Biomedical subjects

Judith Martin

Publications and source records attributed to Judith Martin.

8 recordsLinked to original sources

PubMed2006

Early childhood factors associated with the development of post-traumatic stress disorder: results from a longitudinal birth cohort.

BACKGROUND: Childhood factors have been associated with increased risk of developing post-traumatic stress disorder (PTSD). Previous studies assessed only a limited number of childhood factors retrospectively. We examined the association between childhood neurodevelopmental, temperamental, behavioral and family environmental characteristics assessed before age 11 years and the development of PTSD up to age 32 years in a birth cohort. METHOD: Members of a 1972-73 New Zealand birth cohort (n=1037) who were assessed at ages 26 and 32 years for PTSD as defined by DSM-IV. RESULTS: We identified two sets of childhood risk factors. The first set of risk factors was associated both with increased risk of trauma exposure and with PTSD assessed at age 26. These included childhood externalizing characteristics and family environmental stressors, specifically maternal distress and loss of a parent. The second set of risk factors affected risk for PTSD only and included low IQ and chronic environmental adversity. The effect of cumulative childhood factors on risk of PTSD at age 26 was substantial; over 58% of cohort members in the highest risk quartile for three developmental factors had PTSD as compared to only 25% of those not at high risk on any factors. Low IQ at age 5, antisocial behavior, and poverty before age 11 continued to predict PTSD related to traumatic events that occurred between the ages of 26 and 32. CONCLUSIONS: Developmental capacities and conditions of early childhood may increase both risk of trauma exposure and the risk that individuals will respond adversely to traumatic exposures. Rather than being solely a response to trauma, PTSD may have developmental origins.

Adolescent↗

PubMed2005

Allan-Herndon-Dudley syndrome and the monocarboxylate transporter 8 (MCT8) gene.

Allan-Herndon-Dudley syndrome was among the first of the X-linked mental retardation syndromes to be described (in 1944) and among the first to be regionally mapped on the X chromosome (in 1990). Six large families with the syndrome have been identified, and linkage studies have placed the gene locus in Xq13.2. Mutations in the monocarboxylate transporter 8 gene (MCT8) have been found in each of the six families. One essential function of the protein encoded by this gene appears to be the transport of triiodothyronine into neurons. Abnormal transporter function is reflected in elevated free triiodothyronine and lowered free thyroxine levels in the blood. Infancy and childhood in the Allan-Herndon-Dudley syndrome are marked by hypotonia, weakness, reduced muscle mass, and delay of developmental milestones. Facial manifestations are not distinctive, but the face tends to be elongated with bifrontal narrowing, and the ears are often simply formed or cupped. Some patients have myopathic facies. Generalized weakness is manifested by excessive drooling, forward positioning of the head and neck, failure to ambulate independently, or ataxia in those who do ambulate. Speech is dysarthric or absent altogether. Hypotonia gives way in adult life to spasticity. The hands exhibit dystonic and athetoid posturing and fisting. Cognitive development is severely impaired. No major malformations occur, intrauterine growth is not impaired, and head circumference and genital development are usually normal. Behavior tends to be passive, with little evidence of aggressive or disruptive behavior. Although clinical signs of thyroid dysfunction are usually absent in affected males, the disturbances in blood levels of thyroid hormones suggest the possibility of systematic detection through screening of high-risk populations.

Adolescent↗

PubMed2004

Evolving use of buprenorphine in the treatment of addiction.

Two formulations of buprenorphine were approved in the United States for treatment of opioid dependence in 2002. This newly available treatment offers a safe and effective alternative to addicted individuals who are not currently in treatment. This article focuses on the steps that physicians and patients may take, as of this writing, if they should wish to participate in this new treatment. The content is clinically oriented and intelligible to an audience that is not medically trained. In the article, buprenorphine is placed in context of the standard opioid pharmacotherapy of methadone maintenance, and the expansion of opioid pharmacotherapy into the office setting is described.

Buprenorphine↗

PubMed2004

Faculty development in small-group teaching skills associated with a training course on office-based treatment of opioid dependence.

The Drug Addiction Treatment Act of 2000 (DATA-2000) allows qualified physicians to treat opioid-dependent patients with schedule III-V medications, such as buprenorphine, in practices separate from licensed, accredited opioid treatment programs. Physicians may attain this qualification by completing 8-hours of training in treating opioid dependence. This paper describes the evaluation of a faculty development workshop designed to enhance teaching skills of small-group facilitators involved with DATA-2000 training sessions. This workshop coached the facilitators on their teaching roles in the DATA-2000 session through experiential practice of patient- case discussions related to treatment of opioid-dependence. Descriptive questionnaires evaluated the value of the workshop. Twenty-six facilitators participated in the workshops. Paired mean score responses for specific teaching skill abilities demonstrated statistically significant improvement in all categories. Evaluation of the DATA-2000 training session small-group facilitators was uniformly positive. This faculty development workshop was successful in improving teaching skills for our small-group faculty facilitators.

