• The Korean Journal of Physiology
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• v.19 no.2
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• pp.173-187
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• 1985

Renal compensatory adaptation caused by ablation of a part of renal mass has long been known in the field of the compensatory renal hypertrophy or hyperplasia. Many reports were found on the chronic mechanisms on the compensatory renal hyperfunction after exclusion of the contralateral kidney. However the mechanism(s) of the acute compensatory hyperfunction after contralateral exclusion has not yet been clarified. In the present experiment, we have tried to prove the possibility of the involvement of the renin-angiotensin system and/or prostaglandin system in the control mechanism of the acute compensatory renal hyperfunction after contralateral kidney exclusion. There were found different responses of the renal hyperfunction by contralateral renal pedicle or ureteral occlusion. Contralateral renal pedicle or ureteral occlusion caused a sustained increases of the urinary volume, sodium and potassium excretion, while the magnitude of the changes was different quantitatively by the maneuvers. Blood collection affected on the acute compensatory renal responses after ureteral as well as renal pedicle occlusion. Plasma prostaglandin $E_2$ level was not changed by the contralateral renal pedicle or ureteral occlusion. Urinary excretion of Prostaglandin $E_2$, the indices of renal prostaglandin biosynthesis, was not changed by the contralateral renal pedicle occlusion, but increased without significance by the contralateral ureteral occlusion. Acute renal compensatory responses after contralateral renal pedicle occlusion were blocked by the pretreatment of indomethacin. Plasma renin activity increased after contralateral ureteral occlusion, but the pattern of the increases was the same as in the time-control group. Plasma renin activity after contralateral renal pedicle occlusion did not change by the time sequence. SQ 20,881, an angiotensin I converting enzyme inhibitor, blunted the contralateral renal responses after the renal pedicle occlusion. Bilateral renal denervation abolished the contralateral renal responses after the renal pedicle occlusion. The above data suggest that there is no direct evidence to support the involvement of the renin-angiotensin system and/or prostaglandin system for the acute compensatory renal hyperfunction after contralateral kidney exclusion, and that the functional changes of the intact kidney may be caused by a humoral substances, or other mechanisms by afferent renal nerve activity originating from the treated kidney.

• The Korean Journal of Physiology
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• v.25 no.1
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• pp.81-85
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• 1991

At the fifth day after right lung pneumonectomy in New-Zealand white rabbits $(0.8{\sim}1.1\;kg\;B.W.)$, phospholipid and protein concentration in the left lung lavage fluid were measured for clarification of the effect of unilateral pneumonectomy on the secretory function of the type II pneumocytes in growing rabbits. In an attempt to evaluate the effect of unilateral pneumonectomy on the compensatory growth of the residual lung, left lung weight and left lung weight-body weight ratio and DNA concentration, RNA/DNA and total DNA content in the left lung tissue were measured in pneumonectomized and in sham operated control rabbits. The lung weight of pneumonectomized rabbit was approximately two times heavier than that of the control rabbits. DNA concentration and RNA/DNA of the lung tissue were not changed but total DNA content was increased significantly. Phospholipid concentration in the lung lavage fluid of the pneumonectomized rabbits was over two times higher than that of control rabbits. from these experimental results, It is concluded that unilateral pneumonectomy in growing rabbits might cause to increase the secretion of pulmonary surfactant from type II pneumocyte of the residual lung. The cellular hyperplasia seems to be the primary response of the compensatory growing lung in unilateral pneumonectomized growing rabbits.

• The Korean Journal of Physiology
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• v.17 no.2
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• pp.177-182
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• 1983

