Dolphin interleukin-8 receptor. Map position 18q25-26.
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Biomedical subjects
Publications and source records attributed to J Taylor.
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"Despite the fact that indigenous Australians are known to be frequently mobile over the short term, statistical information regarding this population movement is grossly deficient.... This paper examines various means by which short-term population movement can be quantified to yield aggregate indicators of demographic impact. First, census data are used to establish the rate and pattern of inter-regional, short-term displacement. This reveals regional urban centres as net recipients of temporary residents while most rural areas experience temporary absenteeism. Secondly, results from household surveys are reported stressing the importance of including visitors to households in the estimation of service populations. Thirdly, administrative data on occupancy in urban hostels are used to derive indicators of the duration of movement."
The temporal relationship of serum levels of human immunodeficiency virus (HIV) RNA and of immune activation products in 10 HIV-seropositive persons who showed an accelerated decline (inflection point) in CD4 T cell counts and went on to develop AIDS and in 10 matched controls without inflection point were examined. Cases and controls did not differ statistically at the baseline time point for this study. CD4 cell inflection points occurred 18-30 months before AIDS development. Serum levels of soluble tumor necrosis factor receptor II, soluble interleukin-2 receptor, beta2-microglobulin, and neopterin increased significantly > or = 6 months before the CD4 cell inflection point. In contrast, increases in mean HIV RNA levels occurred at the time of the CD4 cell inflection point. These data are consistent with the view that in vivo immune activation precedes the increases in virus load and is followed by an accelerated and rapid loss of CD4 lymphocytes.
Mutations in the Van Gogh gene result in the altered polarity of adult Drosophila cuticular structures. On the wing, Van Gogh mutations cause an altered polarity pattern that is typical of mutations that inactivate the frizzled signaling/signal transduction pathway. The phenotype however, differs from those seen previously, as the number of wing cells forming more than one hair is intermediate between that seen previously for typical frizzled-like or inturned-like mutations. Consistent with Van Gogh being involved in the function of the frizzled signaling/signal transduction pathway, Van Gogh mutations show strong interactions with mutations in frizzled and prickle. Mitotic clones of Van Gogh display domineering cell nonautonomy. In contrast to frizzled clones, Van Gogh clones alter the polarity of cells proximal (and in part anterior and posterior) but not distal to the clone. In further contrast to frizzled clones, Van Gogh clones cause neighboring wild-type hairs to point away from rather than toward the clone. This anti-frizzled type of domineering nonautonomy and the strong genetic interactions seen between frizzled and Van Gogh suggested the possibility that Van Gogh was required for the noncell autonomous function of frizzled. As a test of this possibility we induced frizzled clones in a Van Gogh mutant background and Van Gogh clones in a frizzled mutant background. In both cases the domineering nonautonomy was suppressed consistent with Van Gogh being essential for frizzled signaling.
Continuous haemofiltration with lactate-based replacement fluid is widely used for the treatment of acute renal failure (ARF). In the presence of lactic acidosis, such treatment exacerbates rather than improves the clinical state. Continuous haemofiltration using a locally-prepared bicarbonate-based replacement fluid was performed in 200 patients over 7 years. All the patients had ARF with concomitant lactic acidosis, or demonstrated lactate intolerance after starting haemofiltration with lactate-based replacement fluids. In every case it was possible to correct the acidosis without inducing either extracellular volume expansion or hypernatraemia. In 89 patients (45%), the lactic acidosis resolved while being treated with bicarbonate-based haemofiltration. Fifty-seven patients (28.5%) survived. Significant differences at presentation in the group who survived, compared with those who died, were seen in age (50.8 vs. 57.1), mean arterial pressure (68.5 vs. 60.0 mmHg) and APACHE II score (32.1 vs. 38.9). Neither the severity of the presenting acidosis nor the arterial blood lactate appeared to predict outcome. Patients who developed ARF and lactic acidosis after cardiac surgery had a low survival rate. The combination of ARF and lactic acidosis that cannot safely be treated by haemofiltration using lactate-based replacement fluids can be managed with bicarbonate-based haemofiltration.
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The optic nerve of rats with EAE was examined at various times to determine the integrity of the blood-brain barrier (BBB) and to assess monocyte-macrophage, T cell, and microglial responses. In naive control animals, leakage of horseradish peroxidase (HRP) and the presence of cells expressing major histocompatibility complex (MHC) class II antigen were evident in the meninges of the retrobulbar optic nerve. In rats with EAE, microglia in the region of the lamina cribrosa and in the regions adjacent to the meninges became activated from day 7 to 8 postinduction (pi). HRP leakage was also evident in the region of the lamina cribrosa from day 7 to 8 pi. On day 8 pi, infiltration of inflammatory cells and Monastral blue leakage were apparent in the myelinated region of the optic nerve. The intensity of these cellular and vascular changes peaked at day 12 pi, when signs of clinical disease became manifest. Monocytes-macrophages expressing MHC class II and the ED1 antigen, together with lymphocytes expressing the alphabetaT cell receptor, constituted the major proportion of cells associated with inflammatory lesions. Thus: (i) the inherent weakness of the BBB as well as the presence of both antigen (myelin) and MHC class II+ cells in the retrobulbar optic nerve are likely susceptibility factors for the frequent involvement of this region in EAE and multiple sclerosis; and (ii) activation of microglia occurs early in the pathogenesis of experimental optic neuritis.
