In Vivo Confocal Microscopy Characterization of Candida parapsilosis Keratitis.

ABSTRACT: The present clinical case concerns two patients with mycotic keratitis because of Candida parapsilosis in which corneal confocal microscopy presented a characteristic feature of this pathogen. Both described patients used a therapeutic contact lens and administered a therapy with steroid eye drops which are well known predisposing factors for the onset of corneal mycoses. This report can be useful for correctly identifying the pathologic condition and quickly directing the therapy.

[Limitations of outpatient vitreoretinal surgery at the Toulouse University hospital between 2016 and 2020: Causes for traditional hospitalization]. / Les limites de l'ambulatoire en chirurgie vitréo-rétinienne au CHU de Toulouse entre 2016 et 2020 : identification des causes d'hospitalisation traditionnelle.

INTRODUCTION: Currently, the majority of patients undergoing vitreoretinal surgery (VRS) are managed on an outpatient basis; this has been made possible by major surgical and anesthetic advances over the past decades. Nevertheless, the conversion to "all outpatient" surgery still poses some problems that are interesting to identify, and traditional hospitalization remains the solution in many situations. METHODS: All patients undergoing VRS at the Toulouse University Hospital between 2016 and 2020 were included retrospectively. For each patient, we analyzed the entire medical, anesthesia and demographic records. We performed a simple descriptive analysis of all parameters studied, followed by a bi-variate analysis between the "Outpatient/Hospitalization" parameter and all other parameters. RESULTS: Three thousand patients were included over the study period; 79.4% of patients were managed on an outpatient basis compared to 20.6% by traditional hospitalization. Failure of ambulatory care was the cause of 41.9% of the traditional hospitalizations, with the absence of an accompanying person on the evening of the surgery being the main reason (47.8%). DISCUSSION: Social isolation is found to be one of the main causes of failure of ambulatory care; improvements might be made at this level, in order to reduce the burden on the inpatient hospital system.

Mindfulness-based stress reduction in cancer patients: impact on overall survival, quality of life and risk factor.

Mindfulness-based stress reduction, a complementary and alternative therapy, is able to decrease cancer-related fatigue, and stress and to improve the quality of life in cancer patients. Some studies evaluated if mindfulness-based stress reduction could improve some cardiometabolic and cancer risk factors, including systemic chemokines, growth factors, and pro-inflammatory biomarkers (e.g., C-reactive protein, Interleukin-1). In this narrative review, we highlight the pleiotropic beneficial effects of mindfulness-based stress reduction and its clinical impact on cardiovascular and cancer risk factors among patients with cancer in different stages. Moreover, improvements in the overall quality of life, sleep quality, and immune functions [changes in plasma levels of interleukin-4 (IL-4), interferon-γ (INF-γ), and interleukin-10 (IL-10)] will also be discussed. Albeit few clinical studies available in the literature, evidenced the beneficial effects of mindfulness-based stress reduction on the immune and cardiometabolic profile in cancer patients, providing important insights into the closest collaboration between psycho-oncologists, oncologists, and cardiologists.

The proposal of an integrated ultrasonographic approach into the ALS algorithm for cardiac arrest: the PEA protocol.

BACKGROUND AND OBJECTIVE: Guidelines on cardiac arrest (CA) recommend the prompt beginning of cardio-pulmonary resuscitation (CPR) and the identification and correction of reversible causes. This article deals with the application of clinical ultrasonography (US) in resuscitation, presenting a simple codified US protocol usable during CPR to recognize reversible causes of CA. EVIDENCE ON US IN CA AND STATE OF THE ART: Emergency US is a bedside, point-of-care, focused diagnostic procedure with aim to complete the physical examination. It is performed by emergency physician everywhere to answer briefly important clinical questions. Several trials recently experimented US employment during advanced life support, demonstrating its feasibility without delaying CPR. PERSPECTIVES: The PEA Protocol: We propose a simplified US protocol for non-shockable rhythms, called "PEA protocol" to remember the applications of the study (CA in Pulseless Electrical Activity, PEA) and the US scan sequence: Pulmonary scans to depict pneumothorax and pleural effusion and to differentiate wet or dry lung; Epigastric for pericardial effusion, left and right ventricular sides and motion, IVC filling; Abdominal and other scans for aortic aneurism and dissection, peritoneal effusion, bowel occlusion or perforation, deep venous thrombosis. The PEA protocol could be performed both during CA in PEA and during periarrest conditions. CONCLUSIONS: Clinical US, using a well codified protocol, could effectively help to identify reversible causes in CA, even improving patients outcome.