In order to clarify the effect of the unilateral pneumonectomy on the compensatory growth of the residual lung, liver and kidney, and serum electrophoresis pattern, right lung pneumonectomy was performed on rabbits under general anesthesia with pentobarbital sodium. On the fifth day after the surgery, the weight of the residual lung, liver and bilateral kidneys was measured and organ weight-body weight ratio was calculated. And in an attempt to know whether the cells in the liver and the kidney were proliferated by unilateral pneumonectomy, DNA content was determined. The quantity(g/100 ml) of serum protein was determined also and serum electrophoresis was performed on cellulose acetate membrane. The results obtained are summarized as following. The weight of the residual lung and lung weight-body weight ratio was significantly increased respectively. The weight of the liver and organ weight-body weight ratio were not changed but the DNA content of the liver and kidney tissue increased significantly, illustrating that unilateral pneumonectomy caused cellular hyperplasia in the liver and in the kidney as well as in the residual lung. The quantity(g/100 ml) of serum protein was significantly increased and in the analysis of the electrophoregram, there was significant difference between the normal and pneumonectomy group. Taken together, these results indicate that unilateral pneumonectomy caused the compensatory hyperplasia of the liver, the kidney and the residual lung as well as the change of electro-phoretic pattern. And it also suggests that a humoral factor, which proliferates the cells in the residual lung, the liver and the kidney, existed in the pneumonectomized rabbits.

• Maxillofacial Plastic and Reconstructive Surgery
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• v.13 no.2
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• pp.191-198
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• 1991

This is a case report and review of literature of the facial asymmetry corrected by various surgical methods. In case 1, facial asymmetry resulted from osteochondroma of condyle and corrected via condylectomy only. In case 2, unilateral condylar hyperplasia with compensatory maxillary growth resulted in severe facial asymmetry. Procedures used in case 2 are vertical ramus osteotomy, condylectomy, genioplasty, mandibular inferior border ostectomy and Le Fort I osteotomy.

• CELLMED
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• v.7 no.2
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• pp.8.1-8.7
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• 2017

Benign prostatic hyperplasia (BPH) is one of the major diseases of the urinary system in older men. WSY-0702 is the extracted from the traditional medicinal plant; Seoritae, and it has effects of anti-obesity, chronic cervical pain, and anti-oxidant. The present study aimed to investigate the therapeutic potential of WSY-0702 in the prevention and treatment of BPH. Several parameters including inflammatory mediators, hormones, and oxidative stress (OS) have been considered to play a role in the development of BPH. Prostate tissue damage and OS may lead to compensatory cellular proliferation with resulting hyperplastic growth. An in vitro study showed that proliferation inhibited the human prostate epithelial cell line RWPE-1 in a dose-dependent manner. In cell line, the cell cycle at the G2/M and G0/G1 phase and downregulated the expression of CyclineB1 (CCNB1) and CyclineD1 (CCND1). In addition, we measured the $H_2O_2$-induced OS damage using RWPE-1 cells. We examined the relative expression of protein involved in the regulation of prostate apoptosis: transforming growth factor (TGF)-${\beta}$, a negative growth factor able to induced prostate apoptosis under physiological conditions. These results suggest that WSY-0702 that can inhibit the growth of prostate epithelial cell by a mechanism that may involve arresting the cell cycle and downregulating CCNB1 and CCND1 expression. In addition, WSY-0702 exposure resulted in significant protective effects in $H_2O_2$-stressed PWPE-1 cells by reduction in TGF-${\beta}$ levels.

• Animal cells and systems
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• v.5 no.2
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• pp.91-99
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• 2001

Vertebrates regenerate tissues in three ways: proliferation of cells that maintain some or all of their differentiated structure and function, redifferentiation of mature cells followed by proliferation and redifferentiation into the same cell type or transdetermination to another cell type, and activation of restricted lineage stem cells, which have the ability to transdetermine to different lineages under the appropriate conditions. The behavior of the cells during regeneration is regulated by growth factors and extracellular matrix molecules. Some non-regenerating tissues are now known to harbor stem cells which, though they form scar tissue in vivo, are capable of producing new tissue-specific cells in vitro, suggesting that the injury environment inhibits latent regenerative capacity. Regenerative medicine seeks to restore tissues via transplantation of stem cell derivatives, implantation of bioartificial tissues, or stimulation of regeneration in vivo. These approaches have been partly successful, but several research issues must be addressed before regenerative medicine becomes a clinical reality.

