Biomedical subjects
Publications and source records attributed to G Galati.
The Authors report a case of Vater's ampulla apudoma and after having examined the characteristics of these neoplasms they discuss clinical presentation, diagnostic and treatment problems of islet cell adenomas. They review the literature and make some remarks.
Surgery remains the preferred therapy for renal cell carcinoma. The various adjunctive or complementary therapies currently yield disappointing results. Identifying reliable prognostic factors could help in selecting patients most likely to benefit from postoperative adjuvant therapies. We reviewed the surgical records of 78 patients who had undergone radical nephrectomy with lymphadenectomy for renal cell carcinoma, matched for type of operation and histology. According to staging (TNM), 5.1% of the patients were classified as stage I, 51.3% as stage II, 29.5% as stage III and 14.5% as stage IV. Of the 78 patients 40 were T2N0 and 21 T3aN0. Tumor grading showed that 39.7% of the patients had well-differentiated tumors(G1), 41.1% moderately-differentiated (G2), and 19.2% poorly-differentiated tumors (G3). Overall actuarial survival at 5 and 10 years was 100% for stage 1; 91.3% at 5 years and 83.1% at 10 years for stage II; 45.5% and 34.1% for stage III; and 29.1% and nil for stage IV (stage II vs stage III p = 0.0001). Patients with tumors confined to the kidney (pT2N0) had better 5- and 10-year survival rates than patients with tumors infiltrating the perirenal fat (pT3aN0) (p = 0.000006). Survival differed according to nuclear grading (G1 vs G3 ; p = 0.000005; G2 vs G3; p = 0.0009). In conclusion our review identified tumor stage, primary-tumor extension, and the grade of nuclear differentiation as reliable prognostic factors in patients with renal cell carcinomas.
The efficacy of short term prophylaxis in the prevention of infection has been tested in 72 patients who underwent surgical treatment for colorectal pathology. General tolerance to the antibiotics was good. The Authors took this remark as a starting point for reviewing the literature and making comments.
GSH was readily depleted by a flavonoid, H(2)O(2), and peroxidase mixture but the products formed were dependent on the redox potential of the flavonoid. Catalytic amounts of apigenin and naringenin but not kaempferol (flavonoids that contain a phenol B ring) when oxidized by H(2)O(2) and peroxidase co-oxidized GSH to GSSG via a thiyl radical which could be trapped by 5,5-dimethyl-1-pyrroline-N-oxide (DMPO) to form a DMPO-glutathionyl radical adduct detected by ESR spectroscopy. On the other hand, quercetin and luteolin (flavonoids that contain a catechol B ring) or kaempferol depleted GSH stoichiometrically without forming a thiyl radical or GSSG. Quercetin, luteolin, and kaempferol formed mono-GSH and bis-GSH conjugates, whereas apigenin and naringenin did not form GSH conjugates. MS/MS electrospray spectroscopy showed that mono-GSH conjugates for quercetin and luteolin had peaks at m/z 608 [M + H](+) and m/z 592 [M + H](+) in the positive-ion mode, respectively. (1)H NMR spectroscopy showed that the GSH was bound to the quercetin A ring. Spectral studies indicated that at a physiological pH the luteolin-SG conjugate was formed from a product with a UV maximum absorbance at 260 nm that was reducible by potassium borohydride. The quercetin-SG conjugate or kaempferol-SG conjugate on the other hand was formed from a product with a UV maximum absorbance at 335 nm that was not reducible by potassium borohydride. These results suggest that GSH was oxidized by apigenin/naringenin phenoxyl radicals, whereas GSH conjugate formation involved the o-quinone metabolite of luteolin or the quinoid (quinone methide) product of quercetin/kaempferol.
