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Minimal reports are available on the relationship between blood lipids such as cholesterol, triglycerides, high-density lipoprotein cholesterol (HDL-C) and low density lipoprotein cholesterol (LDL-C) and acne. Most of available literature was about the effect of drugs used in acne treatment on these parameters. In this work we determined plasma total cholesterol, triglycerides, HDL-C and LDL-C levels in 166 (83 males and 83 females) newly diagnosed untreated Jordanian acne patients and compared with 105 (52 males and 53 females) of age and sex matched healthy controls. Results indicated that acne patients, males and females, had significantly low plasma HDL-C levels ( p = 0.000). Plasma total cholesterol, triglycerides and LDL-C levels were shown to be within the normal range except for triglycerides and LDL-C levels in severe acne cases for both sexes, were shown to be significantly elevated compared with those in healthy controls ( p = 0.004 and 0.000 consequently). It has been noticed that there was a trend for plasma HDL-C of acne patients to decrease as the severity of acne condition increases. Our results indicated that acne patients have significant changes in the plasma lipids profile that should be considered in the pathogenesis as well as in the treatment of acne.

Based on our results, we conclude that low vitamin A and E plasma levels have an important role in the pathogenesis of acne and in the aggravation of this condition.

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Adiponectin is an adipokine involved in the regulation of body metabolism and immune response. Circulating levels and/or activity of adiponectin were reported to influence susceptibility to several diseases, including type 2 diabetes mellitus, cardiovascular disease, and metabolic syndrome. In this study, serum adiponectin levels and the association of adiponectin gene (ADIPQO) single-nucleotide polymorphism (G276T SNP) with hypertension in type 2 diabetic patients were examined. Type 2 diabetic patients (n = 449) were recruited and divided into two groups, normotensive (n = 199) and hypertensive (n = 250). Results demonstrated that serum adiponectin levels were significantly higher in normotensive subjects compared with hypertensive subjects (P < .05). When these results were compared according to gender, only female hypertensive diabetic patients showed significantly higher levels of adiponectin (P < .05). In addition, no significant difference in the genotypes and alleles frequencies of ADIPQO G276T SNP was observed between the two groups (P > .05). In conclusion, high circulating levels of adiponectin were found to be associated with hypertension only in type 2 diabetic female patients which might indicate a gender preference.

BackgroundAlpha-1 antitrypsin (α1-AT) is a member of the serine protease inhibitors (serpins) family. Liver cells are the major source of synthesis and secretion of (α1-AT) into the blood. Moreover, it has been demonstrated that α1-AT is expressed and secreted by many types of malignant cells. Studies have indicated that serum levels of (α1-AT) increase in a good number of malignant diseases. In addition, a significant correlation between serum levels and cancer stage has also been reported. In this work we aimed to test how α1-AT levels behave at the third week after treatment with chemotherapy.MethodsThe α1-AT blood levels were measured using commercially available radial immunodiffusion kit (Kent Laboratory Inc, Bellinham, Washigton) following manufacturer instructions.ResultsThe α1-AT blood levels were significantly decreased after treatment compared with those before the treatment started. The mean difference (before - after) treatment was 127.82 and 137.37 mg/dL with 95% CI of difference 109.06 - 146.57 and 116.08 - 158.65 mg/dL in lung and prostate cancer respectively. When we compared these levels according to the stage of cancer, we found that the mean difference (before - after) treatment was also highly significant as indicated by P-value and the 95% CI of these differences.ConclusionObtained data strongly indicate the value of testing α1-AT blood levels as one of the important indicators for the efficacy of cancer treatment.

There is compelling evidence from transgenic mouse studies and analysis of mutations in human carcinomas indicating that the TGF-β signal transduction pathway is tumor suppressive. We have shown that overexpression of TGF-β1 in mammary epithelial cells suppresses the development of carcinomas and that expression of a dominant negative type II TGF-β receptor (DNIIR) in mammary epithelial cells under control of the MMTV promoter/enhancer increases the incidence of mammary carcinomas. Studies of human tumors have demonstrated inactivating mutations in human tumors of genes encoding proteins involved in TGF-β signal transduction, including DPC4/Smad4, Smad2, and the type II TGF-β receptor (TβRII). There is also evidence that TGF-β can enhance the progression of tumors. This hypothesis is being tested in genetically modified mice. To attain complete loss of TβRII, we have generated mice with loxP sites flanking exon 2 of Tgfbr2 and crossed them with mice expressing Cre recombinase under control of the MMTV promoter/enhancer to obtain Tgfbr2 mgKO mice. These mice show lobuloalveolar hyperplasia. Mice are being followed for mammary tumor development. Tgfbr2 mgKO mice that also express polyoma virus middle T antigen under control of the MMTV promoter (MMTV-PyVmT) develop mammary tumors with a significantly shorter latency than MMTV-PyVmT mice and show a marked increase in pulmonary metastases. Our data do not support the hypothesis that TGF-β signaling in mammary carcinoma cells is important for invasion and metastasis, at least in this model system. The importance of stromal-epithelial interactions in mammary gland development and tumorigenesis is well established. These interactions probably involve autocrine and paracrine action of multiple growth factors, including members of the TGF-β family, which are expressed in both stroma and epithelium. Again, to accomplish complete knockout of the type II TGF-β receptor gene in mammary stromal cells, FSP1-Cre and Tgfbr2 flox/flox mice were crossed to attain Tgfbr2 fspKO mice. The loss of TGF-β responsiveness in fibroblasts resulted in intraepithelial neoplasia in prostate and invasive squamous cell carcinoma of the forestomach with high penetrance by 6 weeks of age. Both epithelial lesions were associated with an increased abundance of stromal cells. Activation of paracrine hepatocyte growth factor (HGF) signaling was identified as one possible mechanism for stimulation of epithelial proliferation. TGF-β signaling in fibroblasts thus modulates the growth and oncogenic potential of adjacent epithelia in selected tissues. More recently, we have examined the effects of Tgfbr2 fspKO fibroblasts on normal and transformed mammary epithelium. We analyzed the role of TGF-β signaling by stromal cells in mammary tumor progression. To avoid the possibility of endogenous wild-type fibroblasts masking potential effects of Tgfbr2 fspKO cells on tumor progression, we implanted PyVmT mammary carcinoma cells with Tgfbr2 fspKO or wildtype fibroblasts in the subrenal capsule of nude mice. Mamm...