Network


Latest external collaboration on country level. Dive into details by clicking on the dots.

Hotspot


Dive into the research topics where Jessica Ross is active.

Publication


Featured researches published by Jessica Ross.


Journal of Biomedical Informatics | 2011

A practical method for transforming free-text eligibility criteria into computable criteria

Samson W. Tu; Mor Peleg; Simona Carini; Michael Bobak; Jessica Ross; Daniel L. Rubin; Ida Sim

Formalizing eligibility criteria in a computer-interpretable language would facilitate eligibility determination for study subjects and the identification of studies on similar patient populations. Because such formalization is extremely labor intensive, we transform the problem from one of fully capturing the semantics of criteria directly in a formal expression language to one of annotating free-text criteria in a format called ERGO annotation. The annotation can be done manually, or it can be partially automated using natural-language processing techniques. We evaluated our approach in three ways. First, we assessed the extent to which ERGO annotations capture the semantics of 1000 eligibility criteria randomly drawn from ClinicalTrials.gov. Second, we demonstrated the practicality of the annotation process in a feasibility study. Finally, we demonstrate the computability of ERGO annotation by using it to (1) structure a library of eligibility criteria, (2) search for studies enrolling specified study populations, and (3) screen patients for potential eligibility for a study. We therefore demonstrate a new and practical method for incrementally capturing the semantics of free-text eligibility criteria into computable form.


Journal of Affective Disorders | 2011

Towards parenthood: An antenatal intervention to reduce depression, anxiety and parenting difficulties

Jeannette Milgrom; Charlene Schembri; Jennifer Ericksen; Jessica Ross; Alan W. Gemmill

BACKGROUND There have been few antenatal interventions aimed at preparing women for the transition to parenthood and previous attempts to intervene antenatally to prevent postnatal depression and anxiety have had limited impact. METHODS We evaluated the effectiveness of an antenatal intervention which targeted risk factors for poor postnatal adjustment, with the dual aim of reducing both postnatal symptoms of depression/anxiety and parenting difficulties (a nine-unit self-guided workbook with weekly telephone support). Based on an initial feasibility study (n=200) which confirmed a low level of help-seeking among distressed women during pregnancy, an additional community networking component was developed aimed at increasing social support and access to health professionals to facilitate treatment of current antenatal depression/anxiety, if present. In the evaluation of a second version of the intervention, pregnant women (n=143) were randomly allocated to receive either the intervention or routine care. RESULTS Following the antenatal intervention there were significantly fewer cases scoring above threshold for mild-to-severe depression/anxiety symptoms postnatally compared to routine care, along with a trend towards reduced parenting stress. The community networking component appeared helpful and women with higher baseline depression scores showed higher levels of help-seeking in both intervention and routine care groups. LIMITATIONS It was not possible to evaluate the efficacy of individual program components separately. CONCLUSIONS The findings provide support for the effectiveness of the Towards Parenthood intervention both as a preparation for parenthood program and in reducing symptoms of postnatal depression/anxiety.


Biological Psychiatry | 2011

Hippocampal Volume Differences in Gulf War Veterans with Current Versus Lifetime Posttraumatic Stress Disorder Symptoms

Brigitte A. Apfel; Jessica Ross; Jennifer Hlavin; Dieter J. Meyerhoff; Thomas J. Metzler; Charles R. Marmar; Michael W. Weiner; Norbert Schuff; Thomas C. Neylan

BACKGROUND Decreased hippocampal volume is described in posttraumatic stress disorder (PTSD) and depression. However, it is not known whether it is a risk factor for the development of PTSD or a consequence of PTSD. We sought to determine the effects of PTSD and depressive symptoms on hippocampal volume. METHODS Clinical and magnetic resonance imaging data were collected in a cross sectional study of 244 Gulf War veterans. Measures included lifetime and current Clinician Administered PTSD Scale, Hamilton Depression Scale, Life Stressor Checklist, and Lifetime Drinking History. Magnetic resonance imaging data were acquired with a 1.5-T scanner and analyzed with automated and semiautomated image processing techniques. RESULTS Eighty-two veterans had lifetime PTSD, 44 had current PTSD, and 38 had current depression. In the linear regression analysis, current PTSD symptoms (standardized coefficient β = -.25, p = .03) but neither lifetime PTSD symptoms nor current depression were associated with smaller hippocampal volume. Gender, age, history of early life trauma, education, lifetime and current alcohol use, current marijuana use, and treatment with antidepressants did not have independent effects. Participants with chronic PTSD had, on average, a smaller hippocampus compared with those with remitted PTSD. CONCLUSIONS The finding that current but not lifetime PTSD symptom severity explains hippocampal size raises two possibilities: either a small hippocampus is a risk factor for lack of recovery from PTSD (trait) or PTSD effects on hippocampal volume are reversible once PTSD symptoms remit and the patient recovers (state).