1. A H2O2 generating system markedly increased the cytotoxicity of catechols, hydroquinone, in isolated hepatocytes, but not in P450 inhibited hepatocytes. 2. H2O2 or NADPH supported microsomal catalysed GSH conjugate formation with catechols or hydroquinone. Cytochrome P450 inhibitors inhibited conjugate formation. However, superoxide dismutase inhibited NADPH, but did not affect H2O2 supported GSH conjugate formation. The conjugate formed with dihydrocaffeic acid was identified as a mono-GSH conjugate indicating that the o-quinone was the major metabolite formed. 3. Dopamine (a catecholamine) induced cytotoxicity was prevented by inhibitors of monoamine oxidase (MAO) or P450, but was markedly increased by hepatocyte catalase inhibition or NAD(P)H:quinone oxidoreductase inhibition. This suggests that H2O2 formed by the mitochondrial metabolism of monoamine oxidase then oxidised dopamine to cytotoxic o-quinone catalysed by P450. Dihydrocaffeic acid cytotoxicity was also increased by the monoamine oxidase substrate tyramine. 4. It is concluded that polyphenolics are oxidised by H2O2/P450 in hepatocytes to form quinone metabolites.
The introduction of functional neuroimaging techniques has contributed to understanding the neural correlates of recovery of motor, sensory and cognitive functions after brain damage. In this paper, we review the literature of the past twenty years, with particular emphasis on quantitative studies of cerebral blood flow and metabolism. Studies are presented that examine recovery from hemiparesis, aphasia, spatial hemineglect and sensory disorders. The contribution of this research is critically discussed in a methodological perspective. A basic distinction is made between cerebral plasticity and recovery of functions. It is also argued that the most frequently used experimental designs do not permit directly relating changes in brain activity to functional recovery. The importance of accurate behavioural measures is underlined. Alternative experimental designs are proposed, based on correlations between behavioural performance and brain activations.
Because sensory systems use different spatial coordinate frames, cross-modal sensory integration and sensory-motor coordinate transformations must occur to build integrated spatial representations. Multimodal neurons using non-retinal body-centred reference frames are found in the posterior parietal and frontal cortices of monkeys. We used functional magnetic resonance imaging to reveal regions of the human brain using body-centred coordinates to code the spatial position of both visual and somatic sensory stimuli. Participants determined whether a visible vertical bar (visual modality) or a location touched by the right index finger (somatic sensory modality) lay to the left or to the right of their body mid-sagittal plane. This task was compared to a spatial control task having the same stimuli and motor responses and comparable difficulty, but not requiring body-centred coding of stimulus position. In both sensory modalities, the body-centred coding task activated a bilateral fronto-parietal network, though more extensively in the right hemisphere, to include posterior parietal regions around the intraparietal sulcus and frontal regions around the precentral and superior frontal sulci, the inferior frontal gyrus and the superior frontal gyrus on the medial wall. The occipito-temporal junction and other extrastriate regions exhibited bilateral activation enhancement related to body-centred coding when driven by visual stimuli. We conclude that posterior parietal and frontal regions of humans, as in monkeys, appear to provide multimodal integrated spatial representations in body-centred coordinates, and these data furnish the first indication of such processing networks in the human brain.
A clinical assessment of protective action of desmoplastic response by limiting tumor aggressiveness has been carried out in 171 patients with gastric carcinoma, surgically treated at the First Surgical Clinic of the University of Rome "La Sapienza" between 1988-1999. A univariate statistical analysis was performed using Kaplan-Meier method for: desmoplastic reaction, age, sex, histologic type, tumor size, stage, lymphonodal status and metastases. To determine the influence of these factors on prognosis, the Cox regression was applied. We found a significant association between desmoplastic reaction extent and presence or absence of metastases (p= 0.026), lymphonodal involvement (p = 0.05), stage (p = 0.036). In the univariate analysis, survival was significantly related to sex (p = 0.012), tumor size (p = 0.009), lymphonodal involvement (p = 0.000), metastases (p = 0.000), stage (p = 0.000), desmoplastic reaction extent (p = 0.05); age and histologic type showed no relationship (p = n.s.). The desmoplastic response extent is not a protective factor against tumor invasiveness in gastric carcinoma, on the contrary it may be considered a negative prognostic factor.
