Modifications of protein Z and interleukin-6 during the acute phase of coronary artery disease.
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Acute Disease↗
Biomedical subjects
Gian Franco Gensini
Publications and source records attributed to Gian Franco Gensini.
Role of glycoprotein Ia gene polymorphisms in determining platelet function in myocardial infarction patients undergoing percutaneous coronary intervention on dual antiplatelet treatment.
Response variability to antiplatelet treatment has been described and the widespread use of acetylsalicylic acid (ASA) and clopidogrel requires clarification of the residual platelet reactivity (RPR). Various glycoprotein Ia (GpIa) polymorphisms have been investigated, but their influence on platelet reactivity in myocardial infarction (MI) patients undergoing percutaneous coronary intervention (PCI) on dual antiplatelet treatment is not still elucidated. Aim of this study was to evaluate the effect of C807T, G873A and T837C polymorphisms of GpIa on modulating platelet function in MI patients on dual antiplatelet treatment undergoing PCI. We measured platelet function by both a point-of-care assay (PFA100) and platelet-rich-plasma aggregation in 289 MI patients undergoing PCI and receiving dual antiplatelet treatment. Our data show that C807T/G873A polymorphisms, but not T837C, are associated with higher platelet reactivity. Carriers of the 807T/873A allele had significantly higher platelet aggregation values after arachidonic acid (AA) and collagen stimuli and, even if they did not reach the statistical significance, after 2 and 10 microM ADP stimuli; 807T/873A allele carriers had also significantly shorter closure times on PFA100/epinephrine membranes. At the multiple analyses, C807T/G873A polymorphisms resulted an independent risk factor for RPR defined by both AA induced platelet aggregation (OR=3.0, 95%CI 1.17-7.89, p=0.022) or by PFA100/epinephrine (OR=4.1, 95%CI 1.53-10.89, p=0.005). In conclusion, this study shows the 807T/873A allele of the GpIa gene is an independent risk factor for the RPR on dual antiplatelet treatment, and extends, in a larger acute coronary syndrome population, the observation that the 807T/873A allele is associated with higher platelet reactivity.
Adult↗
Coffee consumption and risk of coronary heart disease: a meta-analysis.
BACKGROUND AND AIMS: During the past three decades the relationship between habitual coffee drinking and coronary heart disease (CHD) has been assessed in numerous studies, with conflicting results. The aim of this study was to systematically examine the data published on the association between habitual coffee consumption and risk of CHD. METHODS AND RESULTS: Thirteen case-control and 10 cohort studies were included. Case-control studies incorporated 9487 cases of CHD and 27,747 controls, and cohort studies included a total of 403,631 participants that were followed for between 3 and 44 years. The summary of odds ratios (OR) for the case-control studies showed statistically significant associations between coffee consumption and CHD for the highest intake group (>4 cups/day), OR 1.83 (95% CI 1.49-2.24; P<0.0001), and for the second highest category (3-4 cups/day), OR 1.33 (95% CI 1.04-1.71; P<0.0001), while no significant association emerged for low daily coffee intake (< or =2 cups/day), OR 1.03 (95% CI 0.87-1.21; P=0.45). The analysis of long-term follow-up cohort studies did not show any association between the consumption of coffee and CHD, with a relative risk (RR) of 1.16 (95% CI 0.95-1.41; P=0.14) for the highest category, and 1.05 (95% CI 0.90-1.22; P=0.57) and 1.04 (95% CI 0.90-1.19; P=0.60) for the second and third highest categories, respectively. These results did not differ substantially when controlling for region of origin, fatal and non-fatal events, year of publication, and number of years of follow-up. CONCLUSIONS: Despite a significant association between high consumption of coffee and CHD reported among case-control studies, no significant association between daily coffee consumption and CHD emerged from long-term follow-up prospective cohort studies.
Adult↗
Lone and secondary nonvalvular atrial fibrillation: role of a genetic susceptibility.
