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Biomedical subjects

M Aragona

Publications and source records attributed to M Aragona.

At least 19 recordsLinked to original sources
PubMed2006

Association between burnout and anger in oncology versus ophthalmology health care professionals.

The prevalence of burnout in oncology staff was compared with that of the ophthalmology staff, who normally present a low prevalence of burnout as described in this literature. The correlation of burnout with the emotion of anger was also investigated. Thirty-six subjects working in an oncology department and 32 working in an ophthalmology department were examined using the Maslach Burnout Inventory and the State-Trait Anger Expression Inventory. The oncology group showed higher mean scores on the MBI Emotive Exhaustion and Depersonalization scales with respect to ophthalmology staff. Correlation analysis showed that increasing burnout was associated with higher anger expressed towards the environment and loss of anger control. Anger, as a response to frustration, appears to be a feature constantly associated with the clinical expression of burnout and it should not be underestimated in theoretical and preventive contexts.

Adult↗
PubMed2004

Pancreas transplant alone.

Pancreas transplant alone (PTA) represents a growing proportion of overall pancreas transplantations, with 1-year patient and graft survivals of almost 100% and higher than 80%, respectively. PTA can restore normoglycemia without exogenous insulin administration and eliminate acute diabetic complications. In our series of 28 PTA, performed with portal-enteric drainage, 2-year patient and pancreas survivals were 100% and 87%, respectively. In patients with successful transplantation, rapid normalization of blood glucose level and HbA1c concentration was observed, due to restored endogenous insulin secretion. Several classical cardiovascular risk factors were measured before and after transplant, with significant improvements shortly after transplantation. Diabetic retinopathy improved in 58.8% of examined eyes, stabilized in 35.3%, and worsened in 5.9%. In conclusion, PTA represents a clinically relevant option for patients with type 1 diabetes without advanced renal disease. It restores normoglycemia in the vast majority of patients and seems to have a positive impact on late diabetic complications.

Blood Glucose↗
PubMed2003

Reducing insulin resistance with metformin: the evidence today.

Insulin resistance, defined as the inability of insulin to exert a normal biological action at the level of its target tissues, is one of the principal pathogenetic defects of type 2 diabetes. Metformin, the most widely-prescribed insulin-sensitizing agent in current clinical use, improves blood glucose control mainly by improving insulin-mediated suppression of hepatic glucose production, and by enhancing insulin-stimulated glucose disposal in skeletal muscle. Experimental studies show that metformin-mediated improvements in insulin sensitivity may be associated with several mechanisms, including increased insulin receptor tyrosine kinase activity, enhanced glycogen synthesis, and an increase in the recruitment and activity of GLUT4 glucose transporters. In adipose tissue, metformin promotes the re-esterification of free fatty acids and inhibits lipolysis, which may indirectly improve insulin sensitivity through reduced lipotoxicity. The improved glycaemia with metformin is not associated with increased circulating levels of insulin, and the risk of hypoglycaemia with metformin is minimal. The therapeutic profile of metformin supports its use for the control of blood glucose, in diabetic patients and for the prevention of diabetes in subjects with impaired glucose tolerance. Moreover, the improvement by metformin of cardiovascular risk factors associated with the dysmetabolic syndrome may account for the significant improvements in macrovascular outcomes observed in the UK Prospective Diabetes Study.

Adipose Tissue↗
PubMed2003

Dissociation between carotid artery lesions and lipid parameters in recipients of successful kidney graft.

BACKGROUND: The relationships between lipid levels and atherosclerotic lesions of carotid arteries in kidney graft recipients are still unclear. METHODS: We evaluated carotid morphology in 53 recipients of functioning renal transplantation, and studied the relationship of carotid artery wall lesions with relevant clinical and laboratory risk factors for cardiovascular disease. The patients were on stable, cyclosporine-based immunosuppressive therapy. RESULTS: The main clinical characteristics of patients were: age, 46.5 +/- 10.1 years; males/females, 40/13; body mass index, 25.8 +/- 4.4 kg/m2; duration of transplantation, 43 +/- 52 months. Ultrasonographic scanning of carotid arteries showed the presence of lesions (intimal-media thickness and/or plaque) in 28 patients (52.8%). These recipients differed from patients without carotid lesions in terms of age (50.4 +/- 9.0 vs 42.2 +/- 9.7 years, p < 0.01) and duration of pre-transplant dialysis (4.6 +/- 3.4 vs 2.3 +/- 1.9 years, p < 0.01), whereas no statistically significant difference was observed as for total cholesterol (230 +/- 44 vs 235 +/- 35 mg/dl), LDL-cholesterol (142 +/- 32 vs 143 +/- 30 mg/dl), HDL-cholesterol (52 +/- 12 vs 58 +/- 20 mg/dl) and triglycerides (178 +/- 94 vs 167 +/- 89 mg/dl). The percentage of post-transplant diabetes was 3-fold higher in patients with carotid lesions (25 vs 8%). No difference was observed as for the following parameters: body mass index, duration of transplantation, fibrinogen levels, DDimer concentrations, reactive C-protein values, prevalence of hypertension, percentage of smokers vs non-smokers. CONCLUSIONS: The present study supports the view that carotid artery lesions in kidney graft recipients on stable, cyclosporine-based immunosuppressive therapy may not be related to circulating lipid values.

