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Biomedical subjects

S Schild

Publications and source records attributed to S Schild.

7 recordsLinked to original sources
PubMed2006

Cardiac parasympathetic regulation in obese women with binge eating disorder.

OBJECTIVE: Obese individuals with a binge eating disorder (BED) differ from obese non-binge eaters (NBED) with respect to (a) eating behaviour, (b) psychiatric comorbidity and (c) level of psychosocial distress. The aim of the study was to explore whether these three factors have an influence on cardiac parasympathetic function, that is independent of obesity: as alterations in cardiac parasympathetic function may have a role in the higher cardiovascular mortality that is present in obese individuals. METHODS: In total, 38 obese women (BMI>30 kg/m(2)), with a BED and 34 age and BMI matched healthy controls (NBED) completed a laboratory stress protocol that incorporated a baseline resting period, Head-up Tilt Testing (HUT) and two challenging mental tasks. Heart rate and blood pressure were measured continuously during the protocol. Parasympathetic cardiac regulation was assessed as the high frequency component of heart rate variability (HRV-HF). RESULTS: Mental challenge led to an augmented reduction of HRV-HF in obese binge eaters, which was linked to the binge eating frequency and hunger perception, but not to psychiatric comorbidity. During baseline conditions and HUT, no significant differences in parasympathetic measures were observed between the two subject groups. CONCLUSION: Subjects with a BED showed greater reduction in parasympathetic cardiac control (HRV-HF) during mental stress, suggesting higher stress vulnerability in women with a BED. Longitudinal investigations are necessary to evaluate whether this is associated with an increased cardiovascular mortality.

Adult↗
PubMed1995

Multiple polymorphisms, but no mutations, in the WAF1/CIP1 gene in human brain tumours.

The cyclin kinase inhibitor WAF1/CIP1, also termed CDKN1, mediates p53-induced cell cycle arrest in response to DNA damage. This property makes it an attractive tumour-suppressor candidate for a p53-associated tumour-suppressor gene. In order to investigate the role of WAF1/CIP1 in the pathogenesis of primary human brain tumours we performed single-stranded conformation polymorphism (SSCP) analysis and direct sequencing of exon 2 of the gene in a representative series of 158 brain tumours and corresponding blood samples. In addition, all tumours were examined for mutations in exons 5-8 of the p53 gene. Analysis of WAF1/CIP1 revealed multiple polymorphisms, the most abundant being AGC-->AGA (Ser-->Arg) at codon 31 with an allele frequency of 8.5%. Less common polymorphisms included GTG-->GGG (Val-->Gly) at codon 25, GCC-->ACC (Ala-->Thr) at codon 64, CGC-->CTC (Arg-->Leu) at codon 32, GGC-->AGC (Gly-->Ser) at codon 14 and GCG-->GTG (Ala-->Val) at codon 39 each with an allele frequency of 0.3%. These polymorphisms were all located in a conserved region of exon 2. Two of the polymorphisms were also seen in a group of 157 healthy controls indicating that WAF1/CIP1 polymorphisms do not predispose to cancer. None of the tumours included in our series showed a somatic mutation in WAF1/CIP1. All samples were also analysed for loss of heterozygosity on the short arm of chromosome 6 in the region of the WAF1/CIP1 locus. Allelic loss was observed in only one patient with a glioblastoma. Mutations in the p53 gene were found in 22 of 158 tumours. No association was found between any polymorphism of the WAF1/CIP1 gene, p53 mutations and histopathological tumour type. Our data indicate that WAF1/CIP1 mutations are probably not involved in the formation of primary human brain tumours.

Base Sequence↗
PubMed1982

Beyond diagnosis: issues in recurrent counseling of parents of the mentally retarded.

Most of the social work literature on counseling parents of the mentally retarded deals with the initial work around the diagnosis. This paper discusses the nature of problems for which parent counseling may be indicated subsequent to the period of diagnosis. Problem areas fall into four categories: Parent Expectations, Value Dilemmas, Life Transitions and Environmental Transactions. Practice issues are defined and discussed as these relate to the dual world realities faced by the parents, the slowness in learning and developmental progress of the retardate, the uncertainties inherent in the situation, and the pitfalls present in recurrent helping with inevitable crisis as these occur during the lifetime of the parents.

Adolescent↗
PubMed1977

Social work with genetic problems.

The generic utility of social work practice skills and knowledge applies to this field of practice as to any other. What is required is a delineation of the role that social workers are to take, a clear articulation of what they can do and do well, and their acquisition of the specific knowledge related to genetic problems that would provide the framework in which to practice social work in this area. From their practice experience, social workers in genetics are in a unique position to contribute important knowledge about their clients that would help to provide essential and needed services as well as guide social work intervention. The key role for social workers in genetics is the provision of supportive counseling to help clients deal with the social dimensions of their genetic problems. In other words, genetic social work focuses mainly on assisting clients with problems in living that are generated by a genetic diagnosis and that may be more problematic or distressing than the genetic defect itself.

Attitude↗