4 research outputs found
ΠΠΠΠ ΠΠ‘ΠΠ ΠΠΠΠΠΠΠΠ ΠΠΠΠΠΠΠ ΠΠΠ Π’Π ΠΠΠ‘ΠΠΠ Π’ΠΠΠ Π€ΠΠ ΠΠ« Π ΠΠ€ΠΠΠ£Π’ΠΠΠ
Background: One way to increase drug efficacy is to provide a drug delivery transport system to the target organ. A widely used method is to incorporate the drug in a biodegradable polymer composition with forming nanosized drugβs transport forms. Objective: Our aim was to investigate the tissue biodistribution of antibiotic rifabutin transport system based on lactic and glycolic acids copolymer, and to compare it with the pure substance of rifabutin. Methods: These substances were administered to two groups of rats intragastrically in the doses of 10Β mg/kg. After a certain period of time, the animals were sacrificed by cervical dislocation. Samples preparation for analysis was carried out of the liquid-liquid extraction. Active substanceβs concentrations were measured by high performance liquid chromatography method. Results: The study included 8-week-aged Wistar rats of both sexes weighing 0.22Β±0.02 kg. Animals were divided into 2 groups. The study group received polymer form of antibiotic, and the comparison group received substance of rifabutin. In intervals of 10 min, 30 min, 1 h, 2 h, 4 h, 7 h, 15 h, 24 h after drug administration liver, lung, spleen, kidney, intestines, stomach, heart and brain were resected respectively. Organs were measured by their weight. The drug was not detected in the brain. Rifabutin was determined in other examined