Adult↗

PubMed2003

In praise of boundaries. A conversation with Miss Manners. Interview by Diane L. Coutu.

The past three decades have been a time of increasing informality in the American workplace. It's easy to characterize this growing comfort with the casual as a positive step for workplace culture, an outgrowth of the American democratic belief in workers' equality. Informal environments are said to be more trusting and open, and workers who are free to express their personalities are more comfortable and thus more creative--right? According to etiquette guru Judith Martin--known far and wide as Miss Manners--informality in the workplace may do more harm than good. Without some formality in social intercourse, Miss Manners argues, human interactions end up being governed by laws, which are too heavy-handed to serve as a guide through the nuances of personal--or professional--behavior. Since our earliest beginnings, we have developed formal rules to accompany shared human experiences, such as eating and mourning. Yet, says Miss Manners, something in us rebels against form and etiquette, and every so often, an anti-manners movement takes hold, and people come to believe that following etiquette is unnatural. One recent such movement has led to the belief that a distinction between our work life and our professional life is unnecessary. If we hope to reassure our customers that we are indeed professional, however, we need to be aware of the boundaries of professional behavior. On the whole, Miss Manners argues, informality in the workplace leads to a host of problems, from making employees feel pressured to "socialize" with coworkers during weekends and evenings to sexual harassment. Despite the shortcomings of informality in the American workplace, though, Miss Manners believes that we have the best code of manners the world has ever seen-in theory. In practice, American etiquette is undoubtedly still a work in progress.

Efficiency, Organizational↗

PubMed2002

A rec(4) dup 4p inherited from a maternal inv(4)(p15q35): case report and review.

A rec(4) dup 4p inherited from a maternal inv(4)(p15q35) was detected in a four-year-old girl with malformations, developmental delay, and behavioral problems that resemble those for trisomy 4p. A review of eight other liveborns with rec(4) dup 4p shows that about 40% of them also have manifestations in common with trisomy 4p, but the rest have a variable spectrum of malformations. Overall, the rec(4) dup 4p phenotype is not specific, and a diagnosis would not have been feasible without cytogenetic studies. This lack of a clinically recognizable phenotype could reflect the effects of the variable sizes of deletions of 4q, molecular differences in the break points, or the known variable expression of trisomy 4p. The fact that 79% of the recombinants in the offspring of inv(4)(p13-p15q35) carriers are rec(4) dup 4p suggests that meiotic recombination favors its generation or that rec(4) dup 4q are more lethal in utero.

Abnormalities, Multiple↗

PubMed2002

Differences in early childhood risk factors for juvenile-onset and adult-onset depression.

BACKGROUND: Family and twin studies suggest that juvenile-onset major depressive disorder (MDD) may be etiologically distinct from adult-onset MDD. This study is the first to distinguish prospectively between juvenile- and adult-onset cases of MDD in a representative birth cohort followed up from childhood into adulthood. METHOD: The study followed a representative birth cohort prospectively from birth to age 26 years. Early childhood risk factors covered the period from birth to age 9 years. Diagnoses of MDD were made according to DSM criteria at 3 points prior to adulthood (ages 11, 13, and 15 years) and 3 points during adulthood (ages 18, 21, and 26 years). Four groups were defined as (1) individuals first diagnosed as having MDD in childhood, but not in adulthood (n = 21); (2) individuals first diagnosed as having MDD in adulthood (n = 314); (3) individuals first diagnosed in childhood whose depression recurred in adulthood by age 26 years (n = 34); and (4) never-depressed individuals (n = 629). RESULTS: The 2 juvenile-onset groups had similar high-risk profiles on the childhood measures. Compared with the adult-depressed group, the juvenile-onset groups experienced more perinatal insults and motor skill deficits, caretaker instability, criminality, and psychopathology in their family-of-origin, and behavioral and socioemotional problems. The adult-onset group's risk profile was similar to that of the never-depressed group with the exception of elevated childhood sexual abuse. CONCLUSIONS: Heterogeneity within groups of psychiatric patients poses problems for theory, research, and treatment. The present study illustrates that the distinction between juvenile vs adult-onset MDD is important for understanding heterogeneity within depression.

Adolescent↗

PubMed1998

Bioetiquette.

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Authorship↗