Node Synchronization for the Viterbi Decoder

Motivated by the needs of NASA's Voyager 2 mission, in this paper we describe an algorithm which detects and corrects losses of node synchronization in convolutionally encoded data. This algorithm, which would be implemented as a hardware device external to a Viterbi decoder, makes statistical decisions about node synch based on the hard-quantized undecoded data stream. We will show that in a worst-case Voyager environment, our method will detect and correct a true loss of synch (thought to be a very rare event) within several hundred bits; many of the resulting outages will be corrected by the outer Reed-Solomon code. At the same time, the mean time between false alarms is on the order of several years, independent of the signal-to-noise ratio.     

Differential effects on body weight of central 6-hydroxydopamine lesions in obese (ob/ob) and diabetes (db/db) mice.

Obese (ob/ob) and diabetes (db/db) mice are genetic mutants that have been shown to have altered levels of central catecholamines (CAs) as well as syndromes of obesity, hyperphagia, and hyperglycemia. Because the CAs, and particularly norepinephrine (NE), are implicated in the control of feeding, levels of central CAs were experimentally reduced in ob/ob and db/db mice to investigate the role of CAs in these cases of spontaneously occurring obesity. Lesions produced by 6-hydroxydopamine (6-OHDA) were used to produce large depletions of NE and dopamine (DA) in both ob/ob and db/db mice and in lean control Ss of the same background strains. In the db/db but not the ob/ob, central CA depletion was accompanied by a significant and persistent weight loss and by a reduction in plasma glucose levels when compared with vehicle-infused controls. Treatment with the NE uptake blocker desipramine (DI) prior to 6-OHDA infusions attenuated NE but not DA depletion. Diabetes Ss that received DI pretreatment showed a weight loss and decrease in plasma glucose proportional to the amount of NE depletion. Lean Ss that received the 6-OHDA treatments showed only a transient weight loss and no significant change in blood glucose. Abnormalities in central noradrenergic systems may account for part of the obesity syndrome in the diabetes mouse. (29 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Sequential Change-Point Detection Procedures That are Nearly Optimal and Computationally Simple

Abstract

Sequential schemes for detecting a change in distribution often require that all of the observations be stored in memory. Lai (1995 Lai , T. L. ( 1995 ). Sequential Changepoint Detection in Quality Control and Dynamical Systems , Journal of Royal Statistical Society, Series B 57 : 613 – 658 . [Google Scholar], Journal of Royal Statistical Society, Series B 57: 613–658) proposed a class of detection schemes that enable one to retain a finite window of the most recent observations, yet promise first-order optimality. The asymptotics are such that the window size is asymptotically unbounded. We argue that what's of computational importance isn't having a finite window of observations, but rather making do with a finite number of registers. We illustrate in the context of detecting a change in the parameter of an exponential family that one can achieve eventually even second-order asymptotic optimality through using only three registers for storing information of the past. We propose a very simple procedure, and show by simulation that it is highly efficient for typical applications.     

Behavioral and neurochemical effects of neonatal administration of monosodium {l}-glutamate in mice.

Studied the feeding behavior, activity level, and thermoregulatory ability of 117 CL-1 mice made obese by neonatal administration of monosodium {l}-glutamate (MSG). The degree of obesity and other characteristics of the syndrome depended on age, diet, and housing condition. Carcass fat determinations demonstrated the presence of obesity in all MSG Ss; however, body weight was elevated over control levels only in adult mice caged in groups. Group-housed MSG Ss also failed to increase food intake in response to food deprivation and were both hypoactive and hypothermic. Individually caged MSG Ss showed normal activity levels and body temperature, an attenuated response to food deprivation, and an enhanced response to a high-fat diet. Since MSG obesity may be the consequence of damage to the dopamine-rich arcuate nucleus of the hypothalamus, a 2nd goal was to measure central catecholamines and examine any changes in the MSG S's behavioral responses to catecholaminergic drugs. Ss treated with MSG sustained some loss of hypothalamic dopamine, but no systematic relation between central catecholamines and behavioral aspects of the syndrome could be discerned. (46 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Single-unit activity of cerebellar nuclear cells in the awake genetically dystonic rat

We have established a cell culture system that reproduces morphogenic processes in the developing mammary gland. EpH4 mouse mammary epithelial cells cultured in matrigel form branched tubules in the presence of hepatocyte growth factor/scatter factor (HGF/SF), the ligand of the c-met tyrosine kinase receptor. In contrast, alveolar structures are formed in the presence of neuregulin, a ligand of c-erbB tyrosine kinase receptors. These distinct morphogenic responses can also be observed with selected human mammary carcinoma tissue in explant culture. HGF/SF-induced branching was abrogated by the PI3 kinase inhibitors wortmannin and LY294002. In contrast, neuregulin- induced alveolar morphogenesis was inhibited by the MAPK kinase inhibitor PD98059. The c-met-mediated response could also be evoked by transfection of a c-met specific substrate, Gab1, which can activate the PI3 kinase pathway. An activated hybrid receptor that contained the intracellular domain of c-erbB2 receptor suffices to induce alveolar morphogenesis, and was observed in the presence of tyrosine residues Y1028, Y1144, Y1201, and Y1226/27 in the substrate-binding domain of c-erbB2. Our data demonstrate that c-met and c-erbB2 signaling elicit distinct morphogenic programs in mammary epithelial cells: formation of branched tubules relies on a pathway involving PI3 kinase, whereas alveolar morphogenesis requires MAPK kinase.     

