Fusarium sambucinum astA gene expressed during potato infection is a functional orthologue of Aspergillus nidulans astA

Sulfate assimilation plays a vital role in prototrophic organisms. Orthologues of the alternative sulfate transporter (AstA) gene from Aspergillus nidulans were identified in the fungal plant pathogens Fusarium sambucinum and F. graminearum. By physiological and biochemical analyses, the AstA orthologues were determined to be able to uptake sulfate from the environment. Similarly to astA in A. nidulans, the FsastA gene was found to be regulated by sulfur metabolite repression (SMR) in a sulfur-dependent manner. In contrast, the FgastA transcript was undetectable, however, when the FgastA gene was expressed heterologously in A. nidulans, the translated FgAstA protein acted as a sulfate transporter. Interestingly, F. sambucinum astA expression was remarkably augmented in infected potato tubers, despite the presence abundant sulfate and was found not to be correlated with plant resistance

Review of Novel Potential Insulin Resistance Biomarkers in PCOS Patients—The Debate Is Still Open

Research on proteins and peptides that play roles in metabolic regulation, which may be considered potential insulin resistance markers in some medical conditions, such as diabetes mellitus, obesity and polycystic ovarian syndrome (PCOS), has recently gained in interest. PCOS is a common endocrine disorder associated with hyperandrogenemia and failure of ovulation, which is often accompanied by metabolic abnormalities, including obesity, dyslipidemia, hyperinsulinemia, and insulin resistance. In this review, we focus on less commonly known peptides/proteins and investigate their role as potential biomarkers for insulin resistance in females affected by PCOS. We summarize studies comparing the serum fasting concentration of particular agents in PCOS individuals and healthy controls. Based on our analysis, we propose that, in the majority of studies, the levels of nesfastin-1, myonectin, omentin, neudesin were decreased in PCOS patients, while the levels of the other considered agents (e.g., preptin, gremlin-1, neuregulin-4, xenopsin-related peptide, xenin-25, and galectin-3) were increased. However, there also exist studies presenting contrary results; in particular, most data existing for lipocalin-2 are inconsistent. Therefore, further research is required to confirm those hypotheses, as well as to elucidate the involvement of these factors in PCOS-related metabolic complications

Does the Value of FSH Predict Severity of Metabolic Complications in Females with POI?

Premature ovarian insufficiency (POI) is defined as a cessation of ovarian function before the age of 40. Such early deprivation of estrogens in women may be associated with several adverse cardiovascular and metabolic consequences. The aim of this retrospective study was to investigate whether women with POI and a serum follicle-stimulating hormone (FSH) level of 25–40 I/U (Group A) have the same metabolic profile as women with POI and a serum FSH level of >40 I/U (Group B). One hundred twenty-three women were included in the study group (Group A; n = 41; Group B; n = 82). The control group comprised 77 healthy women with regular menstruation. In the age- and BMI-adjusted model, no differences were found between the groups with respect to total cholesterol, high-density lipoproteins, triglycerides, HOMA-IR, glucose, and insulin. The only significant difference was found in terms of low-density lipoprotein cholesterol (LDL-C). The highest serum concentration was found in Group B, the second highest was found in Group A, and the lowest was in the controls. In conclusion, changing the threshold of FSH required to establish a POI diagnosis may have an impact on the level of serum LDL-C

Low frequency of spontaneous rearrangements during plasmid incorporation in CHO-KI mutant cells defective in DNA repair

pLrec plasmid DNA was introduced into Chinese hamster cell lines defective in DNA repair (Pa13, Pb4, xrs6) and the parental CHO-K1 cell line. Clones with stable integrated plasmid were isolated and integrity of the incorporated DNA was checked by Southern blotting and PCR. Intact pLrec plasmid was found in 11% of the isolated CHO-K1 clones. In contrast, intact plasmid copies were found in 68.8%, 50%, 35.7% clones of Pa13, Pb4 and xrs6 cell lines, respectively. We conclude that certain DNA repair defects may facilitate intact plasmid integration. The higher frequency of integration of the intact vector into the genome of cell lines defective in DNA repair as compared to the parental cell line points to two possibilities, not mutually exclusive: (1) these cells possess a mechanism that facilitates the process of plasmid incorporation and hence, plasmid DNA is incorporated into the genome before extrachromosomal recombination takes place; (2) the vector is inserted into a less recombination prone site in the genome

Metabolic syndrome is associated with similar long-term prognosis in non-obese and obese patients. An analysis of 45 615 patients from the nationwide LIPIDOGRAM 2004-2015 cohort studies

Aims We aimed to evaluate the association between metabolic syndrome (MetS) and long-term all-cause mortality. Methods The LIPIDOGRAM studies were carried out in the primary care in Poland in 2004, 2006 and 2015. MetS was diagnosed based on the National Cholesterol Education Program, Adult Treatment Panel III (NCEP/ATP III) and Joint Interim Statement (JIS) criteria. The cohort was divided into four groups: non-obese patients without MetS, obese patients without MetS, non-obese patients with MetS and obese patients with MetS. Differences in all-cause mortality was analyzed using Kaplan-Meier and Cox regression analyses. Results 45,615 participants were enrolled (mean age 56.3, standard deviation: 11.8 years; 61.7% female). MetS was diagnosed in 14,202 (31%) by NCEP/ATP III criteria, and 17,216 (37.7%) by JIS criteria. Follow-up was available for 44,620 (97.8%, median duration 15.3 years) patients. MetS was associated with increased mortality risk among the obese (hazard ratio, HR: 1.88 [95% CI, 1.79-1.99] and HR: 1.93 [95% CI 1.82-2.04], according to NCEP/ATP III and JIS criteria, respectively) and non-obese individuals (HR: 2.11 [95% CI 1.85-2.40] and 1.7 [95% CI, 1.56-1.85] according to NCEP/ATP III and JIS criteria respectively). Obese patients without MetS had a higher mortality risk than non-obese patients without MetS (HR: 1.16 [95% CI 1.10-1.23] and HR: 1.22 [95%CI 1.15-1.30], respectively in subgroups with NCEP/ATP III and JIS criteria applied). Conclusions MetS is associated with increased all-cause mortality risk in non-obese and obese patients. In patients without MetS obesity remains significantly associated with mortality. The concept of metabolically healthy obesity should be revised