BACKGROUND: An involvement of the renin angiotensin system in atrial fibrillation (AF) has been hypothesized, and ACE DD genotype has been suggested to influence the predisposition to AF. The aim of this study was to investigate the role of the ACE I/D polymorphism in relation to the different clinical forms of AF, lone and secondary nonvalvular atrial fibrillation (NVAF). METHODS: 510 consecutive patients with documented NVAF (106 patients had lone, and 404 secondary NVAF), and 520 controls with a negative history of cardiovascular disease have been studied. RESULTS: A significant difference in allele frequency between lone and secondary NVAF (p=0.002) has been found. The ACE D allele was associated with the predisposition to lone NVAF under a dominant, recessive and additive model, both at univariate and multivariate analysis, after adjustment for age and gender (multivariate analysis: dominant OR=2.87, p=0.02; recessive OR=2.01, p=0.003; additive OR=4.47, p<0.0001). ACE D allele was significantly associated with secondary NVAF at both univariate and multivariate analysis under a recessive and additive, but not dominant, model (multivariate analysis: recessive OR=1.89, p=0.001; additive OR=2.50, p<0.0001). CONCLUSIONS: This study highlights the role of ACE gene in predisposing to both lone and secondary NVAF, further contributing to penetrate the genetic mechanisms responsible for this complex disease. The clinical relevance of our results may be related to the possible characterization of subjects predisposed to NVAF in the absence of traditional risk factors, and to the use of ACE-inhibitors therapy able to improve the arrhythmogenic substrate.
Aged↗
Incidence, clinical findings, and outcome of women with left ventricular apical ballooning syndrome.
Left ventricular apical ballooning syndrome (LVABS) is a clinical condition that may mimic ST-elevation acute myocardial infarction (AMI). To assess incidence, clinical findings, and outcome of white women with LVABS, we reviewed 305 consecutive women with chest pain and anterior ST-elevation AMI referred for potential mechanical revascularization; 36 (12%) patients met the diagnostic criteria for LVABS and were compared with the remaining 269 women with angiographic evidence of coronary artery disease (CAD). Patients with LVABS showed a lower incidence of diabetes mellitus (5% vs 21%, p = 0.023), a higher rate of antecedent stressful events (26% vs 3%, p <0.0001), and a higher heart rate at admission (91 +/- 20 vs 82 +/- 19, p = 0.018) than women with CAD. Urgent angiography showed no significant CAD in patients with LVABS and an average of 1.6 +/- 0.7 diseased coronary arteries (>50% stenosis) in the 269 control women (p = 0.0001). Peak creatine kinase-MB value was lower in patients with LVABS (21 +/- 26 mU/ml) than in women with CAD (307 +/- 302 mU/ml, p = 0.0001). The only independent predictors of LVABS among women with anterior AMI were peak creatine kinase-MB value (p = 0.0001) and the presence of an antecedent stressful event (p = 0.001). LV systolic function at admission was similar between women with LVABS and those with CAD (echocardiographic ejection fraction 35.6 +/- 8.4% vs 35.5 +/- 8.0%, p = 0.944) but was significantly different at discharge (ejection fraction 50.1 +/- 9.6% vs 45.2 +/- 13.5%, p = 0.021). Moreover, at 6-month follow-up, women with LVABS showed a better survival rate (97% vs 86%, p = 0.055) and freedom from major cardiac events (death, reinfarction, or rehospitalization 92% vs 69%, p = 0.001) than women with CAD. In conclusion, few women presenting with clinical features of anterior AMI have LVABS. Despite a favorable outcome, LVABS should be considered in the differential diagnosis of women with chest pain and ST-segment elevation in the precordial leads. Peak creatine kinase-MB value and the presence of an antecedent stressful event are strong predictors of LVABS in women with anterior AMI.
Aged↗
Favourable outcome of Streptococcus agalactiae prosthetic valve endocarditis after conservative treatment.
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Aged↗
Abnormal pressure passive dilatation of cerebral arterioles in the elderly with isolated systolic hypertension.