BACKGROUND: The aim of this study was to determine the efficacy and safety of biliary-intestinal bypass in severely obese subjects (Body Mass Index > 35). METHODS: From January to December 1999, 23 patients (8 men and 15 women, mean age 36.6 years: range 20-51) affected with primary morbid obesity (BMI >40: range 40.1-64.7), in whom different attempt using conservative medicine have proved non-resolutive, underwent biliary-intestinal bypass. After the operation all the patients have been followed- up for 12 months. RESULTS: The mean Body Mass Index was reduced to 36.9 (range 27.7-44.1) after 6 months and to 33 (range 24.9-40.1) after 12 months. Peri and postoperative mortality was zero. Excessive malabsorption was efficaciously controlled by adequate replacement therapy. Diarrhoea, common compliance of every operation inducin malabsorbition, was reduced to 2-3 evacuation a day after 2-3 months. CONCLUSIONS: On the basis of personal experience it is underlined that biliary-intestinal bypass, as surgical treatment of morbid obesity refractory to medical therapy, is today a safe and effective operation (up to 80% of excess body weight lose); the presence of biliary-intestinal anastomosis reduces the post-operative loss of bile acids, choleretic diarrhoea and electrolytic disorders.
BACKGROUND: The hemorrhage from breakup of the varix esophageal is a dramatic complication of the hypertension of the circle portal, numerous attempts have stayed performed for identify the patients that present taller risk of hemorrhage, to the purpose of to establish the preventive more proper measures to arrive before the first episode of hemorrhage. The treatment of the patient with high pressure portal stays still today extremely controversial, to concern the choice of the more opportune strategies, that for it as concerns the choice of the better moment for effect the single therapies. METHODS: We have taken 63 patients treatises in urgency for esophageal variceal bleeding in consideration, we of the initial group of the 63 patients have subjected endoscopic 34 patients, subjected elastic binding of the varix 20 patients, and to derivative interventions in urgency 9 patients. RESULTS: The results to distance after surgical treatment for it as concern the rise of encephalopatia it show a percentage of the 60% of patient and the actuarial survival to 5 ages is of the 33.3%. CONCLUSIONS: In conclusion seem us of power affirm that the role of the endoscopic of the esophageal varix is prominent in the management of massive acute esophageal bleeding.
Lipomas are an uncommon cause of small-bowel obstruction. The symptoms are intermittent and nonspecific. The Authors report a case in which intussusception was diagnosed with echography and the obstruction was treated with resection. They conclude that lipomas must always be considered in the differential diagnosis of intrabdominal neoplasms and in intestinal obstructions.
The clearance of apoptotic cells is crucial to avoid chronic inflammation and autoimmunity. Little is known about the factors that regulate it in vivo. We show that granulocyte-macrophage colony-stimulating factor (GM-CSF) administration to carcinoma patients confers to their leukocytes a significantly higher ability to phagocytose apoptotic cells than before (P < 0.005). GM-CSF increased the concentration of monocytes and polymorphonuclear leukocytes in the peripheral blood and activated circulating polymorphonuclear leukocytes. Both effects abated early after treatment, whereas phagocytosis of apoptotic cells was still significantly higher after 18 days compared with basal values (P < 0.005 and P < 0.025 for monocytes and polymorphonuclear leukocytes, respectively). On in vitro phagocytosis of apoptotic cells monocytes, but not polymorphonuclear leukocytes, up-regulated MHC class II membrane expression. These findings are consistent with the possibility that GM-CSF endows both scavenger and antigen-presenting leukocytes with the ability to internalize apoptotic tumor cells.
The spatial location of an object can be represented in the brain with respect to different classes of reference frames, either relative to or independent of the subject's position. We used functional magnetic resonance imaging to identify regions of the healthy human brain subserving mainly egocentric or allocentric (object-based) coordinates by asking subjects to judge the location of a visual stimulus with respect to either their body or an object. A color-judgement task, matched for stimuli, difficulty, motor and oculomotor responses, was used as a control. We identified a bilateral, though mainly right-hemisphere based, fronto-parietal network involved in egocentric processing. A subset of these regions, including a much less extensive unilateral, right fronto-parietal network, was found to be active during object-based processing. The right-hemisphere lateralization and the partial superposition of the egocentric and the object-based networks is discussed in the light of neuropsychological findings in brain-damaged patients with unilateral spatial neglect and of neurophysiological studies in the monkey.
