Association between background parenchymal enhancement and tumor response in patients with breast cancer receiving neoadjuvant chemotherapy.

PURPOSE: To analyze the relationships between background parenchymal enhancement (BPE) of the contralateral healthy breast and tumor response after neoadjuvant chemotherapy (NAC) in women with breast cancer. MATERIALS AND METHODS: A total of 228 women (mean age, 47.6 years±10 [SD]; range: 24-74 years) with invasive breast cancer who underwent NAC were included. All patients underwent breast magnetic resonance imaging (MRI) before and after NAC and 127 patients underwent MRI before, during (after the 4th cycle of NAC) and after NAC. Quantitative semi-automated analysis of BPE of the contralateral healthy breast was performed. Enhancement level on baseline MRI (baseline BPE) and MRI after chemotherapy (final BPE), change in enhancement rate between baseline MRI and final MRI (total BPE change) and between baseline MRI and midline MRI (early BPE change) were recorded. Associations between BPE and tumor response, menopausal status, tumor phenotype, NAC type and tumor stage at diagnosis were searched for. Pathologic complete response (pCR) was defined as the absence of residual invasive cancer cells in the breast and ipsilateral lymph nodes. RESULTS: No differences were found in baseline BPE, final BPE, early and total BPE changes between pCR and non-pCR groups. Early BPE change was higher in non-pCR group in patients with stages 3 and 4 breast cancers (P=0.019) and in human epidermal growth factor receptor 2 (HER2)-negative patients (P=0.020). CONCLUSION: Early reduction of BPE in the contralateral breast during NAC may be an early predictor of loss of tumor response, showing potential as an imaging biomarker of treatment response, especially in women with stages 3 or 4 breast cancers and in HER2 - negative breast cancers.

Effects of losartan on left ventricular mass: a three-year follow-up in elderly hypertensives with myocardial hypertrophy despite successful conventional antihypertensive treatment.

OBJECTIVE: Reversal of left ventricular hypertrophy (LVH) in hypertensive patients appears to be a desirable goal to the reduction cardiac risk. The Renin-Angiotensin System (RAS) seems to play a major role in the establishment and maintenance of LVH through the activated systemic RAS and the Intracardiac Angiotensin System (IAS). We focused on the effects of a three-year treatment with losartan supplement in hypertensive patients with LVH not responding to eight years of an effective previous antihypertensive pharmacological treatment. PATIENTS AND METHODS: Two groups of 28 sex-, age- and therapy-matched subjects with essential hypertension and LVH were taken into consideration. The two groups were in effective pharmacological treatment (BP < 140/90) for eight years previous to their enrollment. Patients of Group A were treated for three years with a losartan (100 mg/die) on-top treatment, whereas patients of Group B continued the follow-up of the previous conventional therapy. Both groups were submitted to an echocardiographic follow-up. RESULTS: Group A, showed a significant reduction of the mean LVH since the first step at six months with a further significant trend during the whole period (variance analysis: p < 0.001). Group B showed a non-significant trend toward LVH reduction during the three-year follow-up. No significant further reduction of systolic or diastolic blood pressure values was observed in both groups. CONCLUSIONS: The effects of losartan in hypertensive and hypertrophic patients are in agreement with the results of LIFE Trial. However, the reduction of left ventricular hypertrophy in our patients seems to be related to changes inducted by losartan on the IAS, since no further hemodynamic effects were observed. Losartan induced both a significant reduction of LVH and an improvement of LV diastolic function with a subsequent expected beneficial shift on the prognosis.

Increased cerebrospinal fluid and plasma levels of ultraweak chemiluminescence are associated with changes in the thiol pool and lipid-soluble fluorescence in multiple sclerosis: the pathogenic role of oxidative stress.

The pathogenesis of multiple sclerosis (MS), the major neurological disease of young adults in the western world, is still poorly understood and no effective therapy to block MS is yet available. It is generally accepted that reactive oxygen species have a major role in the mediation of cell damage and that free sulfhydryl groups are vital in cellular defense against endogenous or exogenous oxidants. Modification of the cellular oxidant/antioxidant balance has been involved in the neuropathogenesis of several diseases, e.g., stroke, Parkinson's disease, Alzheimer's disease and physiological aging. An increasingly important area of antioxidant defense is based on sulfhydryl chemistry, owing to the role of sulfhydryl groups in the function of macromolecular structures such as enzymes and cellular membranes. The chemical composition of human cerebrospinal fluid (CSF) is considered to reflect brain metabolism and in the present study we provided experimental evidence of a decrease in sulfhydryl groups and increased content of products of lipid peroxidation, such as ultraweak chemiluminescence and liposoluble fluorescence, which we found higher in the CSF and plasma of MS patients than in controls, pointing out the role of oxidative stress in the pathogenesis of MS.

[Cerebrovascular accidents. II. Neurologic bases and therapeutic aspects of neurorehabilitation]. / Ictus vascolare cerebrale. Parte II--Basi neurologiche e aspetti terapeutici nel trattamento neuroriabilitativo.

The correct treatment of patients with cerebrovascular accident should be established after understanding the phenomena that affect the cerebral tissue from the beginning of the stroke up to its healing. The cerebral edema pathophysiology, the role played by glutamate and calcium in the brain toxicity, and by neurotrophic factors and neuroplasticity in recovery, are treated. Moreover, changes in mood after a stroke, are related to the side of the lesion. A comment on the different techniques of rehabilitation as part of treatment of patient with brain injury, is given.

Changes in sleep spindle activity of subject with chronic somatosensitive and sensorial deficits. Preliminary results.

