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PubMed2004

Trends from an HIV seroprevalence study among childbearing women in New York State from 1988 through 2000: a valuable epidemiologic tool.

BACKGROUND: Women in New York State are heavily affected by the human immunodeficiency virus (HIV) epidemic. New York has had the largest number of births to HIV-infected pregnant women in the United States. Data collected as part of the Survey of Childbearing Women have been valuable for assessing the impact of the disease on the women of New York. OBJECTIVE: To assess HIV prevalence trends among childbearing women in New York State. DESIGN, SETTING, AND PARTICIPANTS: An unlinked HIV seroprevalence study was conducted among all women residing in and giving birth in New York State from 1988 through 2000. Trend and cohort analyses were conducted. Main Outcome Measure HIV prevalence, defined as the number of HIV-positive specimens divided by the total number of HIV-positive and HIV-negative specimens, by geographic region, racial/ethnic group, and maternal age cohort. RESULTS: Trends indicated a steady decline in HIV prevalence in New York State. New York City had a 49% decrease in prevalence between 1988 through 1989 and 1999 through 2000, and the rest of the state showed a 24% decline. However, birth cohort analysis indicated different patterns in trend by subpopulation, with some groups experiencing little or no decline. CONCLUSION: This study reports on the only statewide population-based HIV prevalence data currently available for childbearing women; these data have been a valuable tool for monitoring trends, targeting resources, and evaluating programs and policies.

Adult↗
PubMed1996

A combined analysis of D22S278 marker alleles in affected sib-pairs: support for a susceptibility locus for schizophrenia at chromosome 22q12. Schizophrenia Collaborative Linkage Group (Chromosome 22).

Several groups have reported weak evidence for linkage between schizophrenia and genetic markers located on chromosome 22q using the lod score method of analysis. However these findings involved different genetic markers and methods of analysis, and so were not directly comparable. To resolve this issue we have performed a combined analysis of genotypic data from the marker D22S278 in multiply affected schizophrenic families derived from 11 independent research groups worldwide. This marker was chosen because it showed maximum evidence for linkage in three independent datasets (Vallada et al., Am J Med Genet 60:139-146, 1995; Polymeropoulos et al., Neuropsychiatr Genet 54:93-99, 1994; Lasseter et al., Am J Med Genet, 60:172-173, 1995. Using the affected sib-pair method as implemented by the program ESPA, the combined dataset showed 252 alleles shared compared with 188 alleles not share (chi-square 9.31, 1df, P = 0.001) where parental genotype data was completely known. When sib-pairs for whom parental data was assigned according to probability were included the number of alleles shared was 514.1 compared with 437.8 not shared (chi-square 6.12, 1df, P = 0.006). Similar results were obtained when a likelihood ratio method for sib-pair analysis was used. These results indicate that may be a susceptibility locus for schizophrenia at 22q12.

Alleles↗
PubMed1999

No evidence for linkage between schizophrenia and markers at chromosome 15q13-14.

Freedman et al. [1997: Proc Natl Acad Sci USA 94:587-592] reported linkage in nine multiplex schizophrenia families to markers on chromosome 15, using impaired neuronal inhibition to repeated auditory stimuli (P50), a neurophysiological deficit associated with schizophrenia, as the phenotype. The highest LOD score obtained (5.3 at theta = 0) was for marker D15S1360 mapped to chromosome 15q13-14, less than 120 kb from the alpha7-nicotinic receptor (CHRNA7) gene. The study also reported a small positive LOD score for D15S1360 when examined for linkage to the schizophrenia phenotype. Following these findings, we examined three polymorphic markers (D15S1360, L76630, and ACTC) on chromosome 15q13-14 near the CHRNA7 gene for linkage to schizophrenia, using 54 pedigrees from an independent study. Alleles for these three markers were genotyped and analyzed using parametric and nonparametric methods. No LOD score above 1.00 was obtained for any marker, and affected sib-pair analysis likewise showed no evidence for linkage. We conclude that in our families the region around the CHRNA7 locus does not contain a major locus for susceptibility to schizophrenia.

Chromosomes, Human, Pair 15↗
PubMed2000

Analysis of Myc/Max/Mad network members in adipogenesis: inhibition of the proliferative burst and differentiation by ectopically expressed Mad1.

