Germination Behavior and Geographical Information System-Based Phenotyping of Root Hairs to Evaluate the Effects of Different Sources of Black Soldier Fly (Hermetia illucens) Larval Frass on Herbaceous Crops.

Insect larval frass has been proposed as a fertilizer and amendment, but methods for testing its effects on plants are poorly developed and need standardization. We obtained different types of black soldier fly (Hermetia illucens) frass via the factorial combination of (a) two insect diets, as follows: G (Gainesville = 50% wheat bran, 30% alfalfa meal, 20% maize meal) and W (43% sheep whey + 57% seeds); (b) two frass thermal treatments: NT = untreated and T = treated at 70 °C for 1 h. We tested the effects on the germination of cress (Lepidium sativum L.) and wheat (Triticum durum Desf.) by applying 1:2 w:w water extracts at 0, 25, 50, 75 and 100% concentration. Standardizing frass water content before extraction affected chemical composition. Frass extracts showed high electrical conductivity (8.88 to 13.78 mS cm-1). The W diet was suppressive towards Escherichia coli and showed a lower content of nitrates (e.g., WNT 40% lower than GNT) and a concentration-dependent phytotoxic effect on germinating plants. At 25% concentration, germination indices of G were 4.5 to 40-fold those at 100%. Root and shoot length and root hair area were affected by diet and concentration of frass extracts (e.g., root and shoot length in cress at 25% were, respectively, 4.53 and 2 times higher than at 100%), whereas the effects of the thermal treatment were few or inconclusive. On barley (Hordeum vulgare L.) grown in micropots on a silty loam soil, root mass was reduced by 37% at high extract concentration. A quick procedure for root hair surface area was developed based on the geographic information system (GIS) and may provide a fast method for incorporating root hair phenotyping in frass evaluation. The results indicate that below-ground structures need to be addressed in research on frass effects. For this, phyotoxicity tests should encompass different extract dilutions, and frass water content should be standardized before extraction in the direction of canonical procedures to allow comparisons.

Metformin administration improves leukocyte count in women with polycystic ovary syndrome: a 6-month prospective study.

INTRODUCTION: Polycystic ovary syndrome (PCOS) is a common disorder associated with a wide range of endocrine and metabolic abnormalities. Low-grade chronic inflammation is a related complication recently observed in PCOS. Increased white blood cell (WBC) count was previously reported in PCOS women. OBJECTIVE: To evaluate the effects of six months metformin administration on WBC count in PCOS women. PATIENTS AND METHODS: Fifty normal-weight PCOS women without additional metabolic or cardiovascular diseases were enrolled and treated with metformin (850 mg twice daily) for 6 months in a prospective baseline-controlled clinical study. At baseline and after treatment, WBC count and C-reactive protein (CRP) were evaluated in each patient. The whole hormonal profile, serum insulin and glucose levels (at fasting and during a 75 g 2-h oral glucose tolerance test), serum lipid profile were also assessed. RESULTS: A significant difference was observed in WBC count (7050 +/- 552 vs 6080 +/- 577 cell/mm(3) +/- s.d., P<0.001) and CRP levels (1.8 +/- 0.9 vs 1.1 +/- 0.6 mg/l +/- s.d., P<0.001) after metformin treatment in comparison with baseline values. SHBG levels and the free androgen index also changed significantly (P<0.001). Finally, high-density lipoproteins and the area under curve for glucose/area under curve for insulin ratio also significantly increased (P<0.001), whereas low-density lipoproteins and area under curve for insulin were significantly reduced (P<0.001). No other change was found in any of the biochemical parameters evaluated. CONCLUSION: A six-month course of metformin reduces WBC count in PCOS women.

Serum aldosterone concentration and cardiovascular risk in women with polycystic ovarian syndrome.

