Volume 39, Issue 2

Background The antidiabetic and antioxidant effects of Trigonella foenum-graceum have been suggested. The effects of hydroalcoholic extract of the plant seeds and metformin against the diabetes-induced memory impairment were investigated. Materials and methods The rats were treated: (1) control, (2) diabetic (3–6) and diabetic rats treated by 50, 100 and 200 mg/kg of the plant extract or metformin. The rats were diabetic by streptozotocin (STZ, 55 mg/kg). After the passive avoidance test, malondialdehyde (MDA), nitric oxide (NO) metabolites, total thiol (SH), catalase (CAT) and superoxide dismutase (SOD) were determined in the brain. Results In the diabetic group, at 3, 24 and 48 h after receiving a shock, the latency to enter the dark room was lower than for the controls (p < 0.001). All doses of the extract and metformin increased the latencies to enter the dark at 3 and 24 h after the shock treatment (p < 0.05–p < 0.001). Additionally, the two higher doses of the extract and metformin increased the latency at 48 h after the shock (p < 0.05–p < 0.001). Diabetes also elevated MDA and NO metabolites, while it reduced thiol, SOD and CAT in the hippocampal and cortical tissues (p < 0.001). Treatment of the diabetic animals by the highest dose of the extract and also metformin reduced the MDA and NO metabolites, while it improved thiols, SOD and CAT (p < 0.01–p < 0.001). Conclusions Based on our findings, metformin and the hydro-alcoholic extract from the T. foenum-graceum seed prevented memory deficits resulting from diabetes. Preventing oxidative damage in the brain may at least, in part, be responsible for the positive effects of the extract and metformin.

Background Inflammation, induced by excessive adiposity, links obesity to disease risk yet little attention has been devoted to the lymphoid tissues embedded within adipose tissue depots. Lymph nodes are the primary site for the development of protective immunity, hence any disease process that affects these tissues will also directly impact immunity. Here we examined how obesity alters secondary lymphatic tissue structure and encapsulated immune cells. Materials and methods Four-month-old C57BL/6 male mice were fed standard rodent chow or a Western high fat diet (HFD) for 6 months. Center regions of visceral and subcutaneous lymph nodes (SQLNS) were observed via transmission electron microscopy (TEM). Results Compared with chow, HFD-induced obesity deleteriously modified the structural microarchitecture and immune cell morphology of visceral and SQLNs. In HFD mice, fibroblastic reticular cells (FRCs) were dysregulated while laying among excessive amounts of disorganized collagen (C). In addition HFD lymph nodes contained a disproportionate amount of cellular debris from damaged or dead cells, increased sinus spacing and decreased immune cell interactions. Specifically, dendritic cells (DCs) that are necessary for adaptive immune response where embedded among extracellular debris with decreased pseudopodia. Similarly, the extraneous fibrous extracellular matrix (ECM) in HFD mice limited contact between lymphocytes (LCs) causing their microvilli extensions to decrease. Discussion Overall, excessive C production within lymph nodes, driven by diet-induced obesity, creates a physical barrier that impedes proper lymph flow and cellular communication. Obesity-induced disorganization of the immune cell guidance network interrupts immune cell adhesion and consequently inhibits travel within cortex regions needed for cell interactions, survival and proliferation.

Beta-thalassemia major is a subtype component of hemoglobinopathies; autosomal recessive disorders complicated with anemia that affect at least 50,000 babies each year. It contributes to problems in reproductive entities such as infertility due to iron deposition in the endocrine organs, which leads to malfunction of the hypothalamus-pituitary axis. Due to this, there have been very few pregnancies discovered and reported with this type of condition as they usually required an ovulation-induction agent with assisted reproductive technique to achieved pregnancy. We report a successful spontaneous pregnancy in a woman with beta-thalassemia major who underwent splenectomy with lifelong transfusion-dependence complicated with myocardial siderosis and osteoporosis. The close monitoring and regular blood transfusion are a core of successful support to this type of pregnancy. The unintentional consumption of Fosamax, hydroxyurea and deferiprone (Ferriprox) up till 20 weeks of gestation did not show any adverse effects on fetal well-being. As expected, this pregnancy ended with the preterm delivery via cesarean section due to intrauterine growth restriction with oligohydramnios, and currently, this child is thriving. We concluded that pregnancy is not a contraindication in beta-thalassemia major; complex individual care is needed to achieve a safe outcome for the mother.

Objective To illustrate the importance of treatment duration with intramuscular testosterone undecanoate (Nebido ® ) for the final spermatogenesis recovery after treatment cessation. Also, to show a subsequent poor efficacy of the selective estrogen receptor modulator (SERM) clomiphene citrate (CC) in treating steroid-induced azoospermia following Nebido ® cessation and describe that initial oligozoospermia, existing before starting Nebido ® , largely contributes to that treatment outcome. Methodology Setting: Department of Human Reproduction and Department of Endocrinology, Clinical Hospital Center Rijeka, Rijeka, and Department of Endocrinology, Clinical Hospital Center Sestre milosrdnice, Zagreb, Croatia. Patient: A male patient having been diagnosed with primary hypogonadotropic hypogonadism, oligozoospermia and low testosterone (T) level, was treated with intramuscular testosterone undecanoate (TU) depot 1 g (Nebido ® ) to prevent further progression of testosterone deficiency symptoms (low mood, energy and concentration, fatigue, muscle weakness). Interventions: Stopping Nebido ® and treatment with CC 50 mg per day 5 days per week for 3–6 month to recover spermatogenesis. Main outcome measures: T levels and semen analyses. Results Semen analyses did not return to values before taking Nebido ® 1 year after cessation nor after 3 months of treatment with CC. Values of T, follicle stimulating hormone (FSH) and luteinizing hormone (LH) dropped even more than before starting Nebido ® , after 1 year of cessation. Conclusions Here we describe a case of initially idiopathic gonadal failure with subsequent secondary gonadal failure and infertility resulting from testosterone replacement therapy (TRT) treatment, and poor spermatogenesis recovery outcome of CC used post Nebido ® cessation.