5 research outputs found
ΠΠΈΠΊΠΎΡΠΈΡΡΠ°Π½Π½Ρ ΠΌΠ΅ΡΠΎΠ΄ΡΠ² ΠΌΠ°ΡΠ΅ΠΌΠ°ΡΠΈΡΠ½ΠΎΠ³ΠΎ ΠΌΠΎΠ΄Π΅Π»ΡΠ²Π°Π½Π½Ρ ΠΏΡΠΈ Π²ΠΈΡΡΡΠ΅Π½Π½Ρ ΠΏΡΠΎΠ±Π»Π΅ΠΌΠΈ ΠΌΠΎΡΡΠΎΠ»ΠΎΠ³ΡΡΠ½ΠΎΡ Π΄ΠΈΡΠ΅ΡΠ΅Π½ΡΡΠΉΠ½ΠΎΡ Π΄ΡΠ°Π³Π½ΠΎΡΡΠΈΠΊΠΈ ΠΌΠ΅Π·Π°Π½Π³ΡΠΎ-ΠΊΠ°ΠΏΡΠ»ΡΡΠ½ΠΎΠ³ΠΎ Π³Π»ΠΎΠΌΠ΅ΡΡΠ»ΠΎΠ½Π΅ΡΡΠΈΡΡ Π ΡΠΈΠΏΡ ΡΠ° Π΄ΠΈΡΡΠ·Π½ΠΎΠ³ΠΎ Π²ΠΎΠ²ΡΠ°ΠΊΠΎΠ²ΠΎΠ³ΠΎ Π³Π»ΠΎΠΌΠ΅ΡΡΠ»ΠΎΠ½Π΅ΡΡΠΈΡΡ.
Background. Diffuse lupus and mesangiocapillary glomerulonephritises have similar morphological appearance which causes difficulties of their differential diagnostics. Objective. To analyze and generalize the data about intravital investigation of renal biopsies of patients with diffuse lupus glomerulonephritis and mesangiocapillary glomerulonephritis type I and identification of their most important morphological features with the help of systematic patomorphological study and statistical methods. Methods. 39 renal biopsies of patients with diffuse lupus glomerulonephritis and 43 of biopsies of patients with mesangiocapillary glomerulonephritis were studied. Polyclonal antibodies to IgA, IgG, IgM, complement fraction Π‘1q, Π‘3, monoclonal antibodies to CD68, CD3, CD20, CD45, Ξ±-SMA, vimentin, desmin and polyclonal antibodies to cytokeratin (AE1/AE3 ΡΠ° Π‘Π18) were used. Analysis of biopsies stained with hisctochemical methods was conducted with the help of development of neuronetwork