Biomedical subjects
Publications and source records attributed to M Maggioni.
Involvement of the liver in cases of Listeria monocytogenes is uncommon. We report a case of hepatitis due to L. monocytogenes, with a pathological finding of multiple abscesses. Blood cultures yielded L. monocytogenes. The patient died a few days after admission.
beta-Endorphin (beta-EP) concentrations were measured in peripheral blood mononuclear cells of 10 elderly women with major depressive disorders, 10 age- and sex-matched healthy controls and 10 young healthy controls. beta-EP values were measured in resting condition and after stimulation with corticotropin-releasing hormone (CRH). In patients, beta-EP values were measured in drug-free condition and after 30 days of treatment with phosphatidylserine (BCPS), 200 mg/day, p.o. Basal and CRH-stimulated beta-EP concentrations were the same in patients and controls; in patients they did not change after BCPS, in spite of significant improvement of the depressive symptomatology.
T-lymphocyte responses to phytohemoagglutinin (PHA) stimulation were examined in 10 elderly women with nonmelancholic Major Depressive Disorders (MDD), in 10 age- and sex-matched controls and in 10 young female controls, before and after in vivo stimulation with corticotropin-releasing hormone (CRH). The tests were repeated in MDD patients after 30 days of therapy with phosphatidylserine (BC-PS), 200 mg/day, p.o. T-lymphocyte responses to PHA stimulation did not differ in the three groups, and were not changed by CRH administration. BC-PS therapy, while significantly improving the depressive symptomatology, did not modify the T-lymphocyte response to PHA, either before or after CRH stimulation.
BACKGROUND: Aberrations of the p53 gene (also known as TP53) frequently lead to the synthesis of mutant proteins that accumulate in the nuclei and/or cytoplasm of neoplastic cells. Intracellular p53 protein accumulation may be an unfavorable prognostic parameter in breast, lung, ovarian, gastric, and colorectal cancers. Specific classes of p53 gene mutations, assayed by characteristic subcellular p53 protein accumulation patterns, may be useful prognostic indicators. PURPOSE: The prognostic value of nuclear and cytoplasmic p53 protein accumulation in the tumor cells of patients with colorectal carcinoma was studied. METHODS: Antibodies PAb 1801 and CM1 were used for immunocytochemical assay of nuclear and cytoplasmic p53 protein accumulation in a retrospective series of colorectal carcinoma samples obtained from 206 patients who were followed for at least 5 years. Results were correlated with the following clinicopathologic parameters: patient sex and age; tumor site, stage, and grade; and DNA ploidy status of the tumors. Overall survival and disease-free survival were analyzed with the Kaplan-Meier method. Differences in distributions were analyzed using the Mantel-Cox method. Multivariate analysis was performed with the Cox proportional hazards model. RESULTS: Immunostaining with PAb 1801 revealed nuclear p53 accumulation in 46% (95) of 206 cases, whereas CM1 immunostaining of 197 cases showed nuclear and cytoplasmic p53 accumulation in 33% (65 cases) and 50% (99 cases) of the cases, respectively. In univariate analysis, both nuclear p53PAb 1801 and cytoplasmic p53CM1 protein accumulations were significantly associated with poor overall survival (P = .0198 and P = .0017, respectively) and with disease-free survival (P = .004 and P = .0016, respectively). When patients were analyzed according to site of their tumors, nuclear p53PAb 1801 protein accumulation was statistically significant only in the right colon (P = .027), whereas cytoplasmic p53CM1 protein accumulation was statistically significant in the left colon and rectum (P = .0016). In multivariate analysis, only cytoplasmic p53CM1 protein accumulation was associated with poor overall survival and with disease-free survival (P = .006 and P = .002, respectively). With the addition of DNA ploidy status, however, cytoplasmic p53CM1 protein accumulation remained significant only for disease-free survival (P = .035). In patients with tumors of the left colon and rectum, cytoplasmic p53CM1 protein accumulation was the most significant prognostic indicator for overall survival (P = .007) and disease-free survival (P = .002) after disease stage. CONCLUSION: Cytoplasmic p53CM1 protein accumulation, but not nuclear p53PAb 1801 protein accumulation, is an independent prognostic parameter in patients with colorectal carcinomas. IMPLICATIONS: Cytoplasmic p53CM1 accumulation may be a useful indicator of patients at high risk for disease recurrence who may benefit from aggressive adjuvant therapy.