tissues within 10 minutes and the maximum drug concentration in organs was fixed in 1.5β3.5 hours after administration. The rifabutin concentrations defined in the lungs were significantly higher in polymer form (pΒ 0.05). The polymer formβs distribution coefficient was higher in the liver and lungs (15.83 and 10.14Β ΞΌg/g respectively) in comparison with the substance one. The minimum amount of the active ingredient was observed in the heart (0.02Β ΞΌg/g). Conclusion: It is shown that the inclusion of the drug in a polymeric form substantially alters its localization in organs and tissues. Extensive biodistribution nanorifabutin in lung tissue, liver and spleen is established.Β Β ΠΠ΄Π½ΠΈΠΌ ΠΈΠ· Π½Π°ΠΏΡΠ°Π²Π»Π΅Π½ΠΈΠΉ ΡΠ²Π΅Π»ΠΈΡΠ΅Π½ΠΈΡ ΡΡΡΠ΅ΠΊΡΠΈΠ²Π½ΠΎΡΡΠΈ Π»Π΅ΠΊΠ°ΡΡΡΠ²Π΅Π½Π½ΡΡ
ΡΡΠ΅Π΄ΡΡΠ² ΡΠ²Π»ΡΠ΅ΡΡΡ ΡΠΎΠ·Π΄Π°Π½ΠΈΠ΅ ΡΡΠ°Π½ΡΠΏΠΎΡΡΠ½ΠΎΠΉ ΡΠΈΡΡΠ΅ΠΌΡ Π΄ΠΎΡΡΠ°Π²ΠΊΠΈ Π»Π΅ΠΊΠ°ΡΡΡΠ² Π² ΡΠ΅Π»Π΅Π²ΠΎΠΉ ΠΎΡΠ³Π°Π½. Π¨ΠΈΡΠΎΠΊΠΎ ΡΠ°ΡΠΏΡΠΎΡΡΡΠ°Π½Π΅Π½Π½ΡΠΉ ΠΌΠ΅ΡΠΎΠ΄ΠΎΠΌ β Π²ΠΊΠ»ΡΡΠ΅Π½ΠΈΠ΅ Π»Π΅ΠΊΠ°ΡΡΡΠ²Π΅Π½Π½ΠΎΠ³ΠΎ Π²Π΅ΡΠ΅ΡΡΠ²Π° Π² ΡΠΎΡΡΠ°Π² Π±ΠΈΠΎΠ΄Π΅Π³ΡΠ°Π΄ΠΈΡΡΠ΅ΠΌΠΎΠ³ΠΎ ΠΏΠΎΠ»ΠΈΠΌΠ΅ΡΠ° Ρ ΠΎΠ±ΡΠ°Π·ΠΎΠ²Π°Π½ΠΈΠ΅ΠΌ Π½Π°Π½ΠΎΡΠ°Π·ΠΌΠ΅ΡΠ½ΠΎΠΉ ΡΡΠ°Π½ΡΠΏΠΎΡΡΠ½ΠΎΠΉ ΡΠΎΡΠΌΡ Π»Π΅ΠΊΠ°ΡΡΡΠ²Π°. Π¦Π΅Π»Ρ ΠΈΡΡΠ»Π΅Π΄ΠΎΠ²Π°Π½ΠΈΡ: ΠΈΠ·ΡΡΠΈΡΡ Π±ΠΈΠΎΡΠ°ΡΠΏΡΠ΅Π΄Π΅Π»Π΅Π½ΠΈΠ΅ ΠΏΠΎ ΡΠΊΠ°Π½ΡΠΌ ΡΡΠ°Π½ΡΠΏΠΎΡΡΠ½ΠΎΠΉ ΡΠΈΡΡΠ΅ΠΌΡ Π°Π½ΡΠΈΠ±ΠΈΠΎΡΠΈΠΊΠ° ΡΠΈΡΠ°Π±ΡΡΠΈΠ½Π° Π½Π° ΠΎΡΠ½ΠΎΠ²Π΅ ΡΠΎΠΏΠΎΠ»ΠΈΠΌΠ΅ΡΠ° ΠΌΠΎΠ»ΠΎΡΠ½ΠΎΠΉ ΠΈ Π³Π»ΠΈΠΊΠΎΠ»Π΅Π²ΠΎΠΉ ΠΊΠΈΡΠ»ΠΎΡΡ, Π° ΡΠ°ΠΊΠΆΠ΅ ΡΡΠ°Π²Π½ΠΈΡΡ Π΅Π΅ Ρ ΡΠΈΡΡΠΎΠΉ ΡΡΠ±ΡΡΠ°Π½ΡΠΈΠ΅ΠΉ ΡΠΈΡΠ°Π±ΡΡΠΈΠ½Π°. ΠΠ΅ΡΠΎΠ΄Ρ: ΠΏΡΠ΅ΠΏΠ°ΡΠ°ΡΡ Π²Π²ΠΎΠ΄ΠΈΠ»ΠΈ ΠΏΠ΅ΡΠΎΡΠ°Π»ΡΠ½ΠΎ, ΡΠ΅ΡΠ΅Π· Π°ΡΡΠ°Π²ΠΌΠ°ΡΠΈΡΠ΅ΡΠΊΠΈΠΉ ΠΌΠ΅ΡΠ°Π»Π»ΠΈΡΠ΅ΡΠΊΠΈΠΉ Π·ΠΎΠ½Π΄ Π² Π΄ΠΎΠ·Π΅ 10Β ΠΌΠ³/ΠΊΠ³. ΠΠ°Π»Π΅Π΅ ΡΠ΅ΡΠ΅Π· ΠΎΠΏΡΠ΅Π΄Π΅Π»Π΅Π½Π½ΡΠ΅ ΠΏΡΠΎΠΌΠ΅ΠΆΡΡΠΊΠΈ Π²ΡΠ΅ΠΌΠ΅Π½ΠΈ ΡΠΊΡΠΏΠ΅ΡΠΈΠΌΠ΅Π½ΡΠ°Π»ΡΠ½ΡΡ
ΠΆΠΈΠ²ΠΎΡΠ½ΡΡ
ΡΠΌΠ΅ΡΡΠ²Π»ΡΠ»ΠΈ ΠΌΠ΅ΡΠΎΠ΄ΠΎΠΌ Π΄ΠΈΡΠ»ΠΎΠΊΠ°ΡΠΈΠΈ ΡΠ΅ΠΉΠ½ΡΡ
ΠΏΠΎΠ·Π²ΠΎΠ½ΠΊΠΎΠ². ΠΡΠΎΠ±ΠΎΠΏΠΎΠ΄Π³ΠΎΡΠΎΠ²ΠΊΠ° ΠΎΡΠ³Π°Π½ΠΎΠ² ΠΊ Π°Π½Π°Π»ΠΈΠ·Ρ ΠΎΡΡΡΠ΅ΡΡΠ²Π»ΡΠ»Π°ΡΡ ΠΆΠΈΠ΄ΠΊΠΎΡΡΡ-ΠΆΠΈΠ΄ΠΊΠΎΡΡΠ½ΠΎΠΉ ΡΠΊΡΡΡΠ°ΠΊΡΠΈΠ΅ΠΉ. ΠΠΎΠ½ΡΠ΅Π½ΡΡΠ°ΡΠΈΡ Π΄Π΅ΠΉΡΡΠ²ΡΡΡΠ΅Π³ΠΎ Π²Π΅ΡΠ΅ΡΡΠ²Π° ΠΈΠ·ΠΌΠ΅ΡΡΠ»ΠΈ Ρ ΠΈΡΠΏΠΎΠ»ΡΠ·ΠΎΠ²Π°Π½ΠΈΠ΅ΠΌ ΠΌΠ΅ΡΠΎΠ΄Π° Π²ΡΡΠΎΠΊΠΎΡΡΡΠ΅ΠΊΡΠΈΠ²Π½ΠΎΠΉ ΠΆΠΈΠ΄ΠΊΠΎΡΡΠ½ΠΎΠΉ Ρ
ΡΠΎΠΌΠ°ΡΠΎΠ³ΡΠ°ΡΠΈΠΈ. Π Π΅Π·ΡΠ»ΡΡΠ°ΡΡ: Π² ΠΈΡΡΠ»Π΅Π΄ΠΎΠ²Π°Π½ΠΈΠ΅ Π²ΠΊΠ»ΡΡΠ°Π»ΠΈ Π²ΠΎΡΡΠΌΠΈΠ½Π΅Π΄Π΅Π»ΡΠ½ΡΡ
ΠΊΡΡΡ Π»ΠΈΠ½ΠΈΠΈ Wistar ΠΎΠ±ΠΎΠ΅Π³ΠΎ ΠΏΠΎΠ»Π° ΠΌΠ°ΡΡΠΎΠΉ 0,22Β±0,02Β ΠΊΠ³. ΠΠΈΠ²ΠΎΡΠ½ΡΠ΅ Π±ΡΠ»ΠΈ ΡΠ°Π·Π΄Π΅Π»Π΅Π½Ρ Π½Π° 2 Π³ΡΡΠΏΠΏΡ. ΠΡΡΠ»Π΅Π΄ΡΠ΅ΠΌΠ°Ρ Π³ΡΡΠΏΠΏΠ° ΠΏΠΎΠ»ΡΡΠ°Π»Π° Π°Π½ΡΠΈΠ±ΠΈΠΎΡΠΈΠΊ Π² ΠΏΠΎΠ»ΠΈΠΌΠ΅ΡΠ½ΠΎΠΉ ΡΠΎΡΠΌΠ΅, Π° Π³ΡΡΠΏΠΏΠ° ΡΡΠ°Π²Π½Π΅Π½ΠΈΡ ΠΏΠΎΠ»ΡΡΠ°Π»Π° ΡΡΠ±ΡΡΠ°Π½ΡΠΈΡ ΡΠΈΡΠ°Π±ΡΡΠΈΠ½Π°. Π§Π΅ΡΠ΅Π· Π²ΡΠ΅ΠΌΠ΅Π½Π½ΡΠ΅ ΠΈΠ½ΡΠ΅ΡΠ²Π°Π»Ρ 10Β ΠΌΠΈΠ½, 30Β ΠΌΠΈΠ½, 1Β Ρ, 2Β Ρ, 4Β Ρ, 7Β Ρ, 15Β Ρ, 24Β Ρ ΠΏΠΎΡΠ»Π΅ Π²Π²Π΅Π΄Π΅Π½ΠΈΡ ΠΏΡΠ΅ΠΏΠ°ΡΠ°ΡΠ° ΠΏΡΠΎΠΈΠ·Π²ΠΎΠ΄ΠΈΠ»ΠΈ ΡΠ΅Π·Π΅ΠΊΡΠΈΡ ΠΏΠ΅ΡΠ΅Π½ΠΈ, Π»Π΅Π³ΠΊΠΈΡ
, ΡΠ΅Π»Π΅Π·Π΅Π½ΠΊΠΈ, ΠΏΠΎΡΠ΅ΠΊ, ΠΊΠΈΡΠ΅ΡΠ½ΠΈΠΊΠ°, ΠΆΠ΅Π»ΡΠ΄ΠΊΠ°, ΡΠ΅ΡΠ΄ΡΠ° ΠΈ ΠΌΠΎΠ·Π³Π°, ΡΠΎΠΎΡΠ²Π΅ΡΡΡΠ²Π΅Π½Π½ΠΎ, ΠΈ ΠΈΠ·ΠΌΠ΅ΡΡΠ»ΠΈ ΠΈΡ
