The Impact of the 1996 SSI Childhood Disability Reforms: Evidence from Matched SIPP-SSA Data

The Personal Responsibility and Work Opportunity Reconciliation Act of 1996 changed the definition of disability used to determine eligibility for disabled children under the Supplemental Security Income (SSI) program and made other changes in the program. The law required the redetermination of eligibility status for children potentially affected by the new definition of disability. As a result, an estimated 100,000 children were expected to lose SSI benefits. The goal of this paper is to understand the impact of benefit loss on affected children and their families. The analysis draws on data from the 1992, 1993 and 1996 panels of the Survey of Income and Program Participation matched with Social Security Administration records on SSI program participation. The data are used to analyze the impact of the loss of SSI income as a result of the 1996 legislation on family labor supply, welfare program participation, and income and poverty. Compared with families that lost SSI benefits due to normal attrition from the program, the excess benefit loss due to the 1996 childhood disability reforms is associated with lower levels of family labor supply, higher levels of participation in AFDC/TANF and food stamps, and lower levels of family income relative to poverty. For some outcomes, these effects—measured one month after benefit loss—persist for up to 12 months.

Characteristics and costs of individuals experiencing severe hypoglycaemia requiring emergency ambulance assistance in the community

Background and aims: Hypoglycaemia causes considerable a burden to individuals the healthcare providers. The aim of this study was to examine clinical characteristics of individuals requiring emergency medical assistance by ambulance services for an episode of severe hypoglycaemia and to estimate provider costs of hypoglycaemia. Materials and methods: Routinely collected information was retrieved for all episodes of severe hypoglycaemia attended to by the emergency ambulance services for a population of 367,051 people, including 75,603 people with diabetes, in Nottinghamshire and Derbyshire, UK, between 01/11/10 to 28/02/11. A total of 90,435 emergency calls were received in the study period, of which 523 (0.6%) were recorded as severe hypoglycaemia. The time to response, on-site treatment and hospitalisation were recorded along with standard clinical and blood glucose (BG) measures. Ambulance services costs were calculated. Results: The mean (SD) [proportion <= 3.2 mmol/L] pre and post-treatment BG levels were 1.9 (0.9) mmol/L [92%] and 6.5 (3.1) mmol/L [3%] respectively, 74% were under insulin treatment, 28% had nocturnal hypoglycaemia, and 153 (32%) individuals were transported to hospital. Lower pre-treatment BG (p<0.01) and Glasgow Coma Scale scores (p=0.05) were observed in insulin treated individuals in comparison to non-insulin treated individuals. No significant differences in individual characteristics were observed for other clinical measurements: post-treatment blood glucose (p=0.39), systolic blood pressure (p=0.28), diastolic blood pressure (p=0.64) and heart rate (p=0.93). Non insulin treatment was an independent predictor of transportation to hospital (p<0.01). Median time from allocation of call to departure of scene by ambulance services was 39 and 59 minutes for those transported and not transported to hospital respectively, translating to costs of £92 and £139 respectively. The median time from allocation to handing over patients to emergency staff was 75 minutes, equating to a cost of £176. Conclusion: The majority of cases of severe hypoglycaemia are successfully treated at the scene by the emergency ambulance services. Insulin treated and non insulin treated individuals do not differ by clinical characteristics, however non insulin treated individuals were more likely to be transported to hospital. Further studies are needed into the effect of prehospital ambulance care by treatment type on subsequent outcomes

Ultrastructural Distribution of the 7 Nicotinic Acetylcholine Receptor Subunit in Rat Hippocampus

