Effects of Rotation, Site, and Clone on the Chemical Composition of Populus Hybrids

Chemical content values were determined for three Populus clones grown on two dissimilar sites by component (wood, bark, and wood/bark specimens), tissue age (1-, 2- and 4-years-old), and rotation. The chemical content values obtained included extractives, holocellulose, alpha-cellulose, and lignin. In general, analysis of the data for the wood, bark, and wood/bark specimens indicated that: 1) wood was high in holocellulose and alpha-cellulose content compared to bark, 2) bark was high in lignin and extractive content values compared to wood, and 3) wood/bark chemical content values were between the values for the wood and bark specimens.The chemical content data were analyzed to identify: 1) significant differences between rotations by component (wood, bark, and wood/bark) for a given age, clone, and site, and 2) significant differences between sites for four-year-old wood, bark and wood/bark specimens of a given rotation, and clone. Statistical analyses indicated that significant differences existed among clones, sites, ages, and rotations. Within the wood, bark and wood/bark specimens, tissue age, rotation, and site influenced the chemical content values more than the parentage. Potential chemical yields derived from the three Populus hybrid clones investigated will depend on component, age, rotation, and site with limited parentage effects

Recovery of Otoacoustic Emission Function in Luetic Endolymphatic Hydrops: A Possible Measure of Improvement in Cochlear Function

Syphilis is a preventable and curable multi-organ disease caused by Treponema pallidum that may also affect the inner ear. First reported in 1887 by Adam Politzer, luetic endolymphatic hydrops (LEH) is a treatable complication of syphilis which causes a potentially reversible sensorineural hearing loss. Symptoms of LEH include fluctuating hearing loss (often low frequency), tinnitus, and vertigo. Though audiometric parameters have been examined in patients with otosyphilis, few studies have examined the use of otoacoustic emissions (OAEs) as a tool to measure improvement in cochlear function. Here we report an improvement in hearing loss, speech discrimination, and OAEs following treatment of LEH

Comparison of Selected Fuel and Chemical Content Values for Seven Populus Hybrid Clones

Fuel and chemical content values were determined for seven Populus clones by component (wood, bark, and wood/bark specimens) and tissue age (1 to 8 years old). The fuel and chemical content values obtained included: gross heat of combustion, extractives, holocellulose, alpha-cellulose, lignin, and ash. In general, analysis of the data for the wood, bark, and wood/bark specimens indicated that: 1) wood was higher in holocellulose and alpha-cellulose content than bark; 2) bark was higher in gross heat of combustion, lignin, extractive, and ash content values than wood; and 3) combined wood/bark fuel and chemical content values were usually between the individual values for the wood and bark.Statistical analyses indicated that significant differences existed within and among clones. Within the wood, bark, and wood/bark specimens, tissue age influenced the chemical content values more than the parentage. Potential chemical yields derived from the seven Populus hybrid clones investigated will depend on component and age with limited parentage effects

Identification of quantitative trait loci for survival in the mutant dynactin p150Glued mouse model of motor neuron disease.

Amyotrophic lateral sclerosis (ALS) is the most common degenerative motor neuron disorder. Although most cases of ALS are sporadic, 5-10% of cases are familial, with mutations associated with over 40 genes. There is variation of ALS symptoms within families carrying the same mutation; the disease may develop in one sibling and not in another despite the presence of the mutation in both. Although the cause of this phenotypic variation is unknown, it is likely related to genetic modifiers of disease expression. The identification of ALS causing genes has led to the development of transgenic mouse models of motor neuron disease. Similar to families with familial ALS, there are background-dependent differences in disease phenotype in transgenic mouse models of ALS suggesting that, as in human ALS, differences in phenotype may be ascribed to genetic modifiers. These genetic modifiers may not cause ALS rather their expression either exacerbates or ameliorates the effect of the mutant ALS causing genes. We have reported that in both the G93A-hSOD1 and G59S-hDCTN1 mouse models, SJL mice demonstrated a more severe phenotype than C57BL6 mice. From reciprocal intercrosses between G93A-hSOD1 transgenic mice on SJL and C57BL6 strains, we identified a major quantitative trait locus (QTL) on mouse chromosome 17 that results in a significant shift in lifespan. In this study we generated reciprocal intercrosses between transgenic G59S-hDCTN1 mice on SJL and C57BL6 strains and identified survival QTLs on mouse chromosomes 17 and 18. The chromosome 17 survival QTL on G93A-hSOD1 and G59S-hDCTN1 mice partly overlap, suggesting that the genetic modifiers located in this region may be shared by these two ALS models despite the fact that motor neuron degeneration is caused by mutations in different proteins. The overlapping region contains eighty-seven genes with non-synonymous variations predicted to be deleterious and/or damaging. Two genes in this segment, NOTCH3 and Safb/SAFB1, have been associated with motor neuron disease. The identification of genetic modifiers of motor neuron disease, especially those modifiers that are shared by SOD1 and dynactin-1 transgenic mice, may result in the identification of novel targets for therapies that can alter the course of this devastating illness

Carotid intimal-media thickness as a surrogate for cardiovascular disease events in trials of HMG-CoA reductase inhibitors

BACKGROUND: Surrogate measures for cardiovascular disease events have the potential to increase greatly the efficiency of clinical trials. A leading candidate for such a surrogate is the progression of intima-media thickness (IMT) of the carotid artery; much experience has been gained with this endpoint in trials of HMG-CoA reductase inhibitors (statins). METHODS AND RESULTS: We examine two separate systems of criteria that have been proposed to define surrogate endpoints, based on clinical and statistical arguments. We use published results and a formal meta-analysis to evaluate whether progression of carotid IMT meets these criteria for HMG-CoA reductase inhibitors (statins). IMT meets clinical-based criteria to serve as a surrogate endpoint for cardiovascular events in statin trials, based on relative efficiency, linkage to endpoints, and congruency of effects. Results from a meta-analysis and post-trial follow-up from a single published study suggest that IMT meets established statistical criteria by accounting for intervention effects in regression models. CONCLUSION: Carotid IMT progression meets accepted definitions of a surrogate for cardiovascular disease endpoints in statin trials. This does not, however, establish that it may serve universally as a surrogate marker in trials of other agents

A genetic locus complements resistance to Bordetella pertussis-induced histamine sensitization.

