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There is a genetic contribution to the risk of suicide, but sparse prior research on the genetics of suicidal ideation.
Active and passive suicidal ideation were assessed in a Sri Lankan population-based twin registry (n = 3906 twins) and a matched non-twin sample (n = 2016). Logistic regression models were used to examine associations with socio-demographic factors, environmental exposures and psychiatric symptoms. The heritability of suicidal ideation was assessed using structural equation modelling.
The lifetime prevalence of any suicidal ideation was 13.0% (11.7–14.3%) for men; 21.8% (20.3–23.2%) for women, with no significant difference between twins and non-twins. Factors that predicted suicidal ideation included female gender, termination of marital relationship, low education level, urban residence, losing a parent whilst young, low standard of living and stressful life events in the preceding 12 months. Suicidal ideation was strongly associated with depression, but also with abnormal fatigue and alcohol and tobacco use. The best fitting structural equation model indicated a substantial contribution from genetic factors (57%; CI 47–66) and from non-shared environmental factors (43%; CI 34–53) in both men and women. In women this genetic component was largely mediated through depression, but in men there was a significant heritable component to suicidal ideation that was independent of depression.
These are the first results to show a genetic contribution to suicidal ideation that is independent of depression outside of a high-income country. These phenomena may be generalizable, because previous research highlights similarities between the aetiology of mental disorders in Sri Lanka and higher-income countries.
Psychiatric research has entered the age of 'Big Data'. Datasets now routinely involve thousands of heterogeneous variables, including clinical, neuroimaging, genomic, proteomic, transcriptomic and other 'omic' measures. The analysis of these datasets is challenging, especially when the number of measurements exceeds the number of individuals, and may be further complicated by missing data for some subjects and variables that are highly correlated. Statistical learning-based models are a natural extension of classical statistical approaches but provide more effective methods to analyse very large datasets. In addition, the predictive capability of such models promises to be useful in developing decision support systems. That is, methods that can be introduced to clinical settings and guide, for example, diagnosis classification or personalized treatment. In this review, we aim to outline the potential benefits of statistical learning methods in clinical research. We first introduce the concept of Big Data in different environments. We then describe how modern statistical learning models can be used in practice on Big Datasets to extract relevant information. Finally, we discuss the strengths of using statistical learning in psychiatric studies, from both research and practical clinical points of view.
Major depressive disorder (MDD) is a common and disabling condition with well-established heritability and environmental risk factors. Gene–environment interaction studies in MDD have typically investigated candidate genes, though the disorder is known to be highly polygenic. This study aims to test for interaction between polygenic risk and stressful life events (SLEs) or childhood trauma (CT) in the aetiology of MDD.
The RADIANT UK sample consists of 1605 MDD cases and 1064 controls with SLE data, and a subset of 240 cases and 272 controls with CT data. Polygenic risk scores (PRS) were constructed using results from a mega-analysis on MDD by the Psychiatric Genomics Consortium. PRS and environmental factors were tested for association with case/control status and for interaction between them.
PRS significantly predicted depression, explaining 1.1% of variance in phenotype (p = 1.9 × 10−6). SLEs and CT were also associated with MDD status (p = 2.19 × 10−4 and p = 5.12 × 10−20, respectively). No interactions were found between PRS and SLEs. Significant PRSxCT interactions were found (p = 0.002), but showed an inverse association with MDD status, as cases who experienced more severe CT tended to have a lower PRS than other cases or controls. This relationship between PRS and CT was not observed in independent replication samples.
CT is a strong risk factor for MDD but may have greater effect in individuals with lower genetic liability for the disorder. Including environmental risk along with genetics is important in studying the aetiology of MDD and PRS provide a useful approach to investigating gene–environment interactions in complex traits.
Strategies to dissect phenotypic and genetic heterogeneity of major depressive disorder (MDD) have mainly relied on subphenotypes, such as age at onset (AAO) and recurrence/episodicity. Yet, evidence on whether these subphenotypes are familial or heritable is scarce. The aims of this study are to investigate the familiality of AAO and episode frequency in MDD and to assess the proportion of their variance explained by common single nucleotide polymorphisms (SNP heritability).
For investigating familiality, we used 691 families with 2–5 full siblings with recurrent MDD from the DeNt study. We fitted (square root) AAO and episode count in a linear and a negative binomial mixed model, respectively, with family as random effect and adjusting for sex, age and center. The strength of familiality was assessed with intraclass correlation coefficients (ICC). For estimating SNP heritabilities, we used 3468 unrelated MDD cases from the RADIANT and GSK Munich studies. After similarly adjusting for covariates, derived residuals were used with the GREML method in GCTA (genome-wide complex trait analysis) software.
Significant familial clustering was found for both AAO (ICC = 0.28) and episodicity (ICC = 0.07). We calculated from respective ICC estimates the maximal additive heritability of AAO (0.56) and episodicity (0.15). SNP heritability of AAO was 0.17 (p = 0.04); analysis was underpowered for calculating SNP heritability of episodicity.
AAO and episodicity aggregate in families to a moderate and small degree, respectively. AAO is under stronger additive genetic control than episodicity. Larger samples are needed to calculate the SNP heritability of episodicity. The described statistical framework could be useful in future analyses.
