Search Results - (Author, Cooperation:P. B. Mortensen)

2013-03-02

American Association for the Advancement of Science (AAAS)

0036-8075

1095-9203

Biology

Chemistry and Pharmacology

Computer Science

Medicine

Natural Sciences in General

Physics

Animals ; Cytokines/immunology ; Disease Models, Animal ; Female ; Humans ; Mental Disorders/*immunology ; Mice ; Mice, Inbred C57BL ; Poly I-C/immunology/pharmacology ; Pregnancy ; Prenatal Exposure Delayed Effects/*immunology/virology ; Puberty/*immunology ; Stress, Physiological/*immunology

1469-7610

Blackwell Publishing Journal Backfiles 1879-2005

Medicine

Psychology

Infantile autism is a heterogenous disorder with unknown aetiology. Evidence from the relatively few family and twin studies suggests a genetic component. Co-occurrence or cosegregation between infantile autism and chromosomal abnormalities may identify candidate regions, which could be tested in linkage or association studies.The purpose of this study was to use the Danish Cytogenetic Central Register in order to detect autosomal chromosome abnormalities associated with infantile autism, and to review the literature for cases of autism associated with autosomal chromosome abnormalities to identify candidate chromosomal regions.The register-based study identified possible candidate regions on chromosome 7q21 and 10q21.2, which have not previously been reported.A few interesting candidate regions, 15q11–13, 16q23, and 17p11.2 were found in the literature survey.

Electronic Resource

1365-2036

Blackwell Publishing Journal Backfiles 1879-2005

Medicine

Background : Many cases of paracetamol poisoning are with suicidal intent, but the association between paracetamol poisoning and subsequent psychiatric disorder is unknown.Aim : To examine the association between poisoning with paracetamol or other weak analgesics and subsequent psychiatric disorder.Methods : The study was set in a nested case–control design and based on nationwide Danish registers. We identified all patients diagnosed with schizophrenia, affective disorder or eating disorder in 1994–1998 and matched population controls. We estimated the relative risk of these psychiatric disorders after admission for paracetamol or nonparacetamol poisoning, adjusting for income, employment and marital status.Results : We included 12 603 cases with psychiatric disorder, and 1.2% had a diagnosis of poisoning compared with 0.2% of the 252 060 matched population controls. Compared with those with no diagnoses of weak analgesic poisoning, the risk of schizophrenia increased 3.9-fold after paracetamol poisoning, and 2.0-fold after nonparacetamol poisoning. The risk of affective disorder increased 12.2-fold after paracetamol poisoning and 2.6-fold after nonparacetamol poisoning. The risk of eating disorder increased 5.0-fold after paracetamol poisoning, and 2.2-fold after nonparacetamol poisoning. The risk of a diagnosis of psychiatric disorder was very high immediately after poisoning and remained increased for more than 10 years.Conclusions : Paracetamol poisoning is a strong risk marker for psychiatric disorder, particularly affective disorders.

Electronic Resource

1433-9285

Springer Online Journal Archives 1860-2000

Medicine

Summary The cohort consists of all psychiatric patients (n=53) admitted for the first time in 1972 from a welldefined catchment area with a population of 582,000 inhabitants aged 15 years and over. Furthermore, they were all registered with the diagnosis schizophrenia in the nation-wide psychiatric register at least once during an observation period from the day of the first admission in 1972 until August 31, 1983. The entire cohort was followed up on average 13 years after their first admission. Poor employment outcome (79%), poor social contact outcome (55%), and poor overall social outcome (76%) characterized the living conditions of the 42 patients alive at follow-up. Good employment outcome was predicted by “born in rural area”. Good social contact outcome was predicted by full remission at first discharge and poor outcome by male sex. Good overall social outcome was predicted by “born in rural area” and of marginal significance by high social status at first admission. A comparison of parents' highest social group and patients' social group at follow-up supports previous findings on social drift.

Electronic Resource

1433-8491

Springer Online Journal Archives 1860-2000

Medicine

Electronic Resource

1573-5117

Springer Online Journal Archives 1860-2000

Biology

Electronic Resource

1573-2568

BUTYRATE ; OXIDATION ; ULCERATIVE COLITIS ; COLONOCYTES

Springer Online Journal Archives 1860-2000

Medicine

Abstract An impaired oxidation of butyrate has beensuggested as a causative factor of ulcerative colitisand, moreover, agents present in colonic luminalcontents impair butyrate oxidation in both rat and human colonocytes. To evaluate the overall effect offeces on the production of CO2 and ketonebodies from butyrate oxidation in rat colonocytes, fecalhomogenates from 10 healthy subjects and 10 patients with quiescent and 10 patients with activeulcerative colitis were sterile filtrated and added torat colonocytes incubated with 2, 4, and 10 mmol/literof stock butyrate, respectively. Addition of fecal filtrate from healthy subjects and patientswith quiescent and active ulcerative colitis tocolonocytes incubated with 2, 4, and 10 mmol/liter ofstock butyrate, respectively, tended to decrease theproduction of CO2 from butyrate oxidation,whereas ketogenesis was unaffected. The decrease inCO2 production was not explained by thesimultaneous addition of fecal short-chain fatty acids(SCFAs). However, a difference in the ability todecrease CO2 production was not found betweenfiltrates from healthy subjects and patients withquiescent and active ulcerative colitis. In conclusion, feces from healthy subjects and patients withquiescent and active ulcerative colitis containinhibitor(s) of the production of CO2 frombutyrate oxidation in colonocytes. However, a specific inhibitory effect of feces from patients withulcerative colitis on the production of CO2could not be identified.

Electronic Resource