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The aim of the four-year field experiment was to determine the effect of the foliar application of auxin, a synthetic growth hormone, used on its own and in combination with various iron concentrations on the yield and forage quality of Medicago× varia T. Martyn, the Kometa cultivar. The research was conducted in three replications at the experimental facility of Siedlce University (52°10'03"N; 22°17'24"E, Poland) between 2014 and 2017. The treatment combinations were as follows: K - control (distilled water); A - indole-3-butyric acid (IBA - synthetic auxin); A+F1 - auxin (indole-3 butyric acid) with iron (II) sulphate (IV) heptahydrate at 3% concentration; A+F2 - auxin (indole-3 butyric acid (IBA)) with iron (II) sulphate heptahydrate at 5% concentration; A+F3 - auxin (indole-3 butyric acid (IBA) with iron (II) sulphate heptahydrate at 7% concentration. Between 2014 and 2017 hybrid alfalfa was harvested at the beginning of the bud stage, three times a growing season. Each growth cycle, plants were sprayed once at the 9-leaf stage. During a harvest 0.5 kg of fresh matter was collected from each plot to determine the content of aboveground dry matter and to perform chemical analyses. The highest yield, 44% higher than for control plants, was noted on the plot treated with auxin applied together with iron sulphate at 5% concentration, and the lowest on the control plot. Foliar application of auxin with iron improved the quality of alfalfa forage, affecting the content of total and digestible protein and crude fibre and dry matter digestibility. [ABSTRACT FROM AUTHOR]

Introduction: Recombinant human growth hormone (rhGH) treatment has been a well-established means of dealing with chronic kidney disease (CKD)-related short-stature for over 25 years. The aim of this study was to evaluate the safety, efficacy, metabolic effects, and factors influencing response to rhGH treatment in Poland. Material and methods: 156 non-dialyzed children with different stages of CKD were analysed regarding anthropometric features, biochemical parameters, calcium-phosphorus metabolism, bone mineral density (BMD), and CKD progression. The analysis comprised 24 months of treatment Results: The median height velocity during the whole course of treatment in the analysed group was 8 cm/year. In the first year of treatment, it was significantly faster than in the second year (9.5 cm/year and 7.6 cm/year, respectively, p < 0.01) and did not differ between children with CKD stage 2-3 (group A) and with CKD stage 4--5 (group B). Age of therapy onset correlated negatively with total ΔheightSDS (r = --0.21, p < 0.05). Throughout the treatment we observed a decrease of hypercalcemia (both groups) and an increase of hyperphosphatemia (group A). In the first year parathyroid hormone (PTH), IGF-1, CaxP, and ALP increased. In the second year PTH, IGF-1, and CaxP stabilized, and ALP decreased. ΔheightSDS correlated negatively with initial and mean serum cholesterol. Serum triglyceride concentration increased in the course of treatment. After 24 months, total body BMD increased in group A, and lumbar spine BMD increased in both groups (A and B). The mean decrease of glomerular filtration rate was 2.5 ml/min/1.73 m2/year. Conclusions: rhGH treatment is safe and effective, and should include the youngest CKD patients. Our results suggest that there might be a relationship between rhGH treatment and lipid profile, which necessitates further research. [ABSTRACT FROM AUTHOR]

Background: Activated PI3K delta syndrome (APDS) belongs to the heterogeneous group of primary immunodeficiency disorders (PIDs). Progress in next-generation sequencing (NGS) enabled identification of gain-of-function mutations in phosphoinositide 3-kinase (PI3K) genes. Depending on the type of causative mutation, APDS is classified into two types: APDS 1 and APDS 2. To date, less than 100 cases of APDS have been reported. Clinical symptoms of APDS result from impaired immune regulation and are clinically manifested by recurrent infections, allergies, lymphoproliferation and autoimmunity. They show similarity to other PIDs. Therefore, many patients were diagnosed incorrectly. The availability of genetic testing has allowed establishing the correct diagnosis in increasing number of patients suffering from APDS. Case presentations: The first male patient presented in infancy with recurrent infections. Subsequently he was found to suffer from hepatosplenomegaly, early portal hypertension, massive lymphoproliferation and hypogammaglobulinemia. The common E1021K mutation in the PI3KCD gene was identified. The patient underwent successful hematopoietic stem cell transplantation with resolution of most symptoms. The second patient suffered from persistent growth retardation since early life, facial dysmorphism and recurrent respiratory infections from early childhood. He was found to have systemic lympho-proliferation, panhypoglobulinemia and impaired antibody responses to vaccines. The introduction of NGS in Poland enabled rapid identification of a mutation in the PI3KR1 gene. Growth hormone administration seemed to have worsened the lymphoproliferation. Conclusions: Patients with suspected common variable immunodeficiency (CVID) and additional symptoms, such as allergy, facial dysmorphia, short stature, enhanced lymphoproliferation and lack of adequate response to human immunoglobulin replacement therapy, should be considered for NGS-based genetic testing. It may substantially shorten the time needed to establish the correct diagnosis, direct appropriate treatment and avoid potentially harmful therapies. To date, few cases of APDS have been described. It is important to report each of them to establish clinical indices and laboratory biomarkers of APDS 1 and APDS 2, to develop the standards of care in these conditions. [ABSTRACT FROM AUTHOR]