Adult↗
PubMed2001

A DNA replication origin and a replication fork barrier used in vivo in the circular plasmid pKD1.

As in other yeasts, ARS-containing plasmids can be maintained extrachromosomally in Kluyveromyces lactis. Although some fragments of K. lactis DNA have ARS activity in both K. lactis and Saccharomyces cerevisiae, it appears that the sequences required for ARS activity in the two yeasts are different. As an approach to a better understanding of ARS structure and function in K. lactis, we analyzed the replication of the circular plasmid pKD1. We identified a 159-bp sequence able to promote autonomous replication of pKD1 in both yeasts; this fragments contains both a sequence related to the S. cerevisiae ARS consensus sequence and a region of 53% identity to the 40-bp sequence essential for K. lactis KARS101 function. By the analysis of in vivo replication intermediates we provide the first direct evidence that DNA replication initiates at or near the K. lactis ARS element. Replication terminates at the cisacting stability locus of pKD1, which functions as a replication fork barrier (RFB) and is necessary for proper plasmid segregation. RFB activity requires the pKDI gene products that are important for plasmid segregation, suggesting a link between DNA replication termination and plasmid segregation in a eukaryotic organism.

Base Sequence↗
PubMed2001

Nerve growth factor receptor immunoreactivity in breast cancer patients.

Nerve growth factor receptor (NGF-R) has been shown to have antiproliferative, differentiative, or apoptotic effects on some types of tumor cells, whereas in others it may have mitogenic activity. The immunohistochemical distribution of NGF-R was analyzed in a series of tissue samples from breast cancer patients and its relationship with other clinical and pathological parameters was studied. The distribution of NGF-R was evaluated by immunohistochemistry in frozen tissue samples of 46 breast cancer patients (ME20-4 monoclonal anti-NGF-R). NGF-R immunoreactivity was localized in the plasma membrane of myoepithelial cells, differentiated ducts, neoplastic cells, blood vessels, and nerve fibers in 26 patients (57%). Less differentiated neoplastic tissues were usually NGF-R negative. NGF-R immunoreactivity was associated with estrogen receptor (ER) status (p = 0.02), small tumor dimension (pT) (p = 0.04), low histologic grade (G1-G2) (p < 0.05), old age (p = 0.02), menopause (p = 0.02), and long disease-free survival (DFS) (median follow up 86 months; p = 0.03; independently from ER, pT, age, menopause by multivariate analysis, p = 0.0078). The expression of NGF-R immunoreactivity by breast cancer patients with long DFS may represent a crucial step both in the differentiation status of neoplasia and in the host immune mechanism controlling tumor growth and metastasization.

Age Factors↗
PubMed2001

Deep venous thrombosis in patients undergoing salvage radical cystectomy.

OBJECTIVE: The possible occurrence of venous thrombosis in tumor-bearing patients had already been reported by Trousseau in the past century. The blood clotting alterations in cancer-bearing patients can cause Deep Venous Thrombosis (DVT), especially in those patients with disseminated metastases. Anti-tumor chemotherapy can increase the risk of thrombosis. Herein we report our past experience on a sample of patients who underwent pelvic surgery to treat infiltrating bladder tumors. METHODS: We have retrospectively analyzed the records of patients with infiltrating bladder tumors who underwent salvage radical cystectomy. RESULTS: We observed the highest incidence of DVT (33.3%; 3 out of 9) in those patients with a higher risk due to anesthesia and an absolute need for extensive surgery. One of our patients died of pulmonary embolism. CONCLUSION: The diagnosis of DVT and Pulmonary Embolism is not always easy to achieve and all possible tests must be performed whenever possible (e.g. clinical examination, hematological test, etc.).

Aged↗
PubMed2000

Telomere length maintenance in aging and carcinogenesis.