Approach to respiratory failure in emergency department.

OBJECTIVES AND BACKGROUND: The goal of this review is to provide update recommendations that can be used by emergency physicians who provide primary cares to patients with Acute Respiratory Failure (ARF), from the admission to an emergency department through the first 24 to 48 hours of hospitalization. This work wants to address the diagnosis and emergency medical care of ARF and the management of medical complications. STATE OF THE ART: A lot of statement has been developed for the early management and treatment of ARF; moreover, over the last fifteen years, we have assisted to the rise of a new technique of ventilation, in the Emergency Department: Non Invasive Ventilation. This kind of ventilation was firsthy applied in intensive Care and in Respiratory Care Unit. Randomized controlled clinical trials have showed its usefulness in the early treatment of several forms of ARF, together with medical therapy.

Nitric oxide synthesis and isoprostane production in subjects with type 1 diabetes and normal urinary albumin excretion.

The role of nitric oxide (NO) and free radicals in the development of microvascular disease in type 1 diabetes remains unclear. We have measured NO and isoprostane (a stable marker of in vivo lipid peroxidation) production in 13 type 1 diabetic subjects with normal urinary albumin excretion and 13 healthy volunteers. Whole-body NO synthesis was quantified by measuring the urinary excretion of 15N-nitrate after the intravenous administration of L-[15N]2-arginine. The urinary excretion of the major urinary metabolite of 15-F2t-isoprostane (8-iso-prostaglandin-F2alpha), 2,3-dinor-5,6-dihydro-F2t-IsoP, was quantified as a marker of in vivo lipid peroxidation. Whole-body NO synthesis was significantly higher in diabetic subjects compared with control subjects (342 vs. 216 nmol 15N-nitrate/mmol creatinine [95% CI of the difference 45-207], P = 0.005). This increase was not explained by a difference in renal function between the 2 groups. There was no difference in 2,3-dinor-5,6-dihydro-F2t-IsoP excretion between diabetic subjects and control subjects (44.8+/-7.8 vs. 41.4+/-10.0 ng/mmol creatinine, mean +/- 95% CI). However, there was an inverse correlation between NO synthesis and free radical activity in subjects with diabetes (r = -0.62, P = 0.012) that was not observed in control subjects (r = 0.37, P = 0.107). We conclude that whole-body NO synthesis is higher in type 1 diabetic subjects with normal urinary albumin excretion than in control subjects. The inverse correlation between isoprostane production and NO synthesis in diabetic subjects is consistent with the hypothesis that NO is being inactivated by reactive oxygen species.

Recent developments in durum wheat chromosome engineering.

Transfer of alien chromosome segments from various Triticeae species into cultivated wheats, commonly referred to as "chromosome engineering", is currently benefiting from the recent, impressive advancements in molecular genetics, cytogenetics and genomics, which are providing new insights into the genetic and physical organization of even complex plant genomes, such as those of the Triticeae. The powerful analytical tools presently available are making the assessment of desired genotypes in the course of chromosome engineering far more precise and effective than in the past, thus giving this transfer strategy renewed and increased potential for meaningful practical achievements. Examples are given here of the application of such tools to the engineering of the durum wheat genome with small alien segments containing genes with beneficial impact on disease resistance and quality traits.

Review of dilated cardiomyopathies. Dilated cardiomyopathies and altered prothrombotic state: a point of view of the literature.

