Dynamic gamma frequency feedback coupling between higher and lower order visual cortices underlies perceptual completion in humans.

To perceive a coherent environment, incomplete or overlapping visual forms must be integrated into meaningful coherent percepts, a process referred to as "Gestalt" formation or perceptual completion. Increasing evidence suggests that this process engages oscillatory neuronal activity in a distributed neuronal assembly. A separate line of evidence suggests that Gestalt formation requires top-down feedback from higher order brain regions to early visual cortex. Here we combine magnetoencephalography (MEG) and effective connectivity analysis in the frequency domain to specifically address the effective coupling between sources of oscillatory brain activity during Gestalt formation. We demonstrate that perceptual completion of two-tone "Mooney" faces induces increased gamma frequency band power (55-71Hz) in human early visual, fusiform and parietal cortices. Within this distributed neuronal assembly fusiform and parietal gamma oscillators are coupled by forward and backward connectivity during Mooney face perception, indicating reciprocal influences of gamma activity between these higher order visual brain regions. Critically, gamma band oscillations in early visual cortex are modulated by top-down feedback connectivity from both fusiform and parietal cortices. Thus, we provide a mechanistic account of Gestalt perception in which gamma oscillations in feature sensitive and spatial attention-relevant brain regions reciprocally drive one another and convey global stimulus aspects to local processing units at low levels of the sensory hierarchy by top-down feedback. Our data therefore support the notion of inverse hierarchical processing within the visual system underlying awareness of coherent percepts.

Event-related potential correlates of visual identity negative priming unbiased by trial-by-trial effects.

Negative priming (NP) refers to slowed reaction times and/or less accurate responses in people responding to a target that was ignored on a previous trial. Although extensive research with behavioral measures has been conducted, little is known about the electrophysiological mechanisms underlying this effect. The few previous studies carried out have led to contradictory results, supporting either episodic-retrieval or inhibition-based theoretical perspectives. In this study, we analyzed the ERP correlates of negative priming by using an experimental global context which, similar to the NP standard context, included Attended repetition trials. In addition, we presented relevant stimuli in separate blocks instead of the more usual randomized design. The NP effect can be biased by strategies adopted by participants when attended and ignored repetition trials are presented randomly. Specifically, we observed an enhanced N2 when a distractor from the previous trial became the target in the next trial. It is supposed that this finding reflects the involvement of additional attentional resources in the selection of a previously inhibited distractor as the new target stimuli.

Myocardial infarction and arterial thrombosis in severe (homozygous) FXII deficiency: no apparent causative relation.

Twenty-one patients (12 female and 9 male) with severe (homozygous) factor XII (FXII) deficiency and 58 (32 female and 26 male) with heterozygous FXII deficiency were observed for an average 16.2 years. No patient with homozygous FXII deficiency experienced myocardial infarction or any other arterial thrombosis. The same was true for heterozygotes. The cases of FXII deficiency and arterial thrombosis reported in the literature were evaluated. In every instance, associated risk factors were present that could justify the arterial thrombosis. Dyslipidemia, hypertension, smoking, and diabetes mellitus were the most frequent findings. The examination of the few papers that dealt with the prevalence of arterial thrombosis in patients with severe FXII deficiency showed that only 1 patient of 61 experienced myocardial infarction. In conclusion, it seems that the role of FXII deficiency in the pathogenesis of arterial thrombosis is minor.

Long term use of oral contraceptives without thrombosis in patients with FV Leiden polymorphism: a study of 37 patients (2 homozygous and 35 heterozygous).

It is commonly accepted that women on oral contraceptive therapy have about a four fold increased incidence of venous thrombosis in comparison to non users. Women with FV Leiden polymorphism have an even higher incidence. The purpose of the paper is to show that women with FV Leiden polymorphism may sometimes remain asymptomatic in spite of long-term use of oral contraceptives. We have studied and followed 37 women with this polymorphism (35 heterozygotes and 2 homozygotes) who remained asymptomatic even after a long use, occasionally up to 10-12 years of oral contraception. Furthermore, these women remained asymptomatic in spite of the fact that the majority of them took preparations containing third generation progestins (gestodene or desogestrel). These progestins are considered to be more thrombogenic as compared to older ones. Finally, several of these women became pregnant before, during interruptions or after the contraceptive therapy and remained also asymptomatic but for one patient with varicose veins who developed superficial phlebitis during one pregnancy. These data indicate that FV Leiden polymorphism, as far as oral contraceptive therapy is concerned, is not a very strong prothrombotic condition and probably does not represent an absolute contraindication to its use. Unfortunately so far there is no sure way to distinguish the women with this polymorphism who will develop venous thrombosis from those who will remain asymptomatic during oral contraceptive therapy.