CONTEXT: Polycystic ovary syndrome (PCOS) is associated with early impairment of vascular structure and a low-grade chronic inflammation. Aldosterone is a well-recognized cardiovascular risk (CVR) factor and is related to inflammatory processes. OBJECTIVE: Our objective was to investigate serum aldosterone levels in PCOS and correlate them to some CVR factors and early atherosclerotic markers. DESIGN AND SETTING: A prospective baseline-controlled clinical study was conducted at the University "Federico II" of Naples School of Medicine (Naples, Italy). PATIENTS: Fifty PCOS women age- and body mass index-matched with 50 healthy women were enrolled. MEAN OUTCOME MEASURES: Anthropometric, hormonal, and metabolic patterns, including plasma aldosterone, renin, and C-reactive protein, were measured in each subject. Intima-media thickness was also evaluated in each patient and control. RESULTS: Aldosterone levels were significantly increased (P < 0.001) in PCOS compared with healthy women (10.5 +/- 3.2 vs. 5.7 +/- 2.5 ng/dl). In PCOS, a significant (P < 0.001) direct correlation between plasma aldosterone and homeostasis model assessment, C-reactive protein, intima-media thickness, and mean blood pressure was found. On the other hand, high-density lipoprotein cholesterol and potassium were inversely (P < 0.001) related to serum aldosterone. Multiple linear regression analysis showed that the area under the curve for insulin and homeostasis model assessment was linearly related to aldosterone in PCOS. CONCLUSION: PCOS women show an insulin resistance related increase in serum aldosterone levels.

The increase of leukocytes as a new putative marker of low-grade chronic inflammation and early cardiovascular risk in polycystic ovary syndrome.

White blood cell (WBC) count is a known risk factor for atherosclerotic vascular disease in adult women. Polycystic ovary syndrome (PCOS) is potentially a risk factor for atherosclerosis and cardiovascular disease. The aim of the present study was to investigate leukocyte count in PCOS. One hundred and fifty PCOS women matched for age and body mass index with 150 healthy women were enrolled. WBC count, C-reactive protein, and a complete anthropometrical, metabolic, and hormonal evaluation were performed in both groups. Serum insulin, glucose level, and lipid profile were also measured in each subject. WBC count was significantly higher (P < 0.0001) in PCOS with (interquartile range in parentheses) 7260 (393) cells/mm(3), compared with controls with 5220 (210) cells/mm(3). C-reactive protein levels were significantly increased (P < 0.0001) in PCOS with 2 (1) mg/liter compared with healthy women with 0.7 (0.8) mg/liter. In both groups, there was a significant (P < 0.0001) linear correlation between WBC count and homeostasis model assessment score (PCOS, r = 0.94; controls, r = 0.91). Multiple linear regression analysis showed that other hormone levels are not predictors of leukocyte count both in PCOS and control women. In conclusion, our data demonstrate that PCOS women have an increased WBC count that correlates with homeostasis model assessment values.

Is plasminogen activator inhibitor-1 a cardiovascular risk factor in young women with polycystic ovary syndrome?

This study aimed to evaluate plasminogen activator inhibitor-1 (PAI-1) activity in PCOS. Thirty women with PCOS - 15 normal-weight and 15 obese - and 30 healthy women matched as a group for age and body mass index (BMI) were recruited. The homeostasis model assessment (HOMA) score was significantly elevated in obese compared with normal-weight women, in both PCOS women and controls. HOMA score was significantly higher in both PCOS groups relative to controls. After further adjustment for BMI, PAI-1 activity (IU/ml +/- SD) was significantly higher in the PCOS groups compared with controls. A significant positive correlation was found between HOMA score and BMI in PCOS and control groups. Serum PAI-1 activity was significantly related to BMI and HOMA score. When considering two BMI subgroups, there was no significant difference in the relationship between serum PAI-1 activity and HOMA score in both the control and PCOS groups. No other significant relationship was found between serum PAI-1 activity and any other hormonal or metabolic parameter. In conclusion, women with PCOS have significantly elevated PAI-1 activity independent of obesity, and it is speculated that elevated PAI-1 activity may be a factor in the increased cardiovascular morbidity seen in PCOS.

Serum homocysteine concentrations in children with growth hormone (GH) deficiency before and after 12 months GH replacement.