Normal somatic cells have a finite number of divisions, a limited capacity to proliferate. Human telomeres, the long DNA TTAGGG repeats at the ends of chromosomes, are considered a molecular clock marker. The gradual and progressive telomere shortening at each replicative cycle is associated, through the activation of pRB and p53 pathways and genomic instability, to the replicative senescence, a non-dividing state and widespread cell death. Activation of telomere maintenance [telomerase; or alternative lengthening of telomeres mechanisms (ALT), or other adaptive responses] can revert this program. Although not completely known, several mechanisms and modulating agents may be able to up and down-regulate telomere length and its maintenance. Chemopreventive therapies for the up-regulation of telomerase activity, able to prolong the life of cell cultures in a phenotypically youthful state, could have important applications in research and medicine. On the contrary the therapeutic down-regulation of telomerase activity may be used in cancer therapy. Telomerase expression per se is not oncogenic, but telomere shortening and maintenance seem to be crucial events in tumor formation. Thus a particular focus has been pointed out relatively to the immortalization of normal or potential pre-cancerous cells. With the extension of life span the probability to get in contact with carcinogens increases, genetic instability, oncogene activation and/or onco-suppressor gene inactivation (i.e. p53, pRB, ras): the cancer transformation can be then induced in predisposed cells, depending on their genetic context, by the activation of telomere maintenance. Pharmacological intervention may be able to modulate the rate of living, by increasing life span of few specific target cells, or decreasing it in proliferating . Because of the unknown state of the enormous cell number of the human organism, is it safe to extend the human life span by therapeutic agents?

Aging↗
PubMed2000

[Unexpected death by leukostasis and lung leukostatic tumors in acute myeloid leukemia. Study of four cases].

Four cases of unexpected death due to acute myeloid leukemia have been studied: myeloblastic M1 (case I and II), promyelocytic M3 (case III), myelomonocytic M4 (case IV). Diagnosis was performed before death only in case III. Histological leukostasis was the most evident feature in all cases, particularly at the lung level, where tumor-like aspects were evident and widely diffused in case II. The last three cases were pregnant at the third trimester. Serious hemorrhagic complications were evident in all cases: CID in the former 3 cases and primary hyperfibrinolysis in the 4th, as demonstrated by the absence of intravascular cloths in many organs and especially in lung and kidney; abundant, on the contrary, in the former three cases. Leukostasis was not associated to hyper-leucocytosis in all 4 cases, but associated to normal number of peripheral white cells (below normal level in case III). This phenomenon, that disagrees with literature data on acute or chronic reactivated myeloid leukemia leukostasis, may be due to the primary confination of the immature granuloblasts in the vascular bed, because of the hemoreologic effects connected with their deficient plasticity, that is essential for normal granulocytes to flow easily in the capillary bed. In all cases death was caused by breathing and cardiocirculatory insufficiency with the associated unceasing hemorrhages.

Adolescent↗
PubMed1998

Psychopathological considerations on the relationship between bulimia and obsessive-compulsive disorder.

The relationship between eating disorders, impulse control disorders and obsessive-compulsive disorder as part of a so-called 'obsessive-compulsive spectrum' is discussed, with particular emphasis on the relationship between eating disorders (particularly bulimia) and obsessive-compulsive disorder. The empirical studies on comorbidity, personality and familiarity are briefly reviewed. Both similarities and differences found in personality, body image, mental rumination, fears, physical exercises, rituals, impulses (bulimic binging and obsessive impulses) and purging behaviors of these patients are discussed from a psychopathological point of view. In particular the importance of distinguishing between obsessive thoughts and prevalent (dominant) thoughts is underlined; the distinctions between repetitive weight controls, physical exercises and purging behaviors of eating disorder patients on the one hand and compulsions on the other, and the distinction between binge impulses and obsessive impulses, are also stressed.

Anorexia Nervosa↗
PubMed1998

[Cellular adaptation and cancerogenesis].