The aim of this study was to investigate the cerebrovascular adaptability to 2 sequential pressor stimuli in elderly patients with isolated systolic hypertension. Ten healthy elderly normotensive subjects (68 to 82 years), 10 elderly subjects with isolated systolic hypertension (63 to 82 years), and 10 young normotensive subjects (24 to 40 years) took part in the study. A pressor reaction, using sequential cold pressor and handgrip stimulation, was induced. The cerebrovascular response to the pressor stimulation was measured by transcranial Doppler determination of the mean flow velocity in the middle cerebral arteries. In all of the subjects, blood pressure increased during handgrip (+12 mm Hg, P<0.001 in the young; +18 mm Hg, P<0.01 in the elderly normotensive subjects; +19 mm Hg, P<0.001 in the hypertensive patients versus baseline). In the hypertensive subjects, the pressure increase persisted well into the recovery period. The pressure increase caused a significant increase in mean flow velocity in the middle cerebral arteries only in the elderly subjects. Cold pressor test increased blood pressure in all of the subjects during stimulation and the first 2 minutes of the recovery period (at whole-curve ANOVA: F=22.03, P<0.001 in the young participants; F=18.3, P<0.001 in the normotensive elderly; and F=13.04, P<0.001 in the hypertensive elderly). Mean flow velocity in the middle cerebral arteries significantly increased only in the hypertensive subjects. In the elderly hypertensive patients, the cerebrovascular reaction to adrenergic stimuli was more impaired than in the elderly normotensive subjects. This event can amplify the pressure insult on cerebral hemodynamics and increase the predisposition to cerebral damage, such as vascular cognitive impairment or stroke.
Adaptation, Physiological↗
Genetic susceptibility to atrial fibrillation (AF) in patients with congestive heart failure.
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Alleles↗
Role of endothelin-1 in exposure to high altitude: Acute Mountain Sickness and Endothelin-1 (ACME-1) study.
BACKGROUND: The degree of pulmonary hypertension in healthy subjects exposed to acute hypobaric hypoxia at high altitude was found to be related to increased plasma endothelin (ET)-1. The aim of the present study was to investigate the effects of ET-1 antagonism on pulmonary hypertension, renal water, and sodium balance under acute and prolonged exposure to high-altitude-associated hypoxia. METHODS AND RESULTS: In a double-blind fashion, healthy volunteers were randomly assigned to receive bosentan (62.5 mg for 1 day and 125 mg for the following 2 days; n=10) or placebo (n=10) at sea level and after rapid ascent to high altitude (4559 m). At sea level, bosentan did not induce any significant changes in hemodynamic or renal parameters. At altitude, bosentan induced a significant reduction of systolic pulmonary artery pressure (21+/-7 versus 31+/-7 mm Hg, P<0.03) and a mild increase in arterial oxygen saturation versus placebo after just 1 day of treatment. However, both urinary volume and free water clearance (H2OCl/glomerular filtration rate) were significantly reduced versus placebo after 2 days of ET-1 antagonism (1100+/-200 versus 1610+/-590 mL; -6.7+/-3.5 versus -1.8+/-4.8 mL/min, P<0.05 versus placebo for both). Sodium clearance and segmental tubular function were not significantly affected by bosentan administration. CONCLUSIONS: The present results indicate that the early beneficial effect of ET-1 antagonism on pulmonary blood pressure is followed by an impairment in volume adaptation. These findings must be considered for the prevention and treatment of acute mountain sickness.
Acute Disease↗
Usefulness of aspirin resistance after percutaneous coronary intervention for acute myocardial infarction in predicting one-year major adverse coronary events.
Recently, great interest has focused on the phenomenon of aspirin resistance, which may be defined as clinical or laboratory resistance. Monitoring the antiplatelet effect appears to be relevant in the presence of clinical implications, but no data are available on the possible clinical implications of the failure of aspirin to inhibit tests of platelet function in the setting of acute coronary syndromes. This study evaluated the role of aspirin resistance in the occurrence of 1-year major adverse coronary events (MACEs) in patients with acute myocardial infarction (AMI) who have undergone percutaneous coronary intervention (PCI). We prospectively evaluated 146 patients (115 men and 31 women; median age 65 years, range 30 to 84) with AMI who underwent primary PCI. Exclusion criteria were the use of glycoprotein IIb/IIIa inhibitors, hematocrit <or=30%, and a platelet count <100,000/mm3. Platelet function analyzer-100 closure times by collagen-epinephrine were used for measuring platelet function in venous blood samples obtained 12 to 15 hours after revascularization. Patients were considered aspirin resistant in the presence of a collagen-epinephrine closure time of <203 seconds. After 1-year follow-up, MACEs were recorded in 44 of 146 patients (30.1%). A significantly higher percentage of patients with MACEs had aspirin resistance (39.1% vs 23.2%, p <0.05). A Kaplan-Meier survival curve showed that the overall risk of MACEs was significantly higher among patients with aspirin resistance (p = 0.02). A Cox regression analysis that adjusted for age, gender, traditional cardiovascular risk factors, systolic left ventricular function, number of stenosed coronary arteries, and previous AMI, PCI, or coronary artery bypass graft showed aspirin resistance to be a significant and independent risk factor for the future MACEs (hazard ratio 2.9, 95% confidence interval 1.1 to 9.2, p <0.05). In conclusion, our data demonstrate that aspirin resistance after PCI is a significant and independent predictor of MACEs in patients with AMI undergoing primary PCI.
