Thyroid-Stimulating Hormone Receptor Autoimmunity and Local Factors in Multiple Risk Factors Are Mainly Involved in the Occurrence of Pretibial Myxedema.

Background: Pretibial myxedema (PTM) is a local mucinous dermopathy associated with thyroid diseases. Since the etiology of PTM is unclear, the aim of this study is to identify the risk factors for PTM and their etiological roles in PTM occurrence.

Methods: A large-scale case-control study (n = 1,200) was performed to identify risk factors for PTM by calculating odds ratio (OR) values and 95% confidential intervals.

Morphological Diversity of Pretibial Myxedema and Its Mechanism of Evolving Process and Outcome: A Retrospective Study of 216 Cases.

Background. Pretibial myxedema (PTM) is a rare dermopathy. The morphologic features and mechanism of its evolving process are not reported in large case series.

A Randomized Controlled Trial of Intralesional Glucocorticoid for Treating Pretibial Myxedema.

Background: Pretibial myxedema (PTM) is an uncommon dermopathy associated with autoimmune thyroid diseases. Now it is thought to be autoimmune and its treatment with glucocorticoid is helpful. However, it has not been evaluated.

A predictive model of the oxygen and heme regulatory network in yeast.

Deciphering gene regulatory mechanisms through the analysis of high-throughput expression data is a challenging computational problem. Previous computational studies have used large expression datasets in order to resolve fine patterns of coexpression, producing clusters or modules of potentially coregulated genes. These methods typically examine promoter sequence information, such as DNA motifs or transcription factor occupancy data, in a separate step after clustering.

Regulation of the HAP1 gene involves positive actions of histone deacetylases.

The yeast transcriptional regulator Hap1 promotes both transcriptional activation and repression. Previous studies have shown that Hap1 binds to the promoter of its own gene and represses its transcription. In this report, we identified the DNA site that allows Hap1-binding with high affinity.

Gene expression profiling of human primary astrocytes exposed to manganese chloride indicates selective effects on several functions of the cells.

Exposure of adult humans to manganese (Mn) has long been known to cause neurotoxicity. Recent evidence also suggests that exposure of children to Mn is associated with developmental neurotoxicity. Astrocytes are critical for the proper functioning of the nervous system, and they play active roles in neurogenesis, synaptogenesis and synaptic neurotransmission.

The common insecticides cyfluthrin and chlorpyrifos alter the expression of a subset of genes with diverse functions in primary human astrocytes.

Given the widespread use of insecticides in the environment, it is important to perform studies evaluating their potential effects on humans. Organophosphate insecticides, such as chlorpyrifos, are being phased out; however, the use of pyrethroids in household pest control is increasing. While chlorpyrifos is relatively well studied, much less is known about the potential neurotoxicity of cyfluthrin and other pyrethroids.

A novel mode of chaperone action: heme activation of Hap1 by enhanced association of Hsp90 with the repressed Hsp70-Hap1 complex.

Molecular chaperones Hsp90 and Hsp70 control many signal transducers, including cyclin-dependent kinases and steroid receptors. The yeast heme-responsive transcriptional activator Hap1 is a native substrate of both Hsp90 and Hsp70. Hsp90 and Hsp70 are critical for the precise regulation of Hap1 activity by heme.

Structural environment dictates the biological significance of heme-responsive motifs and the role of Hsp90 in the activation of the heme activator protein Hap1.

Heme-responsive motifs (HRMs) mediate heme regulation of diverse regulatory proteins. The heme activator protein Hap1 contains seven HRMs, but only one of them, HRM7, is essential for heme activation of Hap1. To better understand the molecular basis underlying the biological significance of HRMs, we examined the effects of various mutations of HRM7 on Hap1.