Differential expression of glutamate decarboxylase messenger RNA in cerebellar Purkinje cells and deep cerebellar nuclei of the genetically dystonic rat

The genetically dystonic rat exhibits a motor syndrome that closely resembles the human disease, generalized idiopathic dystonia. Although in humans dystonia is often the result of pathology in the basal ganglia, previous studies have revealed electrophysiological abnormalities and alterations in glutamate decarboxylase, the synthetic enzyme for GABA, in the cerebellum of dystonic rats. In this study, we further characterized the alterations in cerebellar GABAergic transmission in these mutants by examining the expression of the messenger RNA encoding glutamate decarboxylase (67000 mol. wt) with in situ hybridization histochemistry at the single cell level in Purkinje cells and neurons of the deep cerebellar nuclei. Glutamate decarboxylase (67000 mol. wt) messenger RNA levels were increased in the Purkinje cells and decreased in the deep cerebellar nuclei of dystonic rats compared to control littermates, suggesting opposite changes in GABAergic transmission in Purkinje cells and in their target neurons in the deep cerebellar nuclei. In contrast, levels of glutamate decarboxylase (67000 mol. wt) messenger RNA in the pallidum, and of enkephalin messenger RNA in the striatum, were unaffected in dystonic rats. The data indicate that both the Purkinje cells and GABAergic neurons of the deep cerebellar nuclei are the site of significant functional abnormality in the dystonic rat.     

Central noradrenergic neurons: Differential effects on body weight of electrolytic and 6-hydroxydopamine lesions in rats.

Compared the effects of bilateral electrolytic and 6-hydroxydopamine (6-OHDA) lesions of the ventral noradrenergic bundle (VB) in 2 experiments with a total of 67 female albino rats. When Ss were fed only a standard laboratory diet, no significant differences were found between groups. When a high-fat diet supplement was introduced, the group with electrolytic lesions became significantly heavier than the control group; however, the 6-OHDA group did not differ from the controls. Norepinephrine depletion was significantly greater following the 6-OHDA than the electrolytic lesions. Both lesions reduced telencephalic dopamine and serotonin only slightly. Exp II, in which both types of lesions were placed at a rostral ventromedial hypothalamic site, yielded the same pattern of results. Diet-dependent increased in body weight were attributed to the destruction of a non-noradrenergic system, which was spared by the relatively selective 6-OHDA lesion but damaged by the nonselective electrolytic lesion. (39 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Feeding, activity, and body temperature following 6-hydroxydopamine lesions in diabetes (db/db) mice.

Reductions in central catecholamines produced by intraventricular injections of 6-hydroxydopamine (6-OHDA) cause weight loss and decreased plasma glucose in diabetes (db/db) mice. The present study examined the effects of this treatment in short-term (64-day) and long-term (120-day) survival groups of female diabetes (C57 BL/KsJ-db/db) and lean mice. Phenotypically heterozygotes (db/m) and homozygotes (m/m) were used as controls. Diabetes Ss treated with 6-OHDA decreased food intake, lost weight, and maintained a lower weight than vehicle-treated controls until vehicle-treated Ss began to enter the terminal stages of the syndrome, indicated by a loss of body weight. Diabetes Ss given 6-OHDA lost weight despite reduced body temperatures and activity levels. Blood glucose levels were always lower in 6-OHDA than in ad lib fed vehicle-treated db/db Ss. The 6-OHDA treatment also improved pancreatic islet granulation. Pair feeding vehicle-treated with 6-OHDA-treated db/db Ss did not halt weight gain in the vehicle-treated group. However, measurement of carcass fat indicated similar losses in db/db-6-OHDA Ss and vehicle-treated Ss when the vehicle group was pair-fed with lean controls. Treatment with 6-OHDA produced long-term improvement in the diabetes syndrome, but the decreased body weight of the 6-OHDA-treated diabetes Ss could not be completely accounted for by changes in food intake or energy expenditure. (43 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Effects of lesions of the gustatory neocortex on taste aversion learning in the rat.

In 5 experiments, 110 normal male Long-Evans hooded rats and 125 Ss with lesions of the gustatory neocortex (GN) were compared for their ability to learn aversions to taste cues paired with toxicosis. When the taste presentation was followed immediately by toxicosis, normal Ss and 8 Ss with lesions of the posterior (visual) neocortex learned aversions to sucrose, sodium chloride, quinine hydrochloride, and hydrochloric acid solutions. Ss with GN lesions learned aversions to all solutions except sucrose. In preference tests, all solutions were shown to be discriminable from water by both normal and GN-lesioned Ss. Under conditions in which a 6-hr delay separated taste presentation and toxicosis, normals again learned specific aversions to all 4 solutions, but Ss with GN lesions failed to learn specific aversions to sucrose, sodium chloride, and hydrochloric acid solutions. It was shown that the ability of Ss with GN lesions to learn aversions to sucrose and quinine depended on stimulus concentration. It is proposed that the data can be accounted for by postulating a change in the threshold for taste illness associations following GN lesions. (30 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)