Brain Behavior and Immunity | 2011

Suppressed monocyte gene expression profile in men versus women with PTSD

Thomas C. Neylan; Bing Sun; Hans Rempel; Jessica Ross; Maryann Lenoci; Aoife O’Donovan; Lynn Pulliam

There have been several attempts to use gene microarrays from peripheral blood mononuclear cells to identify new biological pathways or targets for therapy in Posttraumatic Stress Disorder (PTSD). The few studies conducted to date have yielded an unclear pattern of findings, perhaps reflecting the use of heterogeneous samples of circulating immune cells for analysis. We used gene microarrays on a homogeneous sample of circulating monocytes to test the hypothesis that chronic PTSD would be associated with elevated inflammatory activity and to identify new pathways dysregulated in the disorder. Forty-nine men (24 PTSD+ and 25 age-matched trauma-exposed PTSD- controls) and 18 women (10 PTSD+ and 8 age-matched PTSD- controls) were recruited. Gene expression microarray analysis was performed on CD14+ monocytes, immune cells that initiate and respond to inflammatory signaling. Male subjects with PTSD had an overall pattern of under-expression of genes on monocytes (47 under-expressed versus 4 over-expressed genes). A rigorous correction for multiple comparisons and verification with qPCR showed that of only 3 genes that were differentially expressed, all were under-expressed. There was no transcriptional evidence of chronic inflammation in male PTSD+ subjects. In contrast, preliminary data from our pilot female PTSD+ subjects showed a relatively balanced pattern of increased and decreased expression of genes and an increase in activity of pathways related to immune activation. The results indicate differential patterns of monocyte gene expression in PTSD, and the preliminary data from our female pilot subjects are suggestive of gender dimorphism in biologic pathways activated in PTSD. Changes in immune cell gene expression may contribute to medical morbidity in PTSD.


Molecular Psychiatry | 2012

Genome Wide Linkage Analysis of 972 Bipolar Pedigrees Using Single Nucleotide Polymorphisms

Daniel L. Koller; Tatiana Foroud; Howard J. Edenberg; John I. Nurnberger; Peter P. Zandi; Virginia L. Willour; Francis J. McMahon; James B. Potash; Marian Lindsay Hamshere; Detelina Grozeva; Elaine K. Green; George Kirov; Ian Richard Jones; Lisa Jones; Nicholas John Craddock; Derek W. Morris; Ricardo Segurado; Michael Gill; Dessa Sadovnick; Ronald A. Remick; Paul E. Keck; John R. Kelsoe; Muhammad Ayub; Alan Maclean; Douglas Blackwood; Chunyu Liu; Elliot S. Gershon; William M. McMahon; Gholson J. Lyon; Reid Robinson

Because of the high costs associated with ascertainment of families, most linkage studies of Bipolar I disorder (BPI) have used relatively small samples. Moreover, the genetic information content reported in most studies has been less than 0.6. Although microsatellite markers spaced every 10 cM typically extract most of the genetic information content for larger multiplex families, they can be less informative for smaller pedigrees especially for affected sib pair kindreds. For these reasons we collaborated to pool family resources and carried out higher density genotyping. Approximately 1100 pedigrees of European ancestry were initially selected for study and were genotyped by the Center for Inherited Disease Research using the Illumina Linkage Panel 12 set of 6090 single-nucleotide polymorphisms. Of the ∼1100 families, 972 were informative for further analyses, and mean information content was 0.86 after pruning for linkage disequilibrium. The 972 kindreds include 2284 cases of BPI disorder, 498 individuals with bipolar II disorder (BPII) and 702 subjects with recurrent major depression. Three affection status models (ASMs) were considered: ASM1 (BPI and schizoaffective disorder, BP cases (SABP) only), ASM2 (ASM1 cases plus BPII) and ASM3 (ASM2 cases plus recurrent major depression). Both parametric and non-parametric linkage methods were carried out. The strongest findings occurred at 6q21 (non-parametric pairs LOD 3.4 for rs1046943 at 119 cM) and 9q21 (non-parametric pairs logarithm of odds (LOD) 3.4 for rs722642 at 78 cM) using only BPI and schizoaffective (SA), BP cases. Both results met genome-wide significant criteria, although neither was significant after correction for multiple analyses. We also inspected parametric scores for the larger multiplex families to identify possible rare susceptibility loci. In this analysis, we observed 59 parametric LODs of 2 or greater, many of which are likely to be close to maximum possible scores. Although some linkage findings may be false positives, the results could help prioritize the search for rare variants using whole exome or genome sequencing.


