Insights into image contrast from dislocations in ADF-STEM.

Competitive mechanisms contribute to image contrast from dislocations in annular dark-field scanning transmission electron microscopy (ADF-STEM). A clear theoretical understanding of the mechanisms underlying the ADF-STEM contrast is therefore essential for correct interpretation of dislocation images. This paper reports on a systematic study of the ADF-STEM contrast from dislocations in a GaN specimen, both experimentally and computationally. Systematic experimental ADF-STEM images of the edge-character dislocations reveal a number of characteristic contrast features that are shown to depend on both the angular detection range and specific position of the dislocation in the sample. A theoretical model based on electron channelling and Bloch-wave scattering theories, supported by numerical simulations based on Grillo's strain-channelling equation, is proposed to elucidate the physical origin of such complex contrast phenomena.

Myelin-oligodendrocyte-glycoprotein (MOG) autoantibodies as potential markers of severe optic neuritis and subclinical retinal axonal degeneration.

Antibodies against conformation-dependent epitopes of myelin-oligodendrocyte-glycoprotein (MOG-abs) are present in subgroups of neuromyelitis optica spectrum disorder (NMOSD), recurrent optic neuritis (rON), multiple sclerosis (MS), and anti-NMDAR encephalitis. Using optical coherence tomography (OCT) we assessed whether MOG-abs might serve as potential marker of retinal axonal degeneration. We investigated a clinically heterogeneous cohort of 13 MOG-abs-positive patients (4 MOG-abs-positive rON, 4 MOG-abs-positive adult MS, 3 MOG-abs-positive relapsing encephalomyelitis, 2 MOG-abs-positive aquaporin-4-abs-negative NMOSD). As controls, we studied 13 age, sex and ON episode(s)-matched MOG-abs and aquaporin-4-abs-negative (AQP4-abs-negative) MS patients and 13 healthy controls (HC). In addition, we investigated 19 unmatched AQP4-abs-positive MOG-abs-negative NMOSD subjects. Considering all eyes, global pRNFL [in µm, mean (SD)] was significantly reduced in MOG-abs-positive patients [72.56 (22.71)] compared to MOG-abs-negative MS [80.81 (13.55), p = 0.0128], HCs [103.54 (8.529), p = 0.0014] and NMOSD [88.32 (18.43), p = 0.0353]. Non ON eyes from MOG-abs-positive subjects showed significant subclinical atrophy of temporal pRNFL quadrants. Microcystic macular edema (MME) was observed only in eyes of MOG-abs-positive (24%) and AQP4-abs-positive NMOSD (5.6%), but not in MOG-abs-negative MS or HC (p < 0.01). MOG-abs may serve as potential marker of retinal degeneration. Specifically, MOG-abs-related OCT features predominate in temporal pRNFL quadrants (resembling the MS retinal pattern), might be more severe than AQP4-abs-positive NMOSD, indicate subclinical pathology, and may be associated with MME.

A light, nontoxic interleukin 12 protocol inhibits HER-2/neu mammary carcinogenesis in BALB/c transgenic mice with established hyperplasia.

With a slight asynchronous but consistent progression, all of the mammary glands of female BALB/c mice transgenic for the transforming rat HER-2/neu oncogene progress to atypical hyperplasia and to invasive carcinoma. Previous studies have shown that chronic administration of interleukin (IL) 12 started at the 2nd week of age hampers this progression because of its ability to inhibit tumor angiogenesis and activate a nonspecific immune response. Here we show that a similar inhibition is achieved when 7-week-old mice with fully blown atypical hyperplasia receive a weekly injection of 100 ng IL-12 for 16 times. This lower-dose and later IL-12 administration induces high and sustained levels of serum IFN-gamma equivalent to those elicited by more frequent administrations. A lower-dose and less toxic treatment may thus be envisaged as a possible option in the management of preneoplastic mammary lesions.

Contingent negative variation and schizophrenia: a long-term follow-up study.

The CNVs of three disorganized schizophrenics and three paranoid schizophrenics were studied longitudinally over a 5-year period. The CNV of the disorganized-type schizophrenics reached its maximum decrease within 3 years of disease onset. A more gradual and less accentuated decrease was noted in the paranoid group within a span of 5 years.

Brain slow potentials (CNV), prolactin, and schizophrenia.