Although usually thought of as external environmental stressors, a significant heritable component has been reported for measures of stressful life events (SLEs) in twin studies.
We examined the variance in SLEs captured by common genetic variants from a genome-wide association study (GWAS) of 2578 individuals. Genome-wide complex trait analysis (GCTA) was used to estimate the phenotypic variance tagged by single nucleotide polymorphisms (SNPs). We also performed a GWAS on the number of SLEs, and looked at correlations between siblings.
A significant proportion of variance in SLEs was captured by SNPs (30%, p = 0.04). When events were divided into those considered to be dependent or independent, an equal amount of variance was explained for both. This 'heritability' was in part confounded by personality measures of neuroticism and psychoticism. A GWAS for the total number of SLEs revealed one SNP that reached genome-wide significance (p = 4 × 10−8), although this association was not replicated in separate samples. Using available sibling data for 744 individuals, we also found a significant positive correlation of R2 = 0.08 in SLEs (p = 0.03).
These results provide independent validation from molecular data for the heritability of reporting environmental measures, and show that this heritability is in part due to both common variants and the confounding effect of personality.
It has been well established that both genes and non-shared environment contribute substantially to the underlying aetiology of major depressive disorder (MDD). A comprehensive overview of genetic research in MDD is presented.
Papers were retrieved from PubMed up to December 2011, using many keywords including: depression, major depressive disorder, genetics, rare variants, gene–environment, whole genome, epigenetics, and specific candidate genes and variants. These were combined in a variety of permutations.
Linkage studies have yielded some promising chromosomal regions in MDD. However, there is a continued lack of consistency in association studies, in both candidate gene and genome-wide association studies (GWAS). Numerous factors may account for variable results including the use of different diagnostic approaches, small samples in early studies, population stratification, epigenetic phenomena, copy number variation (CNV), rare variation, and phenotypic and allelic heterogeneity. The conflicting results are also probably, in part, a consequence of environmental factors not being considered or controlled for.
Each research group has to identify what issues their sample may best address. We suggest that, where possible, more emphasis should be placed on the environment in molecular behavioural genetics to identify individuals at environmental high risk in addition to genetic high risk. Sequencing should be used to identify rare and alternative variation that may act as a risk factor, and a systems biology approach including gene–gene interactions and pathway analyses would be advantageous. GWAS may require even larger samples with reliably defined (sub)phenotypes.
It has been proposed that non-steroidal anti-inflammatory drugs (NSAIDs) may interfere with the efficacy of antidepressants and contribute to treatment resistance in major depressive disorder (MDD). This effect requires replication and a test of whether it is specific to serotonin-reuptake inhibiting (SRI) antidepressants.
We tested the effect of concomitant medication with NSAIDs on the efficacy of escitalopram, a SRI antidepressant, and nortriptyline, a tricyclic antidepressant, among 811 subjects with MDD treated for up to 12 weeks in the GENDEP study. Effects of NSAIDs on improvement of depressive symptoms were tested in mixed-effect linear models. Effects on remission were tested in logistic regression. Age, sex, baseline severity and centre of recruitment were considered as potential confounding factors.
Ten percent (n=78) of subjects were taking NSAIDs during the antidepressant treatment. Older subjects were significantly more likely to take NSAIDs. After controlling for age, sex, centre of recruitment and baseline severity, concomitant medication with NSAIDs did not significantly influence the efficacy of escitalopram [β=0.035, 95% confidence interval (CI) −0.145 to 0.215, p=0.704] or nortriptyline (β=0.075, 95% CI −0.131 to 0.281, p=0.476). Although slightly fewer subjects who took NSAIDs reached remission [odds ratio (OR) 0.80, 95% CI 0.49–1.31, p=0.383], this non-significant effect was reversed after controlling for age, sex, baseline severity and recruitment centre effects (OR 1.04, 95% CI 0.61–1.77, p=0.882).
NSAIDs are unlikely to affect the efficacy of SRI or other antidepressants. Concurrent use of NSAIDs and antidepressants does not need to be avoided.
Symptom dimensions have not yet been comprehensively tested as predictors of the substantial heterogeneity in outcomes of antidepressant treatment in major depressive disorder.
We tested nine symptom dimensions derived from a previously published factor analysis of depression rating scales as predictors of outcome in 811 adults with moderate to severe depression treated with flexibly dosed escitalopram or nortriptyline in Genome-based Therapeutic Drugs for Depression (GENDEP). The effects of symptom dimensions were tested in mixed-effect regression models that controlled for overall initial depression severity, age, sex and recruitment centre. Significant results were tested for replicability in 3637 adult out-patients with non-psychotic major depression treated with citalopram in level I of Sequenced Treatment Alternatives to Relieve Depression (STAR*D).
The interest-activity symptom dimension (reflecting low interest, reduced activity, indecisiveness and lack of enjoyment) at baseline strongly predicted poor treatment outcome in GENDEP, irrespective of overall depression severity, antidepressant type and outcome measure used. The prediction of poor treatment outcome by the interest-activity dimension was robustly replicated in STAR*D, independent of a comprehensive list of baseline covariates.
