Effect of dietary changes from high-fat diet to normal diet on breast cancer growth and metastasis / 한국영양학회지

Purpose@#It has been previously reported that breast tumor incidence, growth, and metastasis are stimulated by high-fat diet but reduced by caloric restriction. However, few studies have elucidated the effects of dietary change from a high-fat diet after breast cancer initiation. Therefore, in this study, we attempted to provide practical assistance to breast cancer prevention and management by investigating the effects of dietary change from a high-fat diet to normal diet on breast cancer growth and metastasis. @*Methods@#The experimental animals were divided into 2 groups (high-fat diet control [HFC] group and diet restriction [DR] group) and consumed a high-fat diet for 8 weeks. 4T1 cells were transplanted into subcutaneous fat or tail vein to measure the growth and metastasis of breast cancer. The HFC and DR groups continuously ingested either high-fat diet or AIG-93G diet for 5 weeks or 3 weeks, respectively. Cell proliferation and apoptosis markers from tumor tissues were analyzed by Western blot analysis. The data were analyzed using the SPSS 25.0 package program. @*Results@#The results show that the DR group significantly reduced breast tumor initiation, growth, and tumor tissue weight compared to the HFC group. The DR group suppressed tumor growth by decreasing proliferation and inducing apoptosis through down-regulation of Bcl-xL and up-regulation of caspase-3 activity. Furthermore, the DR group significantly reduced numbers of metastasized tumors in lung tissues. @*Conclusion@#These results suggest that dietary change from a high-fat diet to normal diet decreased breast growth by reducing cell proliferation and inducing apoptosis and metastasis. Taken together, these results indicate that dietary change to a low-fat and balanced diet might suppress breast tumor growth and metastasis even after tumor diagnosis.

Valproic Acid Regulates alpha-Synuclein Expression through JNK Pathway in Rat Primary Astrocytes

Although the role of alpha-synuclein aggregation on Parkinson's disease is relatively well known, the physiological role and the regulatory mechanism governing the expression of alpha-synuclein are unclear yet. We recently reported that alpha-synuclein is expressed and secreted from cultured astrocytes. In this study, we investigated the effect of valproic acid (VPA), which has been suggested to provide neuroprotection by increasing alpha-synuclein in neuron, on alpha-synuclein expression in rat primary astrocytes. VPA concentration-dependently increased the protein expression level of alpha-synuclein in cultured rat primary astrocytes with concomitant increase in mRNA expression level. Likewise, the level of secreted alpha-synuclein was also increased by VPA. VPA increased the phosphorylation of Erk1/2 and JNK and pretreatment of a JNK inhibitor SP600125 prevented the VPA-induced increase in alpha-synuclein. Whether the increased alpha-synuclein in astrocytes is involved in the reported neuroprotective effects of VPA awaits further investigation.

Expression and Localization of COMMD1 Proteins in Human Placentas from Women with Preeclampsia

PURPOSE: Recently, COMMD1 has been identified as a novel interactor and regulator of hypoxia-inducible factor-1 and nuclear factor kappa B transcriptional activity. The goal of this study was to determine the difference of COMMD1 expression in the placentas of women with normal and preeclamptic (PE) pregnancies. MATERIALS AND METHODS: Immnoperoxidase and immunofluorescent staining for COMMD1 was performed on nine normal and nine severe PE placental tissues, and COMMD1 mRNA expression was quantified by quantitative reverse transcription polymerase chain reaction. RESULTS: The expression of mRNA of COMMD1 was significantly higher in the study group than in the control group. The immunoreactivity was higher especially in the syncytiotrophoblast of PE placentas than in the control group. CONCLUSION: This study demonstrated increased placental COMMD1 expression in women with severe preeclampsia compared to that found in women with normal pregnancies, and this finding might contribute to a better understanding of the pathophysiology of preeclampsia.