Transcription factors of the Myc/Max/Mad network affect multiple aspects of cellular behavior, including proliferation, differentiation, and apoptosis. Recent studies have shown that Mad proteins can inhibit cellular growth and transformation and thus antagonize the function of Myc proteins. To define further the contribution of these proteins to cellular growth control, we have studied the expression of the respective genes and proteins in 3T3-L1 cells, both upon serum stimulation of quiescent cells and during adipocytic differentiation in response to insulin, dexamethasone, and isobutylmethylxanthine. We found distinct expression patterns for the mad genes. Mad4 was induced when cells exit the cell cycle and, together with mad1, during the late phase of differentiation. In contrast, mad3 expression was associated with progression through S phase and the proliferative burst of differentiating preadipocytes, overlapping in part c-myc expression. DNA binding analyses revealed that the most prominent network complex both in cycling and in differentiating cells was Mnt/Max, whereas c-Myc/Max complexes were detectable only during peak c-Myc expression periods. Ectopic expression of Mad1 in preadipocytes resulted in the inhibition of S phase and the proliferation associated with the proliferative burst; as a consequence, adipocytic differentiation was significantly inhibited. Our findings suggest that the precise temporal regulation of Myc/Max/Mad network proteins is critical for determining cellular behavior.

1-Methyl-3-isobutylxanthine↗
PubMed1996

Analysis of case-control/family sampling design.

A commonly adopted design in genetic epidemiologic studies is the so-called case-control/family sampling design. Here, cases and controls are sampled and response variables, either quantitative or qualitative, for relatives of cases are contrasted with those of control relatives. This design can be used to examine familial aggregation, contribute to identification of genetic subtypes, and test the discrete versus continuous spectrum hypothesis for disorders of unknown etiology. However, the statistical independence assumption required by conventional case-control studies is violated for observations from related individuals who share the same genetic/environmental conditions. Consequently, ignoring dependence among related subjects will lead to incorrect sample size calculations and potentially erratic scientific conclusions. In this paper, we discuss several statistical issues that are relevant to the case-control/family sampling design with a focus on the use of this design in psychiatric research. Specifically, we 1) discuss the relative merit of matched versus unmatched designs; 2) present statistical methods that are useful for analyzing family data and 3) present sample size formulas for studies of quantitative and qualitative traits. A genetic epidemiologic study of schizophrenia is used for illustrative purposes.

Adolescent↗
PubMed1987

Refractory aplastic anemia: concomitant therapy with antithymocyte globulin and high-dose corticosteroids.

Bone marrow transplantation is possible for only a minority of patients with severe aplastic anemia. There has been successful treatment in some patients with immunosuppressive agents: high-dose 6-methylprednisolone, antilymphocyte globulin, and antithymocyte globulin. We report the successful treatment of two patients with severe aplastic anemia with the simultaneous administration of antithymocyte globulin and high-dose 6-methylprednisolone after failure with antithymocyte globulin and low-dose corticosteroids.

Adolescent↗
PubMed1994

Sequential strategy to identify a susceptibility gene for schizophrenia: report of potential linkage on chromosome 22q12-q13.1: Part 1.

To identify genes responsible for the susceptibility for schizophrenia, and to test the hypothesis that schizophrenia is etiologically heterogeneous, we have studied 39 multiplex families from a systematic sample of schizophrenic patients. Using a complex autosomal dominant model, which considers only those with a diagnosis of schizophrenia or schizoaffective disorder as affected, a random search of the genome for detection of linkage was undertaken. Pairwise linkage analyses suggest a potential linkage (LRH = 34.7 or maximum lod score = 1.54) for one region (22q12-q13.1). Reanalyses, varying parameters in the dominant model, maximized the LRH at 660.7 (maximum lod score 2.82). This finding is of sufficient interest to warrant further investigation through collaborative studies.

Adult↗
PubMed1994

Follow-up of a report of a potential linkage for schizophrenia on chromosome 22q12-q13.1: Part 2.