Adult↗
Carotid artery stenting: first consensus document of the ICCS-SPREAD Joint Committee.
BACKGROUND AND PURPOSE: The prevention of stroke and the correct treatment of carotid artery stenosis represent today a major debate in cardiovascular medicine. Beside carotid endarterectomy, carotid angioplasty and stenting is becoming more widely performed for the treatment of severe carotid obstructive disease, and is now accepted as a less invasive technique that may provide an alternative for selected patients, particularly those with significant comorbidities. An Italian multidisciplinary task force, in which converged the most representative scientific societies involved in carotid treatment, was created to provide neurologists, radiologist, cardiologists, vascular surgeons, and all those involved in prevention and treatment of carotid disease with a simple, clear and updated evidence-based consensus document. SUMMARY OF REVIEW: This First Consensus Document of the ICCS (Italian Consensus Carotid Stenting)/SPREAD group addressed the main issues related to methodology, definition of symptomatic and asymptomatic carotid stenosis, indication and procedures for carotid artery stenting, including the use of devices for preventing procedural embolic complications. Special attention was paid to credentials and competency for physicians qualifications to perform vascular angioplasty and stent placement, including training, acceptable complication rates and certification. CONCLUSIONS: As any guideline or consensus statement, also this document is valid as long as the evidence on which it is based remains up-to-date. In such a fast-evolving field of medicine as the management of carotid stenosis, it is mandatory to stimulate a continuous and fruitful discussion among all the professionals involved in this very evolutionary field.
Carotid Artery Diseases↗
A model of anti-angiogenesis: differential transcriptosome profiling of microvascular endothelial cells from diffuse systemic sclerosis patients.
The objective of this work was to identify genes involved in impaired angiogenesis by comparing the transcriptosomes of microvascular endothelial cells from normal subjects and patients affected by systemic sclerosis (SSc), as a unique human model disease characterized by insufficient angiogenesis. Total RNAs, prepared from skin endothelial cells of clinically healthy subjects and SSc patients affected by the diffuse form of the disease, were pooled, labeled with fluorochromes, and hybridized to 14,000 70 mer oligonucleotide microarrays. Genes were analyzed based on gene expression levels and categorized into different functional groups based on the description of the Gene Ontology (GO) consortium to identify statistically significant terms. Quantitative PCR was used to validate the array results. After data processing and application of the filtering criteria, the analyzable features numbered 6,724. About 3% of analyzable transcripts (199) were differentially expressed, 141 more abundantly and 58 less abundantly in SSc endothelial cells. Surprisingly, SSc endothelial cells over-express pro-angiogenic transcripts, but also show up-regulation of genes exerting a powerful negative control, and down-regulation of genes critical to cell migration and extracellular matrix-cytoskeleton coupling, all alterations that provide an impediment to correct angiogenesis. We also identified transcripts controlling haemostasis, inflammation, stimulus transduction, transcription, protein synthesis, and genome organization. An up-regulation of transcripts related to protein degradation and ubiquitination was observed in SSc endothelial cells. We have validated data on the main anti-angiogenesis-related genes by RT-PCR, western blotting, in vitro angiogenesis and immunohistochemistry. These observations indicate that microvascular endothelial cells of patients with SSc show abnormalities in a variety of genes that are able to account for defective angiogenesis.
Biopsy↗
Fat snorers and sleepy-heads: were many distinguished characters of the past affected by the obstructive sleep apnea syndrome?