The small, 195-amino-acid form of the hepatitis delta virus (HDV) antigen (deltaAg-S) is essential for genome replication, i.e., for the transcription, processing, and accumulation of HDV RNAs. To better understand this requirement, we used purified recombinant deltaAg-S and HDV RNA synthesized in vitro to assemble high-molecular-weight ribonucleoprotein (RNP) structures. After transfection of these RNPs into human cells, we detected HDV genome replication, as assayed by Northern analysis or immunofluorescence microscopy. Our interpretation is that the input deltaAg-S is necessary for the RNA to undergo limited amounts of RNA-directed RNA synthesis, RNA processing, and mRNA formation, leading to de novo translation of deltaAg-S. It is this second source of deltaAg-S which then goes on to support genome replication. This assay made it possible to manipulate in vitro the composition of the RNP and then test in vivo the ability of the complex to initiate RNA-directed RNA synthesis and go on to achieve genome replication. For example, both genomic and antigenomic linear RNAs were acceptable. Substitution for deltaAg-S with truncated or modified forms of the deltaAg, and even with HIV nucleocapsid protein and polylysine, was unacceptable; the exception was a form of deltaAg-S with six histidines added at the C terminus. We expect that further in vitro modifications of these RNP complexes should help define the in vivo requirements for what we define as the initiation of HDV genome replication.
OBJECTIVES: To measure the prevalence of HSV-2 antibodies in a birth cohort of 21 year old New Zealanders from whom detailed sexual histories had been obtained, and to assess the potential for HSV-2 serology in characterising a young adult population's risk for sexually transmitted diseases (STD). METHODS: Sera from 784 cohort members were tested using an indirect IgG enzyme linked immunoassay specific to the HSV-2 glycoprotein G. Positive results were confirmed by western blot. RESULTS: In all, 27 subjects were seropositive for HSV-2 (3.4%), only seven of whom gave a history of genital herpes (26%). Risk among females increased with lifetime number of partners, while risk for males increased with having a first partner who was aged 16 years or under. CONCLUSIONS: The seroprevalence of HSV-2 infection in this cohort was low, but similar to that seen in several other populations in this age group. HSV-2 seropositivity did not appear to be a sensitive marker for high risk sexual activity in this young population. This may be because a critical mass of HSV-2 carriers has not accumulated among potential partners by age 21 years.
Macrophage colony stimulating factor (MCSF) is believed to play a key role in one of the earliest events in atherosclerosis, ie, monocyte to macrophage differentiation in the arterial intima. The aim of this study was to examine the biological effects of vascular wall expression of MCSF. A recombinant adenovirus vector encoding human MCSF (AdMCSF) was generated by standard techniques of homologous recombination in 293 cells. The rabbit carotid artery was transduced with AdMCSF. As negative controls, carotid arteries were transduced with either an adenoviral vector encoding beta-galactosidase, an adenoviral vector encoding apolipoprotein E, or diluent alone. Intima-media thickness ratio was calculated 5 and 21 days after transduction. The cell type present in intimal infiltrates was analyzed by immunohistochemistry. MCSF expression was demonstrated in the vessel wall of AdMCSF-transduced vessels by reverse transcription-polymerase chain reaction and immunofluorescence. In contrast to control vessels, adenovirus-mediated MCSF expression was associated with an intimal cellular infiltrate consisting of smooth muscle cells and small numbers of macrophages. Whereas the intima-media thickness ratio was greater in AdMCSF-transduced vessels at 5 days, this difference was no longer statistically significant at 21 days. These results suggest that MCSF may play a role in recruitment of monocytes and macrophages to the vessel wall and may contribute to smooth muscle cell proliferation and migration.