We investigated the effects of the somatosensitive and sensory afferent inputs on the thalamic generators of sleep spindles (SS) in adult subjects affected by posterior funiculi lesions (five subjects), deafness (four subjects) or blindness (four subjects). The density, duration and frequency of SS, as well as the index of spindling, were analyzed during stage 2 NREM. The results show that the subjects with somatosensitive and sensorial lesions spent much more time on SS activity than the control group (eight subjects), and had a significantly increased density (< .0001), duration (< .0005) and index of spindling (< .0001). On the other hand, the frequency of spindling was little modified (< .05). Moreover, among the three groups of patients, those with somatosensitive deficits showed the greatest SS activity. In conclusion, our results suggest that the thalamic generators of SS are markedly modulated by peripheral inputs in man.

On a rare atypical form of metachromatic leukodystrophy (MLD): "neurological non-mld patients with low levels of arylsulphatase A". Description of two cases.

Two young patients (a brother and his sister) with low ASA levels who had myoclonic seizures since the age of eight years, were investigated by means of electrophysiological, neuroradiological and laboratory tests and submitted to a physical examination. In both patients, the disease started at the age of eight years with drug resistent myoclonic seizures. Intelligence was not impaired and ASA levels were lower than normal, but clinical features were not those of classic MLD. Electrophysiological study revealed altered SEPs and normal BAEPs (they are both altered in leukodystrophy). Therefore our findings conclude that tour patients must be considered "Neurological patients non-MLD with low levels of ASA".

Spindle and EEG sleep alterations in subjects affected by cortical cerebellar atrophy.

All-night polygraphic records (EEG, EOG and ECG) were performed on 9 subjects. Four of them were affected by Familiar Cerebellar Atrophy (FCA) whereas the others were their blood relatives without clinical signs of cerebellar deficit. In the former FCA was diagnosed clinically and the cerebellar atrophy was confirmed by computer tomography (CT). In all the latter except one who showed slight cerebellar atrophy, the CTs were negative. The EEG sleep records of the FCA patients were characterized by slowly changing phases between synchronized and desynchronized sleep, instability of the synchronized sleep with frequent modifications of EEG activity, subnormal measurement of both REM and slow-wave sleep and presence of spindles in REM sleep (only in 2 patients). The spindle activity was reduced in two FCA subjects. The electroencephalographic sleep records of two BRs, one of which with small cerebellar atrophy, showed qualitative and quantitative alterations similar to those of FCA patients, even if marked to a lesser degree. Increased spindle densities were present in the same BRs who showed sleep abnormalities. The EEG alterations observed in the two BR subjects could show small cerebellar injuries which would be insufficient to induce clinical signs.

[Electroencephalographic characteristics of sleep in subjects with paleo and neocerebellar lesions]. / Caratteristiche elettroencefalografiche del sonno in soggetti con lesione paleo e neocerebellare.

The research was performed in order to study: 1) paleo and neocerebellar contributions in the sleep organization and 2) the electrical sleep activities at different time intervals during the functional compensation which follows the cerebellar lesion. Polygraphic sleep records (EEG, EMG, EOG) were performed on four subjects with surgical lesions more than 6 months old in cerebellar cortex (two subjects in paleo and two in neocerebellum). Another subject was studied before a surgical paleocerebellar lesion and at different time intervals after that (8th, 30th, 60th, and 90th day). Paleo and neocerebellar lesions showed different sleep abnormalities. The former induced both quantitative and qualitative alterations in the cyclic sleep organization, the latter did not show significant alterations in this organization but rather in transition between sleeping and waking and in sleep maintenance. The acute paleocerebellar lesion showed at the 8th and 30th day a strong reduction of the synchronized sleep (SS) and an increase of the desynchronized one (DS). In the successive records, 30th and 90th day, the SS/DS ratio increased to the values observed in the chronic paleocerebellar lesioned subjects.

[Spindle activity during sleep in subjects with a deficit in pallesthetic sensibility]. / Studio dell'attivita' spindle durante il sonno di soggetti con deficit della sensibilita' pallestesica.

Sleep spindle activity was studied on four subjects affected by pallesthesic deficit due to injury the posterior funiculi of the cord. The spindle activity was studied as density (number of spindles min.), duration and percent of sleep time utilized in spindle activity. The polygraph sleep records included EOG, EMG and 6 monopolar EEG recordings, 3 for each side, on the frontal, parietal and occipital regions. The records showed a spindle activity which was similar in different subjects and that was significantly higher than the physiological values. In fact, the spindle density was about 250%, the duration was about 130% and the spindle percent was about 280%, with respect to the physiological values assumed to be 100%.

[Electroencephalographic changes during nocturnal sleep in subjects with familial cortico-cerebellar atrophy]. / Alterazioni elettroencefalografiche del sonno notturno in soggetti con atrofia cortico-cerebellare familiare.

The purpose of this research was to analyze the qualitative and quantitative EEG sleep alterations in four subjects affected by familiar cerebellar atrophy and in their blood relations, who were clinically healthy. Polygraphic sleep registrations (including EEG, EOG, EMG, ECG and except in two cases, EPG), computerized cranial tomography and clinical evaluation were carried out in all subjects. The EEG sleep records of subjects afflicted by cerebellar atrophy showed quantitative alterations, namely reductions of IV phase and REM, with an increase of the intermediary phase between synchronized and desynchronized sleep. The qualitative characteristic were: slow and recurrent changing phases, instable periods of sleep with frequent fragmentations, numerous arousals, intermediary phases corresponding to the II studies of Barros-Ferreira and in only two cases, presence of spindle activity during REM sleep. Two blood relations showed EEG sleep alterations similar to the atrophy subjects. According to the common genotype and similar EEG sleep abnormalities, we suggest that the latter, in these two subjects, may be produced by small cerebellar lesions, which are insufficient for a clear clinical symptomatology.