ABSTRACT
Objective To investigate the role of Calcineurin binding protein 1(Cabin1)in renal tubular epithelial cells(RTECs)injury. Methods The male Sprague-Dawley rats were randomly divided into Sham-oper-ated and 5/6 nephrectomized group. Nephrectomized rats were further divided into two groups ,which were 4 and 8 weeks after operation,including 6 rats in each group. Rats were sacrificed at 4 or 8 weeks after nephrectomy,then control or remnant kidneys were harvested. 2μm sections of kidney tissues were collected and stained with Masson's trichrome and were graded for tubulointerstitial lesion score (TILS). RTECs mitochondrial morphology changes were detected by electron microscope. Western blot was applied to detect Cabin1 protein level in the renal tissue. Results At 8 weeks after the operation,plenty of RTECs fell off from the basement membrane,accompanied with interstitial fibrosis and the infiltration of inflammatory cells. Moreover ,TILS were significantly increased in rats at 8 weeks after operation while compared to sham-operated rats(7.16 ± 0.52 vs. 0.00 ± 0.00,P<0.05). RTECs mi-tochondria begun to swell at 4 weeks after 5/6 nephrectomy,while the disruption of cristae could be found in rats at 8 weeks. Cabin1 protein expression apparently increased in the remnant kidney. Cabin1 protein obviously increased in rats at 8 weeks after the surgery compared to sham-operated rats(0.97 ± 0.09 vs. 0.22 ± 0.07,P<0.05)and rats at 4 weeks after nephrectomy(0.97 ± 0.09 vs. 0.45 ± 0.03,P<0.05). Conclusions Cabin1 is overexpressed during RTECs injury in 5/6 nephrectomized rats. It can be a crucial factor regulating the damage of RTECs.
ABSTRACT
Objective To investigate the role of Calcineurin binding protein 1(Cabin1)in renal tubular epithelial cells(RTECs)injury. Methods The male Sprague-Dawley rats were randomly divided into Sham-oper-ated and 5/6 nephrectomized group. Nephrectomized rats were further divided into two groups ,which were 4 and 8 weeks after operation,including 6 rats in each group. Rats were sacrificed at 4 or 8 weeks after nephrectomy,then control or remnant kidneys were harvested. 2μm sections of kidney tissues were collected and stained with Masson's trichrome and were graded for tubulointerstitial lesion score (TILS). RTECs mitochondrial morphology changes were detected by electron microscope. Western blot was applied to detect Cabin1 protein level in the renal tissue. Results At 8 weeks after the operation,plenty of RTECs fell off from the basement membrane,accompanied with interstitial fibrosis and the infiltration of inflammatory cells. Moreover ,TILS were significantly increased in rats at 8 weeks after operation while compared to sham-operated rats(7.16 ± 0.52 vs. 0.00 ± 0.00,P<0.05). RTECs mi-tochondria begun to swell at 4 weeks after 5/6 nephrectomy,while the disruption of cristae could be found in rats at 8 weeks. Cabin1 protein expression apparently increased in the remnant kidney. Cabin1 protein obviously increased in rats at 8 weeks after the surgery compared to sham-operated rats(0.97 ± 0.09 vs. 0.22 ± 0.07,P<0.05)and rats at 4 weeks after nephrectomy(0.97 ± 0.09 vs. 0.45 ± 0.03,P<0.05). Conclusions Cabin1 is overexpressed during RTECs injury in 5/6 nephrectomized rats. It can be a crucial factor regulating the damage of RTECs.
ABSTRACT
Objective To study the profiles of decompression sickness(DCS) in various kinds of animals and to find out the target organ of decompression sickness by providing a basic experimental method for establishing animal models.Method Eleven kinds of animals were exposed to different pressures for different times at different compression/decompression rates.They were monitored at the precordial regions with Doppler flow meter for bubble sounds after decompression to normal pressure,to obtain a record about the developing course of the DCS.Pathological examinations of the bulbar conjunctiva were also made. Result Bubble sound of grade IV were recorded at the precordial regions after decompression.Among them,75%~100% incurred DCS with a diverse extent. Animals developed DCS showed vascular spasm,dysfunction and endothelial tumefaction.Conclusion Each of the 11 kinds of animals can serve as a model of DCS and the processes of development of DCS in various animals are similar.Blood vessels are the target organs of decompression sickness.
ABSTRACT
This study represents the first description of structural variations in the globin beta chains of 19 strains of inbred mice. The trypic pep tide mapping of beta chains of globin from BALB/c, BALB/cA, BALB/cJ, BALBcJ-nu, BALB/nu/ + ,BALB/cyJax,B10,B10A/sui,C57BL/6,C57BL/10snJ,SMMC/B,SMMC/C, C3H/He, CFW, DBA/2,SWI,Swars/nu/+,SSB and 129/sv strains of mice was established. The results showed that the position of peptide spots upon fingerprint mapping of beta chains was obviously different in comparison with each other. The different patterns of variability and polymorphism found in the various mouse species may then have come into being as a consequence of the action of selective forces on the various new beta chains which were created by some exchange processes.
ABSTRACT
The separation and purification of beta chains of globm from the inbreeding SMMC/B mice were performed by the dissociation of chains in urea, CMhcellulose column chromatography for the separation of alpha and beta chains, and Sephadex G25 column chromatography for removing salts. The pure beta-chain was digested by trypsin. Digested fragments were resolved by cellulose membrane two-way electrophoresis, thus obtaining the map of spots of beta-chain fragments for B33, B34, Bp(), Bp and Bf. The spots,BTp3, which have the same positions ,were separated and micro-sequences were assayed by DABITC/PITC double coupling technique. According to the genetic code, we might deduce the nucleotide sequence of their mRNA from the known amino acid sequence of BTp3, a piece of beta-chain. By analyzing the altered genetic loci of beta-chain of globin, we might determine the genetic purity of the strain and distinguish objectively the genetic types between species and subspecies.