Encoding databases satisfying a given set of dependencies

Consider a relation schema with a set of dependency constraints. A fundamental question is what is the minimum space where the possible instances of the schema can be "stored". We study the following model. Encode the instances by giving a function which maps the set of possible instances into the set of words of a given length over the binary alphabet in a decodable way. The problem is to find the minimum length needed. This minimum is called the information content of the database. We investigate several cases where the set of dependency constraints consist of relatively simple sets of functional or multivalued dependencies. We also consider the following natural extension. Is it possible to encode the instances such a way that small changes in the instance cause a small change in the code. © 2012 Springer-Verlag

U.S. State Policy Contexts and Physical Health among Midlife Adults

This study examines how state policy contexts may have contributed to unfavorable adult health in recent decades. It merges individual-level data from the 1993–2016 Behavioral Risk Factor Surveillance System (n=2,166,835) with 15 state-level policy domains measured annually on a conservative to liberal continuum. We examined associations between policy domains and health among adults ages 45–64 years and assess how much of the associations is accounted by adults’ socioeconomic, behavioral/lifestyle, and family factors. A more liberal version of the civil rights domain was associated with better health. It was disproportionately important for less-educated adults and women, and its association with adult health was partly accounted by educational attainment, employment, and income. Environment, gun safety, and marijuana policy domains were, to a lesser degree, predictors of health in some model specifications. In sum, health improvements require a greater focus on macro-level factors that shape the conditions in which people live

Mechanisms by which statins protect endothelial cells from radiation-induced injury in the carotid artery

BackgroundThe incidental use of statins during radiation therapy has been associated with a reduced long-term risk of developing atherosclerotic cardiovascular disease. However, the mechanisms by which statins protect the vasculature from irradiation injury remain poorly understood.ObjectivesIdentify the mechanisms by which the hydrophilic and lipophilic statins pravastatin and atorvastatin preserve endothelial function after irradiation.MethodsCultured human coronary and umbilical vein endothelial cells irradiated with 4 Gy and mice subjected to 12 Gy head-and-neck irradiation were pretreated with statins and tested for endothelial dysfunction, nitric oxide production, oxidative stress, and various mitochondrial phenotypes at 24 and 240 h after irradiation.ResultsBoth pravastatin (hydrophilic) and atorvastatin (lipophilic) were sufficient to prevent the loss of endothelium-dependent relaxation of arteries after head-and-neck irradiation, preserve the production of nitric oxide by endothelial cells, and suppress the cytosolic reactive oxidative stress associated with irradiation. However, only pravastatin inhibited irradiation-induced production of mitochondrial superoxide; damage to the mitochondrial DNA; loss of electron transport chain activity; and expression of inflammatory markers.ConclusionsOur findings reveal some mechanistic underpinnings of the vasoprotective effects of statins after irradiation. Whereas both pravastatin and atorvastatin can shield from endothelial dysfunction after irradiation, pravastatin additionally suppresses mitochondrial injury and inflammatory responses involving mitochondria. Clinical follow-up studies will be necessary to determine whether hydrophilic statins are more effective than their lipophilic counterparts in reducing the risk of cardiovascular disease in patients undergoing radiation therapy

SPG10 is a rare cause of spastic paraplegia in European families

Background: SPG10 is an autosomal dominant form of hereditary spastic paraplegia (HSP), which is caused by mutations in the neural kinesin heavy chain KIF5A gene, the neuronal motor of fast anterograde axonal transport. Only four mutations have been identified to date.Objective: To determine the frequency of SPG10 in European families with HSP and to specify the SPG10 phenotype.Patients and methods: 80 index patients from families with autosomal dominant HSP were investigated for SPG10 mutations by direct sequencing of the KIF5A motor domain. Additionally, the whole gene was sequenced in 20 of these families.Results: Three novel KIF5A mutations were detected in German families, including one missense mutation (c.759G>T, p.K253N), one in frame deletion (c.768_770delCAA, p.N256del) and one splice site mutation (c.217G>A). Onset of gait disturbance varied from infancy to 30 years of age. All patients presented clinically with pure HSP, but a subclinical sensory--motor neuropathy was detected by neurophysiology studies.Conclusions: SPG10 accounts for approximately 3% of European autosomal dominant HSP families. All mutations affect the motor domain of kinesin and thus most likely impair axonal transport. Clinically, SPG10 is characterised by spastic paraplegia with mostly subclinical peripheral neuropathy

Ensemble density-functional theory for ab-initio molecular dynamics of metals and finite-temperature insulators

A new method is presented for performing first-principles molecular-dynamics simulations of systems with variable occupancies. We adopt a matrix representation for the one-particle statistical operator Gamma, to introduce a ``projected'' free energy functional G that depends on the Kohn-Sham orbitals only and that is invariant under their unitary transformations. The Liouville equation [ Gamma , H ] = 0 is always satisfied, guaranteeing a very efficient and stable variational minimization algorithm that can be extended to non-conventional entropic formulations or fictitious thermal distributions.Comment: 5 pages, two-column style with 2 postscript figures embedded. Uses REVTEX and epsf macros. Also available at http://www.physics.rutgers.edu/~dhv/preprints/index.html#nm_meta

Identifiers in Registers - Describing Network Algorithms with Logic

We propose a formal model of distributed computing based on register automata that captures a broad class of synchronous network algorithms. The local memory of each process is represented by a finite-state controller and a fixed number of registers, each of which can store the unique identifier of some process in the network. To underline the naturalness of our model, we show that it has the same expressive power as a certain extension of first-order logic on graphs whose nodes are equipped with a total order. Said extension lets us define new functions on the set of nodes by means of a so-called partial fixpoint operator. In spirit, our result bears close resemblance to a classical theorem of descriptive complexity theory that characterizes the complexity class PSPACE in terms of partial fixpoint logic (a proper superclass of the logic we consider here).Comment: 17 pages (+ 17 pages of appendices), 1 figure (+ 1 figure in the appendix

