Work-related allergy in medical doctors: atopy, exposure to domestic animals, eczema induced by common chemicals and membership of the surgical profession as potential risk factors

Purpose To investigate the risk factors associated with work-related allergy-like symptoms in medical doctors. Methods Self-administered questionnaire survey and CAP test were conducted among medical school students in the 4th grade of their 6-year medical course in 1993–1996 and 1999–2001. Follow-up questionnaires were sent in 2004 to the graduates. These questionnaires enquired into personal and family history of allergic diseases, lifestyle, history of allergy-like symptoms including work-relatedness and occupational history as medical doctors. Relationships between allergy-like symptoms and relevant factors were evaluated by multivariate logistic regression analysis. Results Of 261 respondents at the follow-up survey, 139 (53.3%) and 54 (20.7%) had a history of any allergy-like symptoms and any work-related allergy-like symptoms, respectively. Female gender and family history of allergic diseases were signiWcantly associated with any allergy-like symptoms. Personal history of allergic disease, exposure to domestic animals, eczema caused by rubber gloves, metallic accessories, or cosmetics during schooling days, and membership of the surgical profession were signiW- cant risk factors for work-related allergy-like symptoms. On the contrary, to work-related allergy-like symptoms, gender, age, and smoking status were not signiWcantly related, and consumption of prepared foods was inversely related. Conclusions Personal history of atopy and eczema induced by common goods and the history of keeping domestic animals may be predictors of work-related allergy-like symptoms in doctors. After graduation from medical school, physicians start with exposure to various allergens and irritants at work, which relate to work-related allergy-like symptoms, especially for surgeons

Using Kalirin conditional knockout mice to distinguish its role in dopamine receptor mediated behaviors

Abstract Background Mice lacking Kalirin-7 (Kal7KO), a Rho GDP/GTP exchange factor, self-administer cocaine at a higher rate than wildtype mice, and show an exaggerated locomotor response to experimenter-administered cocaine. Kal7, which localizes to post-synaptic densities at glutamatergic synapses, interacts directly with the GluN2B subunit of the N-methyl-d-aspartate (NMDA; GluN) receptor. Consistent with these observations, Kal7 plays an essential role in NMDA receptor dependent long term potentiation and depression, and glutamatergic transmission plays a key role in the response to chronic cocaine. A number of genetic studies have implicated altered Kalirin expression in schizophrenia and other disorders such as Alzheimer’s Disease. Results A comparison of the effects of experimenter-administered cocaine on mice lacking all Kalirin isoforms to its effects on mice lacking only Kalirin-7 identified Kal7 as the key isoform whose deletion produces exaggerated locomotor responses to cocaine. Pretreatment of Kal7KO mice with a low dose of ifenprodil, a selective GluN2B antagonist, eliminated their enhanced locomotor response to cocaine, revealing an important role for GluN2B in this behavior. Selective knockout of Kalirin in dopamine transporter expressing neurons produced a transient enhancement of cocaine-induced locomotion, while knockout of Kalirin in Drd1a- or Drd2-dopamine receptor expressing neurons was without effect. As observed in Kalirin global knockout mice, eliminating Kalirin expression in Drd2-expressing neurons increased exploratory behavior in the elevated zero maze, an effect eliminated by pretreatment with ifenprodil. Conclusions The cocaine-sensitive neuronal pathways which are most sensitive to altered Kalirin function may be the pathways most dependent on GluN2B and Drd2

Primers Table Females-S.Table_1

qPCR primers tabl

Suppl.Table.4_RegulatedTranscripts

Supplemental Table 4 Regulated Transcript

Supplemental Table 3

Supplemental Table

Data from: Sex-specific gene expression in the mouse nucleus accumbens before and after cocaine exposure

Females are more sensitive than males to the addictive effects of cocaine and are more likely to relapse. The nucleus accumbens has a well-established major role in the response to cocaine, and sex-specific differential expression of key transcripts at baseline and after cocaine withdrawal could underlie some of these differences. To address this hypothesis, four groups of mice (cycling females, ovariectomized females treated with estradiol or placebo and males) were evaluated for open field activity following 7 daily injections of saline or cocaine. Sensitization to the locomotor effects of cocaine was most pronounced in ovariectomized mice receiving estradiol, was greater in cycling females than in males, and failed to occur in ovariectomized/placebo mice. After a 28-day period of withdrawal, RNA prepared from the nucleus accumbens of individual cocaine or saline injected mice was subjected to RNASeq analysis. Expression of a substantial fraction of the transcripts expressed in the nucleus accumbens (~3%) differed in cycling female mice when compared to male mice, was altered by ovariectomy or was responsive to estradiol treatment. The transcripts differentially expressed in the nucleus accumbens of cycling female mice withdrawn from cocaine for 28-days exhibited substantial overlap with those differentially expressed in the nucleus accumbens of male mice withdrawn for 7-days. A small set of transcripts were similarly affected by cocaine in placebo or estradiol treated ovariectomized mice. Transcripts differentially expressed after 28-days of withdrawal encoded neprilysin, which degrades enkephalin and other neuropeptides, G protein coupled receptors and secreted proteins such as Wnt2, Fst and Igfbp4

FPKM_AllMice_AllTranscripts-S.Table_2

FPKM All Transcript

SUPPLEMENTARY MATERIAL LEGENDS

legends for Supplementary file