OBJECTIVE: This open, prospective study was designed to evaluate the effect of growth hormone deficiency (GHD) and GH replacement therapy on serum homocysteine (Hcy) concentration in children with GHD. SUBJECTS: Seventeen prepubertal children with GHD (11 boys and six girls) aged 8.6 +/- 1.9 years were studied before and after 12 months of GH replacement therapy at a dose of GH of 30 microg/kg/day. Seventeen healthy children acted as controls and were matched for age, sex and body mass index (BMI). METHODS: At study entry, height, weight, blood pressure, serum Hcy, serum IGF-I, total-low density lipoprotein (LDL)- and high density lipoprotein (HDL) cholesterol, triglycerides, free T4, free T3, vitamin B12, folate, glucose and creatinine were measured in all subjects. The atherogenic index (AI) was also calculated as the ratio of total cholesterol/HDL cholesterol (T/HDL). In GHD children these parameters were also revaluated after 12 months of GH therapy. RESULTS: At study entry height and serum IGF-I were significantly lower, as expected, in GHD patients than in controls (P < 0.0001 and P < 0.007, respectively). Serum Hcy levels were significantly higher in GHD patients than in healthy children (8.4 +/- 2.9 vs. 6.0 +/- 2.9 micromol/l; P < 0.03), although the absolute values were within the normal values for age and sex. There were no significant differences at baseline with respect to blood pressure, serum vitamin B12, folate, fT3, fT4, lipid profile, creatinine and glucose levels. After 12 months of GH replacement therapy height and serum IGF-I increased significantly compared to pretreatment values (P < 0.0001); serum Hcy levels decreased significantly (6.0 +/- 3.3 micromol/l; P < 0.002) compared to baseline values, becoming similar to control values. Total cholesterol (3.5 +/- 0.6 mmol/l) and the AI (2.5 +/- 0.8) decreased significantly with respect to both pretreatment (4.2 +/- 1.0 mmol/l; P < 0.0002 and 3.4 +/- 0.8; < 0.002, respectively) and control values (4.2 +/- 0.4 mmol/l; P < 0.0005 and 3.3 +/- 1.1; P = 0.02, respectively). CONCLUSIONS: GHD in children is associated with higher serum levels of Hcy compared to controls, without significantly affecting the lipid profile. GH replacement for 12 months significantly decreased the Hcy levels and improved the lipid profile with a decrease of total cholesterol and the total/HDL cholesterol ratio, compared to pretreatment values. Given the small number of patients, further larger studies are needed to clarify whether these results may have significant effects in the prevention of cardiovascular disease in adulthood.

Lack of an association between peroxisome proliferator-activated receptor-gamma gene Pro12Ala polymorphism and adiponectin levels in the polycystic ovary syndrome.

Polycystic ovary syndrome (PCOS) is one of the most common endocrine metabolic diseases and is characterized by obesity in approximately 50% of those affected. Adiponectin is an adipocyte-derived protein that possesses an antiatherosclerotic action and improves insulin sensitivity. Peroxisome proliferator-activated receptor-gamma (PPAR-gamma) regulates the transcription of several adipocyte-specific genes. The aim of this study was to investigate the putative influence of the PPAR-gamma gene Pro12Ala polymorphism on the adiponectin levels in PCOS and healthy women. One hundred twenty women with PCOS and 120 healthy women whose ages and body mass indexes matched those of the PCOS patients were investigated. The genetic analysis of PPAR-gamma gene Pro12Ala polymorphism was performed by restriction fragment of polymorphisms. Serum adiponectin levels were evaluated, and the homeostasis model assessment score was also calculated. No subject was homozygous for the Ala12 allele of the PPAR-gamma gene. No significant differences in body mass index, plasma glucose and lipid levels, and homeostasis model assessment scores were observed between and within genotype groups in PCOS and control women. No significant differences in serum adiponectin concentrations were observed between and within genotype groups in PCOS and control women. In conclusion, our results confirm that adiponectin concentrations are similar in PCOS and controls and demonstrate no effect of the PPAR-gamma gene Pro12Ala polymorphism on serum adiponectin levels.

Early impairment of endothelial structure and function in young normal-weight women with polycystic ovary syndrome.