ΠΌΠ°ΡΡΡ. Π ΠΌΠΎΠ·Π³Π΅ ΠΏΡΠ΅ΠΏΠ°ΡΠ°Ρ Π½Π΅ ΠΎΠ±Π½Π°ΡΡΠΆΠΈΠ²Π°Π»ΡΡ. Π ΠΎΡΡΠ°Π»ΡΠ½ΡΡ
ΠΈΡΡΠ»Π΅Π΄ΡΠ΅ΠΌΡΡ
ΡΠΊΠ°Π½ΡΡ
ΡΠΈΡΠ°Π±ΡΡΠΈΠ½ ΠΎΠΏΡΠ΅Π΄Π΅Π»ΡΠ»ΡΡ ΡΠΆΠ΅ ΡΠ΅ΡΠ΅Π· 10Β ΠΌΠΈΠ½ ΠΏΠΎΡΠ»Π΅ Π²Π²Π΅Π΄Π΅Π½ΠΈΡ, Π° ΠΌΠ°ΠΊΡΠΈΠΌΠ°Π»ΡΠ½Π°Ρ ΠΊΠΎΠ½ΡΠ΅Π½ΡΡΠ°ΡΠΈΡ ΠΏΡΠ΅ΠΏΠ°ΡΠ°ΡΠ° Π΄ΠΎΡΡΠΈΠ³Π°Π»Π°ΡΡ Π² ΠΎΡΠ³Π°Π½Π°Ρ
ΡΠΏΡΡΡΡ 1,5β3,5Β Ρ. ΠΠΎΠ½ΡΠ΅Π½ΡΡΠ°ΡΠΈΠΈ ΡΠΈΡΠ°Π±ΡΡΠΈΠ½Π°, ΠΎΠΏΡΠ΅Π΄Π΅Π»ΡΠ΅ΠΌΡΠ΅ Π² Π»Π΅Π³ΠΊΠΈΡ
, ΠΎΠΊΠ°Π·Π°Π»ΠΈΡΡ ΡΡΠ°ΡΠΈΡΡΠΈΡΠ΅ΡΠΊΠΈ Π·Π½Π°ΡΠΈΠΌΠΎ (pΒ 0,05) Π²ΡΡΠ΅ ΠΏΠΎΡΠ»Π΅ Π²Π²Π΅Π΄Π΅Π½ΠΈΡ ΠΏΠΎΠ»ΠΈΠΌΠ΅ΡΠ½ΠΎΠΉ ΡΠΎΡΠΌΡ ΠΏΡΠ΅ΠΏΠ°ΡΠ°ΡΠ°. ΠΠΎΡΡΡΠΈΡΠΈΠ΅Π½Ρ ΡΠ°ΡΠΏΡΠ΅Π΄Π΅Π»Π΅Π½ΠΈΡ ΠΏΠΎΠ»ΠΈΠΌΠ΅ΡΠ½ΠΎΠΉ ΡΠΎΡΠΌΡ Π² ΠΏΠ΅ΡΠ΅Π½ΠΈ ΠΈ Π»Π΅Π³ΠΊΠΈΡ
Π±ΡΠ» ΠΌΠ°ΠΊΡΠΈΠΌΠ°Π»ΡΠ½ΡΠΌ (15,83 ΠΈ 10,14Β ΠΌΠΊΠ³/Π³, ΡΠΎΠΎΡΠ²Π΅ΡΡΡΠ²Π΅Π½Π½ΠΎ) ΠΏΠΎ ΡΡΠ°Π²Π½Π΅Π½ΠΈΡ Ρ ΡΡΠ±ΡΡΠ°Π½ΡΠΈΠ΅ΠΉ. ΠΠΈΠ½ΠΈΠΌΠ°Π»ΡΠ½ΠΎΠ΅ ΠΊΠΎΠ»ΠΈΡΠ΅ΡΡΠ²ΠΎ (0,02Β ΠΌΠΊΠ³/Π³) Π΄Π΅ΠΉΡΡΠ²ΡΡΡΠ΅Π³ΠΎ Π²Π΅ΡΠ΅ΡΡΠ²Π° Π½Π°Π±Π»ΡΠ΄Π°Π»ΠΈ Π² ΡΠ΅ΡΠ΄ΡΠ΅. ΠΠ°ΠΊΠ»ΡΡΠ΅Π½ΠΈΠ΅: ΠΏΠΎΠΊΠ°Π·Π°Π½ΠΎ, ΡΡΠΎ Π²ΠΊΠ»ΡΡΠ΅Π½ΠΈΠ΅ ΡΠΈΡΠ°Π±ΡΡΠΈΠ½Π° Π² ΠΏΠΎΠ»ΠΈΠΌΠ΅ΡΠ½ΡΡ ΡΠΎΡΠΌΡ Π·Π½Π°ΡΠΈΡΠ΅Π»ΡΠ½ΠΎ ΠΈΠ·ΠΌΠ΅Π½ΡΠ΅Ρ Π΅Π³ΠΎ Π»ΠΎΠΊΠ°Π»ΠΈΠ·Π°ΡΠΈΡ ΠΏΠΎ ΠΎΡΠ³Π°Π½Π°ΠΌ ΠΈ ΡΠΊΠ°Π½ΡΠΌ. Π£ΡΡΠ°Π½ΠΎΠ²Π»Π΅Π½ΠΎ ΠΏΠΎΠ²ΡΡΠ΅Π½Π½ΠΎΠ΅ Π½Π°ΠΊΠΎΠΏΠ»Π΅Π½ΠΈΠ΅ Π½Π°Π½ΠΎΠΊΠΎΠΌΠΏΠΎΠ·ΠΈΡΠΈΠΈ ΡΠΈΡΠ°Π±ΡΡΠΈΠ½Π° Π² ΡΠΊΠ°Π½ΠΈ Π»Π΅Π³ΠΊΠΈΡ
, ΠΏΠ΅ΡΠ΅Π½ΠΈ ΠΈ ΡΠ΅Π»Π΅Π·Π΅Π½ΠΊΠΈ.
Parity Mixed Doublets in A = 36 Nuclei
The -circular polarizations () and asymmetries
() of the parity forbidden M1 + E2 -decays: MeV) and MeV)
MeV) are investigated theoretically. We use the recently proposed
Warburton-Becker-Brown shell-model interaction. For the weak forces we discuss