Role of bile acids and metabolic activity of colonic bacteria in increased risk of colon cancer after cholecystectomy.

Since the metabolic activity of the colonic flora plays a definite role in colon cancer and an increased incidence of this disease is reported after cholecystectomy, we studied the metabolic activity of the colonic flora in a group of postcholecystectomy patients and matched controls by measuring, as representative end products of the bacterial metabolism, their fecal bile acids (BA), fecal 3-methylindole (SK) and indole (IN), and respiratory methane and hydrogen. Patients had significantly higher SK and lower IN, and, among BA, higher lithocholic (LCA) and chenodeoxycholic acid concentrations and LCA/deoxycholic acid ratio in the stools than controls. Similar differences from controls were reported for colon cancer. Comparable bacterial metabolic activities are thus operative in the large bowel of postcholecystectomized and colon cancer patients. This supports the biological plausibility of the association of cholecystectomy and colon cancer.

The effects of S(-) and R(+) sulpiride, metoclopramide, cisapride and domperidone on the small intestine suggest DA2-receptors are involved in the control of small intestinal transit time in rats.

To study the effect of intraperitoneal S(-)sulpiride (1-15 mg/kg), R(+)sulpiride (5-10 mg/kg), metoclopramide (1-15 mg/kg), cisapride (10 mg/kg) and domperidone (5-10 mg/kg) on intestinal progression, rats were given the test drug followed by oral lactulose. Their hydrogen excretion was used to calculate the small bowel transit time (SBTT) and maximum peak time (MPT). Metoclopramide (7.5 mg/kg) had the greatest effect on SBTT (-25%), followed by S(-)sulpiride and domperidone. S(-)sulpiride (10 mg/kg) had the greatest activity on the MPT (-35.2%) followed by metoclopramide. R(+)sulpiride and cisapride did not modify SBTT and MPT. In conclusion S(-)sulpiride is the isomer active on intestinal transit and DA2-receptors seem important targets in the modulation of intestinal progression, since S(-)sulpiride, metoclopramide and domperidone are DA2-receptor antagonists, and R(+)sulpiride and cisapride are not. The H2 breath test proved a valid method for measuring the effect of drugs on the small intestine in animals.

Indomethacin-induced enteropathy: effect of the drug regimen on intestinal permeability in rats.

To set up and characterize reproducible, long-standing small intestinal inflammation in rats, animals were given three different oral regimens of indomethacin (Ind): a bolus of 10 mg/kg in water and three daily doses of 2, 4, and 8 mg/kg Ind in (a) the drinking water or (b) the standard diet. The effect of Ind on the small intestine was monitored by measuring intestinal permeability (IP). The three-day regimen seemed more suitable than a bolus dose to induce long-standing inflammatory modifications in the rat small intestine and Ind administered in the drinking water gave more consistent modifications of IP and more reproducible results than Ind in food. IP seemed a suitable tool for detecting these inflammatory changes in the small-intestinal physiology. This model could be used to assess the effect of new drugs on inflammation.

Hemorheological study in patients with coronary artery disease.

Hemorheological parameters (viscosity of whole blood, plasma viscosity, hematocrit, velocity of red blood cells) were studied in 30 patients with coronary artery disease (15 patients with acute myocardial infarction, 15 patients with chronic angina), 14 subjects at high risk for ischemic heart disease and 14 normal volunteers matched for sex and age. Viscosity of whole blood was high in all coronary disease patients and in high-risk subjects as compared with controls. Velocity of red blood cells was significantly decreased in these patients. On the other hand, plasma viscosity and fibrinogen values were in the normal range in both groups and hematocrit was only slightly elevated in patients with angina. Furthermore, there were no changes in rheological parameters during the period of observation (1 week). We can suppose that the hyperviscosity is due, above all, to the decreased red blood cell deformability both in coronary disease patients but also in high-risk subjects. It is probable that red blood cell damage is present before the acute ischemic event, and that is a preexisting cause and not a consequence of it.

Variability of plasma viscosity in monoclonal IgM gammopathies.

Hyperviscosity syndromes can caused by both plasmatic and cellular factors. We have studied 20 patients affected by IgM gammopathy of different origin and 12 healthy subjects matched for sex and age, in order to evaluate the relation between paraprotein levels and plasma viscosity. We have observed a significant plasma viscosity increase only in 14 patients with monoclonal IgMk gammopathy. In the same patients was also evident an hyperviscosity syndrome. In the other 6 patients, with monoclonal IgM or polyclonal gammopathy and without clinical symptoms, plasma viscosity was only slightly increased. We have also observed a significant correlation between IgM and light chains (kappa, lambda) serum level and increased plasma viscosity. These results suggest that one can't consider all IgM gammopathies as cause of hyperviscosity syndrome.