Loss of interest, diminished activity and inability to make decisions predict poor outcome of antidepressant treatment even after adjustment for overall depression severity and other clinical covariates. The prominence of such symptoms may require additional treatment strategies and should be accounted for in future investigations of antidepressant response.
Childhood adversity has been associated with onset of psychosis in adulthood but these studies have used only general definitions of this environmental risk indicator. Therefore, we sought to explore the prevalence of more specific adverse childhood experiences amongst those with and without psychotic disorders using detailed assessments in a large epidemiological case-control sample (AESOP).
Data were collected on 182 first-presentation psychosis cases and 246 geographically matched controls in two UK centres. Information relating to the timing and frequency of exposure to different types of childhood adversity (neglect, antipathy, physical and sexual abuse, local authority care, disrupted living arrangements and lack of supportive figure) was obtained using the Childhood Experience of Care and Abuse Questionnaire.
Psychosis cases were three times more likely to report severe physical abuse from the mother that commenced prior to 12 years of age, even after adjustment for other significant forms of adversity and demographic confounders. A non-significant trend was also evident for greater prevalence of reported severe maternal antipathy amongst those with psychosis. Associations with maternal neglect and childhood sexual abuse disappeared after adjusting for maternal physical abuse and antipathy. Paternal maltreatment and other forms of adversity were not associated with psychosis nor was there evidence of a dose–response effect.
These findings suggest that only specific adverse childhood experiences are associated with psychotic disorders and only in a minority of cases. If replicated, this greater precision will ensure that research into the mechanisms underlying the pathway from childhood adversity to psychosis is more fruitful.
Studies exploring gene–environment interplay in affective disorders now include very large numbers of participants. Methods for evaluating the role of adversity in such studies need to be developed that do not rely on lengthy and labour-intensive interviews. In the present study, a brief questionnaire method for measuring 11 adverse events reported before interview and before their worst illness episodes by bipolar, unipolar and healthy control participants, participating in genetic association studies, was evaluated.
Five hundred and twelve bipolar disorder (BD) participants, 1447 participants with recurrent unipolar depression (UPD) and 1346 psychiatrically healthy control participants underwent the researcher-administered version of the List of Threatening Experiences Questionnaire (LTE-Q) for the 6 months before their worst affective episodes for UPD and BD participants, and for the 6 months before interview for the UPD participants and controls.
UPD and BD cases were significantly more likely to report at least one event, as well as more events in the 6 months before interview and before their worst illness episodes, than healthy controls. Both manic and depressive episodes were significantly associated with adverse events in the BD cases. Depressed mood at the time of interview influenced event reporting in UPD and control participants but not the BD cases. Age was negatively correlated with the number of events reported by controls.
The researcher-administered LTE-Q provides a measure of case-control differences for adversity that is applicable in large genetic association studies. Confounding factors for event reporting include present mood and age.
Response and remission defined by cut-off values on the last observed depression severity score are commonly used as outcome criteria in clinical trials, but ignore the time course of symptomatic change and may lead to inefficient analyses. We explore alternative categorization of outcome by naturally occurring trajectories of symptom change.
Growth mixture models were applied to repeated measurements of depression severity in 807 participants with major depression treated for 12 weeks with escitalopram or nortriptyline in the part-randomized Genome-based Therapeutic Drugs for Depression study. Latent trajectory classes were validated as outcomes in drug efficacy comparison and pharmacogenetic analyses.
The final two-piece growth mixture model categorized participants into a majority (75%) following a gradual improvement trajectory and the remainder following a trajectory with rapid initial improvement. The rapid improvement trajectory was over-represented among nortriptyline-treated participants and showed an antidepressant-specific pattern of pharmacogenetic associations. In contrast, conventional response and remission favoured escitalopram and produced chance results in pharmacogenetic analyses. Controlling for drop-out reduced drug differences on response and remission but did not affect latent trajectory results.
Latent trajectory mixture models capture heterogeneity in the development of clinical response after the initiation of antidepressants and provide an outcome that is distinct from traditional endpoint measures. It differentiates between antidepressants with different modes of action and is robust against bias due to differential discontinuation.
Many studies have used negative mood induction techniques to investigate the effect of emotional state on cognitive performance but positive mood induction paradigms have been used less frequently. The objective of this study was to investigate the effect of positive mood induction on emotional processing in euthymic individuals with bipolar disorder (BD) and controls.
Previously, we reported that positive mood induction using a novel technique based on feedback produced a longer-lasting effect in euthymic individuals with BD than controls (Farmer et al. 2006). Here we report the effect of mood induction on two tests of emotional processing, the Affective Go/No-go test (AGNG) and the Cambridge Gamble task (CGT), on which BD patients in the manic phase differ in their performance from controls.
Following positive mood induction, bipolar cases exhibited a positive emotional bias on the AGNG and performed more slowly than controls on the CGT, particularly when making more difficult decisions.
These data confirm that positive mood induction is more effective in individuals with BD than controls. They also suggest that alterations in decision making and attentional biases occur even with transient and subtle changes in mood in bipolar disorder.
A number of scales are used to estimate the severity of depression. However, differences between self-report and clinician rating, multi-dimensionality and different weighting of individual symptoms in summed scores may affect the validity of measurement. In this study we examined and integrated the psychometric properties of three commonly used rating scales.
