The strong self-damped Lyman α absorption systems present in the spectra of high redshift QSOs represent a unique population of absorber which has recently been associated with the precursors of current disk galaxies. In a low resolution survey for what we have come to call “Lyman α disk systems” performed at Lick Observatory (Wolfe, et al. 1986, Ap. J. Suppl. 61, 249) approximately 18 systems with confirmed damped Lyman α profiles and rest frame equivalent widths greater than 5 Å were detected in a sample of 68 high redshift QSOs (Smith, Cohen and Bradley 1986, Ap. J. 310, 583). Subsequent higher resolution study has shown these systems to have the following properties (Turnshek, et al. 1988, Ap. J., in press):

1. 1.Neutral hydrogen column densities, 2 × 1020 ≤ NHI ≤ 8 × 1021 cm−2.
2. 2.Low-mixed ionization state. Typically the low ionization states dominate the high ionization states (e.g. CII ≫ CIV). Some enrichment has occurred, −2≲[X/H]⊙ ≲0.
3. 3.Gas density, n ≲ 1 cm−3.
4. 4.The gas shows two components, a quiescent (disk) component, σν ≲ 10 km s−1, and a turbulent (halo) component, σν ≲ 20 km s−1. Some systems show only the low velocity dispersion component.
5. 5.At least one system intervening toward a radio QSO (Pks 0458-020) shows 21-cm absorption. The system shows multiple cloud structure with σν ≈ 6 km s−1, Ts ≈ 100 K, and structure extended over several kpc on the sky.
6. 6.There is evidence that these systems may be self gravitating with scale height of the order of 300 pc.
7. 7.These systems represent a unique population of absorber (distinct from the ‘Lyman a forest’ and heavy element systems) covering approximately 20% of the sky to z ≈ 3 and accounting for all of the baryonic matter at that redshift.

Benzodiazepines are widely prescribed to manage sleep disorders, anxiety and muscular tension. While providing short-term relief, continued use induces tolerance and withdrawal, and in older users, increases the risk of falls. However, long-term prescription remains common, and effective interventions are not widely available. This study developed a self-managed cognitive behaviour therapy package for cessation of benzodiazepine use delivered to participants via mail (M-CBT) and trialled its effectiveness as an adjunct to a general practitioner (GP)-managed dose reduction schedule. In the pilot trial, participants were randomly assigned to GP management with immediate or delayed M-CBT. Significant recruitment and engagement problems were experienced, and only three participants were allocated to each condition. After immediate M-CBT, two participants ceased use, while none receiving delayed treatment reduced daily intake by more than 50%. Across the sample, doses at 12 months remained significantly lower than baseline, and qualitative feedback from participants was positive. While M-CBT may have promise, improved engagement of GPs and participants is needed for this approach to substantially impact on community-wide benzodiazepine use.

We have used thermal desorption spectroscopy to carry out a comparative study of potassium adsorption on Al(111) and on the fivefold Al-Pd-Mn surface. Potassium adsorption on the quasicrystal was found to be different than on Al(111). The potassium monolayer desorbed from fivefold Al-Pd-Mn at lower temperatures than from Al(111). Potassium is known to form a dense monolayer on Al(111), with an ideal coverage of 0.33, but for the monolayer on fivefold Al Pd Mn we find that the saturation coverage is only one twelfth.

The cognitive profile of early onset Parkinson’s disease (EOPD) has not been clearly defined. Mutations in the parkin gene are the most common genetic risk factor for EOPD and may offer information about the neuropsychological pattern of performance in both symptomatic and asymptomatic mutation carriers. EOPD probands and their first-degree relatives who did not have Parkinson’s disease (PD) were genotyped for mutations in the parkin gene and administered a comprehensive neuropsychological battery. Performance was compared between EOPD probands with (N = 43) and without (N = 52) parkin mutations. The same neuropsychological battery was administered to 217 first-degree relatives to assess neuropsychological function in individuals who carry parkin mutations but do not have PD. No significant differences in neuropsychological test performance were found between parkin carrier and noncarrier probands. Performance also did not differ between EOPD noncarriers and carrier subgroups (i.e., heterozygotes, compound heterozygotes/homozygotes). Similarly, no differences were found among unaffected family members across genotypes. Mean neuropsychological test performance was within normal range in all probands and relatives. Carriers of parkin mutations, whether or not they have PD, do not perform differently on neuropsychological measures as compared to noncarriers. The cognitive functioning of parkin carriers over time warrants further study. (JINS, 2011, 17, 1–10)

A 60-year-old patient with a clinical diagnosis of schizophrenia underwent a magnetic resonance imaging (MRI) scan related to the evaluation of isolated seizures that emerged while medicated with clozapine. Unexpectedly, the MRI scan revealed evidence of asymmetric and enlarged cerebral ventricles that were interpreted as congenital in origin. The presence of both congenital lateral ventricular asymmetry and ventriculomegaly may interact to increase risk of schizophrenia. The history and clinical features, including cognitive testing, of the illustrative patient are presented.

Williams syndrome is a neurodevelopmental disorder that results from the deletion of ~25-30 genes spanning about 1.5 megabases in the q11.23 region of chromosome 7. Patients with this syndrome present with a combination of a distinctive elfin-like facial appearance; growth retardation; mild mental retardation; an inconsistent cognitive profile that includes visuospatial impairments with good facial discrimination and relatively preserved expressive language skills; and cardiovascular abnormalities. In addition, a striking behavioral feature of the syndrome is the high sociability and empathy that these patients show for others. The study of patients with “partial” deletions of the chromosome band 7q11.23, mutated genes in this region and knockout mice with deletions of specific genes in the homologous G1–G2 region of mouse chromosome 5 are clarifying some genotype/phenotype relationships. Futhermore, genes located in this region that are prominently expressed have been implicated in brain development and function.The neuropsychological profile of patients with Williams syndrome is heterogeneous, highlights important dissociations between cognitive functions and suggests that the behavioral dimensions of sociability, empathy, engageability, and talkativeness may be independent of, or not easily explained by, the cognitive deficits. Williams syndrome has enormous heuristic value because its pathological feature of heightened “sociability” can be a “deficit” symptom of major complex neuropsychiatrie disorders, such as schizophrenia and autism. Data consistent with a core inability of patients with Williams syndrome to inhibit social approach suggest that this disorder may afford an opportunity to study the biological basis of the “drive” toward socialization. From a research perspective, the syndrome lends itself to neurobiological studies of sociability as a dimension that varies independently of cognition (or at least many separable cognitive processes). Importantly, from a clinical perspective, the syndrome challenges us to administer strategic psychosocial interventions that take advantage of the opportunities that “pathological” sociability provide, while avoiding its threats. An illustrative example of an effective strategically planned psychosocial intervention for a patient with Williams syndrome is briefly presented.