M

Matthew Adams

University of Brighton

ORCID: 0000-0001-8473-5044

Publishes on Semiconductor Lasers and Optical Devices, Photonic and Optical Devices, Optical Network Technologies. 242 papers and 8.3k citations.

242Publications
8.3kTotal Citations

Is this you? Claim your profile.

Add your photo, update your bio, and get notified when your ranking changes.

Top publicationsby citations

Activators of peroxisome proliferator-activated receptor gamma have depot-specific effects on human preadipocyte differentiation.
Matthew Adams, Carl Montague, Johannes B. Prins et al.|Journal of Clinical Investigation|1997
Cited by 520Open Access

Activation of peroxisome proliferator-activated receptor (PPAR) gamma, a nuclear receptor highly expressed in adipocytes, induces the differentiation of murine preadipocyte cell lines. Recently, thiazolidinediones (TZDs), a novel class of insulin-sensitizing compounds effective in the treatment of non-insulin-dependent diabetes mellitus (NIDDM) have been shown to bind to PPARgamma with high affinity. We have examined the effects of these compounds on the differentiation of human preadipocytes derived from subcutaneous (SC) and omental (Om) fat. Assessed by lipid accumulation, glycerol 3-phosphate dehydrogenase activity, and mRNA levels, subcultured preadipocytes isolated from either SC or Om depots did not differentiate in defined serum-free medium. Addition of TZDs (BRL49653 or troglitazone) or 15-deoxyDelta12,14prostaglandin J2 (a natural PPARgamma ligand) enhanced markedly the differentiation of preadipocytes from SC sites, assessed by all three criteria. The rank order of potency of these agents in inducing differentiation matched their ability to activate transcription via human PPARgamma. In contrast, preadipocytes from Om sites in the same individuals were refractory to TZDs, although PPARgamma was expressed at similar levels in both depots. The mechanism of this depot-specific TZD response is unknown. However, given the association between Om adiposity and NIDDM, the site-specific responsiveness of human preadipocytes to TZDs may be involved in the beneficial effects of these compounds on in vivo insulin sensitivity.

Hybridizing Habitus and Reflexivity:
Matthew Adams|Sociology|2006
Cited by 412

This article initially summarizes two dominant tropes in the sociology of identity in recent years, centred on the concepts of self-reflexivity and habitus, followed by an overview of extensive critical debate to which both have been subjected. It is claimed that the key criticisms of the extended reflexivity thesis gather around accusations of excessive voluntarism in accounting for contemporary identity, while critiques of Bourdieu's conceptualization of habitus deem it overly deterministic. In an attempt to move beyond the conceptual stalemate of two distinct approaches to identity, a number of hybridized accounts have emerged in social theory.The remainder of the article discusses a number of these accounts in relation to social change, and offers an initial consideration of their strengths and limitations. It is argued that the importance of post-reflexive choice must remain integral to any attempt at hybridization of these important terms, particularly in relation to the contemporary workings of social stratification.

Genetic analysis of 29 kindreds with generalized and pituitary resistance to thyroid hormone. Identification of thirteen novel mutations in the thyroid hormone receptor beta gene.
Matthew Adams, Charles H. Matthews, Trevor N. Collingwood et al.|Journal of Clinical Investigation|1994
Cited by 230Open Access

Resistance to thyroid hormone (RTH), with elevated serum free thyroid hormones and nonsuppressed thyrotropin levels, is either relatively asymptomatic, suggesting a generalized disorder (GRTH) or associated with thyrotoxic features, indicating possible selective pituitary resistance (PRTH). 20 GRTH and 9 PRTH cases, sporadic or dominantly inherited, were analyzed. Affected individuals were heterozygous for single nucleotide substitutions in the thyroid hormone receptor beta gene, except for a single case of a seven nucleotide insertion. With one exception, the corresponding 13 novel and 7 known codon changes localized to and extended the boundaries of two mutation clusters in the hormone-binding domain of the receptor. 15 kindreds shared 6 different mutations, and haplotype analyses of the mutant allele showed that they occurred independently. The majority (14 out of 19) of the recurrent but a minority (1 out of 10) of unique mutations were transitions of CpG dinucleotides. Mutant receptor binding to ligand was moderately or severely impaired and did not correlate with the magnitude of thyroid dysfunction. There was no association between clinical features and the nature or location of a receptor mutation. These observations suggest that GRTH and PRTH are phenotypic variants of the same genetic disorder, whose clinical expression may be modulated by other non-mutation-related factors.