models. Results. It was revealed a number of morphological findings that play the most important role in the cases of complicated differential diagnosis between mesangiocapillary type I and diffuse lupus glomerulonephritises, such as the following: deposition of IgM in stroma, subepithelial and subendothelial deposition of complement C3 fraction, deposition of complement C3 within cylinders, deposition of complement C1q fractions inside the tubular basal membrane at the focuses with sclerosis. Conclusion. Immunohistochemical analysis with the method of neuronetwork mathematical modeling helped to reveal the most important factor evidences for differential diagnostics of glomerulonephritis.Π¦Π΅Π»Ρ β ΠΏΡΠΎΠ°Π½Π°Π»ΠΈΠ·ΠΈΡΠΎΠ²Π°ΡΡ ΠΈ ΠΎΠ±ΠΎΠ±ΡΠΈΡΡ Π΄Π°Π½Π½ΡΠ΅ ΠΎ ΠΏΡΠΈΠΆΠΈΠ·Π½Π΅Π½Π½ΠΎΠΌ ΠΈΡΡΠ»Π΅Π΄ΠΎΠ²Π°Π½ΠΈΠΈ Π±ΠΈΠΎΠΏΡΠΈΠΈ ΠΏΠΎΡΠ΅ΠΊ Ρ ΠΏΠ°ΡΠΈΠ΅Π½ΡΠΎΠ² Ρ Π²ΠΎΠ»ΡΠ°Π½ΡΠΌ Π΄ΠΈΡΡΡΠ·Π½ΡΠΌ Π³Π»ΠΎΠΌΠ΅ΡΡΠ»ΠΎΠ½Π΅ΡΡΠΈΡΠΎΠΌ ΠΈ ΠΌΠ΅Π·Π°Π½Π³ΠΈΠΎΠΊΠ°ΠΏΠΈΠ»Π»ΡΡΠ½ΡΠΌ Π³Π»ΠΎΠΌΠ΅ΡΡΠ»ΠΎΠ½Π΅ΡΡΠΈΡΠΎΠΌ I ΡΠΈΠΏΠ° ΠΈ Π²ΡΡΠ²Π»Π΅Π½ΠΈΠ΅ Π½Π°ΠΈΠ±ΠΎΠ»Π΅Π΅ Π²Π°ΠΆΠ½ΡΡ
ΠΌΠΎΡΡΠΎΠ»ΠΎΠ³ΠΈΡΠ΅ΡΠΊΠΈΡ
ΠΏΡΠΈΠ·Π½Π°ΠΊΠΎΠ² Ρ ΠΏΠΎΠΌΠΎΡΡΡ ΡΠΈΡΡΠ΅ΠΌΠ°ΡΠΈΡΠ΅ΡΠΊΠΎΠ³ΠΎ ΠΏΠ°ΡΠΎΠΌΠΎΡΡΠΎΠ»ΠΎΠ³ΠΈΡΠ΅ΡΠΊΠΎΠ³ΠΎ ΠΈΡΡΠ»Π΅Π΄ΠΎΠ²Π°Π½ΠΈΡ ΠΈ ΡΡΠ°ΡΠΈΡΡΠΈΡΠ΅ΡΠΊΠΈΡ
ΠΌΠ΅ΡΠΎΠ΄ΠΎΠ². ΠΠ½Π°Π»ΠΈΠ· Π±ΠΈΠΎΠΏΡΠΈΠΉ ΠΎΠΊΡΠ°ΡΠ΅Π½Π½ΡΡ
ΠΈΠΌΠΌΡΠ½ΠΎΠ³ΠΈΡΡΠΎΡ
ΠΈΠΌΠΈΡΠ΅ΡΠΊΠΈΠΌΠΈ ΠΌΠ΅ΡΠΎΠ΄Π°ΠΌΠΈ ΠΏΡΠΎΠ²ΠΎΠ΄ΠΈΠ»ΡΡ Ρ ΠΏΠΎΠΌΠΎΡΡΡ Π½Π΅ΠΉΡΠΎΡΠ΅ΡΠ΅Π²ΡΡ
