Acylation stimulating protein: a female lipogenic factor?

Acylation stimulating protein (ASP) is a potent lipogenic factor produced from adipocytes. Plasma ASP levels were shown to increase in obesity, diabetes mellitus type II and dyslipidemia, and decrease after weight loss and fasting. Growing evidence suggests that ASP may significantly contribute to subcutaneous fat storage in females. In vitro, ASP stimulated triglyceride synthesis to a larger extent in subcutaneous compared with omental adipocytes. The ASP receptor binding affinity to plasma membranes prepared from adipose tissue showed higher binding affinity to plasma membranes from female adipose tissue compared with male adipose tissue, and was more pronounced to subcutaneous compared with omental plasma membranes. Human studies demonstrated that postprandial triglyceride clearance predicted by ASP levels was more efficient in women than in men. In mice, postprandial triglyceride clearance, with intraperitoneal ASP administration, was faster in females compared with males. The ASP deficient mice were resistant to weight gain and had reduced fat mass that was more pronounced in females. Recent findings in humans and mice point to a significant association between progesterone and ASP variations in females. In this review, we highlight findings, to date, linking ASP to physiological and hormonal alterations that may contribute to subcutaneous fat distribution typical to females.

Undergraduate medical education in the Gulf Cooperation Council: a multi-countries study (Part 1).

BACKGROUND: The Gulf Cooperation Council (GCC) countries have witnessed over the last 40 years a rapid and major social, cultural, and economic transformation. The development of medical education in the region is relatively new, dating from the late 1960s. An important goal among the medical colleges in the region is to graduate national physicians who can populate the healthcare service of each country. AIM: The aim of this study is to provide understanding of undergraduate medical education in each of the six GCC countries and the challenges that each face. METHODS: This is a descriptive cross-sectional study. Fourteen senior medical faculty were requested to submit information about undergraduate medical education in their own countries, focusing on its historical background, student selection, curriculum, faculty, and challenges. RESULTS: The information provided was about 27 medical colleges: 16 from the Kingdom of Saudi Arabia (KSA), five from the United Arab Emirates (UAE), two from the Kingdom of Bahrain, two from Sultanate of Oman, one from Kuwait, and one from the State of Qatar. It was found that older colleges are reviewing their curriculum while new colleges are developing their programs following current trends in medical education, particularly problem-based learning and integrated curricula. The programs as described 'on paper' look good but what needs to be evaluated is the curriculum 'in action'. Faculty development in medical education is taking place in most of the region's medical colleges. CONCLUSION: The challenges reported were mainly related to shortages of faculty, availability of clinical training facilities and the need to more integration with the National Health Care services. Attention to quality, standards, and accreditation is considered essential by all colleges.

Absence of deafness-associated connexin-26 (GJB2) gene mutations in the Omani population.

We have investigated the prevalence of mutations in the connexin 26 (GJB2) gene in Omani population using both PCR-RFLP and direct DNA sequencing methods. Two common GJB2 gene mutations (35delG and 167delT) were screened in 280 healthy controls and 95 deaf patients using two different PCR-RFLP methods. To investigate other GJB2 mutations, we have amplified and sequenced DNA from 51 unrelated deaf patients and 17 control subjects. None of the samples studied, either by RFLP or sequencing, revealed any deafness-associated mutations in the coding region of the GJB2 gene. These findings disagree with many reports on the GJB2 gene, describing various mutations as the cause of congenital recessive deafness. Although, an amino acid substitution (S86T) was identified by sequencing, we conclude that this change could not be associated with deafness since it was present in all the control and patient samples sequenced.

A seminested PCR test for simultaneous detection of two common mutations (35delG and 167delT) in the connexin-26 gene.

BACKGROUND: Several mutations described in the connexin-26 gene cause nonsyndromic autosomal recessive deafness (NARD). The prevalence of two frame-shift mutations, known as 35delG and 167delT, was relatively high in patients with NARD from different populations. METHODS AND RESULTS: A seminested PCR test has been developed for simultaneous detection of two common mutations in the connexin-26 gene. The test is based on PCR amplification of a 285-bp DNA fragment that covers both the 35delG and 167delT mutations. The latter mutation destroys a Pst I site and is easily detected by Pst I digestion of the 285-bp DNA fragment. However, the 35delG mutation does not destroy or create a restriction site. To create a site, we designed a mismatched primer that generated an EcoN I site in an 87-bp DNA fragment, but only if the 35delG mutation was present. The test was validated using five DNA samples previously characterized for the connexin-26 mutations. After validation, we screened 45 unrelated patients with NARD and 280 healthy Omani subjects for the presence or absence of the 35delG and 167delT mutations. Neither mutation was found to be present in patients or control subjects. CONCLUSION: We developed a seminested PCR test for the simultaneous detection of both common mutations in the connexin-26 gene. In our analysis of 45 patients and 280 control subjects, the 35delG and 167delT mutations were absent in both groups.