Proliferation and differentiation of villous trophoblast during placental development, from an early stage to full-term, were investigated in routinely fixed and processed tissues, by means of the immunocytochemical localization of the cell cycle-related proto-oncogene c-myc and the p53 and retinoblastoma susceptibility (Rb) tumour-suppressor gene products. The proliferative activity of the trophoblast was determined using an antibody against proliferating cell nuclear antigen (PCNA) which stains all proliferating cells in paraffin-embedded tissues. Diffuse nuclear immunoreactivity for PCNA, c-myc and Rb gene products was a consistent finding in early cytotrophoblast; c-myc product expression was also detectable in both layers of mid-gestation trophoblast. Only scattered cytotrophoblastic nuclei of early gestational placenta displayed immunostaining for p53 gene product. In full-term placenta c-myc expression was undetectable while Rb gene product and PCNA immunoreactivity declined markedly. These results indicate that the expression of the above genes is spatio-temporally regulated during placental development. A potential involvement of the oncosuppressor gene products p53 and Rb in the control of trophoblastic proliferation and of c-myc in the control of both the proliferative and differentiation pathways of trophoblastic cells is suggested.
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Morphologic changes are reported to occur in rat lung vasculature after 3 days of hypoxia. We have previously shown that immunoreactivity for the vasodilator calcitonin gene-related peptide (CGRP) is increased in pulmonary endocrine cells by 7 days of hypoxia. Because these cells may be among the earliest mediators of the hypoxic response, we examined endocrine cell CGRP content in rat lung after 0, 2, 4, and 8 h and 1, 5, 10, 15, 20, 28, and 35 days of normobaric hypoxia, using optimal and supraoptimal dilutions of CGRP antibodies to demonstrate changes in CGRP immunoreactivity. This was compared with temporal changes in pulmonary vascular smooth muscle after 1, 5, and 20 days of hypoxia exposure by evaluating vascular immunoreactivity for alpha-smooth muscle actin (alpha-SM actin), platelet-derived growth factor (PDGF) beta-receptor, and proliferating cell nuclear antigen (PCNA). Significant increases in endocrine cell CGRP immunoreactivity were found after 4 h of hypoxia, and levels increased up to 1 day, followed by a decrease (at 5 days) and then a progressive increase up to 35 days. After 1 day of hypoxia, the number of vessels displaying immunoreactivity for alpha-SM actin, PDGF beta-receptor, and PCNA were also significantly increased. Whereas PDGF beta-receptor and PCNA returned to control values by day 20, alpha-SM actin reached a plateau that persisted until 20 days. The results indicate that modulation of endocrine cell CGRP content in response to hypoxia is rapid and characterized by a significant and persistent increase, paralleled by a proliferation of vascular cells leading to vascular muscularization.(ABSTRACT TRUNCATED AT 250 WORDS)
Zolpidem is a new imidazopyridine hypnotic with a pharmacological profile substantially different from benzodiazepines. In this observational multicenter study the possibility of shifting to zolpidem (10 mg at N1, 15 or 20 after N1) insomniac patients previously taking (for at least 15 days and not longer than 3 months) standard posology of triazolam (0.125-0.25 mg), lorazepam (1 mg) or lormetazepam (1 mg) was assessed. For ethical reasons the patients were mandatorily to be insomniacs despite their taking hypnotics or not tolerating them. Patients enrolled were 299 of whom 276 evaluable (139 males and 136 females; mean age 48.67 +/- 14.64, range 18-83). Study duration was 7 nights with visits at N0 (baseline), N1 (after 1st night), N3 (after 3rd night) and N7 (final evaluation); on each visit the Saint Mary Hospital Sleep Questionnaire and the benzodiazepine withdrawal symptom's rating scale were administered; moreover, after N7, investigators were asked a judgement of feasibility of such a shift. In 229 (83.5%) out of 274 patients such a shift to zolpidem was considered successfully (no occurrence of symptoms and/or signs of previously taken hypnotic withdrawal); in the remaining 45 patients, just 17 (6.2%) seemed to be real unsuccessful cases (reactions mild and transient, anyhow). In conclusion abrupt shift to zolpidem appeared to be largely feasible in the patients studied.
Baseline follicle stimulating hormone (FSH) and luteinizing hormone (LH) plasma levels and their responses to luteinizing hormone releasing hormone (LHRH) stimulation were investigated in 72 patients who met Research Diagnostic Criteria for affective disorders and in 72 healthy volunteers. Fifty-six patients were examined during a depressive phase and 16 during a normothymic phase. LH-FSH basal levels were significantly lower in postmenopausal depressed and normothymic women than in controls. In fertile women and men, concentrations of the two gonadotropins were also lower in patients than in controls, but the phenomenon did not generally reach statistical significance. LHRH-induced LH rises were lower in postmenopausal and fertile depressed and normothymic women than in controls, while FSH rises were reduced only in postmenopausal depressive women in both depressed and normothymic phases. The impairment underlying the gonadotropin secretory deficiency remains to be elucidated.