ΠΌΠΎΠ΄Π΅Π»Π΅ΠΉ. ΠΡΠ»ΠΎ Π²ΡΡΠ²Π»Π΅Π½ΠΎ ΡΡΠ΄ ΠΌΠΎΡΡΠΎΠ»ΠΎΠ³ΠΈΡΠ΅ΡΠΊΠΈΡ
Π΄Π°Π½Π½ΡΡ
, ΠΊΠΎΡΠΎΡΡΠ΅ ΠΈΠ³ΡΠ°ΡΡ Π½Π°ΠΈΠ±ΠΎΠ»Π΅Π΅ Π²Π°ΠΆΠ½ΡΡ ΡΠΎΠ»Ρ Π² ΡΠ»ΠΎΠΆΠ½ΡΡ
ΡΠ»ΡΡΠ°ΡΡ
Π΄ΠΈΡΡΠ΅ΡΠ΅Π½ΡΠΈΠ°Π»ΡΠ½ΠΎΠΉ Π΄ΠΈΠ°Π³Π½ΠΎΡΡΠΈΠΊΠΈ ΠΌΠ΅ΠΆΠ΄Ρ ΠΌΠ΅Π·Π°Π½Π³ΠΈΠΎΠΊΠ°ΠΏΠΈΠ»Π»ΡΡΠ½ΡΠΌ ΡΠΈΠΏΠΎΠΌ I ΠΈ Π΄ΠΈΡΡΡΠ·Π½ΡΠΌ Π²ΠΎΠ»ΡΠ°Π½ΠΎΡΠ½ΡΠΌ Π³Π»ΠΎΠΌΠ΅ΡΡΠ»ΠΎΠ½Π΅ΡΡΠΈΡΠ°ΠΌΠΈ, ΡΠ°ΠΊΠΈΠ΅ ΠΊΠ°ΠΊ: ΠΎΡΠ»ΠΎΠΆΠ΅Π½ΠΈΡ IgM Π² ΡΡΡΠΎΠΌΠ΅, ΡΡΠ±ΡΠΏΠΈΡΠ΅Π»ΠΈΠ°Π»ΡΠ½Π°Ρ ΠΈ ΡΡΠ±ΡΠ½Π΄ΠΎΡΠ΅Π»ΠΈΠ°Π»ΡΠ½Π°Ρ Π΄Π΅ΠΏΠΎΠ·ΠΈΡΠΈΡ ΡΡΠ°ΠΊΡΠΈΠΈ ΠΊΠΎΠΌΠΏΠ»Π΅ΠΌΠ΅Π½ΡΠ° Π‘3, ΠΎΡΠ»ΠΎΠΆΠ΅Π½ΠΈΠ΅ ΠΊΠΎΠΌΠΏΠ»Π΅ΠΌΠ΅Π½ΡΠ° C3 Π²Π½ΡΡΡΠΈ ΡΠΈΠ»ΠΈΠ½Π΄ΡΠΎΠ², ΠΎΡΠ»ΠΎΠΆΠ΅Π½ΠΈΠ΅ ΠΊΠΎΠΌΠΏΠ»Π΅ΠΌΠ΅Π½ΡΠ° ΡΡΠ°ΠΊΡΠΈΠΉ C1q Π² ΡΡΠ±ΡΠ»ΡΡΠ½ΠΎΠΉ Π±Π°Π·Π°Π»ΡΠ½ΠΎΠΉ ΠΌΠ΅ΠΌΠ±ΡΠ°Π½Π΅ Π² ΡΠΎΠΊΡΡΠ΅ ΡΠΊΠ»Π΅ΡΠΎΠ·Π°. ΠΠΌΠΌΡΠ½ΠΎΡΠΈΡΠΎΡ
ΠΈΠΌΠΈΡΠ΅ΡΠΊΠΈΠΉ Π°Π½Π°Π»ΠΈΠ· Ρ ΠΌΠ΅ΡΠΎΠ΄ΠΎΠΌ Π½Π΅ΠΉΡΠΎΡΠ΅ΡΠ΅Π²ΠΎΠ³ΠΎ ΠΌΠ°ΡΠ΅ΠΌΠ°ΡΠΈΡΠ΅ΡΠΊΠΎΠ³ΠΎ ΠΌΠΎΠ΄Π΅Π»ΠΈΡΠΎΠ²Π°Π½ΠΈΡ ΠΏΠΎΠ·Π²ΠΎΠ»ΠΈΠ» Π²ΡΡΠ²ΠΈΡΡ Π½Π°ΠΈΠ±ΠΎΠ»Π΅Π΅ Π²Π°ΠΆΠ½ΡΠ΅ ΡΠ²ΠΈΠ΄Π΅ΡΠ΅Π»ΡΡΡΠ²Π° ΡΠ°ΠΊΡΠΎΡΠΎΠΌ Π΄Π»Ρ Π΄ΠΈΡΡΠ΅ΡΠ΅Π½ΡΠΈΠ°Π»ΡΠ½ΠΎΠΉ Π΄ΠΈΠ°Π³Π½ΠΎΡΡΠΈΠΊΠΈ Π³Π»ΠΎΠΌΠ΅ΡΡΠ»ΠΎΠ½Π΅ΡΡΠΈΡΠ°.ΠΠ΅ΡΠ° β ΠΏΡΠΎΠ°Π½Π°Π»ΡΠ·ΡΠ²Π°ΡΠΈ ΡΠ° ΡΠ·Π°Π³Π°Π»ΡΠ½ΠΈΡΠΈ Π΄Π°Π½Ρ ΠΏΡΠΎ ΠΏΡΠΈΠΆΠΈΡΡΡΠ²Ρ Π΄ΠΎΡΠ»ΡΠ΄ΠΆΠ΅Π½Π½Ρ Π±ΡΠΎΠΏΡΡΠΉ Π½ΠΈΡΠΎΠΊ Ρ ΠΏΠ°ΡΡΡΠ½ΡΡΠ² Π· Π²ΠΎΠ²ΡΠ°ΠΊΠΎΠ²ΠΈΠΌ Π΄ΠΈΡΡΠ·Π½ΠΈΠΌ Π³Π»ΠΎΠΌΠ΅ΡΡΠ»ΠΎΠ½Π΅ΡΡΠΈΡΠΎΠΌ Ρ ΠΌΠ΅Π·Π°Π½Π³ΡΠΎΠΊΠ°ΠΏΡΠ»ΡΡΠ½ΠΈΠΌ Π³Π»ΠΎΠΌΠ΅ΡΡΠ»ΠΎΠ½Π΅ΡΡΠΈΡΠΎΠΌ I ΡΠΈΠΏΡ Ρ Π²ΠΈΡΠ²Π»Π΅Π½Π½Ρ Π½Π°ΠΉΠ±ΡΠ»ΡΡ Π²Π°ΠΆΠ»ΠΈΠ²ΠΈΡ