Acetylcholine (ACh) is an important neurotransmitter in the mammalian brain; it is implicated in arousal, learning, and other cognitive functions. Recent studies indicate that nicotinic receptors contribute to these cholinergic effects, in addition to the established role of muscarinic receptors. In the hippocampus, where cholinergic involvement in learning and memory is particularly well documented, 7 nicotinic acetylcholine receptor subunits (7 nAChRs) are highly expressed, but their precise ultrastructural localization has not been determined. Here, we describe the results of immunogold labeling of serial ultrathin sections through stratum radiatum of area CA1 in the rat. Using both anti-7 nAChR immunolabeling and -bungarotoxin binding, we find that 7 nAChRs are present at nearly all synapses in CA1 stratum radiatum, with immunolabeling present at both presynaptic and postsynaptic elements. Morphological considerations and double immunolabeling indicate that GABAergic as well as glutamatergic synapses bear 7 nAChRs, at densities approaching those observed for glutamate receptors in CA1 stratum radiatum. Postsynaptically, 7 nAChRs often are distributed at dendritic spines in a perisynaptic annulus. In the postsynaptic cytoplasm, immunolabeling is associated with spine apparatus and other membranous structures, suggesting that 7 nAChRs may undergo dynamic regulation, with insertion into the synapse and subsequent internalization. The widespread and substantial expression of 7 nAChRs at synapses in the hippocampus is consistent with an important role in mediating and/or modulating synaptic transmission, plasticity, and neurodegeneration

The structure of classical extensions of quantum probability theory

On the basis of a suggestive definition of a classical extension of quantum mechanics in terms of statistical models, we prove that every such classical extension is essentially given by the so-called Misra–Bugajski reduction map. We consider how this map enables one to understand quantum mechanics as a reduced classical statistical theory on the projective Hilbert space as phase space and discuss features of the induced hidden-variable model. Moreover, some relevant technical results on the topology and Borel structure of the projective Hilbert space are reviewed

ZAC in GtoPdb v.2023.1

The zinc-activated channel (ZAC, nomenclature as agreed by the NC-IUPHAR Subcommittee for the Zinc Activated Channel) is a member of the Cys-loop family that includes the nicotinic ACh, 5-HT3, GABAA and strychnine-sensitive glycine receptors [2, 3, 5]. The channel is likely to exist as a homopentamer of 4TM subunits that form an intrinsic cation selective channel equipermeable to Na+, K+ and Cs+, but impermeable to Ca2+ and Mg2+ [5]. ZAC displays constitutive activity that can be blocked by tubocurarine, TTFB and high concentrations of Ca2+ [5]. Although denoted ZAC, the channel is more potently activated by H+ and Cu2+, with greater and lesser efficacy than Zn2+, respectively [5]. Orthologs of the human ZACN gene are present in a wide range of mammalian genomes, but notably not in the mouse or rat genomes. [2, 3]

ZAC in GtoPdb v.2021.3

The zinc-activated channel (ZAC, nomenclature as agreed by the NC-IUPHAR Subcommittee for the Zinc Activated Channel) is a member of the Cys-loop family that includes the nicotinic ACh, 5-HT3, GABAA and strychnine-sensitive glycine receptors [2, 3, 4]. The channel is likely to exist as a homopentamer of 4TM subunits that form an intrinsic cation selective channel equipermeable to Na+, K+ and Cs+, but impermeable to Ca2+ and Mg2+ [4]. ZAC displays constitutive activity that can be blocked by tubocurarine and high concentrations of Ca2+ [4]. Although denoted ZAC, the channel is more potently activated by H+ and Cu2+, with greater and lesser efficacy than Zn2+, respectively [4]. ZAC is present in the human, chimpanzee, dog, cow and opossum genomes, but is functionally absent from mouse, or rat, genomes [2, 3]

ZAC (version 2019.4) in the IUPHAR/BPS Guide to Pharmacology Database

The zinc-activated channel (ZAC, nomenclature as agreed by the NC-IUPHAR Subcommittee for the Zinc Activated Channel) is a member of the Cys-loop family that includes the nicotinic ACh, 5-HT3, GABAA and strychnine-sensitive glycine receptors [1, 2, 3]. The channel is likely to exist as a homopentamer of 4TM subunits that form an intrinsic cation selective channel equipermeable to Na+, K+ and Cs+, but impermeable to Ca2+ and Mg2+ [3]. ZAC displays constitutive activity that can be blocked by tubocurarine and high concentrations of Ca2+ [3]. Although denoted ZAC, the channel is more potently activated by protons and copper, with greater and lesser efficacy than zinc, respectively [3]. ZAC is present in the human, chimpanzee, dog, cow and opossum genomes, but is functionally absent from mouse, or rat, genomes [1, 2]