comparatively different weak interaction models based on different assumptions
for evaluating the weak meson-hadron coupling constants. The results determine
a range of values from which we find the most probable values:
= for and = for .Comment: RevTeX, 17 pages; to appear in Phys. Rev.
Mutation of Ser172 in Yeast Ξ² Tubulin Induces Defects in Microtubule Dynamics and Cell Division
Ser172 of Ξ² tubulin is an important residue that is mutated in a human brain disease and phosphorylated by the cyclin-dependent kinase Cdk1 in mammalian cells. To examine the role of this residue, we used the yeast S. cerevisiae as a model and produced two different mutations (S172A and S172E) of the conserved Ser172 in the yeast Ξ² tubulin Tub2p. The two mutants showed impaired cell growth on benomyl-containing medium and at cold temperatures, altered microtubule (MT) dynamics, and altered nucleus positioning and segregation. When cytoplasmic MT effectors Dyn1p or Kar9p were deleted in S172A and S172E mutants, cells were viable but presented increased ploidy. Furthermore, the two Ξ² tubulin mutations exhibited synthetic lethal interactions with Bik1p, Bim1p or Kar3p, which are effectors of cytoplasmic and spindle MTs. In the absence of Mad2p-dependent spindle checkpoint, both mutations are deleterious. These findings show the importance of Ser172 for the correct function of both cytoplasmic and spindle MTs and for normal cell division