The 17-item Hamilton Depression Rating Scale (HAMD-17), the Montgomery–Asberg Depression Rating Scale (MADRS) and the Beck Depression Inventory (BDI) were administered to 660 adult patients with unipolar depression in a multi-centre pharmacogenetic study. Item response theory (IRT) and factor analysis were used to evaluate their psychometric properties and estimate true depression severity, as well as to group items and derive factor scores.
The MADRS and the BDI provide internally consistent but mutually distinct estimates of depression severity. The HAMD-17 is not internally consistent and contains several items less suitable for out-patients. Factor analyses indicated a dominant depression factor. A model comprising three dimensions, namely 'observed mood and anxiety', 'cognitive' and 'neurovegetative', provided a more detailed description of depression severity.
The MADRS and the BDI can be recommended as complementary measures of depression severity. The three factor scores are proposed for external validation.
Background. We describe the development, reliability and applications of the Diagnostic Interview for Psychoses (DIP), a comprehensive interview schedule for psychotic disorders.
Method. The DIP is intended for use by interviewers with a clinical background and was designed to occupy the middle ground between fully structured, lay-administered schedules, and semi-structured, psychiatrist-administered interviews. It encompasses four main domains: (a) demographic data; (b) social functioning and disability; (c) a diagnostic module comprising symptoms, signs and past history ratings; and (d) patterns of service utilization and patient-perceived need for services. It generates diagnoses according to several sets of criteria using the OPCRIT computerized diagnostic algorithm and can be administered either on-screen or in a hard-copy format.
Results. The DIP proved easy to use and was well accepted in the field. For the diagnostic module, inter-rater reliability was assessed on 20 cases rated by 24 clinicians: good reliability was demonstrated for both ICD-10 and DSM-III-R diagnoses. Seven cases were interviewed 2–11 weeks apart to determine test–retest reliability, with pairwise agreement of 0·8–1·0 for most items. Diagnostic validity was assessed in 10 cases, interviewed with the DIP and using the SCAN as 'gold standard': in nine cases clinical diagnoses were in agreement.
Conclusions. The DIP is suitable for use in large-scale epidemiological studies of psychotic disorders, as well as in smaller studies where time is at a premium. While the diagnostic module stands on its own, the full DIP schedule, covering demography, social functioning and service utilization makes it a versatile multi-purpose tool.
Background. Current cognitive theories propose that depression develops as a result of the interaction between dysfunctional cognitive schemata and environmental stressors. There is also consistent evidence of a substantial genetic contribution to depression. This study examines the familiality and stability of dysfunctional attitudes and attempts to distinguish whether they reflect trait vulnerability to depression or the state of being depressed.
Method. The 24-item Dysfunctional Attitude Scale (DAS-24) was completed by 108 depressed probands and their nearest-aged siblings and 105 healthy control probands and their nearest-age siblings, at the time of a semi-structured clinical interview and 10–12 months later. Subjects also completed self-report measures of depressed mood on both occasions.
Results. Measures of clinical depression were significantly correlated with DAS scores. At retest, DAS scores remained elevated despite improvement in mood, giving support for earlier findings, that dysfunctional attitudes remain active following recovery.
The dependency subscale (DAS-D) of the DAS showed modest familiality, although there were no significant differences for DAS-D scores between the two groups of siblings. In a multiple regression analysis, current mood-state was the overwhelming predictor of DAS scores. However for DAS-D, gender as well as current mood influenced scores on this subscale.
Conclusion. Although there was modest evidence for temporal stability and familiality for some DAS-24 subscale scores, dysfunctional attitudes were predominantly influenced by current low mood, and therefore reflect the state of being depressed rather than a familial vulnerability trait underpinning depression.
Background. The overall aim of the GENESiS project is to identify quantitative trait loci (QTLs) for anxiety/depression, and to examine the interaction between these loci and psychosocial adversity. Here we present life-events data with the aim of clarifying: (i) the aetiology of life events as inferred from sibling correlations; (ii) the relationship between life events and measures of anxiety and depression, as well as neuroticism; and (iii) the interaction between life events and neuroticism on anxiety/depression indices.
Methods. We assessed the occurrence of one network and three personal life-event categories and multiple indices of anxiety/depression including General Health Questionnaire, Anhedonic Depression, Anxious Arousal and Neuroticism in a large community-based sample of 2150 sib pairs, 410 trios and 81 quads. Liability threshold models and raw ordinal maximum likelihood were used to estimate within-individual and between-sibling correlations of life events. The relationship between life events and indices of emotional states and personality were assessed by multiple linear regression and canonical correlations.
Results. Life events showed sibling correlations of 0·37 for network events and between 0·10 and 0·19 for personal events. Adverse life events were related to anxiety and depression and, to a less extent, neuroticism. Trait-vulnerability (as indexed by co-sib's neuroticism, anxiety and depression) accounted for 11% and life events for 3% of the variance in emotional states. There were no interaction effects.
Conclusions. Life events show moderate familiality and are significantly related to symptoms of anxiety and depression in the community. Appropriate modelling of life events in linkage and association analyses should help to identify QTLs for depression and anxiety.