A collaboration involving four groups of investigators (Johns Hopkins University/Massachusetts Institute of Technology; Medical College of Virginia/The Health Research Board, Dublin; Institute of Psychiatry, London/University of Wales, Cardiff; Centre National de la Recherche Scientifique, Paris) was organized to confirm results suggestive of a schizophrenia susceptibility locus on chromosome 22 identified by the JHU/MIT group after a random search of the genome. Diagnostic, laboratory, and analytical reliability exercises were conducted among the groups to ensure uniformity of procedures. Data from genotyping of 3 dinucleotide repeat polymorphisms (at the loci D22S268, IL2RB, D22S307) for a combined replication sample of 256 families, each having 2 or more affected individuals with DNA, were analysed using a complex autosomal dominant model. This study provided no evidence for linkage or heterogeneity for the region 22q12-q13 under this model. We conclude that if this region confers susceptibility to schizophrenia, it must be in only a small proportion of families. Collaborative efforts to obtain large samples must continue to play an important role in the genetic search for clues to complex psychiatric disorders such as schizophrenia.

Adult↗
PubMed1995

Schizophrenia: a genome scan targets chromosomes 3p and 8p as potential sites of susceptibility genes.

Using a systematically ascertained sample of 57 families, each having 2 or more members with a consensus diagnosis of schizophrenia (DSM-III-R criteria), we have carried out linkage studies of 520 loci, covering approximately 70% of the genome for susceptibility loci for schizophrenia. A two-stage strategy based on lod score thresholds from simulation studies of our sample identified regions for further exploration. In each region, a dense map of highly informative dinucleotide repeat polymorphisms (heterozygosity greater than .70) was analyzed using dominant, recessive, and "affected only" models and nonparametric sib pair identity-by-descent methods. For one region, 8p22-p21, affected sib-pair analyses gave a P value = .0001, corresponding to a lod score approximately equal to 3.00. For 8p22-p21, the maximum two-point lod score occurred using the "affected only" recessive model (ZMAX = 2.35; theta M = theta F); allowing for a constant sex difference in recombination fractions found in reference pedigrees, ZMAX = 2.78 (theta M/theta F = 3). For a second region, 3p26-p24, the maximum two-point lod score was 2.34 ("affected only" dominant model), and the affected sib-pair P value was .01. These two regions are worthy of further exploration as potential sites of susceptibility genes for schizophrenia.

Biomarkers↗
PubMed2004

An indirect test of the new mutation hypothesis associating advanced paternal age with the etiology of schizophrenia.

Two studies by Malaspina et al. [2001: Arch Gen Psychiatr 58:361-367]; [2002: Am J Med Genet 114:299-303] have put forward the hypothesis that advanced paternal age with concomitant mutations in the male germ line is associated with sporadic schizophrenia in offspring. The hypothesis was supported by an observation of a monotonic increase in the risk for schizophrenia with increased paternal age, and a second observation in a separate sample of greater paternal mean age at birth among cases of apparent sporadic schizophrenia. The present study did not test the association of the risk of schizophrenia with advanced paternal age, but repeated the test of paternal age at birth among sporadic versus familial schizophrenic probands. We also examined the risk of schizophrenia, psychosis, and broad psychosis among paternal 1st and 2nd degree relatives of schizophrenic probands as a function of paternal age at birth of the proband, reasoning that if probands born to older fathers are more likely to be sporadic cases, the risk of schizophrenia (or psychosis) should be lower on the paternal side of the family. Results indicate a lack of support for the previous finding that sporadic probands tend to have older fathers at birth than familial probands. Results also failed to support the related hypothesis that increased paternal age is associated with the lower risk of schizophrenia (or psychosis) in the relatives of schizophrenic probands. The failure to support the paternal age hypothesis may be a function of heterogeneous samples, but calls for further research in the context of family studies.

Family Health↗
PubMed2002

Orcokinin peptides in developing and adult crustacean stomatogastric nervous systems and pericardial organs.