Journal of Medical Internet Research | 2016

Internet Cognitive Behavioral Therapy for Women With Postnatal Depression: A Randomized Controlled Trial of MumMoodBooster

Jeannette Milgrom; Brian G. Danaher; Alan W. Gemmill; Charlene Holt; Christopher J. Holt; John R. Seeley; Milagra S Tyler; Jessica Ross; Jennifer Ericksen

Background There are few published controlled trials examining the efficacy of Internet-based treatment for postnatal depression (PND) and none that assess diagnostic status (clinical remission) as the primary outcome. This is despite the need to improve treatment uptake and accessibility because fewer than 50% of postnatally depressed women seek help, even when identified as depressed. Objective In a randomized controlled trial (RCT), we aimed to test the efficacy of a 6-session Internet intervention (the MumMoodBooster program, previously evaluated in a feasibility trial) in a sample of postnatal women with a clinical diagnosis of depression. The MumMoodBooster program is a cognitive behavioral therapy (CBT) intervention, is highly interactive, includes a partner website, and was supported by low-intensity telephone coaching. Methods This was a parallel 2-group RCT (N=43) comparing the Internet CBT treatment (n=21) to treatment as usual (n=22). At baseline and at 12 weeks after enrollment, women’s diagnostic status was assessed by telephone with the Standardized Clinical Interview for DSM-IV (SCID-IV) and symptom severity with the Beck Depression Inventory (BDI-II). Depression symptoms were measured repeatedly throughout the study period with the Patient Health Questionnaire (PHQ-9). Results At the end of the study, 79% (15/19) of women who received the Internet CBT treatment no longer met diagnostic criteria for depression on the SCID-IV (these outcome data were missing for 2 intervention participants). This contrasted with only 18% (4/22) remission in the treatment as usual condition. Depression scores on the BDI-II showed a large effect favoring the intervention group (d=.83, 95% CI 0.20-1.45). Small to medium effects were found on the PHQ-9 and on measures of anxiety and stress. Adherence to the program was very good with 86% (18/21) of users completing all sessions; satisfaction with the program was rated 3.1 out of 4 on average. Conclusions Our results suggest that our Internet CBT program, MumMoodBooster, is an effective treatment option for women clinically diagnosed with PND. This is one of only two controlled evaluations of specialized online psychological treatment among women clinically diagnosed with PND. MumMoodBooster appears to be a feasible, effective treatment option, which is potentially accessible to large numbers of women in metropolitan, rural, and remote areas. Future work might be focused profitably on establishing comparability with face-to-face treatments and purely self-guided delivery. We have commenced a larger RCT comparing MumMoodBooster with face-to-face CBT. Trial Registration Australian and New Zealand Clinical Trials Registry (ANZCTR): ACTRN12613000113752; https://www.anzctr.org.au/Trial/Registration/TrialReview.aspx?id=363561 (Archived by WebCite® at http://www.webcitation.org/6f64kuyLf).


Psychiatric Genetics | 2008

Genome-wide parametric linkage analyses of 644 bipolar pedigrees suggest susceptibility loci at chromosomes 16 and 20

Jessica Ross; Wade H. Berrettini; William Coryell; Elliot S. Gershon; John R. Kelsoe; Melvin G. McInnis; Francis J. McMahon; Dennis L. Murphy; John I. Nurnberger; Tatiana Foroud; John P. Rice; W. Scheftner; Peter P. Zandi; Howard J. Edenberg; William Byerley

Objective Our aim is to map chromosomal regions that harbor loci that increase susceptibility to bipolar disorder. Methods We analyzed 644 bipolar families ascertained by the National Institute of Mental Health Human Genetics Initiative for bipolar disorder. The families have been genotyped with microsatellite loci spaced every approximately 10 cM or less across the genome. Earlier analyses of these pedigrees have been limited to nonparametric (model-free) methods and thus, information from unaffected subjects with genotypes was not considered. In this study, we used parametric analyses assuming dominant and recessive transmission and specifying a maximum penetrance of 70%, so that information from unaffecteds could be weighed in the linkage analyses. As in previous linkage analyses of these pedigrees, we analyzed three diagnostic categories: model 1 included only bipolar I and schizoaffective, bipolar cases (1565 patients of whom approximately 4% were schizoaffective, bipolar); model 2 included all individuals in model 1 plus bipolar II patients (1764 total individuals); and model 3 included all individuals in model 2 with the addition of patients with recurrent major depressive disorder (2046 total persons). Results Assuming dominant inheritance the highest genome-wide pair-wise logarithm of the odds (LOD) score was 3.2 with D16S749 using model 2 patients. Multipoint analyses of this region yielded a maximum LOD score of 4.91. Under recessive transmission a number of chromosome 20 markers were positive and multipoint analyses of the area gave a maximum LOD of 3.0 with model 2 cases. Conclusion The chromosome 16p and 20 regions have been implicated by some studies and the data reported herein provide additional suggestive evidence of bipolar susceptibility genes in these regions.