Most forms of behaviour whether normal or abnormal, show a tendency to run in families. However, these can range from symptoms of dementia and movement disorder caused by the comparatively rare autosomal dominant Huntington's disease to common everyday aspects of behaviour such as religious persuasion or career choice. Normal behaviours and most common disorders do not show simple mendelian inheritance but instead have more complex patterns of transmission involving either major genes with incomplete penetrance, multiple genes of small effect, or a combination of the two. In addition, common complex phenotypes usually involve the combination of genetic and environmental factors. Therefore once family studies have shown that a disorder or trait is familial the next stage is to perform twin studies and, if possible adoption studies to investigate whether this results from shared genes, shared environment or a combination of the two.
Background. Medically unexplained chronic fatigue in childhood
may cause considerable disability
and (by definition) its cause remains unclear. A study of fatigue in healthy
twins has been
undertaken to examine whether or not genetic factors play a part.
Method. A questionnaire survey of the main carers of an epidemiological
population-based sample
of 670 twin pairs who were asked about periods of unexplained and disabling
fatigue in their twins.
Out of 1340 individuals a period of disabling fatigue was reported for
92 (6·9%). Thirty-three
(2·5%) reported disabling fatigue for more than 1 month. Zygosity
could be confidently assigned
in 98% of the sample providing 278 monozygotic (MZ) and 378 dizygotic (DZ)
pairs. These data
were analysed using a structural equation modelling approach.
Results. The results showed that disabling fatigue in childhood
is highly familial with an MZ
tetrachoric correlation (rMZ) of 0·81 and a DZ tetrachoric correlation
(rDZ) of 0·59, for fatigue
lasting at least a week. The most acceptable model using Akaike's
information criteria, was one
containing additive genetic effects (A) and shared environment (C) plus
residual (or non-shared)
environment (E). For fatigue lasting at least a month rMZ was 0·75
and rDZ 0·47. The most
acceptable model included just A and E. However, the role of shared environment
could not be
conclusively rejected.
Conclusions. Unexplained disabling fatigue in childhood is
substantially familial. Both genetic and
shared environmental factors are worth further exploration in a search
for the causes.
Background. Affected sibling pairs provide a valuable
means of investigating the familial basis of
clinical heterogeneity in schizophrenia.
Methods. Associations of schizophrenia subtypes, psychotic
symptoms (defined by SAPS/SANS
and OPCRIT), affective episodes and demographic variables were studied
in 109 sibling pairs with
DSM-IV schizophrenia or schizoaffective disorder.
Results. None of the subtypes or affective episodes were
significantly associated within pairs. A
broad definition of positive formal thought disorder, grandiose
delusions and delusions of influence
(all from OPCRIT) were modestly associated. There was no excess of same-sex
pairs. There were
modest associations for age of illness onset, pre-morbid adjustment
and illness severity. Caution is
required in interpreting the results because many statistical tests were
carried out.
Conclusions. None of the variables appears to be closely
associated with specific genetic or shared
environmental factors that contribute liability to schizophrenia. They
are at best only weakly
associated with such factors, and/or are associated with factors unrelated
to the aetiology of
Recent studies have suggested that expanded CAG/CTG repeats contribute to the genetic aetiology of schizophrenia and bipolar disorder. However, the nature of this contribution is uncertain and difficult to predict from other known trinucleotide repeat diseases that display much simpler patterns of inheritance. We have sought to replicate and extend earlier findings using Repeat Expansion Detection in an enlarged sample of 152 patients with schizophrenia, 143 patients with bipolar disorder, and 160 controls. We have also examined DNA from the parents of 62 probands with schizophrenia or bipolar disorder. Our results confirm our earlier, preliminary findings of an association between expanded trinucleotide repeats and both schizophrenia and bipolar disorder. However, our data do not support the hypothesis that trinucleotide repeat expansion can alone explain the complex patterns of inheritance of the functional psychoses neither can this mechanism fully explain apparent anticipation.
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PDF Death and the Detective (The Death Series Book 2)
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Three County Cork road workers were returning from a job in Carrigaline, Ireland, when they saw a pothole. They stopped and repaired the pothole. A Health and Safety worker saw them, and the three men were consequently suspended from their jobs because they had not filed the proper paperwork for this particular pothole before repairing it.
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The holidays have arrived and do we have some treats for you!
We all know that the minute Halloween is over, everyone begins planning their holidays. Not to be out done, Chef Andres has a few treats up his sleeve.
First off, he has decided to host his 2nd annual Thanksgiving Wine Dinner on Thursday November 16th! But no worries...there will be no turkey (since we know you all will be getting enough of that on the actual day of Thanksgiving). Check out our events page for more information.
For the 4th year, Chef Andres will be doing what almost no Italian Restaurant in Fort Lauderdale is doing....a full "Feast of the Seven Fishes" dinner for Christmas Eve. He is currently finalizing the menu...so stay tuned here for details as they are available. But make sure to call to reserve your table because this dinner sells out quickly!
And we save the best for last! We can't give away too many details at the moment, but make sure to follow us on social media as we release details on some up coming pop-up dinners and collaborations with other local Chefs. We are thrilled and can't wait to share all the deliciousness with you all!
Cheers and Happy Holidays!


