Ultrastructural aberrations, histological disruption and upregulation of the VEGF, CD34 and ASMA immunoexpression in the myocardium of anemic albino rats.

Iron deficiency anemia (IDA) is a global health problem affecting various body systems and tissues including the cardiovascular system. Several literatures described the associated physiological and clinical changes in the cardiovascular system and heart. However, the associated structural changes were poorly investigated. Therefore, the main aim of the present work was to elucidate whether IDA induces structural changes and alterations in the VEGF, CD34 and ASMA immunoexpression in the myocardium of albino rats. Thirty adult male albino rats were divided into two groups (fifteen rats each); control and anemic. Hematological data for all animals were assessed weekly and statistically analyzed. Three weeks later, animals were sacrificed, and heart specimens were obtained and processed for light and electron microscopy. All hematological parameters showed a statistically significant decrease in the anemic group. Structurally, the anemic group showed markedly degenerated, disrupted and disorganized cardiomyocytes in addition to markedly congested blood vessels, fibroblasts, collagen fibers deposition and perivascular cellular infiltration were noted. Also, positive immunostaining for VEGF, CD34 and ASMA was observed. Ultra-structurally, the myocardium of the anemic group showed disrupted and degenerated myofibrils with degenerated nuclei, perinuclear edema, widened interstitial spaces and marked collagen deposition. Mitochondria markedly increased with abnormal shapes. IDA induced myocardial injury that may propagate to regeneration through activated CD34 progenitor cells and increased VEGF or to degeneration and fibrosis through collagen fibers deposition and enhanced ASMA. So, early diagnosis and treatment of IDA is mandatory to avoid the associated myocardial structural changes.

Morphometric analysis of vastus medialis oblique muscle and its influence on anterior knee pain.

Healthy knees require full range squatting movements. Vastus medialis (VM) muscle regulates and adjusts the extensor apparatus that influences the patellofemoral function. This work was designed to investigate the anatomy and morphometry of vastus medialis oblique (VMO) muscle by widely used imaging techniques and investigate how VMO muscle participates in anterior knee pain. Ten dissected cadaveric specimens were examined, focusing on fiber orientations, origin, insertions and nerve supply of VMO muscle. Magnetic resonance imaging and ultrasound of VMO muscle were recorded. Anatomical cross-sectional areas of VMO muscle were determined in painless and painful knees and statistically analyzed. In cadaveric specimens, there was distinct separation between VM longus and VMO (change in fiber angle or fibro-fascial plane). VMO inserted directly into the medial proximal margin of the patella, capsule of the knee joint and continuous with the patellar tendon. Separate branch of femoral nerve run along the anteromedial border of the muscle. Anatomical cross-sectional area was significantly decreased in painful knee by -17.2%±11.0% at lower end of shaft of femur, -21.1%±6.0% at upper border of patella, -36.7%±11.0% at mid-patellar level. VMO is distinct muscle within quadriceps femoris group. VMO muscle would track the patella medially and participate in last phase of knee extension. Assessment of the VMO muscle anatomical cross-sectional area by ultrasonography may constitute promising and reliable tool to evaluate patellofemoral pain syndrome staging.

Histomorphological, VEGF and TGF-ß immunoexpression changes in the diabetic rats' ovary and the potential amelioration following treatment with metformin and insulin.

Diabetes mellitus (DM) affects the ovary by reducing the number and diameters of ovarian follicles and increasing atretic follicles. Follicular growth and diameters depend on VEGF production. Hyperglycemia causes ovarian stromal and follicular degeneration then fibrosis by activating TGF-ß. Insulin and metformin promote development of ovarian follicles and reduce atretic follicles. Therefore, the present study investigates the ovarian VEGF and TGF-ß immune-expression and its variations in diabetic, insulin and metformin-treated rats. Forty adult female albino rats were divided equally into four groups: control, diabetic (STZ-induced diabetes), diabetic metformin-treated group (100 mg/kg/day orally/eight weeks) and diabetic insulin-treated group (5 U insulin /day). Ovarian sections were stained with hematoxylin and eosin, Masson's trichrome, immunohistochemistry for VEGF and TGF-ß. The diabetic group showed noticeable atrophic and degenerative changes in cortex and medulla as well as increased density and distribution of the collagenous fibers. The number and diameter of primary, secondary and tertiary follicles were decreased. However, the number of atretic follicles and corpus luteum was increased. Significant decrease in the surface area percentage of VEGF immuno-expression and significant increase in TGF-ß immuno-expression surface area percentage were detected. By treating animals with metformin and insulin, there was restoration of the ovarian histological structure more or less as in control. DM negatively affects the histological and morphometric parameters of ovaries. Furthermore, insulin showed more beneficial effects than metformin in hindering these complications by modifying the expression of VEGF and TGF-ß.