This is a study of possible CNV correlations to schizophrenia. Three groups of schizophrenic patients were examined: 14 patients with an initial acute psychotic illness, before and after neuroleptic therapy; 9 subjects with chronic schizophrenia, who did not require continuous neuroleptic therapy; 18 patients with chronic schizophrenia under almost continuous neuroleptic therapy for many years. The results were compared with CNV parameters of a control group. On the basis of the results obtained, the authors advance the view that the different modes of manifestation of cerebral bioelectric reactivity (CNV) are independent of treatment and are related to the different stages of the evolution of the disorder.

A longitudinal CNV study in a group of five bipolar cyclothymic patients.

The authors carried out a longitudinal study in five subjects with bipolar cyclothymic psychosis, recording contingent negative variations in the same patients in the different phases of illness and under normal clinical conditions. An average voltage decrease was found in the depressive phases and a more conspicuous decrease in the manic phases. Furthermore, an evident postimperative negative variation was present in four subjects during the manic phase. The authors set forth tentative psychological and neurophysiological interpretation of their results.

Brain slow potentials and hypnosis.

Contingent negative variation behavior was studied in 12 voluntary normal subjects in basal conditions and in the hypnotic trance state under different emotional suggestions. A CNV voltage decrease and the appearance of a PINV were observed in the hypnotic state. Furthermore 12 nonhypnotizable control subjects were tested under the same experimental conditions and no CNV modification was found.

A one-year study on the pharmacodynamic profile of interferon-beta1a in MS.

Interferon (IFN)-beta1a induction of neopterin and beta2-microglobulin (beta2-MG) were evaluated over 1 year in patients with MS. Neopterin and beta2-MG levels peaked 24 to 48 hours after weekly injections of IFNbeta1a over the entire study period. Predose levels of neopterin decreased significantly, consistent with a long-term decrease in IFNgamma expression and macrophage activation during IFNbeta-1a treatment. Predose levels of beta2-MG increased, the significance of which is as yet unclear.

Correlation between morphological and functional retinal impairment in multiple sclerosis patients.

PURPOSE: To assess whether a correlation exists between optic nerve fiber layer (NFL) thickness and the retinal or visual pathway function in multiple sclerosis (MS) patients previously affected by optic neuritis. METHODS: Fourteen patients with a diagnosis of definite MS were examined. All had been affected by optic neuritis (MSON) with complete recovery of visual acuity (14 eyes included in study). These were compared with 14 eyes from 14 age-matched control subjects. NFL thickness was measured by optical coherence tomography (OCT). Three different measurements in each quadrant (superior, inferior, nasal, and temporal) were taken and averaged. The data in all quadrants (12 values averaged) were identified as NFL Overall, whereas the data obtained in the temporal quadrant only (3 values averaged) were identified as NFL Temporal. Retinal and visual pathway function was assessed by simultaneously recording pattern electroretinograms (PERGs) and visual evoked potentials (VEPs) using high-contrast (80%) checkerboard stimuli subtending 15 minutes and 60 minutes of the visual arc (min arc) and reversed at the rate of two reversals per second. RESULTS: In MSON eyes there was a significant (P < 0.01) reduction in NFL thickness in both NFL Overall and NFL Temporal evaluations compared with the values observed in control eyes. PERG, (15-min arc checks) and VEP (15-min arc and 60-min arc checks), showed a significant (P < 0.01) delay in latency and reduction in amplitude. NFL Overall and NFL Temporal values were significantly correlated (P < 0.01) to the PERG P50 latency and P50 to N95 amplitude recorded with 15-min arc checks. No correlations (P > 0.01) between NFL values and the other electrophysiological data (PERG recorded with 60-min arc checks and VEP recorded with 15-min arc and 60-min arc checks) were found. CONCLUSIONS: There is a correlation between PERG changes and NFL thickness in MS patients previously affected by optic neuritis, but there is no correlation between VEP changes and NFL thickness.

Electrophysiological study (VEP, BAEP) in HIV-1 seropositive patients with and without AIDS.