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The SCCBA Family Law Section presents an MCLE Brown Bag:
This seminar is designed to acquaint attendees with the types of experts that are used in family law cases and how to choose one.
It can be difficult to select an expert. The panelists will cover what experts have been helpful. How and when to use as expert, how to find an expert and how to work with an expert.
MCLE CREDIT: 1.0 General Substantive Law; 1.0 Family Law Specialization (A) Dissolution of Marriage
Robert Redding, Madden & ReddingKathryn Schlepphorst, Law Offices of Kathyrn SchlepphorstLynne Yates-Carter, Law Offices of Lynne Yates-Carter
Cancellations and refunds will be accepted only 48 hours prior to the event. *State Bar of California Approved MCLE: The Santa Clara County Bar Association is a State Bar of California approved MCLE provider. This program is approved for California MCLE credit.
11/20/2017November 20 Digest
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12/1/20172017 Annual Family Law Holiday Luncheon
12/7/20172017 Annual Women Lawyers' Holiday Lunch
31 North 2nd St., Ste. 400, San Jose, CA 95113


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Love this DIY high heel cupcake idea for a bachelorette party!
3 Ingredient Nutella Brownies - Bake at for around 30 minutes (less time for cupcake form, more time if the centers aren't baked through). Good for school bake sales - taste more like chocolate cake than brownie though
Tiny Cherry Almond tea Cake - looks delicious. fun for tea, soak cherries in liquor of choice first


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people are pretending in every possible way. The person who is pretending to be a saint may be just the opposite, and the person who is pretending to be awake may be asleep, and the person who is pretending to be asleep may be awake...all kinds of pretensions, because the society creates the context where it allows you only either to live an utterly condemned life, the life of a criminal. The society gives you only two alternatives: either be honest and be a criminal, or be dishonest and be respectable. It does not allow you the third alternative. Why does it not allow you the third alternative? -- because the third alternative creates an extra ordinary person and their presence makes the crowd feel very mediocre, very insulted, humiliated. So please don't decide by looking at people's appearances. More are the chances, almost ninety-nine point nine percent, that whatsoever they appear on the surface they will not be deep down. You can be certain about it; I say almost completely certain, because only point one percent can you miss -- which is not much.
Only once in a while will you come across an enlightened, whose appearance is the same as his inwardness; otherwise you will come across people who are one thing on the outside and another on the inside. Don't be deceived by appearances.


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I had outstanding service from Israel-Catalog.com. I had several questions before purchasing the item, and they were answered clearly, promptly, and courteously. During the shipment, I received notices regarding the tracking, assuring me that Israel-Catalog.com was on top of the matter. The item (Hebrew-English dictionary) arrived in pristine condition.
List of songs:
1. Lu yehi (All ewe pray for)
2. Shir mishmar (take care)
3. lahafoch et haanavim leyain(Turn the grapes into wine)
4. Haderech leey sham (Will he return)
5. Lepetach har gash (Living on a volcano)
6. Shir nolad (A song is born)
7. Tvi et hatzemer (Spin the wool)
8. Solveg (Solveig)
9. Ma mutar (What more is there)
10. Keshetigdeli tavini (sometime you'll understand)
11. Balada al sus im ketem al hametzach (Balad of th horse with a spot on his forehead )
- Genre: Chava Alberstein
- Media: Music CD


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Question about Computers & Internet
I have an old facebook account that i want deleted .i cant get into my account because i have forgotten my password and have a new email account .how do i delete this facebook aacount
Posted by suzi precanica on
From your new account go on to the old account and on 'options' in the bottom right corner of where the cover photo would be. > press 'report/block.' > at the bottom of the box that should come up scroll your mouse down to 'this is my old profile'. > and select 'close this account'. Your request will be reviewed and eventually deleted.
Posted on Feb 15, 2014
SOURCE: I have freestanding Series 8 dishwasher. Lately during the filling cycle water hammer is occurring. How can this be resolved
a 6ya expert can help you resolve that issue over the phone in a minute or two.
Best thing about this new service is that you are never placed on hold and get to talk to real repairmen in the US.
New users get to try the service completely Free afterwhich it costs $6 per call and covers almost anything you can think of (from cars to computers, handyman, and even drones).
click here to download the app (for users in the US for now) and get all the help you need.
Posted on Jan 02, 2017
I had the same problem when someone guessed my facebook password and started writing messages to my friends. I found out that I couldn't fully delete the Facebook profile, but I deleted all the information/photos etc and applications and friends from it.
That was before Facebook changed over to the new look, though, but you should still be able to delete all the information..
Hope this helps
Chris (ziraffa)
Posted on Jan 17, 2009
SOURCE: I am NOT getting an email to reset my facebook password
e-mail them or call them. I can suggest nothing further because I do not have access to there servers. Tell them your problem.
Ryan Frame
Creative Energy Associates Technical Center
Posted on Aug 05, 2009
SOURCE: I can't remember my email to my old facebook
Tell your friends who were in the friends list of your old facebook account to look at your profile info for email id. That would be your login mail id. Enter that mail id in 'Forgot password' link and get confirmation code. Paste that as per mail instructions and get new password. Login with that password and mail id you received from friends and enjoy your facebook.