The paper describes the main adaptive mechanisms involved in the carcinogenic process. As a result of the action of carcinogenic agents (physical, chemical, biological), and in relation to the functional status of the affected cells, a number of systems are triggered off: detoxification and conjugation systems, the metabolisation of the said agents, DNA repairing enzymes, increased shock proteins (HSP), the induction of clonal proliferation. All these systems are valuable to the survival of the body and the species and culminate in the apoptosis of damaged cells as the last attempt at adaptation of a social kind for the good of the body. When these compensation mechanisms prove ineffective, imprecise or are exceeded by cell adaptive capacity, the resulting structural and functional alterations trigger off (induction) a very long process which often lasts between one and two thirds of the body's life, in various stages, multistep and multifactorial: this neoplastic transformation leads to a purposeless, egoistic, anarchic proliferation of cells which wish to survive at all costs, even to the detriment of the body of which they form part. Following the exhaustion of cell adaptive defences, there is an accumulation of additional genetic alterations (promotion and progression), the cells become manifestly neoplastic and continue their egoistic adaptation, according to the laws of natural selection: the cells which survive are those which adapt best to the hostile environment of the host's body, which are unaffected by proliferation control mechanisms (contact inhibition, differentiation factors, apoptosis, etc.), which make the best of the growth factors present in their microenvironment, which accomplish the so-called decathlon of the metastatization process, namely acquiring new capacities which can overcome the basal membrane, invade tissues to which they are attracted and continue to proliferate. Manifestly neoplastic cells become not self at a later stage, managing to escape the immune system using various adaptive mechanisms which induce immune tolerance/anergy. From this point of view, cancer may be regarded as an incidental factor in the host's cell adaptation processes; the latter are much more important from a biological point of view and their absence is incompatible with life: cancer might therefore be regarded as a cell adaptation pathology.

Adaptation, Physiological↗
PubMed1997

Depressive mood disorders in patients with operable breast cancer.

We studied 149 subjects admitted to hospital with operable, untreated breast cancer (108) or benign (41) breast disease (control group). Depression was evaluated before diagnosis and surgery, using MMPI and Rorschach tests, HDRS scale, and DSM-III-R diagnostic criteria during a semistructured interview. 62% of patients and 34% of controls (p<0.005) presented some depressive symptoms, whereas only 55% of patients and 18% of controls (p<0.001) met criteria for depressive mood disorders: 2% of patients and 0% of controls for major depression, 13% and 5% for dysthymia (p<0.05), 40% and 13% for depressive disorders NOS (p<0.001). No correlation was observed with respect to stage of disease, histopathologic grade, age and menopause except for ER status (p=0.03). During interview, 89% of patients and 65% of controls reported severe stressful life events 5+/-4 years before the clinical onset of the breast node. No differences were observed in the depression rating scales mean value whereas patients resulted more inhibited in their affection and emotionally controlled (Rorschach data) compared to controls (p<0.05). In conclusion, although the depression diagnostic criteria used may not be strictly correlated higher prevalence of depressive mood disorders and stressful life events were observed in patients in the pre-clinical phase of operable breast cancer. This may suggest an involvement of depression in the natural history of breast cancer.

Adjustment Disorders↗
PubMed1997

[Increase of oxygen free radicals and their derivatives in chemo- and radiation treated neoplasm patients].

BACKGROUND: Radical oxygen species (ROS) are known to mediate cytotoxic anticancer activity by modifying the cellular homeostatic redox balance. The aim of the study is to evaluate whether cancer patients show more ROS after radio/chemotherapy. METHODS: ROS were evaluated in 32 oncologic untreated patients. Blood samples were collected both before and after the end of radio/chemotherapy. Spectrophotometric detection of ROS was performed by using d-ROMs test (Diacron). RESULTS: After therapy all patients showed a marked increase in ROS (378 +/- 35 U Carr) compared to values measured before therapy (269 +/- 62 U Carr, p < 0.0001). This result was more evident during the first course of therapy. No significant differences were observed between patients who received radio or chemotherapy. CONCLUSIONS: In conclusion both radio and chemotherapy induce oxidative stress by increasing radical oxygen species, exceeding the antioxidative capacities of cancer patients. This is useful for therapeutic purposes but may enhance the cytotoxicity induced by therapy.

Adenocarcinoma↗
PubMed1997

[Role of free radicals, telomeres, and telomerases in aging and cancerogenesis].

After a rapid examination of a few basic concepts concerning cellular aging and programmed cell death, the aging of the tissues and organs, the authors discuss the principal theories on senescence. They underline that it is necessary to agree in considering the various genetic and epigenetic, endogenous and exogenous mechanisms that lead to the complex aging phenomenon multiple and interrelated. In particular they stress the hypothesis that senescence can be due to a sum of molecular damages caused by free radicals, and to the loss of telomeric DNA. Radical reactions can cause mutations, inactivation or a decrease in the turnover of mitochondrial DNA which is more vulnerable than the nuclear genoma to the attack of mutagenic agents, acting also as a continuous source of initial and/or promoting factors of the carcinogenetic process. The somatic cells become senescent because during cell division, they lose the mechanisms for the lengthening of the telomere. The telomerase prevents the shortening of telomeres in neoplastic cells and therefore renders them immortal. Paradoxically the protection of the telomere is exactly what must be avoided in the case of tumor cells. Recently the demonstration that telomerase is not always involved in the restoration of telomere length shows the complexity of the problems connected to the cause of senescence.

Cellular Senescence↗