Histamine plays pivotal role in normal physiology and dysregulated production of histamine or signaling through histamine receptors (HRH) can promote pathology. Previously, we showed that Bordetella pertussis or pertussis toxin can induce histamine sensitization in laboratory inbred mice and is genetically controlled by Hrh1/HRH1. HRH1 allotypes differ at three amino acid residues with

5-Thia-5-Deazaflavin, a 1e − -Transferring Flavin Analog

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/65939/1/j.1432-1033.1979.tb12952.x.pd

Genetic dissection reveals diabetes loci proximal to the gimap5 lymphopenia gene

rats are protected from type 1 diabetes (T1D) by 34 Mb of F344 DNA introgressed proximal to the gimap5 lymphopenia gene. To dissect the genetic factor(s) that confer protection from T1D in the DRF. f/f rat line, DRF. f/f rats were crossed to inbred BBDR or DR. lyp/lyp rats to generate congenic sublines that were genotyped and monitored for T1D, and positional candidate genes were sequenced. All (100%) DR. f/f congenic sublines further refined the RNO4 region 1 interval to ϳ670 kb and region 2 to the 340 kb proximal to gimap5. All congenic DRF. f/f sublines were prone to low-grade pancreatic mononuclear cell infiltration around ducts and vessels, but Ͻ20% of islets in nondiabetic rats showed islet infiltration. Coding sequence analysis revealed TCR V␤ 8E, 12, and 13 as candidate genes in region 1 and znf467 and atp6v0e2 as candidate genes in region 2. Our results show that spontaneous T1D is controlled by at least two genetic loci 7 Mb apart on rat chromosome 4. type 1 diabetes; BB rat; T cell receptor; autoimmune CHARACTERISTICS OF TYPE 1 DIABETES (T1D) in both human and the BioBreeding spontaneously diabetes-prone (BBDP) rat include polyuria, hyperglycemia, ketoacidosis, insulitis, and insulin dependency for life. As in human T1D, islets are infiltrated by mononuclear cells at the time of onset with rapid hyperglycemia due to a complete loss of islet ␤-cells (32). The genetic etiology of human T1D remains complex and although the major histocompatibility complex (MHC) (HLA DQ) on chromosome 6 accounts for ϳ40% of T1D risk, the number of non-HLA genetic factors is increasing steadily (2, 7). The BB rat offers a powerful model to dissect both genetic contributions and mechanisms by which immunemediated beta cell killing induces T1D (3, 4, 15, 17-21, 27, 28, 46). As in humans, the major genetic determinant of susceptibility in the BB rat is the MHC (Iddm1) on rat chromosome (RNO) 20. The class II MHC locus RT1B/D. u/u ), an ortholog of human HLA DQ (9), is necessary but not sufficient for T1D in the BBDP rat and other RT1. u/u -related rat strains with spontaneous (24, 47) or induced T1D (8, 43). In BBDP, a null mutation in the gimap5 gene (lyp; Iddm2) on RNO4 (14, 27) causes lymphopenia and is tightly linked to spontaneous T1D development. The DR. lyp/lyp rat with 2 Mb of BBDP DNA encompassing gimap5 introgressed into the genome of related BBDR rats (BioBreeding resistant to spontaneous T1D) are also 100% lymphopenic and 100% spontaneously diabetic (11). With complete T1D penetrance and tight regulation of onset, the congenic DR. lyp/lyp rat line offers distinct advantages in identification of genes responsible for disease progression. It is possible to induce T1D in BBDR rats (32) and related RT1 u/u rats (8) by administration of polyinosinic: polycytidylic acid (poly I:C, an activator of innate immunity), the T reg depleting cytotoxic DS4.23 anti-ART2.1 (formerly RT6) monoclonal antibody or by viral infection (34). This indicates that the BBDR has an underlying genetic susceptibility to T1D. In crosses between WF and either BBDP or BBDR rats, a quantitative trait locus (QTL) important for induced T1D (Iddm14, previously designated Iddm4) was mapped to RNO4 (6, Interestingly, F344 DNA introgressed between D4Rat253 and D4Rhw6 into the congenic DR. lyp/lyp genetic background resulted in a lymphopenic but nondiabetic rat (designated DRF. f/f ) (11). Protection from T1D in the DRF. f/f congenic rat line led us to conclude that spontaneous T1D in the BB rat is controlled, in part, by a diabetogenic factor(s) independent of the gimap5 mutation (76.84 Mb) on RNO4. This congenic interval is encompassed within Iddm14, raising the possibility that the Iddm14 locus could be required for both spontaneous and induced T1D in the BB rat. The aim of this study was to cross the DRF. f/f rat to BBDR and DR. lyp/lyp rats and produce recombinant sublines that could be assessed for both lymphopenia and diabetes and to estimate the number of independent genes on RNO4 that control spontaneous T1D