Fatigue is a common symptom found in the adult oncology literature. However, little is known about its occurrence, causes, conceptual and operational definitions, and effective interventions in children and adolescents with cancer. The purpose of this study was to define and describe fatigue experienced by children and adolescents receiving treatment for cancer. A focus group approach was used to reveal the contextual understanding of fatigue through discussions. Eleven focus groups were convened during a 2-month period at two major children's cancer centers. Twenty-nine children participated in the focus groups: 14 were 7 to 12 years of age and 15 were 13 to 16 years of age. Focus groups were held separately for each age group, lasted from 30 to 45 minutes, and were audiotaped. The audiotapes were transcribed verbatim, and Ethnograph software was used to number the data to sort and code the information. Researchers at both study sites coded the data independently within the context of the unit of analyses, which, in this study, were the study questions. Codes and descriptions were developed for the definitions of fatigue, causes of fatigue, and what helps. Eight codes emerged from the children groups and 12 from the adolescent groups to define fatigue. Six codes were developed from the children groups and 12 from the adolescent groups to describe causes of fatigue. Three codes from the children groups and eight from the adolescent groups described what helps. This study is the first to evaluate fatigue as a symptom in children and adolescents with cancer. Findings from this study will provide the foundation for developing a conceptual model for cancer-related fatigue in children and adolescents.
Genetic obesity is associated with increased neuropeptide Y (NPY) messenger RNA (mRNA) and decreased POMC mRNA in the hypothalamus of ob/ob and db/db mice, or impaired sensitivity to alphaMSH (derived from POMC) in the yellow agouti mouse. Acquired obesity can be produced by chemically lesioning the hypothalamus with either monosodium glutamate (MSG) in neonates or gold thioglucose (GTG) in adult mice. The present study examined whether elevated NPY mRNA and/or decreased POMC mRNA in the hypothalamus are associated with obesity due to hypothalamic lesions. GTG injection into adult mice produced a profound obese phenotype, including hyperphagia, increased body weight, and increased leptin mRNA and peptide, in association with reduced hypothalamic NPY mRNA and POMC mRNA. MSG treatment produced virtual elimination of NPY mRNA in the arcuate nucleus and a reduction of hypothalamic POMC mRNA, and led to elevated leptin. MSG pretreatment did not attenuate GTG-induced hyperphagia and obese phenotype. These results do not support a role for NPY-synthesizing neurons in the arcuate nucleus in mediating hypothalamic acquired obesity, but are consistent with the hypothesis that decreased activity of hypothalamic neurons synthesizing POMC play a role in mediating hypothalamic obesity.
The role of gene expression of the estrogen receptor-alpha form (ER alpha) in the regulation of female reproductive behavior was investigated in estrogen receptor knockout (ERKO) mice, deficient specifically for the ER alpha, but not the ER beta, gene. Estrogen- or estrogen- plus progesterone-treated gonadectomized ERKO mice did not show any lordosis response. Detailed behavioral analysis revealed that ERKO females were also deficient in sexual behavioral interactions preceding the lordosis response. They were extremely rejective toward attempted mounts by stud male mice, which could not show any intromissions. During resident-intruder aggression tests, gonadally intact ERKO females were more aggressive toward female intruder mice than wild-type (WT) mice. Gonadectomy did not influence the levels of aggressive behavior, and their genotype differences when mice were tested both before and after gonadectomy. However, when mice were tested after gonadectomy for the first time, very few ERKO mice showed aggression. In contrast to aggression, male-type sexual behavior shown by resident mice toward female intruder mice during aggression tests was not different between ERKO and WT mice and was completely abolished after gonadectomy of the resident mice. Finally, it was also found that ERKO females showed greatly reduced levels of parental behavior toward newborn pups placed in their home cage. These changes in parental behavior were not influenced by gonadectomy. ERKO females retrieved significantly fewer numbers of pups with longer latencies compared with wild-type (WT) or heterozygous (HZ) littermates when they were tested as gonadally intact or 20-65 days after gonadectomy. In addition, during parental behavior tests, a significantly higher percentage of ERKO mice exhibited infanticide compared with WT and HZ mice, which rarely showed infanticide. Taken together, these findings suggest that ER alpha gene expression plays a key role in female mice, not only for sexual behavior but also for other interrelated behaviors, such as parental and aggressive behaviors. In addition, persistence of genotype differences in parental and aggressive behavior after gonadectomy indicates that ER alpha activation during neural developmental processes may also be involved in the regulation of these behaviors.