Current Opinion in Pulmonary Medicine | 2002

The molecular biology of lung cancer

Jessica Ross; Glenn D. Rosen

Lung cancer is the result of molecular changes that occur in the cell, resulting in the deregulation of pathways which control normal cellular growth, differentiation, and apoptosis. Several of these pathways contain well-characterized proto-oncogenes and tumor suppressor genes which are found to be mutated or have abnormal expression patterns in lung cancer. The molecular changes that characterize lung cancer are complex, but it is known that cigarette smoking causes most squamous cell and small-cell carcinomas. However, the association between cigarette smoke and adenocarcinoma is less clear. Environmental factors, such as air pollutants, radon, and asbestos, likely contribute to the development of lung cancer. In this review, we discuss the major molecular abnormalities in lung cancer with a review of recent studies that begin to decipher the role that different tumor suppressor genes and oncogenes play in the pathogenesis of lung cancer. Also, we highlight the research that has identified new genes which may play a role in lung cancer pathogenesis or progression.


Molecular Neuropsychiatry | 2016

A Rare Variant in CACNA1D Segregates with 7 Bipolar I Disorder Cases in a Large Pedigree

Jessica Ross; Erika Gedvilaite; Carolyn Erdman; Lisa Baird; Nori Matsunami; M. Leppert; Jinchuan Xing; William Byerley

Whole-genome sequencing was performed on 3 bipolar I disorder (BPI) cases from a multiplex pedigree of European ancestry with 7 BPI cases. Within CACNA1D, a gene implicated by genome-wide association studies, a G to C nucleotide transversion at 53,835,340 base pairs (bps) was found predicting the substitution of proline for alanine at amino acid position 1751 (A1751P). Using Sanger sequencing, the DNA variant was shown to co-segregate with the remaining 4 BPI cases within the pedigree. A high-resolution DNA denaturing curve method was then used to screen for the presence of the A1751P change in 4,150 BPI cases from the NIMH Genetics Initiative. The A1751P variant was found in 4 BPI cases. A second variant within exon 43, a C to T nucleotide transition, was found in 1 case at 53,835,355 bps, predicting the substitution of tryptophan for arginine at amino acid position 1771 (R1771W). In the NHLBI Exome Sequencing Project database, the heterozygous A1751P variant was present in 3 of 4,300 subjects of European ancestry, and the R1771W change was not present in any subject. Given the rarity of these variants, large-scale case/control rare variant sequencing studies will be required for definitive conclusions.


Psychiatry Research-neuroimaging | 2018

The effects of early trauma and the FKBP5 gene on PTSD and the HPA axis in a clinical sample of Gulf War veterans

Dmitri A. Young; Sabra S. Inslicht; Thomas J. Metzler; Thomas C. Neylan; Jessica Ross

Previous research indicates that interactions between FKBP5 single nucleotide polymorphisms (SNPs) and child abuse are associated with posttraumatic stress disorder (PTSD) in adulthood. We examined the relationship between the T-allele of the rs1360780 FKBP5 SNP and child abuse on PTSD and the HPA axis in a clinical sample of Gulf War veterans. Genotyping was completed on 266 veterans and 174 veterans additionally participated in a low dose dexamethasone suppression test (DST). The CAPS was used to determine PTSD status and the THQ was used to determine child abuse operationalized as either childhood physical or sexual abuse. Hierarchical regression models were used to assess FKBP5 × child abuse interactions on PTSD, basal cortisol levels, and post DST cortisol levels. The FKBP5 risk allele and child abuse were separately associated with PTSD diagnosis. The risk allele was also associated with significantly lower cortisol levels at baseline. However, no significant FKBP5 × child abuse interaction on PTSD diagnosis, basal cortisol levels, or greater cortisol suppression was observed. Our results suggest that FKBP5 may be a viable biomarker for PTSD. Nonetheless, further work will be required to reconcile our findings with previous reports of an FKBP5 × child abuse interaction on posttraumatic stress response.

Collaboration


Dive into the Jessica Ross's collaboration.

Top Co-Authors

Avatar
Top Co-Authors

Avatar

Ida Sim

University of California

View shared research outputs
Top Co-Authors

Avatar

Thomas J. Metzler

San Francisco VA Medical Center

View shared research outputs
Top Co-Authors

Avatar

Glenn D. Rosen

Beth Israel Deaconess Medical Center

View shared research outputs
Top Co-Authors

Avatar
Top Co-Authors

Avatar

Simona Carini

University of California

View shared research outputs
Top Co-Authors

Avatar
Top Co-Authors

Avatar
Top Co-Authors

Avatar
Top Co-Authors

Avatar

Charles R. Marmar

San Francisco VA Medical Center

View shared research outputs
Researchain Logo
Decentralizing Knowledge