypertension in office normotensives received a confirmatory certainty in other consecutive investigations, performed by me from 1997 to 2002, dealing with minimal signs respectively of: 1. interventricular septum hypertrophy in native hearts, 2. interventricular septum hypertrophy in novel transplanted hearts, 3. gestational impaired blood flow uterine arteries, 4. intrauterine growth retardation, 5. endothelial dysfunction. In all these clinical pictures, I could demonstrate that the initial tensive TOD was associated to a significant elevation of DML(SBP/DBP) just in between normotension and hypertension as per a <em>monitoring prehypertension</em>. Accordingly, I enlarged the appellative of the syndromic picture in &ldquo;Minimal signs of TOD/monitoring prehypertension&rdquo;, <em>alias</em> &ldquo;Tensive target organ damage/Monitoring prehypertension&rdquo;. Importantly, in 2007 and 2009 this clinical association has been eponimically called: &ldquo;Cugini&rsquo;s syndrome&rdquo; in an international context

Circadian rhythm of the renin-angiotensin-aldosterone system: a summary of our research studies.

The renin-angiotensin-aldosterone system (RAAS) is characterized by a circadian rhythm (CR) whose acrophase is detectable early in the morning. The prorenin and angiotensin converting enzyme (ACE) show a CR as well. However, while the prorenin is in phase with the RAAS the ACE shows its circadian acrophase in the afternoon suggesting a negative feed-back. The RAAS CR is influenced by many factors. Its mesor is modified by sodium intake. The physical activity and rest affect both the mesor and acrophase. The variations in mesor amplitude and acrophase in aged subjects are conditioned by sex and physical activity. Moreover, the RAAS CR seems to be influenced by the race. In addition, it is abolished by the beta-adrenergic blockade, suggesting the existence of an adrenergic clock. Interestingly, the RAAS CR seems not to be a pacemaker for the blood pressure CR, whose acrophase is early in the afternoon. The RAAS CR is not substantially modified has in essential hypertension. However, the CR of plasma renin activity is disappeared in the low-renin essential hypertension, while the CR of plasma aldosterone is detectable. On the contrary, the aldosterone CR is not detectable in ascitic liver cirrhosis; but, it is restored when the ascites is removed by peritoneal-jugular shunt. No significant variation of the RAAS CR seems to occur in obesity and Cushing's syndrome. The RAAS CR has disappeared in Conn's disease as well as in Bartter's syndrome and Liddle's syndrome. The administration of indomethacine in Bartter's syndrome and of triamterene in Liddle's syndrome is able to restore the RAAS CR. Finally, the RAAS CR is not detectable in the heart or kidney transplanted patients; such a phenomenon could be attributed to cyclosporine and corticosteroids administration and to the denervation of the transplanted organs