Heart failure is an enormously important clinical problem that, if not faced, may overwhelm health care resources. Primary and secondary cardiomyopathies cause the majority of cases of clinical heart failure, which is thus better approached from the utility point of view of myocardial failure. Furthermore, the risk of thromboembolic complications presenting in such disease may be higher than in ischemic cardiomyopathy. Intracardiac thrombi and mural endocardial plaques (from the organization of thrombi) are present at necropsy in more than 50% of patients with dilated cardiomyopathy (DCM). Several studies have shown that systemic and pulmonary emboli are more frequent in patients with ventricular thrombi or plaques. Dilated cardiomyopathy has been associated with left ventricular thrombosis which leads to substantial morbidity and mortality as a site for peripheral emboli. There are some studies on patients with dilated cardiomyopathy showing altered hemostasis and platelet behavior despite sinus rhythm. Platelet activation, thrombin activation and fibrinolytic activity are increased in patients with DCM compared to normal subjects. However, these markers reflecting coagulation activation in patients with left ventricle thrombus are comparable to those in patients without thrombus in the left ventricle. The pathophysiology and clinical issues concerning the susceptibility to develop left ventricular (LV) thrombosis and its complications like cerebrovascular disease in patients with DCM are summarized and the most recent articles present in the medical literature are reviewed.

Brain natriuretic peptide and acute coronary syndrome.

The natriuretic peptide system (atrial natriuretic peptide, brain natriuretic peptide, BNP, and C natriuretic peptide) is an important marker of cardiac failure. These peptides are synthesized in atrial or ventricular myocytes in response to wall tension. In several studies the correlation between high BNP levels and mortality, in patients with acute coronary syndrome and heart failure, has been demonstrated. On the other hand, plasma levels of BNP could be considered as independent predictors of mortality in patients with heart failure. BNP could be used, for instance, as an early diagnostic marker for the differential diagnosis between cardiogenic and non cardiogenic dyspnea. In the Emergency Department its use will be important in the diagnosis of thoracic pain origin since it may help in the diagnostic and therapeutic course of this patient and to define the modality of hospitalization. Moreover, it can be used as a marker of heart failure severity and as an important negative prognostic factor. Some studies have confirmed that plasma BNP reflects the degree of left ventricular dysfunction and the prognostic significance after acute myocardial infarction and chronic heart failure.

Heart failure and therapy.

The clinical syndrome of heart failure is the final outcome of a number of diseases affecting the heart. Several studies undertaken over the past decade, have led to a significant change in the therapies available and a growing understanding of the physiopathological mechanisms. Increasingly, the current treatment of heart failure, is not just symptomatic but also etiologic and physiopathologic. In this paper we will try to furnish guidelines, as practical as possible, for the treatment of this syndrome, addressing the physiopathologic and experimental principles which underlie it. The present suggestions are based on the updated literature review, they conform to the latest guidelines of the European Society of Cardiology and are in agreement with the classification in grades, proposed by the American Heart Association and the American College of Cardiology.

Evidence for a difference in nitric oxide biosynthesis between healthy women and men.

There is indirect evidence for a gender difference in nitric oxide (NO) synthesis from vascular endothelium. The aim of the present study was to determine NO production more directly in healthy women and men by the measurement of 15N nitrate excreted in urine after the intravenous administration of L-[15N]2-guanidino arginine. Twenty-four healthy volunteers (13 men aged 22 to 40 years and 11 women aged 23 to 42 years) participated in this study. No subjects were receiving any medication. Women were studied between the 7th and 14th days of their menstrual cycles. Arterial blood pressure was measured oscillometrically, and 1.13 micromol L-[15N]2 arginine was administered intravenously after an overnight fast. Urine was collected for the next 36 hours in separate 12-hour periods. Urinary 15N/14N nitrate ratio was assessed by dry combustion in an isotope ratio mass spectrometer. Mean 36-hour urinary 15N nitrate excretion was greater in women than in men (2111+/-139 versus 1682+/-87 etamol; P<0.05). Furthermore, total urinary 15N nitrate excretion was associated inversely with the mean arterial blood pressure in the whole group of subjects (coefficient of correlation, 0.47; P=0.022). The present data show that whole-body production of NO is greater in healthy premenopausal women than in men under ambulatory conditions. The cellular origin of NO measured in this study is unknown, but differences in endothelial production could underlie differences in vascular function between men and women.

