Effect of experimental type 2 diabetes complicated by pyelonephritis on ultrastructural changes in the choroid, retina and nephrons

The clinical and morphological picture of diabetic microangiopathy is rather specific. Diabetic retinal ischemia can lead to irreversible damage to retinal neural elements and choroidal capillaries. Diabetic nephropathy can lead to progressive renal dysfunction and chronic renal failure. Choroidal and retinal capillaries are structurally and functionally similar to those of the intestinal mucosa and renal tissue. Purpose: To assess vascular ultrastructural changes in the choroid, retina, and renal glomerular and tubular system in a rat model of pyelonephritis in the presence of type 2 diabetes. Material and Methods: Samples were obtained from 95 Wistar rats divided into three groups: group 1 (or control group) of 30 intact animals; group 2 of 15 animals with type 2 diabetes induced by intraperitoneal streptozotocin 15.0 mg/ kg for 5 consecutive days; and group 3 of 50 animals with acute pyelonephritis in the presence of type 2 diabetes (streptozotocin 35.0 mg/kg on 2 days spaced by a week). Acute pyelonephritis was induced by Escherichia coli administration (107 CFU/kg) rectally. The ultrastructure of rat choroidal, retinal and renal glomerular-and-tubular vessels was examined with electron microscopy (PEM- 100-01 electron microscope). Results: In rats with induced type 2 diabetes, the most significant ocular vascular changes and renal vascular changes were found in endothelial cells. These changes included findings of vacuolar degeneration in some epithelial cells, basal membrane thickening and focal necrosis of individual epithelial cells. Vessel lumens appeared focally narrowed or expanded, with red blood cells forming clumps or sludge in lumens. Some capillaries were obliterated. These changes obviously caused secondary changes in the surrounding structures. Common ocular changes included focal destruction in retinal pigment epithelium cells, destruction of retinal photoreceptor inner segments and choroidal stromal edema. Common renal changes included destruction of the podocytes of the glomerular capillary network and homogenization of the basal membrane. Vascular ultrastructural changes in the renal glomerular system were more marked in rats with experimental type 2 diabetes and pyelonephritis than in those with type 2 diabetes only. Conclusion: Electron microscopy micrographs demonstrated the ultrastructural changes in the retinal and uveal vascular systems which were of a similar type to those in the renal glomerular-and-tubular system in rats with experimental pyelonephritis in the presence of type 2 diabetes

Effect of experimental type 2 diabetes complicated by pyelonephritis on ltrastructural changes in the choroid, retina and nephrons

Background: The clinical and morphological picture of diabetic microangiopathy is rather specific. Diabetic retinal ischemia can lead to irreversible damage to retinal neural elements and choroidal capillaries. Diabetic nephropathy can lead to progressive renal dysfunction and chronic renal failure. Choroidal and retinal capillaries are structurally and functionally similar to those of the intestinal mucosa and renal tissue. Purpose: To assess vascular ultrastructural changes in the choroid, retina, and renal glomerular and tubular system in a rat model of pyelonephritis in the presence of type 2 diabetes. Material and Methods: Samples were obtained from 95 Wistar rats divided into three groups: group 1 (or control group) of 30 intact animals; group 2 of 15 animals with type 2 diabetes induced by intraperitoneal streptozotocin 15.0 mg/kg for 5 consecutive days; and group 3 of 50 animals with acute pyelonephritis in the presence of type 2 diabetes (streptozotocin 35.0 mg/kg on 2 days spaced by a week). Acute pyelonephritis was induced by Escherichia coli administration (107 CFU/kg) rectally. The ultrastructure of rat choroidal, retinal and renal glomerular-and-tubular vessels was examined with electron microscopy (PEM-100-01 electron microscope). Results: In rats with induced type 2 diabetes, the most significant ocular vascular changes and renal vascular changes were found in endothelial cells. These changes included findings of vacuolar degeneration in some epithelial cells, basal membrane thickening and focal necrosis of individual epithelial cells. Vessel lumens appeared focally narrowed or expanded, with red blood cells forming clumps or sludge in lumens. Some capillaries were obliterated. These changes obviously caused secondary changes in the surrounding structures. Common ocular changes included focal destruction in retinal pigment epithelium cells, destruction of retinal photoreceptor inner segments and choroidal stromal edema. Common renal changes included destruction of the podocytes of the glomerular capillary network and homogenization of the basal membrane. Vascular ultrastructural changes in the renal glomerular system were more marked in rats with experimental type 2 diabetes and pyelonephritis than in those with type 2 diabetes only. Conclusion: Electron microscopy micrographs demonstrated the ultrastructural changes in the retinal and uveal vascular systems which were of a similar type to those in the renal glomerular-and-tubular system in rats with experimental pyelonephritis in the presence of type 2 diabetes

Theoretical and experimental studies of residual stresses, deformations and displacements during induction cladding of thin structural elements

The paper proposes a mathematical model for determining the fields of residual stresses, deformations and displacements that occur in the process of induction cladding, taking into account the fact that the product of the modulus of elasticity and the coefficient of thermal expansion of base metal and deposited metal is-Simplified calculation formulas were obtained and corresponding algorithms were built, which allow determining residual stresses and displacements. Based on this, it is necessary to use lowgradient temperature fields, which allow to avoid the operation of preheating or tempering

Search for MSSM Higgs bosons decaying to μ+μ-in proton-proton collisions at √s=13TeV

A search is performed for neutral non-standard-model Higgs bosons decaying to two muons in the context of the minimal supersymmetric standard model (MSSM). Proton-proton collision data recorded by the CMS experiment at the CERN Large Hadron Collider at a center-of-mass energy of 13TeVwere used, corresponding to an integrated luminosity of 35.9fb-1. The search is sensitive to neutral Higgs bosons produced via the gluon fusion process or in association with a bbquark pair. No significant deviations from the standard model expectation are observed. Upper limits at 95% confidence level are set in the context of the mmod+hand phenomenological MSSM scenarios on the parameter tanβas a function of the mass of the pseudoscalar Aboson, in the range from 130 to 600GeV. The results are also used to set a model-independent limit on the product of the branching fraction for the decay into a muon pair and the cross section for the production of a scalar neutral boson, either via gluon fusion, or in association with bquarks, in the mass range from 130 to 1000GeV

Studies of Bs2∗(5840)0 and Bs1(5830)0 mesons including the observation of the Bs2∗(5840)0→B0KS0 decay in proton-proton collisions at s=8TeV.

Measurements of Bs2∗(5840)0 and Bs1(5830)0 mesons are performed using a data sample of proton-proton collisions corresponding to an integrated luminosity of , collected with the CMS detector at the LHC at a centre-of-mass energy of 8TeV . The analysis studies P-wave Bs0 meson decays into B(∗)+K- and B(∗)0KS0 , where the B+ and B0 mesons are identified using the decays B+→J/ψK+ and B0→J/ψK∗(892)0 . The masses of the P-wave Bs0 meson states are measured and the natural width of the Bs2∗(5840)0 state is determined. The first measurement of the mass difference between the charged and neutral B∗ mesons is also presented. The Bs2∗(5840)0 decay to B0KS0 is observed, together with a measurement of its branching fraction relative to the Bs2∗(5840)0→B+K- decay