Performance and Reliability Analysis of Cross-Layer Optimizations of NAND Flash Controllers

NAND flash memories are becoming the predominant technology in the implementation of mass storage systems for both embedded and high-performance applications. However, when considering data and code storage in non-volatile memories (NVMs), such as NAND flash memories, reliability and performance be- come a serious concern for systems' designer. Designing NAND flash based systems based on worst-case scenarios leads to waste of resources in terms of performance, power consumption, and storage capacity. This is clearly in contrast with the request for run-time reconfigurability, adaptivity, and resource optimiza- tion in nowadays computing systems. There is a clear trend toward supporting differentiated access modes in flash memory controllers, each one setting a differentiated trade-off point in the performance-reliability optimization space. This is supported by the possibility of tuning the NAND flash memory performance, reli- ability and power consumption acting on several tuning knobs such as the flash programming algorithm and the flash error correcting code. However, to successfully exploit these degrees of freedom, it is mandatory to clearly understand the effect the combined tuning of these parameters have on the full NVM sub-system. This paper performs a comprehensive quantitative analysis of the benefits provided by the run-time reconfigurability of an MLC NAND flash controller through the combined effect of an adaptable memory programming circuitry coupled with run-time adaptation of the ECC correction capability. The full non- volatile memory (NVM) sub-system is taken into account, starting from the characterization of the low level circuitry to the effect of the adaptation on a wide set of realistic benchmarks in order to provide the readers a clear figure of the benefit this combined adaptation would provide at the system leve

MM2-thalamic Creutzfeldt-Jakob disease-Neuropathological, biochemical and transmission studies identify a distinctive prion strain

In Creutzfeldt-Jakob disease (CJD), molecular typing based on the size of the protease resistant core of the disease-associated prion protein (PrP(Sc) ) and the M/V polymorphism at codon 129 of the PRNP gene correlates with the clinico-pathologic subtypes. Approximately 95% of the sporadic 129MM CJD patients are characterized by cerebral deposition of type 1 PrP(Sc) and correspond to the classic clinical CJD phenotype. The rare 129MM CJD patients with type 2 PrP(Sc) are further subdivided in a cortical and a thalamic form also indicated as sporadic fatal insomnia. We observed two young patients with MM2-thalamic CJD. Main neuropathological features were diffuse, synaptic PrP immunoreactivity in the cerebral cortex and severe neuronal loss and gliosis in the thalamus and olivary nucleus. Western blot analysis showed the presence of type 2A PrP(Sc) . Challenge of transgenic mice expressing 129MM human PrP showed that MM2-thalamic sporadic CJD (sCJD) was able to transmit the disease, at variance with MM2-cortical sCJD. The affected mice showed deposition of type 2A PrP(Sc) , a scenario that is unprecedented in this mouse line. These data indicate that MM2-thalamic sCJD is caused by a prion strain distinct from the other sCJD subtypes including the MM2-cortical form

Su un caso di infrequente lesione del nervo sciatico da colpo d’arma da fuoco

Dopo una breve rassegna dei diversi meccanismi etiopatogenetici delle lesioni d’arma da fuoco dei nervi periferici gli AA. Descrivono un caso di lesione poco frequente del nervo sciatico popliteo esterno e dei suoi due rami terminali da ferita transfossa alla gamba. Le strutture nervose, pur non interessate direttamente del proiettile, furono inglobate e quindi lese funzionalmente da briglie cicatriziali a partenza dal tramite. La lesione fu irreversibile nonostante il trattamento chirurgico attuato e diede luogo nella valutazione penale del danno ad un giudizio di indebolimento permanente dell’organo della deambulazione

Amitriptyline in the treatment of headache in patients with Parkinson's disease: a double-blind placebo-controlled study.

We evaluated the effect of 25 mg bid amitriptyline on muscle contraction headache in 36 patients with Parkinson's disease in a randomized double-blind placebo-controlled study. Treatment lasted 12 weeks, and we assessed the efficacy by number of days with headache, sum-of-severity score (intensity X number of days with headache), and consumption of analgesics. We also administered Hoehn-Yahr staging, the Webster Rating Scale, the Mini-Mental State, and the Zung Self-Rating Depression Scale. We assessed the patients after a 4-week run-in period and after 4, 8, and 12 weeks of treatment. Thirty-one patients (15 in the amitriptyline group and 16 in the placebo group) completed the trial. Amitriptyline reduced the intensity and the frequency of headache, whereas the placebo did not. The Zung Depression Scale and the Webster Rating Scale findings remained unchanged

No effect of acetylsalicylic acid on B-thromboglobulin and platelet factor 4 plasma levels in patients with transient ischaemic attacks.

We studied the effect of acetylsalicylic acid (ASA) versus placebo on B-thromboglobulin (B-TG) and platelet factor 4 (PF4) plasma levels and ADP-induced platelet aggregation in 25 male patients with transient ischaemic attacks (TIA). The patients were allocated randomly to two groups: 14 patients received oral treatment with ASA 500 mg b.i.d. for 14 days, 11 patients placebo b.i.d. for the same period. B-TG and PF4 plasma levels and ADP-induced platelet aggregation were determined in basal conditions, and two hours, and seven and fourteen days after starting with ASA or placebo. In addition, the same parameters were studied in a group of 20 healthy males of matched age. Basal levels of plasma B-TG and PF4 and the maximal amplitude of ADP-induced platelet aggregation were abnormally high in TIA patients. ASA caused a significant reduction of B-TG plasma levels in TIA patients 2 hours after the first administration, but no effect was observed at the 7th and 14th day of treatment. PF4 plasma levels were unaffected by ASA treatment. It is concluded that ASA, at the dose conventionally used in clinical trials, does not affect the release of two alpha-granule proteins