Search Results - (Author, Cooperation:J. Hallmayer)

2011-02-11

Nature Publishing Group (NPG)

0028-0836

1476-4687

Biology

Chemistry and Pharmacology

Medicine

Natural Sciences in General

Physics

Action Potentials/drug effects ; Autistic Disorder ; Calcium Channels, L-Type/genetics/metabolism ; Calcium Signaling/drug effects ; Cell Transdifferentiation ; Cellular Reprogramming/genetics ; Drug Evaluation, Preclinical/*methods ; Fibroblasts/cytology ; HEK293 Cells ; Humans ; Induced Pluripotent Stem Cells/*pathology ; Long QT Syndrome/drug therapy/genetics/metabolism/pathology ; Mutation, Missense/genetics ; Myocytes, Cardiac/*drug effects/metabolism/*pathology ; Patch-Clamp Techniques ; Phenotype ; Purines/pharmacology ; Single-Cell Analysis ; Syndactyly/drug therapy/genetics/metabolism/pathology

0165-0327

Age at onset ; Family study ; Geriatric depression ; Recurrent depression ; Unipolar depression

Elsevier Journal Backfiles on ScienceDirect 1907 - 2002

Medicine

Psychology

Electronic Resource

0920-9964

Affected sib pair ; Family study ; Sex effect

Elsevier Journal Backfiles on ScienceDirect 1907 - 2002

Medicine

Electronic Resource

0920-9964

Elsevier Journal Backfiles on ScienceDirect 1907 - 2002

Medicine

Electronic Resource

0920-9964

Elsevier Journal Backfiles on ScienceDirect 1907 - 2002

Medicine

Electronic Resource

0165-1781

Genetics ; schizoaffective disorder ; tyrosine hydroxylase gene

Elsevier Journal Backfiles on ScienceDirect 1907 - 2002

Medicine

Electronic Resource

0165-1781

Genetics ; affective disorder ; family studies ; schizoaffective disorder

Elsevier Journal Backfiles on ScienceDirect 1907 - 2002

Medicine

Electronic Resource

1432-0533

Barbiturate ; Ischemic cell necrosis ; Mongolian gerbil ; Nimodipine ; Putrescine

Springer Online Journal Archives 1860-2000

Medicine

Summary Twenty mongolian gerbils were anesthetized (1.5% halothane) and severe forebrain ischemia was produced in 15 animals by occluding both common carotid arteries. After 5 min ischemia brains were recirculated spontaneously. Immediately after ischemia nimodipine (1.5 mg/kg) or pentobarbital (50 mg/kg) was injected intraperitoneally into five animals. Four days later animals were reanesthetized (1.5% halothane); the brains were frozen with liquid nitrogen and cut in a cryostat. Ten-micrometer-thick coronal cryostat sections were stained with cresyl violet to assess the extent of ischemic cell damage in the lateral striatum, the CA1-layer of the hippocampus, and the thalamus. In addition, tissue samples (about 4 mg each) were taken from the lateral striatum, CA1 layer of the hippocampus and the thalamus. Putrescine levels were measured in these samples using reversed-phase high performance liquid chromatography and fluorescence detection. Reversible cerebral ischemia produced a significant increase in putrescine in the lateral striatum (from 11.15±0.79 to 44.83±11.76 nmol/g,P≤0.05), the CA1 subfield of the hippocampus (from 11.27±0.64 to 41.80±3.62 nmol/g,P≤0.05) and less so in the thalamus (from 11.28±0.70 to 16.50±1.71 nmol/g). Both postischemic nimodipine and barbiturate treatment of animals markedly reduced this increase in the lateral striatum to 14.09±1.41 and 15.75±1.38 nmol/g, respectively (P≤0.05 cf. untreated animals), to 29.82±6.04 and 23.21±3.12 nmol/g in the CA1-subfield of the hippocampus (P≤0.05 barbiturate-treated cf. untreated animals), and to 11.92±1.37 and 11.76±0.64 in the thalamus (P〈0.05 barbiturate-treated cf. untreated animals). Severe neuronal necroses were apparent in the lateral striatum in four out of five animals but in none of the nimodipine- or barbiturate-treated animals. In the CA1 subfield of the hippocampus the number of necrotic cells/mm stratum pyramidale amounted to 202.1±9.8, 141.9±4.2 and 78.0±33.4 in untreated, nimodipine- or barbiturate-treated animals, respectively (P≤0.05 barbiturate-treated cf. control animals). It is suggested that putrescine, produced during recirculation following ischemia, contributes to the manifestation of ischemic cell injury. Putrescine may thus be taken as a significant biochemical correlate of ischemic cell damage.

Electronic Resource

1432-0533

Gerbil ; Pentobarbital ; Morphometry ; Selective vulnerability ; Ischemia

Springer Online Journal Archives 1860-2000

Medicine

Summary Male Mongolian gerbils were subjected to bilateral carotid occlusion for 5 and 10 min, followed by 7 days of recirculation. After this interval, serial sections were made of the posterior region of the dorsal hippocampus, and the number of surviving neurons was determined per mm length of CA1 sector. In halothane-anesthetized animals only 21.1% of CA1 neurons survived 5-min ischemia, but this percentage could be raised to 78.6% when animals were pretreated with 25 mg/kg pentobarbital before ischemia. Pretreatment with 50 mg/kg pentobarbital before 5-min ischemia or pretreatment with 25 mg/kg pentobarbital before 10-min ischemia did not reduce CA1 lesions. It is concluded that a non-anesthetic dose of barbiturates is able to prevent selective vulnerability of CA1 sector, but that this effect is limited to the initial 5 min of ischemia.

Electronic Resource

1432-1203

Springer Online Journal Archives 1860-2000

Biology

Medicine

Abstract Linkage analysis was performed on 22 Bulgarian families with polycystic kidney disease (PKD) ascertained through the hemodialysis centers of two medical schools. A total of 128 affected and 59 unaffected individuals, and 54 spouses have been investigated using eight polymorphic markers linked to PKD1 and nine markers to PKD2. The results demonstrate locus heterogeneity with 0.67 as the maximum likelihood value of alpha, i.e., the proportion of families linked to PKD1. In five families, the results suggest linkage to PKD2, and observed recombinants place the gene between loci D4S1544 and D4S1542. In one family, two double recombinants for closely linked markers on chromosome 16 and on chromosome 4 give evidence for the lack of link-age to either PKD1 or PKD2, thus suggesting the involvement of a third locus. Analysis of clinical data in the PKD1 group versus the unlinked group shows no significant differences in the severity of the disease.

Electronic Resource

1433-8491

Springer Online Journal Archives 1860-2000

Medicine

Summary Some recent family studies have shown that the familial risk for schizophrenia is higher in female than in male schizophrenics. It is debated whether the risks for the other disorders, such as schizotypal personality disorder or affective disorders in families of schizophrenics are similarly influenced by the proband's gender. Also, the reason for the effect of proband's gender on the recurrence risk for schizophrenia has not been clarified. This family study (159 probands, 589 first degree relatives) confirms that schizophrenia, but also schizophrenia spectrum disorders were more frequent in families of female compared with male schizophrenics. Neither age at onset in probands nor the interaction between gender and age at onset in probands had a relevant impact on the risk figures in relatives. Affective disorders occurred in families independently of the probands' gender. Aetiological heterogeneity or ascertainment bias may account for the modifying effect of proband's gender in schizophrenia.

Electronic Resource