Gastrointestinal Tract Abnormalities Induced by Prenatal Valproic Acid Exposure in Rat Offspring

In-utero exposure to valproic acid (VPA) has been known as a potent inducer of autism spectrum disorder (ASD), not only in humans, but also in animals. In addition to the defects in communication and social interaction as well as repetitive behaviors, ASD patients usually suffer from gastrointestinal (GI) problems. However, the exact mechanism underlying these disorders is not known. In this study, we examined the gross GI tract structure and GI motility in a VPA animal model of ASD. On embryonic day 12 (E12), 4 pregnant Sprague-Dawley (SD) rats were subcutaneously injected with VPA (400 mg/kg) in the treatment group, and with phosphate buffered saline (PBS) in the control group; the resulting male offspring were analyzed at 4 weeks of age. VPA exposure decreased the thickness of tunica mucosa and tunica muscularis in the stomach and ileum. Other regions such as duodenum, jejunum, and colon did not show a significant difference. In high-resolution microscopic observation, atrophy of the parietal and chief cells in the stomach and absorptive cells in the ileum was observed. In addition, decreased staining of the epithelial cells was observed in the hematoxylin and eosin (H&E)-stained ileum section. Furthermore, decreased motility in GI tract was also observed in rat offspring prenatally exposed to VPA. However, the mechanism underlying GI tract defects in VPA animal model as well as the association between abnormal GI structure and function with ASD is yet to be clearly understood. Nevertheless, the results from the present study suggest that this VPA ASD model undergoes abnormal changes in the GI structure and function, which in turn could provide beneficial clues pertaining to the pathophysiological relevance of GI complications and ASD phenotypes.

Alternations of Septal-hippocampal System in the Adult Wistar Rat with Spatial Memory Impairments Induced by Chronic Cerebral Hypoperfusion

In the current investigation, the status of the septo-hippocampal cholinergic pathway and hippocampal mitogen-activated protein kinase (MAPK) signaling was examined in male Wistar rats with chronic cerebral hypoperfusion, which showed cognitive deficits based on assessment on a version of the Morris water maze. Chronic cerebral hypoperfusion was induced by bilateral common artery occlusion and maintained for 12 weeks until behavioral testing. Chronic cerebral hypoperfusion was shown to induce memory impairments and microglial activation in regions of white matter, including the fimbria of hippocampus. Choline acetyltransferase expression of the basal forebrain and expression of hippocampal MAPKs was decreased in rats with BCCAo compared to control rats. The results of this study suggest that cognitive decline induced by chronic cerebral hypoperfusion could be related to dysfunction of the basal forebrain cholinergic system and reduction of hippocampal MAPK activities.

Transmission of Synucleinopathies in the Enteric Nervous System of A53T Alpha-Synuclein Transgenic Mice

Parkinson's disease (PD) and dementia with Lewy bodies (DLB) are characterized by abnormal deposition of alpha-synuclein aggregates in many regions of the central and peripheral nervous systems. Accumulating evidence suggests that the alpha-synuclein pathology initiates in a few discrete regions and spreads to larger areas in the nervous system. Recent pathological studies of PD patients have raised the possibility that the enteric nervous system is one of the initial sites of alpha-synuclein aggregation and propagation. Here, we evaluated the induction and propagation of alpha-synuclein aggregates in the enteric nervous system of the A53T alpha-synuclein transgenic mice after injection of human brain tissue extracts into the gastric walls of the mice. Western analysis of the brain extracts showed that the DLB extract contained detergent-stable alpha-synuclein aggregates, but the normal brain extract did not. Injection of the DLB extract resulted in an increased deposition of alpha-synuclein in the myenteric neurons, in which alpha-synuclein formed punctate aggregates over time up to 4 months. In these mice, inflammatory responses were increased transiently at early time points. None of these changes were observed in the A53T mice injected with saline or the normal brain extract, nor were these found in the wild type mice injected with the DLB extract. These results demonstrate that pathological alpha-synuclein aggregates present in the brain of DLB patient can induce the aggregation of endogenous alpha-synuclein in the myenteric neurons in A53T mice, suggesting the transmission of synucleinopathy lesions in the enteric nervous system.