The Role of Medical Education in Reducing Health Care Disparities: The First Ten Years of the UCLA/Drew Medical Education Program

BACKGROUND: The University of California, Los Angeles (UCLA)/Charles R. Drew University Medical Education Program was developed to train physicians for practice in underserved areas. The UCLA/Drew Medical Education Program students receive basic science instruction at UCLA and complete their required clinical rotations in South Los Angeles, an impoverished urban community. We have previously shown that, in comparison to their UCLA counterparts, students in the Drew program had greater odds of maintaining their commitment to medically disadvantaged populations over the course of medical education. OBJECTIVE: To examine the independent association of graduation from the UCLA/Drew program with subsequent choice of physician practice location. We hypothesized that participation in the UCLA/Drew program predicts future practice in medically disadvantaged areas, controlling for student demographics such as race/ethnicity and gender, indicators of socioeconomic status, and specialty choice. DESIGN: Retrospective cohort study. PARTICIPANTS: Graduates (1,071) of the UCLA School of Medicine and the UCLA/Drew Medical Education Program from 1985–1995, practicing in California in 2003 based on the address listed in the American Medical Association (AMA) Physician Masterfile. MEASUREMENTS: Physician address was geocoded to a California Medical Service Study Area (MSSA). A medically disadvantaged community was defined as meeting any one of the following criteria: (a) federally designated HPSA or MUA; (b) rural area; (c) high minority area; or (d) high poverty area. RESULTS: Fifty-three percent of UCLA/Drew graduates are located in medically disadvantaged areas, in contrast to 26.1% of UCLA graduates. In multivariate analyses, underrepresented minority race/ethnicity (OR: 1.57; 95% CI: 1.10–2.25) and participation in the Drew program (OR: 2.47; 95% CI: 1.59–3.83) were independent predictors of future practice in disadvantaged areas. CONCLUSIONS: Physicians who graduated from the UCLA/Drew Medical Education Program have higher odds of practicing in underserved areas than those who completed the traditional UCLA curriculum, even after controlling for other factors such as race/ethnicity. The association between participation in the UCLA/Drew Medical Education Program and physician practice location suggests that medical education programs may reinforce student goals to practice in disadvantaged communities

Hereditary sensory neuropathy type I

Hereditary sensory neuropathy type I (HSN I) is a slowly progressive neurological disorder characterised by prominent predominantly distal sensory loss, autonomic disturbances, autosomal dominant inheritance, and juvenile or adulthood disease onset. The exact prevalence is unknown, but is estimated as very low. Disease onset varies between the 2nd and 5th decade of life. The main clinical feature of HSN I is the reduction of sensation sense mainly distributed to the distal parts of the upper and lower limbs. Variable distal muscle weakness and wasting, and chronic skin ulcers are characteristic. Autonomic features (usually sweating disturbances) are invariably observed. Serious and common complications are spontaneous fractures, osteomyelitis and necrosis, as well as neuropathic arthropathy which may even necessitate amputations. Some patients suffer from severe pain attacks. Hypacusis or deafness, or cough and gastrooesophageal reflux have been observed in rare cases. HSN I is a genetically heterogenous condition with three loci and mutations in two genes (SPTLC1 and RAB7) identified so far. Diagnosis is based on the clinical observation and is supported by a family history. Nerve conduction studies confirm a sensory and motor neuropathy predominantly affecting the lower limbs. Radiological studies, including magnetic resonance imaging, are useful when bone infections or necrosis are suspected. Definitive diagnosis is based on the detection of mutations by direct sequencing of the SPTLC1 and RAB7 genes. Correct clinical assessment and genetic confirmation of the diagnosis are important for appropriate genetic counselling and prognosis. Differential diagnosis includes the other hereditary sensory and autonomic neuropathies (HSAN), especially HSAN II, as well as diabetic foot syndrome, alcoholic neuropathy, neuropathies caused by other neurotoxins/drugs, immune mediated neuropathy, amyloidosis, spinal cord diseases, tabes dorsalis, lepra neuropathy, or decaying skin tumours like amelanotic melanoma. Management of HSN I follows the guidelines given for diabetic foot care (removal of pressure to the ulcer and eradication of infection, followed by the use of specific protective footwear) and starts with early and accurate counselling of patients about risk factors for developing foot ulcerations. The disorder is slowly progressive and does not influence life expectancy but is often severely disabling after a long duration of the disease

Molecular genetics and pathophysiology of 17 beta-hydroxysteroid dehydrogenase 3 deficiency.

Autosomal recessive mutations in the 17 beta-hydroxysteroid dehydrogenase 3 gene impair the formation of testosterone in the fetal testis and give rise to genetic males with female external genitalia. Such individuals are usually raised as females, but virilize at the time of expected puberty as the result of increases in serum testosterone. Here we describe mutations in 12 additional subjects/families with this disorder. The 14 mutations characterized to date include 10 missense mutations, 3 splice junction abnormalities, and 1 small deletion that results in a frame shift. Three of these mutations have occurred in more than 1 family. Complementary DNAs incorporating 9 of the 10 missense mutations have been constructed and expressed in reporter cells; 8 of the 9 missense mutations cause almost complete loss of enzymatic activity. In 2 subjects with loss of function, missense mutations testosterone levels in testicular venous blood were very low. Considered together, these findings strongly suggest that the common mechanism for testosterone formation in postpubertal subjects with this disorder is the conversion of circulating androstenedione to testosterone by one or more of the unaffected 17 beta-hydroxysteroid dehydrogenase isoenzymes