The role of the a form of estrogen receptor (ER alpha) gene expression in the regulation of testosterone-dependent male reproductive behaviors was investigated using ER knockout mice (ERKO), which are specifically deficient in functional ER alpha, but not ER beta, gene expression. Previous studies in gonadally intact ERKO mice revealed that male aggressive behavior was greatly reduced by the lack of a functional ER alpha gene. In the present study the almost complete suppression of male-typical offensive attacks was further confirmed in ERKO mice that had been singly housed since weaning. Regarding aggression, it was also found that ER alpha gene disruption virtually abolished the propensity to initiate offensive attacks, even though ERKO mice could elicit attacks from resident C57BL/6J mice as wild-type (WT) and heterozygous littermates. Daily injection of testosterone propionate (TP) was completely ineffective in inducing aggressive behavior in gonadectomized ERKO mice, whereas it successfully restored aggression in WT mice. In contrast, male sexual behaviors, mounts and intromissions, were induced by daily injection of TP in both gonadectomized ERKO and WT mice. In addition to TP, dihydrotestosterone propionate (DHTP) was also effective in restoring mounts in ERKO mice, although DHTP was much more potent in WT mice than in ERKO mice. Neither TP nor DHTP, however, ever induced ejaculation in ERKO mice. These results together with previous findings in gonadally intact ERKO mice suggest that ER alpha may be responsible for the regulation by testosterone of consummatory, but not motivational, aspects of male sexual behavior. Finally, ERKO male mice retrieved newborn pups placed in their home cage with similar latencies to males of the two other genotypes. During parental behavior tests, however, a higher percentage of ERKO mice (70%) showed infanticide compared with WT mice (35%). The latter result was interpreted as showing that ER alpha activation by testosterone during the perinatal period may exert a suppressive effect on testosterone-inducible infanticide in adulthood. With respect to three major testosterone-dependent behavioral systems reflecting masculinization, these findings demonstrate three different types of effects due to ER alpha gene disruption.
OBJECTIVE: To describe the clinical and histopathologic picture of a childhood-onset, severe variant of scapuloperoneal MD with rigidity of the spine. BACKGROUND: Rigidity of the spine is a feature of numerous syndromes, including X-linked Emery-Dreifuss MD, Bethlem myopathy, and the rigid spine syndrome. These are, however, relatively static or very slowly progressive neuromuscular disorders, usually associated with preserved ambulation into adult life. PATIENTS AND METHODS: Five unrelated children (three boys and two girls) presented in the first 2 years of life with poor neck control, waddling gait, and frequent falls. Early wasting of the distal leg muscles, biceps, triceps, and neck muscles was noted in all patients, and all had contractures and severe rigidity of the spine. The condition progressed rapidly, and all patients lost ambulation before the age of 8 years. Cardiac function was normal in all. RESULTS: Creatine kinase was moderately elevated in all, and muscle biopsy specimens showed nonspecific dystrophic changes with normal expression of dystrophin, the sarcoglycans, and laminin alpha2, alpha5, beta1, and gamma1 chains. Emerin expression was normal in two of the boys whose tissue was available for study. CONCLUSIONS: The distribution of weakness, wasting, and contractures of the patients described resembled Emery-Dreifuss MD, but the rapid progression of weakness and contractures and the involvement of both sexes together with normal emerin expression suggest that this form is not X-linked Emery-Dreifuss MD. We suggest that these patients represent a severe MD characterized by early onset distal wasting and severe rigidity of the spine, with probable autosomal recessive inheritance.
This study was designed to determine the ability of quantitative ultrasound (QUS) of the heel to predict fracture risk at different sites in postmenopausal women between the ages of 45 and 75 years. Heel QUS was measured at baseline using a Lunar Achilles scanner, and subsequent fractures were identified over 3 yr. The results were analyzed graphically after age adjustment and using Cox's proportional regression to estimate odds ratios for fracture risk; 3180 women were scanned (79% of sample). Sixty-three wrist, 12 hip, 4 vertebral, 7 proximal humerus, 3 pelvic, and 61 other fractures were identified over a mean followup of 31 mo. There was a fivefold difference in numbers of wrist and osteoporosis-related fractures (hip, vertebra, pelvis, and humerus combined) between the lowest and highest quartiles of QUS results adjusted for age. The odds ratios per 1 SD decline in QUS parameters adjusted for age were: wrist fractures BUA = 1.6, SOS = 1.5, stiffness = 1.8, osteoporosis-related fractures BUA = 1.9, speed of sound (SOS) = 1.6, stiffness = 2.2, and other fractures, BUA = 1.0, SOS = 1.1, stiffness = 1.1. When analyzed for each 10-yr age group, the odds ratios were generally higher in the 56-65 yr group than the other decades. In women between 45 and 75 yr, heel QUS can predict wrist and osteoporosis- related fractures at about the same level that dual-energy X-ray absorptiometry (DXA) of various sites can predict wrist fractures. This extends the current evidence that heel QUS can predict hip fracture risk in women over 75 yr to include other fracture sites in younger women. Heel QUS may be useful in the primary care assessment of osteoporotic fracture risk in women after the menopause.
Based on visual inspection of data, reinforcement procedures, namely, use of verbal praise and verbal praise plus token exchange, were at least mildly influential in improving performance of 5 youth with moderate mental retardation compared to their initial performance without reinforcers. These findings suggest specific reinforcement may improve the time for aerobic activity by adolescents with moderate mental retardation.