ΠΌΠΎΡΡΠΎΠ»ΠΎΠ³ΡΡΠ½ΠΈΡ
ΠΎΠ·Π½Π°ΠΊ Π· Π΄ΠΎΠΏΠΎΠΌΠΎΠ³ΠΎΡ ΡΠΈΡΡΠ΅ΠΌΠ°ΡΠΈΡΠ½ΠΎΠ³ΠΎ ΠΏΠ°ΡΠΎΠΌΠΎΡΡΠΎΠ»ΠΎΠ³ΡΡΠ½ΠΎΠ³ΠΎ Π΄ΠΎΡΠ»ΡΠ΄ΠΆΠ΅Π½Π½Ρ ΡΠ° ΡΡΠ°ΡΠΈΡΡΠΈΡΠ½ΠΈΡ
ΠΌΠ΅ΡΠΎΠ΄ΡΠ². ΠΡΠ»ΠΎ Π²ΠΈΡΠ²Π»Π΅Π½ΠΎ ΡΡΠ΄ ΠΌΠΎΡΡΠΎΠ»ΠΎΠ³ΡΡΠ½ΠΈΡ
Π΄Π°Π½ΠΈΡ
, ΡΠΊΡ Π²ΡΠ΄ΡΠ³ΡΠ°ΡΡΡ Π½Π°ΠΉΠ±ΡΠ»ΡΡ Π²Π°ΠΆΠ»ΠΈΠ²Ρ ΡΠΎΠ»Ρ Ρ ΡΠΊΠ»Π°Π΄Π½ΠΈΡ
Π²ΠΈΠΏΠ°Π΄ΠΊΠ°Ρ
Π΄ΠΈΡΠ΅ΡΠ΅Π½ΡΡΠ°Π»ΡΠ½ΠΎΡ Π΄ΡΠ°Π³Π½ΠΎΡΡΠΈΠΊΠΈ ΠΌΡΠΆ ΠΌΠ΅Π·Π°Π½Π³ΡΠΎΠΊΠ°ΠΏΡΠ»ΡΡΠ½ΠΈΠΌ ΡΠΈΠΏΠΎΠΌ I Ρ Π΄ΠΈΡΡΠ·Π½ΠΈΠΌ Π²ΠΎΠ²ΡΠ°ΠΊΠΎΠ²ΠΈΠΌ Π³Π»ΠΎΠΌΠ΅ΡΡΠ»ΠΎΠ½Π΅ΡΡΠΈΡΠΎΠΌ, ΡΠ°ΠΊΡ ΡΠΊ: Π²ΡΠ΄ΠΊΠ»Π°Π΄Π΅Π½Π½Ρ IgM Π² ΡΡΡΠΎΠΌΡ, ΡΡΠ±Π΅ΠΏΡΡΠ΅Π»ΡΠ°Π»ΡΠ½Π° ΡΠ° ΡΡΠ±Π΅Π½Π΄ΠΎΡΠ΅Π»ΡΠ°Π»ΡΠ½Π° Π΄Π΅ΠΏΠΎΠ·ΠΈΡΡΡ ΡΡΠ°ΠΊΡΡΠΉ ΠΊΠΎΠΌΠΏΠ»Π΅ΠΌΠ΅Π½ΡΡ Π‘3, Π²ΡΠ΄ΠΊΠ»Π°Π΄Π΅Π½Π½Ρ ΠΊΠΎΠΌΠΏΠ»Π΅ΠΌΠ΅Π½ΡΡ C3 Π²ΡΠ΅ΡΠ΅Π΄ΠΈΠ½Ρ ΡΠΈΠ»ΡΠ½Π΄ΡΡΠ², Π²ΡΠ΄ΠΊΠ»Π°Π΄Π΅Π½Π½Ρ ΠΊΠΎΠΌΠΏΠ»Π΅ΠΌΠ΅Π½ΡΡ ΡΡΠ°ΠΊΡΡΠΉ C1q Π² ΡΡΠ±ΡΠ»ΡΡΠ½ΡΠΉ Π±Π°Π·Π°Π»ΡΠ½ΡΠΉ ΠΌΠ΅ΠΌΠ±ΡΠ°Π½Ρ Ρ ΡΠΎΠΊΡΡΡ ΡΠΊΠ»Π΅ΡΠΎΠ·Ρ. ΠΠΌΠΌΡΠ½ΠΎΠ³ΡΡΡΠΎΡ
ΡΠΌΡΡΠ½ΠΈΠΉ Π°Π½Π°Π»ΡΠ· Π· ΠΌΠ΅ΡΠΎΠ΄ΠΎΠΌ Π½Π΅ΠΉΡΠΎΠΌΠ΅ΡΠ΅ΠΆΠ΅Π²ΠΎΠ³ΠΎ ΠΌΠ°ΡΠ΅ΠΌΠ°ΡΠΈΡΠ½ΠΎΠ³ΠΎ ΠΌΠΎΠ΄Π΅Π»ΡΠ²Π°Π½Π½Ρ Π΄ΠΎΠ·Π²ΠΎΠ»ΠΈΠ² Π²ΠΈΡΠ²ΠΈΡΠΈ Π½Π°ΠΉΠ±ΡΠ»ΡΡ Π²Π°ΠΆΠ»ΠΈΠ²Ρ ΡΠ²ΡΠ΄ΠΎΡΡΠ²Π° ΡΠ°ΠΊΡΠΎΡΠΎΠΌ Π΄Π»Ρ Π΄ΠΈΡΠ΅ΡΠ΅Π½ΡΡΠ°Π»ΡΠ½ΠΎΡ Π΄ΡΠ°Π³Π½ΠΎΡΡΠΈΠΊΠΈ Π³Π»ΠΎΠΌΠ΅ΡΡΠ»ΠΎΠ½Π΅ΡΡΠΈΡΡ
The calcium-sensing receptor in physiology and in calcitropic and noncalcitropic diseases
The Ca2+-sensing receptor (CaSR) is a dimeric family C G protein-coupled receptor that is expressed in calcitropic tissues such as the parathyroid glands and the kidneys and signals via G proteins and Ξ²-arrestin. The CaSR has a pivotal role in bone and mineral metabolism, as it regulates parathyroid hormone secretion, urinary Ca2+ excretion, skeletal development and lactation. The importance of the CaSR for these calcitropic processes is highlighted by loss-of-function and gain-of-function CaSR mutations that cause familial hypocalciuric hypercalcaemia and autosomal dominant hypocalcaemia, respectively, and also by the fact that alterations in parathyroid CaSR expression contribute to the pathogenesis of primary and secondary hyperparathyroidism. Moreover, the CaSR is an established therapeutic target for hyperparathyroid disorders. The CaSR is also expressed in organs not involved in Ca2+ homeostasis: it has noncalcitropic roles in lung and neuronal development, vascular tone, gastrointestinal nutrient sensing, wound healing and secretion of insulin and enteroendocrine hormones. Furthermore, the abnormal expression or function of the CaSR is implicated in cardiovascular and neurological diseases, as well as in asthma, and the CaSR is reported to protect against colorectal cancer and neuroblastoma but increase the malignant potential of prostate and breast cancers