Still Too Fat to Fight

The problem of junk food sold in schools is not just a national health issue. It is a national security issue.Over the past 40 years, obesity rates have more than tripled for children and teens. About 1 in 4 young American adults is now too overweight to join the military. Being overweight or obese is the number one medical reason why young adults cannot enlist. When weight problems are combined with poor education, criminal backgrounds, and other disqualifiers, an estimated 75 percent of young Americans could not serve in the military if they wanted to

Safer Streets: Cutting Repeat Crimes by Juvenile Offenders.

FIGHT CRIME: INVEST IN KIDS is an anti-crime organization led by more than 3,500 law enforcement leaders -- chiefs, sheriffs and prosecutors -- and survivors of crime. Most of the survivors are parents of murdered children. Crime requires punishment. Punishment may be placing a young offender in custody, or, depending on the crime, imposing a range of other tough sanctions. The bottom line is that residents must be safe walking the streets. Research shows, however, that punishment alone will often not be enough; troubled teens will need help to stop their aggression, substance abuse, or other anti-social behaviors. It is usually not too late to change anti-social patterns of behavior. Sanctions that include strict and effective interventions can direct anti-social and dangerous juveniles onto a different path that will make Americans safer

Pion-proton scattering and isospin breaking in the Δ0−Δ++\Delta^0-\Delta^{++} system

We determine the mass and width of the $\Delta^{++}\ (\Delta^0)$ resonance from data on $\pi^+ p\ (\pi^- p)$ scattering both, in the pole of the $S$-matrix and conventional Breit-Wigner approaches to the scattering amplitude. We provide a simple formula that relates the two definitions for the parameters of the $\Delta$. Isospin symmetry breaking in the \d0-\dm system depends on the definition of the resonant properties: we find $M_0-M_{++} = 0.40 \pm 0.57\ {\rm MeV},\ \Gamma_0 -\Gamma_{++} = 6.89 \pm 0.95\ {\rm MeV}$ in the pole approach while $\wt{M}_0-\wt{M}_{++} = 2.25 \pm 0.68\ {\rm MeV},\ \wt{\Gamma}_0 - \wt{\Gamma}_{++} = 8.45 \pm 1.11\ {\rm MeV}$ in the conventional approach.Comment: Latex, 23 pages, two figures upon reques

Electromagnetic form factors of hadrons

A vector meson dominance model of the electromagnetic form factors of hadrons is developed which is based on the use of unstable particle propagators. Least-square fits are made to the proton, neutron, pion and kaon form factor data in both the space and time-like regions. A good fit to the low-energy nucleon form factor data is obtained using only rho, $omega$, and phi dominance, and leads to a determination of the vector meson resonance parameters in good agreement with experiment. The nucleon-vector meson coupling constants obey simple sum rules indicating that there exists no hard core contribution to the form factors within theoretical uncertainties. The prediction for the electromagnetic radii of the proton is in reasonable agreement with recent experiments. The pion and kaon charge form factors as deduced from the nucleon form factors assuming vector meson universality are compared to the data. The pion form factor agrees with the data in both the space and time-like regions. The pion charge radius is in agreement with the recent Dubna result, but the isovector P-wave pion-pion phase shift calculated from the theory disagrees with experiment. A possible contribution to the form factors from a heavy rho meson is also evaluated. (auth

Is There a Housing Bubble in Humboldt County?

This analysis is the first look into the housing market in Humboldt County since the rapid increase in national house prices in the early 2000s. The data we present for Humboldt County 1989-2004 is consistent with housing price movements in other coastal regions of the U.S. where some believe that a "housing bubble" has formed. In the three years from January, 2002 to December, 2004, the median house price appreciated by 72% or $113,750, with the most rapid increase in 2004. More importantly, the P/E ratio never rose or fell by more than one point from 1989-2002. In both 2003 and 2004, however, the P/E ratio climbed by three points, so that it was 23.8 in December 2004 while it averaged 15.4 from 1989-2002.Research Paperapplication/pd

A simple dye-coupling assay for evaluating gap junctional communication: The importance of transcription and translation on the establishment of dye-coupling

A simple dye-coupling assay has been developed to study gap junctional communication using a uterine cell line. The new dye-coupling assay was found to be of comparable sensitivity to an autoradiographic assay for transfer of radiolabelled nucleotide. To investigate the importance of protein synthesis in the establishment of dye-coupling under the conditions of this assay, cultures were treated with actinomycin-D and cycloheximide to inhibit transcription and translation, respectively. Inhibition of transcription had no significant effect on dye-coupling. The protein synthesis inhibitor, cycloheximide, also had no significant effect on dye-coupling at concentrations up to 1 uM, even though protein synthesis was inhibited to 19% of control.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/28513/1/0000310.pd

The P_33(1232) resonance contribution into the amplitudes M_{1+}^{3/2},E_{1+}^{3/2},S_{1+}^{3/2} from an analysis of the p(e,e'p)\pi^0 data at Q^2 = 2.8, 3.2, and 4 (GeV/c)^2 within dispersion relation approach