The effects of phosphatidylserine (BC-PS) on cognitive, affective and behavioural symptoms were studied in a group of 10 elderly women with depressive disorders. Patients were treated with placebo for 15 days, followed by BC-PS (300 mg/day) for 30 days. The Hamilton Rating Scale for Depression, Gottfries-Bråne-Steen Rating Scale, Nurse's Observation Scale for Inpatient Evaluation and Buschke Selective Reminding Test were administered before and after placebo and after BC-PS therapy, to monitor changes in depression, memory and general behaviour. At the same time, basal plasma levels of noradrenaline, MHPG, DOPAC, HVA and 5-HIAA, and GH/beta-endorphin/beta-lipotropin responses to clonidine stimulation were measured. BC-PS induced consistent improvement of depressive symptoms, memory and behaviour. No changes in amine metabolite levels or in hormonal responses to alpha 2-adrenoceptor stimulation were observed.
The efficacy of zolpidem 20 mg was compared to that of flunitrazepam 2 mg. Forty-two insomniac female in-patients between 30 and 65 years of age were included in a double blind, parallel group trial and were randomly allocated to the two treatments. Study duration was 9 days with 2 days of placebo run-in, 5 days of active medication and 2 days of placebo withdrawal. Sleep latency, sleep duration, number of awakenings and time spent asleep during the night were given an ordinal score; condition in the morning was evaluated by Visual Analogue Scales and the psychomotor performance was evaluated by the tests: night-day for anterograde amnesia, digit span for verbal recall and Grünberger's fine motor function test. There was no significant difference between zolpidem and flunitrazepam for any of the variables; the drugs were significantly better than placebo baseline for all the sleep efficacy variables. The results of this study indicate that zolpidem is as effective as flunitrazepam in inducing and maintaining sleep but it does not induce a sense of weakness in the morning and does not impair memory.
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Ten chronic undifferentiated schizophrenics, 6 men and 4 women, aged 28-63, with 6- to 31-year histories of the disease were given DDAVP to observe the effects of this neuropeptide on the prevalent negative symptoms of their illness. Patients were maintained on neuroleptic therapy and first given a 20-day course of placebo followed by 20 days of DDAVP i.m., 4 micrograms Andreasen Scale for assessment of negative symptoms, the Brief Psychiatric Rating Scale, the NOSIE Rating Scale and the Luria-Nebraska Rating Scale were administered to monitor negative symptomatology, behavior and memory before the study began, after placebo and after DDAVP administration. Patients were also given a growth hormone-clonidine test and in addition plasma basal concentrations of 3-methoxy-4-hydroxyphenylglycol (MHPG), homovanillic acid, 3,4-dihydroxyphenylacetic acid (DOPAC) and 5-hydroxyindoleacetic acid (5-HIAA) were measured at the same intervals. DDAVP therapy induced a significant improvement of negative symptomatology and a trend toward improvement of short- to medium-term memory. No changes in homovanillic acid, MHPG, 5-HIAA and DOPAC, nor of growth hormone response to clonidine stimulation were observed.
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Clinical and biochemical findings link anorexia nervosa (AN) and primary effective disorders (PAD). Clonidine, an alpha 2-adrenoceptor agonist, has been shown to blunt growth hormone (GH) response and greatly lower plasma cortisol in PAD patients. We examined the GH, cortisol, and beta-endorphin (beta-EP) responses to an acute clonidine challenge (150 micrograms i.v. as a bolus) before and after 30 days of treatment with desmethylimipramine in 14 women with AN. Both before and after treatment, the AN patients showed normal plasma GH and cortisol responses, but an increased plasma beta-EP response. The increased beta-EP response in AN was independent of weight and depressive symptomatology. Our data indicate that alpha 2-adrenoceptors involved in the control of GH and adrenocorticotropic hormone are not altered in AN. The increased beta-EP response may indicate elevated opioid activity in the hypothalamo-pituitary system of AN patients.
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Twenty-three chronic undifferentiated schizophrenics, 13 women and 10 men, aged 37-64 years with 15-to 40-year histories of the disease were given either thyrotropin-releasing hormone (TRH) (10 subjects) or DDAVP (13 subjects) with the aim to improve the negative symptoms of the disease and memory. TRH (600 micrograms i.v.) and DDAVP (4 micrograms i.m.) were administered every other day for 30 days. Negative symptoms were monitored by the Andreasen rating scale and by the Honingfeld NOSIE rating scale, memory by the Folstein 'Mini mental State' rating scale and by the Luria-Nebraska rating scale before therapy and then at days 15, 16, 30 and 31 of treatment. Both therapies significantly improved negative symptoms. Memory was significantly improved in all the patients treated with TRH and in 9 of the 13 patients treated with DDAVP, who presented less severe cognitive impairments. A peripheral mechanism of action of DDAVP was excluded by the observation that plasma electrolytes and osmolality, blood pressure, ECG patterns, 24-hour urine volume and specific gravity, basal plasma cortisol and growth hormone levels and weight of the patients were unchanged during therapy. TRH treatment induced a transient borderline hyperthyroidism at day 15 and a progressive decrease of the thyrotropin response to TRH stimulation. A common mechanism of action of the two peptides on the central noradrenergic system is suggested.