Differential Expression of Proteins Related with Penile Apoptosis in a Rat after Cavernous Nerve Resection / 대한남성과학회지

PURPOSE: The mechanism including changes of proteome within cavernosal tissue after cavernous nerve injury were not evaluated. We performed proteomics and functional analysis to identify proteins of penile corpus cavernosum whose expression was or was not altered by cavernous nerve resection (CNR). MATERIALS AND METHODS: Using 8-week-old male WKY rats, sham and CNR operation under microscope were performed. After 8 weeks, penile tissues of sham and CNR group were harvested. We used 2-DE and MALDI-TOF/TOF (AB 4700) to identify of differently expressed penile proteins. 2-DE gels were stained with silver nitrate and the gels were analyzed with PDQuest. RESULTS: We isolated more than 950 proteins on silver-stained gels of whole protein extracts from normal rat penile corpus cavernous. Of these proteins, 48 prominent proteins were identified using MALDI-TOF/TOF. Protein characterization revealed that the most prominent penile corpus cavernous proteins were those with antioxidant, chaperone, or cytoskeletal structure. Moreover, 11 proteins having levels elevated by CNR were annexin proteins, endoplasmic reticulum protein 29, glutathione s-transferase w-1, and others. In addition, Rho-GDP dissociation inhibitor (RhoGDI), a regulator of Rho proteins, was also increased in CNR rats compared with sham-operated control rats. CONCLUSIONS: The apoptotic signals observed in penile tissues was greatly increased in CNR rats than in sham-operated rats. These results suggest that RhoGDI is one of the proteins regulated by CNR in penile smooth muscle strips, and has a crucial role in the early stage of penile apoptosis.

Gene Expression Profiling using Oligonucleotide Microarray in Atrophic Gastritis and Intestinal Metaplasia / 대한소화기학회지

BACKGROUND/AIMS: The atrophic gastritis with intestinal metaplasia of gastric mucosa has been considered to be the major factor of carcinogenesis in the stomach. However, the key molecules are still poorly understood. To elucidate the molecular genetic basis, we report the results of our initial microarray data to analyze the genome pattern in patients with atrophic gastritis and intestinal metaplasia of the stomach. METHODS: We used oligonucleotide microarray technique to evaluate the gene expression profiles in atrophic gastritis with intestinal metaplasia, in comparison with those of normal mucosa. For the identification of differentially expressed genes, Significance Analysis of Microarrays (SAM) package method was used. The results were analyzed using global normalization, intensity dependent normalization, and box plot normalization. RESULTS: Eight genes including FABP, REG, OR6C1, MEP1, SLC6A1, SI, Mucin 1, and RAB23 in mucosa of atrophic gastritis and intestinal metaplasia were up-regulated by more than 10 times as compared with normal gastric mucosa. Only one gene, LOC44119 was down-regulated by more than 10 times of the expression as compared with normal gastric mucosa. In respect to the expression of known genes related to gastric carcinogenesis, 8 genes including FN1, SRMS, TP53, TP53IMP2, TP53I3, FGFR4, TGFB1, and TGFA showed up- and down-regulations more than 2 folds in expression pattern. CONCLUSIONS: We could identify a total genome pattern in patient with atrophic gastritis and intestinal metaplasia using oligonucleotide microarray. We believe that the current results will serve as a fundamental bioinformative basis for clinical applications in diagnosis and treatment of gastric cancer and precancerous lesion in the future.

The Morphometric Changes of the Enteric Nervous System in the Intestinal Transection-reanastomosis Model / 체질인류학회지

This study was performed to investigate the morphometric changes of myenteric plexus and type 1 interstitial cells of Cajal (ICC-I) in regeneration process of small intestine transection. Sprague Dawley rats (200~250 g) were anesthetized with ether; then the full thickness of ileal wall were semitransected; and subsequent end-to-end anastomosis were performed by using 6-0 silk suture thread. Sham-operated rats, which only underwent the laparotomy, were used for control group. Experimental animals were sacrificed at 3 days, 7 days, 15 days, and 30 days after the operation. In each group myenteric plexus and ICC-Is were prepared by histochemical method (NADH-TR stain for myenteric plexus, ZIO stain for ICC-Is) and cell numbers were counted by image analyzer (Image plus pro-5.0, Media Cybermedics, USA). Degeneration of myenteric neurons and ICC-Is occurred simultaneously and it was similar in oral and anal to the site of transection. Degeneration effects were most prominent at 3 days and 7 days after intestinal transection. In myenteric plexus, many neurons had degenerated appearances and about 40% of them were lost. Most of ICC-Is had cytoplasmic vacuoles and 20~37% of the cells were lost. At 15 days after transection, there were no more degeneration in myenteric neurons (20~25% cell loss) and ICC-Is (20~13% cell loss). At 30 days after transection, numbers of myenteric neurons were not recovered as that of the control group. However numbers of ICC-Is were as similar as that of the control group. In conclusion, we confirmed that degeneration effects of intestinal transection are more severe in myenteric plexus than in ICC-Is, and recovery of cell loss occurs more slowly in myenteric plexus.