The orcokinins are a family of neuropeptides recently isolated from several crustacean species. We found orcokinin-like immunoreactivity in the stomatogastric nervous systems and pericardial organs of three decapod crustacean species, Homarus americanus, Cancer borealis, and Panulirus interruptus. The neuropil of the stomatogastric ganglion was stained in adults of all three species as well as in embryonic and larval H. americanus. In H. americanus, the somata giving rise to this projection were found in the inferior ventricular nerve. Matrix-assisted laser desorption/ionization mass spectrometry mass profiling and sequencing with postsource decay led to the identification of six different orcokinin family peptides, including those previously described in other decapods and two novel shorter peptides. Application of exogenous [Ala(13)]orcokinin to the stomatogastric ganglion of H. americanus resulted in changes in the pyloric rhythm. Specifically, the number of lateral pyloric (LP) neuron spikes/burst decreased, and the phase of firing of the pyloric neurons was altered. Together, these data indicate that the orcokinins are likely to function as modulators of the crustacean stomatogastric ganglion.

Aging↗
PubMed2002

Neuromodulatory complement of the pericardial organs in the embryonic lobster, Homarus americanus.

The pericardial organs (POs) are a pair of neurosecretory organs that surround the crustacean heart and release neuromodulators into the hemolymph. In adult crustaceans, the POs are known to contain a wide array of peptide and amine modulators. However, little is known about the modulatory content of POs early in development. We characterize the morphology and modulatory content of pericardial organs in the embryonic lobster, Homarus americanus. The POs are well developed by midway through embryonic (E50) life and contain a wide array of neuromodulatory substances. Immunoreactivities to orcokinin, extended FLRFamide peptides, tyrosine hydroxylase, proctolin, allatostatin, serotonin, Cancer borealis tachykinin-related peptide, cholecystokinin, and crustacean cardioactive peptide are present in the POs by approximately midway through embryonic life. There are two classes of projection patterns to the POs. Immunoreactivities to orcokinin, extended FLRFamide peptides, and tyrosine hydroxylase project solely from the subesophageal ganglion (SEG), whereas the remaining modulators project from the SEG as well as from the thoracic ganglia. Double-labeling experiments with a subset of modulators did not reveal any colocalized peptides in the POs. These results suggest that the POs could be a major source of neuromodulators early in development.

Animals↗
PubMed2003

Dopamine and histamine in the developing stomatogastric system of the lobster Homarus americanus.

Dopamine and histamine are neuromodulators found in the adult stomatogastric nervous system (STNS) of several crustacean species. We used antibodies against tyrosine hydroxylase (TH) and histamine to map the distribution and developmental acquisition of the dopamine and histamine neurons in the STNS of the lobster, Homarus americanus. Embryos, larvae, juvenile and adult animals were studied. TH labeling was present in the STNS as early as E80-85 (80-85% of embryonic development). A subset of preparations in embryos, larvae, juveniles, and adults contained 1-5 labeled somata in the stomatogastric ganglion. Histamine staining appeared in the STNS as early as E50. The distribution of both TH and histamine staining remained relatively constant through development. Electrophysiological recordings demonstrated that receptors for both amines are present in the embryo. Bath application of dopamine increased the frequency of the pyloric rhythm in embryos, and evidence for dopaminergic activation of peripherally initiated spiking in motor axons was seen. In embryos and adults, histamine inhibited the motor patterns produced by the stomatogastric ganglion (STG). These data suggest that the dopaminergic and histaminergic systems in H. americanus appear relatively early in development and that the effects of each are largely maintained through development.

Animals↗
PubMed1988

Application of plasminogen polymorphism to forensic hemogenetics.

Plasminogen polymorphism (PLG) has attained considerable importance in forensic hemogenetics. PLG comprises two common, codominant autosomal alleles, PLG*A and PLG*B, more than 18 variants, and the silent allele PLG*Q0. Isoelectric focusing followed by functional or immunochemical detection seems to be the optimal method for the determination of phenotypes. PLG*A is the most common allele in all populations, having its highest frequency in Mongoloids, Amerindians and Eskimos, the lowest in Caucasoids. The functionally inactive plasminogen M5 so far has been seen exclusively in Japanese individuals. Silent PLG alleles were only observed in the heterozygous state. No clear differences in functional activity or plasma level could be ascertained for any of the other allotypes. PLG polymorphism is now widely used for many haemogenetic investigations. From the allele distribution in European Caucasoids a single exclusion chance of 17.2% for non-fathers in paternity testing may be calculated. The major prerequisites of a new genetic marker in the parentage expertise, established Mendelian inheritance, favorable distribution of common alleles, low frequency of silent alleles, and simple reproducible typing technology, are fulfilled.

Alleles↗