One hundred-twenty nine HIV-1 seropositive patients (39 females, 90 males) were studied by means of pattern visual evoked potential (VEP) and brainstem auditory evoked potential (BAEP) recording. Utilizing the criteria of the Centers for Disease Control the patients were clinically defined and then subdivided into four groups: group A included patients of category II (n:11); group B patients of category III (n:29); group C patients of category IVa and IVc2 (n:55) and group D patients belonging to the other subgroups of category IV (n:34). EP were altered in 26.35% of the entire group with a marked prevalence of BAEP alterations (21.7%) rather than of VEP (4.65%). A considerable amount of BAEP abnormalities (24.13%) were found in patients with persistent generalized lymphadenopathy (group B). A significant increase of BAEP mean interpeak latencies were observed in group B, C, D patients when compared with those of the control group. On the whole, EP were altered in 20.65% of the neurologically asymptomatic patients. EP alterations may precede any clinical manifestation and can be found during the earlier phases of HIV-1 infection.

Ultrasound as a possible screening method in ovarian cancer.

Ultrasound is a diagnostic method suitable for first level screening of ovarian cancer. The results in 4350 patients confirmed that ultrasound examination, both transabdominal and transvaginal, can be considered quite satisfactory because the sensibility was 100%.

Ultrastructural sperm abnormalities and cerebellar atrophy: does a correlation exist? Report of two cases without endocrine hypogonadism.

Spermiograms were performed in two young patients with cerebellar ataxia, one familial and the other sporadic. The subjects did not have endocrine abnormalities, but there was MRI evidence of cerebellar atrophy. Light and electron microscope examination revealed sperm abnormalities similar to those described in Purkinje cell degeneration (PCD). PCD is an autosomal recessive mutation observed only in the mouse, characterized by mild ataxia due to the postnatal degeneration of cerebellar Purkinje cells and male sterility due to morphological sperm abnormalities.

[Slow cerebral potentials after administration of flunitrazepam to subjects with sleep disorders]. / Potenziali lenti cerebrali dopo somministrazione di flunitrazepam a soggetti con disturbi del sonno.

12 patients admitted for neurological diseases and suffering from sleep disturbances, were given Flunitrazepam and placebo (double blind test) in a single evening dose of 1 and 2 mg. Morning recordings of the expectation wave according to G. Walter's technique did not reveal significant changes in wave morphology, amplitude and latency. The psychophysical conditions of patients and their reaction times did not differ after Flunitrazepam and placebo. The research shows, on the one hand the value of the electrophysiological investigation method and, on the other, the absence of residual effects in the morning after Flunitrazepam administration.

Riluzole in cerebellar ataxia: a randomized, double-blind, placebo-controlled pilot trial.

BACKGROUND: The pleiotropic effects of riluzole may antagonize common mechanisms underlying chronic cerebellar ataxia, a debilitating and untreatable consequence of various diseases. METHODS: In a randomized, double-blind, placebo-controlled pilot trial, 40 patients presenting with cerebellar ataxias of different etiologies were randomly assigned to riluzole (100 mg/day) or placebo for 8 weeks. The following outcome measures were compared: proportion of patients with a decrease of at least 5 points in the International Cooperative Ataxia Rating Scale (ICARS) total score after 4 and 8 weeks compared with the baseline score; mean changes from the baseline to posttreatment ICARS (total score and subscores at 8 weeks); and occurrence of adverse events. RESULTS: Riluzole and placebo groups did not differ in baseline characteristics. The number of patients with a 5-point ICARS drop was significantly higher in the riluzole group than in the placebo group after 4 weeks (9/19 vs 1/19; odds ratio [OR] = 16.2; 95% confidence interval [CI ] 1.8-147.1) and 8 weeks (13/19 vs 1/19; OR = 39.0; 95% CI 4.2-364.2). The mean change in the riluzole group ICARS after treatment revealed a decrease (p < 0.001) in the total score (-7.05 [4.96] vs 0.16 [2.65]) and major subscores (-2.11 [2.75] vs 0.68 [1.94] for static function, -4.11 [2.96] vs 0.37 [2.0] for kinetic function, and -0.74 [0.81] vs 0.05 [0.40] for dysarthria). Sporadic, mild adverse events occurred. CONCLUSIONS: These findings indicate the potential effectiveness of riluzole as symptomatic therapy in diverse forms of cerebellar ataxia. CLASSIFICATION OF EVIDENCE: This study provides Class I evidence that riluzole reduces, by at least 5 points, the ICARS score in patients with a wide range of disorders that cause cerebellar ataxia (risk difference 63.2%, 95% CI 33.5%-79.9%).