The obstructive sleep apnea syndrome (OSAS) is a clinical condition characterized by the coexistence of irregular breathing at night with excessive daytime sleepiness, and it represents a major social health issue because of its high prevalence and of the growing public awareness of it. The XIX century description of "Fat Joe", the famous character of Charles Dickens's Pickwick Papers, is often retained the first presentation of a person affected by OSAS, since Joe was an obese individual who fell asleep during daytime while performing even extremely simple tasks. However, apart from the fact that Joe's Picwickian syndrome ("the obesity hypoventilation syndrome") needs to be differentiated from true OSAS, already in the Hippocratic Corpus (V-IV century BC) many clues regarding apnea and sleepiness are present, and in 79 AD the Roman author Pliny the Younger clearly reported the death of a man in whom obesity, sleepiness and snoring were co-present in a unique clinical picture. In this paper, elements suggesting OSAS are traced back and evidenced in the XIX and XX centuries in distinguished figures, including Emperor Napoleon Bonaparte, Queen Victoria and President Franklin D. Roosevelt. A posteriori reconstruction of the health status of characters of the past is difficult, and, to an extent, speculative, but the elements here provided appear relevant, since the possible presence of disabling OSAS in important personages of the past may have negatively influenced not only their health status, but also their social life and their work activity.
Humans↗
Analysis of minK and eNOS genes as candidate loci for predisposition to non-valvular atrial fibrillation.
AIM: Mink protein, a beta-subunit of I(ks) potassium channels modulate cardiac cellular electrophysiology, and experimental data demonstrated that NO is involved in cardiac vagal activity and in the inhibition of sympathetic activity. We evaluated the role of eNOS -786T>C, 894G>T, 4a/4b and of minK S38G polymorphisms as predisposing factors to non-valvular atrial fibrillation (NVAF). METHODS AND RESULTS: We studied 331 consecutive patients with documented NVAF and in 441 control subjects, comparable for age and gender. A significant difference in allele frequencies between patients and controls for minK S38G and eNOS -786T>C, but not for eNOS 894G>T and 4a/4b polymorphisms, was observed. The minK 38G allele was significantly associated with susceptibility to NVAF at both univariate and multivariable analysis, according to dominant and recessive genetic model (multivariable analysis, dominant: OR=1.73, P=0.004 and recessive: OR=1.59, P=0.006). The eNOS -786C allele weakly influenced NVAF at univariate analysis, according to the dominant model (OR=1.50, P=0.01). The contemporary presence of minK 38G and eNOS -786C alleles increased the predisposition to NVAF, after adjustment with cardiovascular risk factors (OR minK 38G*eNOS -786C=2.11, P<0.0001; OR=2.58, P=0.003; OR=3.08, P=0.002, according to dominant, recessive, and additive model, respectively). CONCLUSION: Our findings suggest a role for minK and eNOS genes as predisposing factors to NVAF.
Aged↗
Predictors of in-hospital mortality after percutaneous coronary intervention for cardiogenic shock.
OBJECTIVES: The mortality of patients with cardiogenic shock (CS) complicating ST elevation acute myocardial infarction (STEMI) remains high, despite early revascularization. Current knowledge of predictors of death is limited. BACKGROUND: The pathophysiologic understanding of CS after acute myocardial infarction has shifted from a mere hemodynamic disorder to a more complex approach including imbalance in metabolic functions. METHODS: In 45 consecutive patients (71.4+/-13 years) with CS complicating STEMI treated with primary percutaneous coronary intervention (PCI) serum levels of lactate, glucose and uric acid on coronary care unit (CCU) admission were measured. The end-point was in-hospital death. RESULTS: The following parameters, on CCU admission, were univariate predictors of in-hospital mortality: serum glucose >200 mg/dl (OR=11.3, p=0.002), serum creatinine >1.5 mg/dl (OR=12.7, p=0.003), uric acid >6.5 mg/dl (OR=6.7, p=0.016), lactate >6.5 mmol/l (OR=54, p<0.0001), age > or =75 years (OR=8.5, p=0.002), history of hypertension (OR=8.3, p=0.003) and TIMI flow post PCI < or = 2 (OR=12.9, p=0.02). At multivariate analysis, after adjustment for sex, age, hypertension and diabetes, lactate >6.5 mmol/l and TIMI flow post PCI < or = 2 were still independent predictors of in-hospital mortality (OR=295, p=0.01; OR=19.5, p=0.04, respectively). CONCLUSIONS: Hyperlactatemia, hyperglycemia and increased levels of uric acid on CCU admission are univariate predictors of in-hospital death. Moreover, at multivariate analysis, hyperlactatemia (>6.5 mmol/l) is an independent indicator of in-hospital death in CS patients complicating STEMI.
Aged↗
Predictors of vitamin B6 and folate concentrations in older persons: the InCHIANTI study.