Posted on Oct 19, 2010
SOURCE: cant delete old account on facebook as they have
Facebook Social Network don't delete accounts, instead they disable them to let other people know that the accounts that were disabled are not available. This will also enable you to activate the account without doing all the registration process and so on.
Posted on Feb 01, 2011
SOURCE: HOw do i delete account
Hi Maya, You can delete your account here. Also, do not put your personal information on FixYa, especially your password/
Posted on Mar 01, 2011
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We used a lit joint as a candle for her birthday cake
Managed to get through family dinner without anyone knowing I was tripping balls. Christmas miracle. He exists.
I will not hesitate to go down on a dick for some cream soda.
I had to make out with him. He bought me a few drinks and he was an Angels fan. As a Yankee fan that was my way of saying good game and sorry we beat the shit out of you
These Dirty People Haven't Told Their SO About Their Kinky Fetish
blew off easter dinner with the fam to go play shot roulette. woke up in nothing but my boxers in the back of a random pickup truck.
I just had to take a picture of someone whose testicles are bigger than my fists combined. Living the dream.
I look like i have multiple stab wounds in my foot and there are footprints from the elevator to my room. What happened?
All I know for sure is, I went to bed drunk and I woke up in a relationship..I think I need to reevaluate my drinking skills.
If a clean cut ginger with a flannel and tattoos shows up at the apartment, he is allowed inside.
This is Why People Stop Sex Halfway Through
I'll tell you that it involved a pair of pliers and a trip to the ER.
I demand a full explanation right now.
Godammit I caught my hair on fire taking a bong rip
It's not my fault you decided to fall in love with a Frodo Baggins lookalike
All I wanted was a couple of orgasms before work, is that too much to ask?!
you never keep up with shots anymore
I'm trying to be more responsible these days
you fucking tried to take your pants off and pee in Taco Bell's parking lot
My favorite bra is missing and I smell like beer and bad decisions. This is definitely a sign that hoe mode is activated.


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SCOTT WITKOWSKI, Wellington
SCOTT WITKOWSKI, Wellington Whos your favorite basketball player and why: Lebron James because hes a well-round player. Pre-game meal or superstition: I always put on my right shoe first.
Scott Fisher, Correspondent
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Gov. Malloy Cuts Municipal Aid by $91 Million, Stunning Legislators And Local Leaders
Connecticut's First Board Game Cafe, The Board Room holds Grand Opening in Middletown
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My husband and I went to Provence about 10 years ago and want to plan another trip there for May. We plan to go for about 12 days (flexible). Last time, we went to Paris, took the train to Avignon and then rented a car--we stayed in St. Remy, day tripped to the surrounding towns. We then went to Aix on Provence and toured around there, ending up in St. Tropez and Cannes, returning home from Nice.
Should we follow the same basic route (except that we wouldn't want to stay in Aix) or are there some variations we could make for Provence/surrounding area ? (We are active, like to walk, love the food, exploring, experiencing, etc)
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Return to Provence in May
My husband and I went to Provence about 10 years ago and want to plan another trip there for May. We plan to go for about 12 days (flexible). Last time, we went to Paris, took the train to Avignon and then rented a car--we stayed in St. Remy, day tripped to the surrounding towns. We then went to Aix on Provence and toured around there, ending up in St. Tropez and Cannes, returning home from Nice.
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You could do the reverse-fly into Nice and out of Paris!
We stayed in Monpellier one time and found it great--a nice city to come "home" to, and a super base for train travel. We trained to Arles and Avignon from there. Ran out of time for going to Collioure. Can't help with car rental though--other Fodorites can.
I believe a TGV line to/from Paris was getting ready to open. You can google to see if it's there now,
On the above trip we flew into Barcelona and then took the train to Monpellier, then to Nice and finished in Paris. Good to not backtrack.
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You did say much about your "day trips to the surrounding towns". Did you visit Uzes, Lourmarin, Vaison, Buis les Baronnis, Simiane la Rotunde, Seguret, Sault, Dieulefit, Grignan, Montbrun les Bains, Brantes, St Paul Trois Chateau, Crillon la Brave, Venasque, Grambois, Pertuis, Ansoois, Cuuceron, Lauris, Mirabeau - just to name a few interesting towns that you may not have visited. Did you explore the lavender fields around Sault, the Gorges de l'Ardeche, Aven d'Orgnac, the Baronnies, Gorges de la Nesque, the dentelles?? Near Aix, did you visit the villages in the Var - Cotignac, Entrecasteaux, Aups, Tourtour, Salneres, Correns, Lorgues, Chateaudouble, Tourrettes, Fayence, Seillans?
Lots to see !!!
Do you have my 27 page itinerary that I've sent to over 3,000 people on Fodors & aol?. E-mail me at [email protected] & I'll attach a copy to the reply e-mail.
Stu Dudley
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Visit the vineyards,museums galore to see,
You can hire the car at the airport, drive through
burgundy before Provence.
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Looking forward to receiving the itinerary Stu. Most of those little towns don't sound familiar so I am excited to learn about checking them out. Sounds like we will have a great time and a new experience.
Although we did some exploration of little towns--I remember Gordes, Bonnieux, Rousillon, Chateauneuf-du-pape I think we mostly saw the bigger places.