Within the fixed-t dispersion relation approach we have analysed the TJNAF and DESY data on the exclusive p(e,e'p)\pi^0 reaction in order to find the P_{33}(1232) resonance contribution into the multipole amplitudes M_{1+}^{3/2},E_{1+}^{3/2},S_{1+}^{3/2}. As an input for the resonance and nonresonance contributions into these amplitudes the earlier obtained solutions of the integral equations which follow from dispersion relations are used. The obtained values of the ratio E2/M1 for the \gamma^* N \to P_{33}(1232) transition are: 0.039\pm 0.029, 0.121\pm 0.032, 0.04\pm 0.031 for Q^2= 2.8, 3.2, and 4 (GeV/c)^2, respectively. The comparison with the data at low Q^2 shows that there is no evidence for the presence of the visible pQCD contribution into the transition \gamma N \to P_{33}(1232) at Q^2=3-4 GeV^2. The ratio S_{1+}^{3/2}/M_{1+}^{3/2} for the resonance parts of multipoles is: -0.049\pm 0.029, -0.099\pm 0.041, -0.085\pm 0.021 for Q^2= 2.8, 3.2, and 4 (GeV/c)^2, respectively. Our results for the transverse form factor G_T(Q^2) of the \gamma^* N \to P_{33}(1232) transition are lower than the values obtained from the inclusive data. With increasing Q^2, Q^4G_T(Q^2) decreases, so there is no evidence for the presence of the pQCD contribution here too

The IGSF1 deficiency syndrome may present with normal free T4 levels, severe obesity, or premature testicular growth

Our objective was to further expand the spectrum of clinical characteristics of the IGSF1 deficiency syndrome in affected males. These characteristic include almost universal congenital central hypothyroidism (CeH) with disharmonious pubertal development (normally timed testicular growth, but delayed rise of serum testosterone), macroorchidism, increased body mass index (BMI), and decreased attentional control. In addition, a subset of patients show prolactin deficiency, transient partial growth hormone deficiency in childhood and increased growth hormone secretion in adulthood. We present a family in which the proband was diagnosed with CeH and low serum prolactin. Severe weight gain started at two years old, with a BMI of 42.3 at 13.9 years. Testicular enlargement (5-6 mL, 3.8-4.3 standard deviation score) started aged three years. A pathogenic variant was found in the IGSF1 gene: c.3411_3412del, p.(Tyr1137*). His brother was referred for short stature at age 13 years and was diagnosed with CeH, normal serum prolactin and IGF-1, and disharmonious puberty. In four male relatives (the proband's brother and three cousins) with the variant (one adult), free thyroxine (fT4) was below the lower limit of the reference range in two, and just above this limit in the other two. Three were overweight or obese, adolescents had disharmonious pubertal development and the adult had profound macroorchidism. In conclusion, male hemizygous carriers of a pathogenic IGSF1 variant can present with fT4 concentration above the lower limit of the reference range while severe early onset obesity or premature testicular growth are part of the phenotypic spectrum.Genetics of disease, diagnosis and treatmen

SPTLC1 variants associated with ALS produce distinct sphingolipid signatures through impaired interaction with ORMDL proteins

Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disease that affects motor neurons. Mutations in the SPTLC1 subunit of serine palmitoyltransferase (SPT), which catalyzes the first step in the de novo synthesis of sphingolipids (SLs), cause childhood-onset ALS. SPTLC1-ALS variants map to a transmembrane domain that interacts with ORMDL proteins, negative regulators of SPT activity. We show that ORMDL binding to the holoenzyme complex is impaired in cells expressing pathogenic SPTLC1-ALS alleles, resulting in increased SL synthesis and a distinct lipid signature. C-terminal SPTLC1 variants cause peripheral hereditary sensory and autonomic neuropathy type 1 (HSAN1) due to the synthesis of 1-deoxysphingolipids (1-deoxySLs) that form when SPT metabolizes L-alanine instead of L-serine. Limiting L-serine availability in SPTLC1-ALS-expressing cells increased 1-deoxySL and shifted the SL profile from an ALS to an HSAN1-like signature. This effect was corroborated in an SPTLC1-ALS pedigree in which the index patient uniquely presented with an HSAN1 phenotype, increased 1-deoxySL levels, and an L-serine deficiency. These data demonstrate how pathogenic variants in different domains of SPTLC1 give rise to distinct clinical presentations that are nonetheless modifiable by substrate availability

SPTLC1 variants associated with ALS produce distinct sphingolipid signatures through impaired interaction with ORMDL proteins

Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disease that affects motor neurons. Mutations in the SPTLC1 subunit of serine palmitoyltransferase (SPT), which catalyzes the first step in the de novo synthesis of sphingolipids (SLs), cause childhood-onset ALS. SPTLC1-ALS variants map to a transmembrane domain that interacts with ORMDL proteins, negative regulators of SPT activity. We show that ORMDL binding to the holoenzyme complex is impaired in cells expressing pathogenic SPTLC1-ALS alleles, resulting in increased SL synthesis and a distinct lipid signature. C-terminal SPTLC1 variants cause peripheral hereditary sensory and autonomic neuropathy type 1 (HSAN1) due to the synthesis of 1-deoxysphingolipids (1-deoxySLs) that form when SPT metabolizes L-alanine instead of L-serine. Limiting L-serine availability in SPTLC1-ALS-expressing cells increased 1-deoxySL and shifted the SL profile from an ALS to an HSAN1-like signature. This effect was corroborated in an SPTLC1-ALS pedigree in which the index patient uniquely presented with an HSAN1 phenotype, increased 1-deoxySL levels, and an L-serine deficiency. These data demonstrate how pathogenic variants in different domains of SPTLC1 give rise to distinct clinical presentations that are nonetheless modifiable by substrate availability