Porcine aortic endothelial cells transfected with HLA-G are partially protected from xenogeneic human NK cytotoxicity.

In this study we tested whether the expression of HLA-G protects porcine endothelial cells (PEC) from the lysis mediated by human natural killer (NK) cells. Because HLA-E is not present in PEC, this model provides an ideal tool to study the direct role of HLA-G in NK inhibition. Immortalized porcine aortic endothelial cells (PED) were stably transfected with a vector coding for the HLA-G1 protein and surface expression was demonstrated by flow cytometry analysis. Although the adhesion of human NK cells to PED was not compromised by HLA-G, the expression of HLA-G partially protected PED from the lysis mediated by polyclonal NK lines derived from different donors. A decrease of the surface expression of HLA-G on PED corresponded to a loss of the capacity of PED to inhibit NK cytotoxicity, indicating that the surface density of HLA-G molecules must exceed a certain threshold to protect target cells. In summary, these data show that HLA-G, independent from the presence of HLA-E, can only partially and inefficiently protect PED from human NK cell-mediated cytotoxicity. Because ILT-2/LIR-1 expression did not correlate with HLA-G mediated inhibition, we hypothesize that other yet unidentified receptors expressed by peripheral blood NK cells are involved in the recognition of HLA-G.

Efficacy and safety of fluvastatin, a new HMG CoA reductase inhibitor, in elderly hypercholesterolaemic women.

This multicentre open 6-week study evaluated the efficacy, safety and tolerability of fluvastatin, the first fully synthetic 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase inhibitor, in elderly women with type IIa hypercholesterolaemia. After a 4-week single-blind placebo period, 22 elderly women (mean age 68 +/- 5 years) with primary hypercholesterolaemia [low density lipoprotein (LDL) cholesterol > 160 mg/dl] were enrolled in the trial. Fluvastatin 40 mg was administered once in the evening. At baseline, and after 3 and 6 weeks of treatment, total cholesterol, LDL cholesterol, high density lipoprotein (HDL) cholesterol, triglycerides, apolipoproteins B (apo B) and A-I (apo A-I) were measured. Safety and tolerability were assessed by monitoring routine laboratory parameters and by recording spontaneously reported side effects. The mean (+/- SD) baseline total cholesterol, LDL cholesterol, triglyceride, HDL cholesterol, apo B and apo A-I levels were 325 +/- 43, 236 +/- 43, 128 +/- 56, 61 +/- 16, 221 +/- 60 and 164 +/- 28 mg/dl, respectively. After 6 weeks, fluvastatin significantly (p < 0.001, ANOVA test) reduced total cholesterol, LDL cholesterol and apo B levels by 22%, 29% and 23%, respectively. These significant reductions were already reached at week 3 (total cholesterol, -21%; LDL cholesterol, -27%). The total cholesterol: HDL cholesterol ratio was reduced by 22% at week 3 and by 21% at week 6 (from 5.3 to 4.2). 78% of the patients showed a reduction > or = 20% for LDL cholesterol. Triglycerides were reduced by 16% (not significant).(ABSTRACT TRUNCATED AT 250 WORDS)

Dopamine-induced antihypertensive effects and plasma insulin rise are blocked by metoclopramide in labetalol-treated patients.