Past research associated unilateral neglect with a systematic ipsilesional shift of the perceived position of the body midline; however, this was not confirmed by recent experiments. We used the constant stimuli method to control for potential artifacts intrinsic to the techniques used in previous studies. Body midline perception was measured in the visual and proprioceptive modalities in ten patients with left unilateral neglect, ten control patients and ten normal subjects and compared with a visual line bisection task, also using the constant stimuli method. Neglect patients showed a significant rightward bias in the line bisection task, but no consistent directional bias either in the proprioceptive or in the visual body midline task. These results clearly counter the association between neglect and an ipsilesional shift of the body midline. However, in the body midline tasks neglect patients made more errors in judgement on both sides of their subjective midline, both with respect to the control groups and with respect to the line bisection task. This may imply that a specific impairment of body-centered representations is indeed present and manifests as a non directional increase in response variability, rather than as a systematic shift. It is suggested that body- and object-related tasks (such as line bisection) may be processed by independent cognitive computations. This interpretation is discussed with reference to a recent neuroimaging study investigating the same kinds of tasks.
It is well documented that right brain damaged patients with left unilateral neglect may show unconscious processing of contralesional stimuli. However, the anatomical correlates of this phenomenon are still not well defined. Here we report the case of a neglect patient with a circumscribed lesion of the dorsal parietal-occipital white matter showing clear implicit processing of the contralesional side of line drawings and object based neglect. The patient was able to perform correct semantic analysis of the symmetry (or asymmetry) of the drawings. Additional testing disclosed denial of the existence of the contralesional side of asymmetrical geometrical shapes with correct perception of symmetrical ones and of shapes without the left side. These findings provide direct evidence supporting a critical role of the dorsal visual system in the activation of conscious representations of visual stimuli.
Isolated intestinal neurofibromatosis of the colon is a most unusual disease: from 1937 to 1999 only 12 cases have been reported. The differential diagnosis and treatment of this lesion are very difficult. A review of the literature is made and personal experience in the diagnosis and treatment of a case in a 68-year-old female is described.
This review summarises current knowledge on the various molecular chemopreventive or therapeutic mechanisms that may be involved when the administration of flavonoids or polyphenols prevented chemical carcinogenesis in animal models. These mechanisms can be subdivided into the following: 1) the molecular mechanisms involved in preventing carcinogen metabolic activation, 2) the molecular mechanisms for preventing tumour cell proliferation by inactivation or downregulation of prooxidant enzymes or signal transduction enzymes, 3) the molecular cell death mechanisms for the induction of tumour cell death (apoptosis) and the molecular mechanisms for the inhibition of isolated mitochondria functions. Many of the flavonoids and polyphenols found in diets, supplements or herbal medicine were also ranked using "accelerated cytotoxic mechanism screening" by a combinatorial approach utilising isolated rat hepatocytes. A strong correlation of an early collapse of the mitochondrial membrane potential and cell death was found for most of the cytotoxic polyphenols but did not occur with non-toxic polyphenols. This screening could prove useful for eliminating polyphenols that have the potential for adverse health effects and for selecting safe and effective polyphenolic candidates for further development as supplements for preventing cancer or cardiovascular disease. Safety concerns of flavonoid/polyphenol supplements are also reviewed.
Flavonoids containing phenol B rings, e.g. naringenin, naringin, hesperetin and apigenin, formed prooxidant metabolites that oxidised NADH upon oxidation by peroxidase/H2O2. Extensive oxygen uptake occurred which was proportional to the NADH oxidised and was increased up to twofold by superoxide dismutase. Only catalytic amounts of flavonoids and H2O2 were required indicating a redox cycling mechanism that activates oxygen and generates H2O2. NADH also prevented the oxidative destruction of flavonoids by peroxidase/H2O2 until the NADH was depleted. These results suggest that prooxidant phenoxyl radicals formed by these flavonoids cooxidise NADH to form NAD radicals which then activated oxygen. Similar oxygen activation mechanisms by other phenoxyl radicals have been implicated in the initiation of atherosclerosis and carcinogenesis by xenobiotic phenolic metabolites. This is the first time that a group of flavonoids have been identified as prooxidants independent of transition metal catalysed autoxidation reactions.