• Korean Journal of Veterinary Research
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• v.16 no.1
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• pp.77-96
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• 1976

In order to investigate the effects and acting mechanism on ovaries, thyroid glands and hypophyses of rabbits in short term administration of sulfadimethoxine (SDM) as medical dose, a total of 90 virgin albino rabbits (mean body weight, 1,362g) were selected at random and alloted to two groups. Rabbits in one group served as controls and the others were administered SDM of 50 mg/kg/day for 5 weeks, and then reared without medication for 4 weeks. Pathological changes of the three organs were observed each week for 9 weeks and the results obtained were summarized as follows: 1. Mean body weights of both groups manifested slow increasing tendency but mean hypophysis weights fluctuated throughout the experimental term. Mean ovary weights of experiments were decreased significantly from the 3rd to 6th week but mean thyroid weights of experiments were increased significantly from the 1st to 6th week compared with those of controls. 2. Many ovarian follicles of each developing stage showed follicular atresia accompanying atrophy or necrosis of oocytes and of disintegrated follicular cells. Theca interna cells and sudanophilic interstitial cells showed atrophy and diminished sudanophilic granules and also liquor folliculi were diminished. These changes icreased from the 1st week, remaining so for 5 weeks and returned to normal status in the 8th or 9th week. 3. The thyroid gland showed a typical hyperplastic goiter. Hypertrophic and hyperplastic epithelia follicular manifested cuboidal or columnar form showing tiny or small vacuoles in cytoplasm. The follicles showed atrophy and decreasing colloidal materials. Necrotic and regenerative changes were also present. The interfollicular vessels showed congestion and hemorrhage. These changes increased from the 1st week, remaining so for 5 weeks and returned to normal status in the 9th week. 4. The rates of differential cell counts of hypophyses revealed increase of basophils (gonadotrophs and thyrotrophs) and decrease of chromophobes. Basophils which had diminished granules stainable with HE, PAS and AF revealed hypertrophy, hyperplasia, and increasing of tiny or small vacuoles in cytoplasm. These changes increased from the 1st week, remaining so for 5 weeks and returned to normal status in the 8th or 9th week. As summarized above histologically, administration of SDM led thyrotrophs and gonadotrophs of pituitary glands to hyperactivity but revealed retrogressive and compensatory changes with functional disturbance in ovaries and thyroid glands. These changes were transitional and attributed to direct actions of the drugs on the ovaries and thyroid glands.

• Journal of Yeungnam Medical Science
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• v.1 no.1
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• pp.59-66
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• 1984

Although it is well established that steroid is effective for treatment of neonatal respiratory distress syndrome (NRDS), the action mechanism of steroid on NRDS is not well known. Several authors have insisted that steroid increases secretion of pulmonary surfactant from type II pneumocyte, but others have insisted that steroid does not affect the secretory function of the type II pneumocyte. And some authors have suggested that steroid may ca use compositional change of pulmonary surfactant phospholipid. From these aspects, it is desirable to confirm the effect of steroid on (he secretory function of the type II pneumocyte. In order to know the effect of steroid on pulmonary surfactant activity, phospholipid phosphorus of lung lavage was measured and composition of pulmonary surfactant phospholipid of lung lavage was analyzed by thin layer chromatography (TLC) in control (C), pneumonectomized (PN), and pneumonectomized with betamethasone treated (PNS) rabbits. And lung weight and lung weight-body weight ratio were measured in each experimental group also. In PN group, right lung pneumonectomy was performed under general anesthesia with pentobarbital sodium (30mg/kg). On the fifth day after the surgery, the left lung was excised and measured above parameters. In PNS group, pneumonectomy was performed as PN group, and one day after the surgery, betamethasone was injected for four days intramusculary (4mg/day) and rabbits were sacrificed. The experiment yielded following results. PNS group's lung weight was significantly (p<0.01) heavier than C group's, but in comparison with PN group's it showed no significant change. PNS group's L/B ratio was significantly (p<0.05) higher than C group's, but compared with PN group's it showed no significant change. The value of phospholipid phosphorus content of PNS group was significantly (p<0.01) higher than that of C group. Even if the value of phospholipid phosphorus content in PNS group was not significantly higher than that of PN group, it showed increasing tendency compared with that of PN group. And in an analysis of the thin layer chromatogram, quantity (${\mu}mol/gm$ of wet weight lung) of phosphatidylcholine in PNS group decreased significantly (p<0.05) compared with C and PN group. From these results, it may be suggested that though steroid inhibits cellular hyperplasia in the compensatory growing lung, it auguments the secretory function of type II pneumocyte and causes compositional change of pulmonary surfactant phospholipid.