Eleven patients with moderate to severe hypertension were studied at the Vargas Hospital of Caracas. The patients were pretreated with labetalol, 800 to 1200 mg/day, orally, over a period of 1 week, after which an intravenous infusion of dopamine, .5 to 3 micrograms/kg/minute, was given. Two intravenous dopamine infusions (30 minutes each) were performed before and after the injection of metoclopramide (30 mg, intravenous bolus). Two washout periods were also included before and after metoclopramide administration. Dopamine induced a decrease of blood pressure from 171.9 + 6.35/103.6 +/- 3.12 to 152.7 +/- 7.55/93.8 +/- 2.97 mm Hg (P < .001) without altering heart rate, and it increased plasma insulin levels from 8.29 +/- .70 microU/mL to 12.09 +/- 1.83 microU/mL (P < .01). Metoclopramide caused no changes of blood pressure or plasma insulin levels. Hypotensive responses and plasma insulin increases due to dopamine were blocked by metoclopramide, however. The authors conclude that a dopaminergic receptor may be involved in some cardiovascular responses and in modulating insulin secretion in humans.

Metoclopramide blocks bromocriptine induced antihypertensive effect in hypertensive patients.

Two groups of patients with essential hypertension were studied at the Vargas Hospital of Caracas. The first group of 9 patients under placebo treatment for 1 week received a single 2.5 mg oral dose of bromocriptine. Cardiovascular and biochemical parameters including arterial pressure, heart rate, plasma renin activity, and plasma aldosterone levels were evaluated during the 6-hour period before and after the administration of drugs. The second experimental design was as follows: 9 patients received 30 mg metoclopramide daily (divided in 3 doses) for 1 week. At the end of the period a single oral dose of 2.5 mg of bromocriptine was given to each patient. The cardiovascular and biochemical parameters were also determined. Bromocriptine reduced both systolic and diastolic arterial pressure. The peak antihypertensive effect was shown 3 hours after administration of the drug, but the reduction of arterial pressure lasted approximately 6 hours. At the same time bromocriptine reduced plasma aldosterone levels and plasma renin activity. This reduction persisted 6 hours after its administration. Metoclopramide reversed the antihypertensive effect of bromocriptine and its effect on aldosterone secretion and plasma renin activity. We conclude from these findings that bromocriptine acts as an antihypertensive agent by stimulating DA2 dopaminergic receptor, the dopaminergic receptor involved in aldosterone and renin secretion is possibly DA2.

[Humoral and cellular inflammatory mediators in acute lung injury: friends or enemies? ]. / Mediatori infiammatori umorali e cellulari dell'Acute Lung Injury: amici o nemici?

Diffuse lung injury (DLI) is characterised by damage to the alveolar and endothelial epithelium that leads to acute respiratory insufficiency. From the histological point of view, this pathological process proceeds through an initial exudative phase which is followed by the organisation of the inflammatory infiltrate up to the deposit of collagen and fibrin which seriously compromises gaseous exchanges. The clinical expression typical of this pathology consists of Acute Lung Injury/Acute Respiratory Distress Syndrome (ALI/ARDS) characterised by hypoxemia resistant to oxygen therapy, tachypnea and the presence of bilateral infiltrates on conventional X-ray of the thorax. Although the etiology is multifactorial, the pathogenesis depends on the uncontrolled activation of the inflammation system in its humoral and cellular components. The present paper examines the principal studies regarding the most important mediators. From an analysis of the literature it emerges that some cytokines (IL-1betha, IL-6, IL-6ra) and cellular mediators (NF-kB, sFasL) are responsible for the epithelial damage by way of complex mechanisms that include apoptosis. Studies carried out up to the present have not however evidenced any independent pathway decisive for pathogenesis. This shows that inflammation is in effect a multiform process that originates precisely as a result of the mutual interaction of the factors implicated in it. The humoral and cell mediators can, however, be used as clinical indicators correlatable with the clinical and physiopathological outcome.

[Association of pulmonary and portal hypertension]. / Associazione tra ipertensione arteriosa polmonare ed ipertensione portale.