The aim of this study was to evaluate the presence of early vascular damage in young normal-weight women with polycystic ovary syndrome (PCOS). Thirty young normal-weight women with PCOS, who had no additional metabolic or cardiovascular diseases, and 30 healthy women (controls) matched for age and body mass index were studied. A complete hormonal assay was performed in each subject. Serum insulin and glucose levels were measured at baseline and after the oral glucose tolerance test. Plasma endothelin-1 levels and serum lipid profile were also assessed. The endothelial function was studied by flow-mediated dilation on the brachial artery, and arterial structure was evaluated by intima-media thickness measurement using Doppler ultrasound of both common carotid arteries.A significant (P < 0.05) difference in flow-mediated dilation (14.3 +/- 1.9% vs. 18.1 +/- 2.0% for PCOS patients and controls, respectively) and in intima-media thickness (0.53 +/- 0.09 mm vs. 0.39 +/- 0.08 mm for PCOS patients and controls, respectively) was found between PCOS and control subjects. Serum endothelin-1 levels were also significantly (P < 0.05) higher in PCOS patients compared with controls (1.1 +/- 0.4 pmol/liter vs. 0.5 +/- 0.2 pmol/liter for PCOS patients and controls, respectively).In conclusion, our data show that young, normal-weight, nondyslipidemic, nonhypertensive women with PCOS have an early impairment of endothelial structure and function.

Exon 6 and 2 peroxisome proliferator-activated receptor-gamma polymorphisms in polycystic ovary syndrome.

Obesity affects about 44% of women with polycystic ovary syndrome (PCOS). Peroxisome proliferator-activated receptor-gamma (PPAR-gamma) is one of the genes involved in the differentiation of adipose tissue. In an attempt to shed light on the high percentage of obesity in PCOS, we examined polymorphisms at exons 6 and 2 of the PPAR-gamma gene in 100 PCOS patients and in 100 healthy controls matched for age and body mass index (BMI). The T allele frequency of exon 6 was significantly higher (P < 0.05) in PCOS patients compared with control women. In addition, the BMI and leptin levels were significantly higher (P < 0.05) in PCOS patients carrying the C-->T substitution than in controls. There was no significant difference in leptin levels after normalization for BMI. The Pro(12)Ala polymorphism at exon 2 was unrelated to BMI and/or leptin levels in PCOS women. In conclusion, the higher frequency of the C-->T substitution in exon 6 of the PPAR-gamma gene in PCOS women suggests that it plays a role in the complex pathogenetic mechanism of obesity in PCOS, whereas the Pro(12)Ala polymorphism does not seem to affect BMI in PCOS women.

Homocysteine levels and C677T polymorphism of methylenetetrahydrofolate reductase in women with polycystic ovary syndrome.

The aim of this study was to investigate the homocysteine (Hcy) levels and the C677T polymorphism of 5,10-methylenetetrahydrofolate reductase (MTHFR), a crucial factor of the Hcy metabolism in young women with polycystic ovary syndrome (PCOS). Seventy young women with PCOS and another 70 healthy women with low folate intake were enrolled. Cases and controls were matched for age, body mass index, and allele frequency. Hcy, vitamin B(12), and folate levels were measured, and a genetic analysis of 5,10-MTHFR at nucleotide 677 was performed in all subjects. No difference in mean Hcy levels was observed between PCOS women in comparison to the control group. Considering the different MTHFR polymorphism, no significant difference was found in serum Hcy levels between subjects with PCOS and controls showing CC (10.4 +/- 3.1 vs. 9.7 +/- 2.9 micromol/liter +/- SD) and CT genotypes (10.9 +/- 3.8 vs. 11.0 +/- 3.2 micromol/liter +/- SD). In subjects with a TT homozygous state, a significant (P < 0.05) difference was observed between PCOS and control women (11.5 +/- 3.9 vs. 22.0 +/- 7.8 micromol/liter +/- SD). In conclusion, our data show that in PCOS women, the serum Hcy levels are normal, and the C677T polymorphism of MTHFR does not influence the Hcy levels like in controls.