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Don't Expect Authentic Eats From Dale Talde
The Brooklyn chef, who runs five restaurants, talks fried chicken, Spam and why his food is never 'authentic'
Dale Talde is working on a new restaurant, Rice & Gold, that will soon open on the Lower East Side, and the menu items aren't likely to be ones you've seen before.
"Why can't, like, tuna poke be served on a really bomb, chewy, everything bagel?" the 37-year-old chef said. "And if there's a cart with a guy doing it, even better."
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Interjet 4O2132 Flight Status Tracker
4O2132 is a domestic flight operated by Interjet. 4O2132 is departing from Mexico City (MEX), Mexico and arriving at Monterrey (MTY), Mexico. The flight distance is about 712 km or 442.42 miles and flight time is 1h 30 minutes . Get the latest status update for 4O2132 / AIJ2132 here.
Update on Oct 28 2017, 01:45
Lastest Status
Distance: 712 km / 442.42 miles or 384.45 nautical miles.
|Departure Mexico City International Airport
|Arrival Monterrey Gen Mariano Escobedo Airport
Scheduled Departure: 17:50
Departure Terminal: 1
Scheduled Arrival: 17:50
Arrival Terminal: A
Flight 4O2132 detail information
|Domestic Flight
|From ( MEX) Mexico City, Mexico to ( MTY) Monterrey, Mexico
|Interjet (4O /AIJ)
|Flight Duration
|1h 30 minutes
|Flight Distance
|712 km / 442.42 miles
4O2132 Departures and Arrivals
|Airport: Mexico City International Airport, Mexico
|ICAO Code: MMMX
|MEX Current time: 22:27:30, Friday 17-11
|Mexico City International Airport Departures
Flights from Mexico City to Monterrey
|Airport: Monterrey Gen Mariano Escobedo Airport, Mexico
|ICAO Code: MMMY
|MTY Current time: 22:27:30, Friday 17-11
|Monterrey Gen Mariano Escobedo Airport Arrivals
|Flights from Monterrey to Mexico City
Check Interjet Status
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Nahcotta, WA Whole Life Insurance Quotes
Are you looking for Nahcotta, WA whole life insurance. We can help you compare the best life insurance options in your Pacific area. To begin simply enter your Zip Code at the top of the page and press "Compare Options". The search engine will take you to a page listing all life insurance companies that are recommended and have proven to be reputable in Nahcotta, WA.If you have not yet decided to get a life insurance policy, it is something that you should consider. Whether you are single with a significant other, or a family person, is nice to have a policy like this so that you can give them something if you unexpectedly depart. We never know about the future, and this can protect us, regardless of what the odds actually are. Having a life insurance policy is a guarantee that in your absence after death, the people that you care about are going to be financially okay. The question that most people ask is what type of policy is best. For some people, a whole life insurance policy is the best way to go. The following suggestions will allow you to quickly get whole life insurance quotes in Nahcotta, WA, helping you to quickly get your policy started and active.
Why Choose Whole Life?
How Do You Get Quotes For Whole Life Insurance?
There are a couple different strategies that you can use in order to get Nahcotta, WA whole life insurance policy estimates. For example, you may see companies that are advertising online, and you can give them a call. The same is true for any of the insurance companies that you see that are advertising in your local paper. Doing it this way, however, can be very time-consuming. That's why you need to find a website that will submit information that you provide for them to multiple companies, all for free, allowing you to simply wait for" to come in.
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The policy that you select should be one that originates from a reliable company. This can be verified through the Better Business Bureau or online comments that you can read. If there is no problem with the reputation of the company, it's just a matter of choosing one that is going to provide you with a large death benefit, and a sizable annuity, all provided to you for a reasonable price.
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Do not obtain a lot more daily life insurance coverage than is needed for your family's requirements. The larger your protection is, the higher your rates will be. A million dollar policy seems wonderful, but odds are you are going to in no way even have to income it out. Save your self the income and just select a policy that covers your wants.
Disclose almost everything relating to your existence and your well being when buying life insurance policy. If something that you unsuccessful to point out contributes to your passing, you may possibly have rendered your insurance coverage null and keep away from. The most pricey insurance coverage plan in the entire world is the one that does not pay out when it really is essential.
As you store for a plan, you need to keep in mind to contain concerns for each ongoing and fastened expenditures. Preserve in head that life insurance coverage funds can be used for pricey one-time costs as well, like estate taxes or funeral expenses which can include up.
In some situations, you can help save cash by buying much more existence insurance policy protection. Even though it might look peculiar, several organizations will offer large discount rates to folks who acquire better coverage. This not only will save income, but is also a god way to guarantee your family is adequately protected.
View out for insurance policy salesman that make unrealistic promises about their knowledge or overall performance. Any agent that seems obscure, or who will not give straight data with regards to scores, ought to not be dealt with. Also, get the time to lodge a complaint about the agent with their superiors.
As stated from the above article, acquiring lifestyle insurance coverage is dependent on educating yourself and inquiring a lot of concerns. You have to maintain going in get to make positive you get the right coverage. By retaining the preceding guidance in thoughts, you will have no difficulties browsing for that ideal coverage.