The association between portal venous hypertension and pulmonary arterial hypertension has received scarce attention in the italian medical literature. Nevertheless the association is relatively frequent, it needs a multidisciplinary approach and it is a stimulus for the search of causes of so-called primary pulmonary hypertension. The purpose of the article is to review the frequency of the association, the main pathogenetic hypothesis formulated to explain the appearance of pulmonary hypertension, the clinical and the laboratory findings, the evolution of the association and to present briefly a personal series of cases. The pulmonary arterial hypertension has been found in approximately 2% of patients with portal hypertension due to either hepatic cirrhosis or extraepatic lesions. Microembolism from the portocavat system or a number of vasoactive substances which enter the pulmonary circulation without being inactivated by the liver have been held responsible for the appearance of pulmonary hypertension in predisposed patients. Clinical and laboratory findings do not differ from those a patients with primary pulmonary hypertension. Also the prognosis is similar. In conclusion on accurate examination of the pulmonary circulation by noninvasive methods, in particular by echocardiography, appears to be mandatory in patients with chronic hepatic lesions. When pulmonary arterial hypertension is detected the study of the biochemical factors which at present are known to determine pulmonary hypertension may be warranted. The study may enhance our knowledge of the pathogenesis of the so-called primary pulmonary hypertension.

[Usefulness of magnetic resonance imaging for the diagnosis of acute myocarditis. A case of acute myocarditis as myocardial infarction-like]. / Ruolo della risonanza magnetica nucleare nella diagnosi di miocardite acute. Un caso di miocardite acuta ad esordio simil-infartuale.

According to the Dallas criteria, myocarditis is defined histologically as an inflammatory process involving the myocardium with an inflammatory infiltrate and myocyte necrosis or damage. Clinically, myocarditis is an insidious disease that is usually asymptomatic and commonly underdiagnosed. Infact, the symptoms are often non-specific and the majority of cases recover fully with no sequelae. At present, endomyocardial biopsy remains the gold standard for the diagnosis of myocarditis, despite its limited sensitivity and specificity. However, the lack of an association between biopsy evidence of myocarditis and the presence of autoantibodies in patients with clinical signs of myocarditis, the paucity of the positive biopsy findings in large cohorts of patients with suspected myocarditis, the potential discordance between clinical and histologic features and the inherent limitation of histologic diagnosis, suggest that the diagnosis shouldn't be based on histologic examination alone. The magnetic resonance imaging (MRI) with gadolinium can be useful to visualize the localization, activity and extent of inflammation and may be a powerful noninvasive diagnostic tool in acute myocarditis. Infact, MRI achieves a 100% sensitivity and a 90% specificity. We report the case of a 31-year-old male patient with an acute myocarditis with electrocardiographic manifestations like to acute myocardial infarction, whose diagnosis was based on the clinical signs and on the characteristic pattern of the MRI with paramagnetic contrast. The MRI with gadolinium is suggested as noninvasive study to support the diagnosis of acute myocarditis in the correct clinical setting.

The high cost of conflict.

Conflict is inevitable, especially in highly stressed environments. Clinical environments marked by nurse-physician conflict (and nurse withdrawal related to conflict avoidance) have been proven to be counterproductive to patients. Clinical environments with nurse-physician professional collegiality and respectful communication show decreased patient morbidity and mortality, thus enhancing outcomes. The growth of managed care, and the organizational turmoil associated with rapid change, makes it imperative to structure the health care environment so that conflict can be dealt with in a safe and healthy manner. Professional health care education programs and employers have a responsibility to provide interactive opportunities for multidisciplinary audiences through which conflict management skills can be learned and truly change the interpersonal environment. Professionals must be free to focus their energy on the needs of the patient, not on staff difficulties.

Rapid removal of sealer following root canal treatment.

A case of acute exacerbation following nonsurgical root canal treatment is presented. Clinical symptoms of acute inflammation superimposed on chronic inflammation were initiated, presumably from root canal treatment and overfilling of AH-26. Unusually rapid removal of the root canal sealer overfilling was observed. Possible mechanisms of resolution, including inflammation and immune response, were discussed.