BACKGROUND: Low dietary intake and low serum concentrations of vitamin B6 and/or folate are associated with increased risk of vascular events, possibly because of their association with inflammation, which plays a crucial role in the pathogenesis of cardiovascular diseases. METHODS: Using data from 1320 participants in the population-based InCHIANTI study (586 men and 734 women; median age, 69 years; range, 21-102 years) for whom complete data on folate, vitamin B6, inflammatory markers, 5,10-methylenetetrahydrofolate reductase (MTHFR) C677T sequence variant, and important covariates were available, we evaluated the association of inflammatory markers with circulating concentrations of vitamin B6 and folate, independently of dietary vitamin intake, circulating vitamin concentrations, and MTHFR C677T sequence variant. RESULTS: According to multiple linear regression analysis, C-reactive protein and interleukin-6 receptor were strongly and negatively associated with circulating vitamin B6 but not with folate concentrations, independent of age, sex, serum creatinine, serum albumin, total energy intake, smoking history, dietary nutrient intake, and circulating homocysteine and vitamin concentrations. Serum folate concentrations were related to MTHFR 677 TT genotype in persons with folate intake in the lowest tertile (< 221.2 microg/day). Vitamin C and retinol intakes were strongly and positively associated with serum folate concentrations independent of age, sex, serum creatinine, serum albumin, total energy intake, smoking history, homocysteine plasma concentrations, dietary nutrient intakes, serum vitamin B6 and vitamin B12 concentrations, and MTHFR C677T sequence variant. CONCLUSIONS: Low serum vitamin B6, but not serum folate, concentrations are independent correlates of the proinflammatory state, and both are influenced by antioxidant reserves.
Adult↗
Hyperviscosity as a possible risk factor for cerebral ischemic complications in atrial fibrillation patients.
Recent studies have suggested that hyperviscosity is frequent in patients with atrial fibrillation (AF). The aims of this study were to evaluate if hemorheologic alterations play a role in the occurrence of cerebral ischemic events in patients with AF and to explore a possible association between inflammation and hyperviscosity in these patients. Sixty-two patients with AF with a history of >or=1 cerebral ischemic event and 94 patients with AF without cerebral ischemic events were studied. A control population included 130 age- and gender-matched healthy volunteers. Hemorheologic variables (whole-blood viscosity, plasma viscosity, the erythrocyte deformability index, and hematocrit), fibrinogen, and high-sensitivity C-reactive protein levels were assayed. An alteration in whole blood viscosity at 94.5 seconds(-1) and the erythrocyte deformability index were found more frequently in patients with previous ischemic events on univariate and multivariate analyses (odds ratio 3.19, p=0.023 and odds ratio 4.26, p=0.002, respectively) adjusted for age, gender, hypertension, diabetes, history of coronary artery disease, left ventricular dysfunction, smoking habit, dyslipidemia, hematocrit, fibrinogen, high-sensitivity C-reactive protein, and hemorheologic parameters. These results should stimulate prospective studies on the role of hemorheologic alterations in the occurrence of cerebral ischemic complications in patients with AF.
Aged↗
The contributions of Paul Ehrlich to infectious disease.
Paul Ehrlich (1854-1915) is nowadays considered a pioneer in a number of medical fields, and in the course of time his role in the establishment and development of disciplines such as histology, immunology, oncology and haematology has been acknowledged. Aim of this historical note is to illustrate, in the area of chemotherapy, the special importance of this brilliant scientist whose 150th anniversary of birth occurred in 2004. Already as a medical student, Ehrlich was obsessed by structural organic chemistry and dyes, and, continually studying these issues, he elaborated his theory regarding the discovery of a "magic bullet", able to specifically destroy tumour cells and micro-organisms. In practice he applied methylene blue to the treatment of malaria patients, following his intuition that such a dye could destroy parasites. However, his culminating achievements in the chemotherapic field, reached even at the expense of his health, were the concept of the one-dose treatment of Helicobacter pylori infection, and the creation of arsphenamine (compound 606, or Salvarsan), the first really effective compound in controlling human syphilis. Within the many and various contributions of Ehrlich to the development of experimental and clinical medicine, a special mention of his experimental studies and clinical applications in the area of chemotherapy is essential, since his achievements in this biomedical area remain a paramount legacy in the history of the therapy of infections.
Allergy and Immunology↗