Introduction: Silver-Russell syndrome (SRS) is characterized by clinical and genetic heterogeneity. SRS is the only disease entity associated with (epi)genetic abnormalities of 2 different chromosomes: 7 and 11. In SRS, the 2 most frequent molecular abnormalities are hypomethylation (loss of methylation) of region H19/IGF2:IG-DMR on chromosome 11p15.5 (11p15 LOM) and maternal uniparental disomy of chromosome 7 (upd(7)mat). Therapy with recombinant human growth hormone (rhGH) is implemented to increase body height in children with SRS. The effect of the administered rhGH on height, weight, body mass index (BMI), body composition, and height velocity in patients with SRS during 3 years of rhGH therapy was analysed., Material and Methods: 31 SRS patients (23 with 11p15 LOM, 8 with upd(7)mat) and 16 patients small for gestational age (SGA) as a control group were diagnosed and followed up in The Children's Memorial Health Institute. Patients were eligible for the 2 Polish rhGH treatment programmes [for patients with SGA or with growth hormone deficiency (GHD)]. Anthropometric parameters were collected in all patients. Body composition using bioelectrical impedance was measured in 13 SRS and 14 SGA patients., Results: Height, weight, and weight for height (SDS) at baseline of rhGH therapy were lower in SRS patients than in the SGA control group: -3.3 ± 1.2 vs. -2.6 ± 06 (p = 0.012), -2.5 vs. -1.9 (p = 0.037), -1.7 vs. -1.1 (p = 0.038), respectively. Height SDS was increased from -3.3 ± 1.2 to -1.8 ± 1.0 and from -2.6 ± 0.6 to -1.3 ± 0.7 in the SRS and SGA groups, respectively. Patients with 11p15 LOM and upd(7) mat achieved similar height, 127.0 ± 15.7 vs. 128.9 ± 21.6 cm, and -2.0 ± 1.3 vs. -1.7 ± 1.0 SDS, respectively. Fat mass percentage decreased in SRS patients from 4.2% to 3.0% (p < 0.05) and in SGA patients from 7.6% to 6.6% (p < 0.05)., Conclusions: Growth hormone therapy has a positive influence on the growth of SRS patients. Regardless of molecular abnormality type (11p15 LOM vs. upd(7)mat), height velocity was similar in SRS patients during 3 years of rhGH therapy.

Several studies in patients with acromegaly or growth hormone (GH) deficiency suggest a stimulatory effect of the growth hormone (GH)/insulin-like growth factor I (IGF-I) axis on the renin-angiotensin-aldosterone system (RAAS). We analyzed the association of serum IGF-I with plasma aldosterone and the aldosterone-to-renin ratio in a large sample from the general population. In addition to serum IGF-I levels, we also considered the IGF-I-to-IGF binding protein (IGFBP)-3 ratio. A total of 1 504 men and 1 566 women aged 25-88 were selected from the first follow-up of the population-based Study of Health in Pomerania. Plasma aldosterone and renin concentrations, as well as serum IGF-I and IGFBP-3 levels were determined with immunoassays. Analyses of variance and linear regression analyses were performed. We found positive associations between serum IGF-I or the IGF-I/IGFBP-3 ratio with plasma aldosterone in women but not in men. Plasma aldosterone levels increased by 2.91 ng/l per IGF-I standard deviation (SD) and by 2.17 ng/l per IGF-I/IGFBP-3 SD. The associations remained significant after exclusion of subjects taking RAAS-altering medication and of subjects with serum IGF-I levels and aldosterone-to-renin ratios outside the reference range. We conclude that, serum IGF-I and the IGF-I/IGFBP-3 ratio are associated with plasma aldosterone levels in women but not in men from the general population. [ABSTRACT FROM AUTHOR]

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Purpose: Short stature in children is a significant medical problem which, without proper diagnosis and treatment, can lead to long-term consequences for physical and psychological health in adult life. Since human height is a polygenic and highly heritable trait, numerous variants in the genes involved in growth-including the growth hormone (GH1) gene-have been identified as causes of short stature., Methods: In this study, we performed for the first time molecular analysis of the GH1 gene in a cohort (n = 186) of Polish children and adolescents with short stature, suffering from growth hormone deficiency (GHD) or idiopathic short stature (ISS), and a control cohort (n = 178)., Results: Thirteen SNP variants were identified, including four missense variants, six in 5'UTR, and three in introns. The frequency of minor missense variants was low (<0.02) and similar in the compared cohorts. However, two of these variants, Ala39Val (rs151263636) and Arg42Leu (rs371953554), were found (heterozygote status) in only two GHD patients. These substitutions, according to databases, can potentially be deleterious., Conclusions: Mutations of GH1 causing short stature are very rare in the Polish population, but two potentially causative variants need further studies in a larger cohort of GHD patients.