Effects of Coriandrum sativum on distant organ inflammation and apoptosis due to liver ischemia/reperfusion injury.

Liver ischemia/reperfusion (IR) often affects distant organs, such as small intestine, kidney, and lung. Coriandrum sativum (CS) has an antioxidant and anti-inflammatory effect on liver damage. The aim of this study was to investigate the anti-inflammatory and antiapoptotic effects of CS extract on small intestine, lung, and kidney after the liver IR injury. Small intestine, lung, and kidney tissues were evaluated and scored in terms of cell degeneration, inflammation, and congestion, as well as caspase-3 (Cas-3) and cluster of differentiation 31 (CD31) immunostainings were carried out. Renal enzymes, creatinine and urea levels were measured biochemically in serum. After IR, a decrease in villi size, diffuse degeneration, epithelial cell shedding and extensive congestion in the capillaries were observed. Meanwhile, the number of degenerated villi and congestion decreased in the IR+CS group. Due to IR, increased congestion was detected in the interalveolar septum of the lungs and in the capillaries between the kidney tubules. It was also observed that the positively stained cells with Cas-3 and CD31 were increased in the lung, kidney, and small intestine tissues of the IR group, and decreased in the IR+CS group. Kidney enzymes, urea and creatinine levels were significantly increased in the IR group and decreased in the IR+CS group. In conclusion, it was observed that liver IR caused changes in distant organs, especially in the small intestine, lung, and kidneys. Damaging effects of IR as well as apoptosis and inflammation were found to be decreased in the groups treated with CS.

Does asporin have a role in polycystic ovary syndrome? A pilot study.

OBJECTIVE: Asporin is secreted by theca cells in the mouse ovaries and is an effective marker at the gonadotropin-independent stage in secondary follicle development. It has an inhibitory effect on transforming growth factor beta and bone morphogenic proteins, which are involved in androgenesis process. Our aim was to compare serum asporin levels of polycystic ovary syndrome and control groups and examine the relationship between asporin and hyperandrogenism. METHODS: A total of 60 patients, i.e., 30 polycystic ovary syndrome group and 30 controls, were included in the study. The demographic characteristics, hormonal status, and serum asporin levels of patients were evaluated and compared for each group. In addition, polycystic ovary syndrome patients were analyzed according to the presence of hyperandrogenism. Receiver operating characteristic curve analysis was performed for asporin levels in order to distinguish polycystic ovary syndrome patients from controls. RESULTS: Body mass index, serum asporin and androgen levels, free androgen index, and insulin resistance values were statistically significantly higher in polycystic ovary syndrome group. Serum asporin levels were statistically significantly higher in hyperandrogenic polycystic ovary syndrome patients compared to non-hyperandrogenic polycystic ovary syndrome women (p=0.010). Receiver operating characteristic curve analysis was done for serum asporin levels to distinguish between polycystic ovary syndrome patients and healthy controls (area under the curve=0.676, standard error: 0.070, 95%CI: 0.539-0.812, p=0.019, 63.3% sensitivity, and 70% specificity). CONCLUSION: The elevation of serum asporin levels in patients with polycystic ovary syndrome may be associated with the pathogenesis of this syndrome, or it may be the consequence of the disease. This relationship may be explained through the androgen mechanism.

Is there any link between vitamin D deficiency and vasovagal syncope?

BACKGROUND: This study aimed to investigate serum 25[OH]D levels between patients with vasovagal syncope (VVS) diagnosed with head-up tilt table test (HUTT) and age-matched healthy people. METHODS: The study included 75 consecutive patients (32.3 ± 10.7 years), who presented with syncope and underwent HUTT and 52 healthy controls (32.9 ± 14.1 years). HUTT patients were divided into two groups according to whether there was syncope response to the test. Patients underwent cardiac, psychiatric, and neurological investigation. Serum 25[OH]D levels were measured by chemiluminescent microparticle immunoassay method. RESULTS: There was no difference between the two groups in terms of age, gender, body mass index (BMI), echocardiographic findings (P > .05). Mean serum 25[OH]D (24.5 ± 6.3 vs 20.1 ± 8.8 ng/mL, P = .003) and vitamin B12 levels (436.4 ± 199.2 vs 363.1 ± 107.6 pg/mL, P = .009) was lower in syncope patients when compared to the control group. In correlation analyses, syncope was shown as correlated with the vitamin D (r = -264, P = .003) and vitamin B12 levels (r = -233, P = .009). But, multivariate regression analyses showed that only vitamin D increased risk of syncope [OR: 0.946, 95% CI (0.901-0.994)]. There was no difference in terms of age, gender, BMI, echocardiographic findings between the in HUTT positive (n = 45) and negative groups (n = 29). Only vitamin D level was significantly lower in HUTT positive group (17.5 ± 7.7 vs 24.4 ± 9.1 ng/mL, P = .002). There was no difference among in the vasovagal subgroups in terms of vitamin D level and other features. CONCLUSION: Vitamin D and B12 levels were reasonably low in syncope patients, but especially low Vitamin D levels were associated with VVS diagnosed in HUTT.