Changes of Immunoreactivities of Calcium Channel alpha(1B)Subunit in Myenteric Plexus of Capsaicin Treated Adult Rats / 체질인류학회지

This study was performed to investigate the changes of immunoreactivities of calcium channel alpha(1B) subunit in myenteric plexus of capsaicin treated adult rats. Sprague Dawley rats (about 200 g) were injected with capsaicin (50 mg/kg) subcutaneously. Ileal myenteric plexus was prepared by whole mount preparation method in 1 day, 2 days, 1 week and 4 weeks after capsaicin treated adult rats. Each myenteric plexus was reacted with NADH-TR and immunostained with alpha(1B) subunit. Myenteric ganglion cell numbers were counted by image analyzer. In control group myenteric plexus was arranged in rectangular appearance; myenteric ganglia and internodal strand were immunoreacted with alpha(1B) subunit. Immunoreactive cells were 56.0% of total myenteric neurons. Total numbers of immunoreactive cells decreased by 19.0%, 37.9% and 64.9% in 1 day, 2 days, and 1 week after capsaicn treated group respectively. In 4 weeks after capsaicin treated group, immunoreactivities of alpha(1B) subunit were increased compared to that of the 1 week after group. However total numbers of immuoreactive cells decreased by 43.9% compared to that of the control group. In conclusion, we confirmed that immunoreactivities of alpha(1B) subunit were decreased until 1 week after capsaicin treatment and recovered progressively after that time. It will take more than 4 weeks latency to recover the control immunoreactivities of alpha(1B) subunit.

A Pilot Study as the Biochip Based Gene Expression Profiling in Patients with Hyperplastic Colonic Polyp

PURPOSE: A microarray-based gene expression analysis may offer a rapid and efficient means for assessing. However, the molecular genetic change in nonneoplastic colonic polyp is still poorly understood. To elucidate the molecular genetic basis, We now report the results of our initial microarray data to analyze the genom pattern in patients with hyperplastic polyps of colon. METHODS: 36 samples (18 pairs of colonic polyps and normal colonic mucosa were) harvested from colonoscopic biopsy. 3 of 18 colonic polyps were pathologically identified as the serrated type of hyperplastic polyp. We used the oligonucleotide microarray technique for analysis of the expression profiles of serrated polyps and normal mucosa. For the identification of differentially expressed genes, SAM (Significance Analysis of Microarray) package method was used. The result was analysed by using global normalization, intensity dependent normalization and block-wise normalization. RESULTS: Polypectomy specimens microscopically showed the pathologically characteristic serration with a saw-teeth like luminal border (branching of the crypts). 8 genes including RHEB (Ras homolog enriched in brain), WASF2 (WAS protein family, member 2), TYRP1 (Tyrosinase-related protein 1), VSX1 (Visual system homeobox 1 homolog), ROS1 (V-ros UR2 sarcoma virus oncogene homolog 1), WEE1 (WEE1 homolog), TEC (Tec protein tyrosine kinase), TNFRSF10A (Tumor necrosis factor receptor superfamily, member 10a) in serrated polyp were up-regulated by more than 10 times as compared with normal colonic mucosa. On the other hand, 6 genes including SIAT7D (Sialyltransferase 7D), DRD1 (Dopamine receptor D1), SIAT1 (Sialyltransferase 1), ITSN1 (Intersectin 1), TNFSF12 (Tumor necrosis factor superfamily, member 12), CHES1 (Checkpoint suppressor 1) were down-regulated by less than a tenth of the expression as compared with normal colonic mucosa. CONCLUSIONS: Serrated polyps as a subset of hyperplastic colonic polyps were analyzed with the oligonucleotide microarray technique. We authors could identify 14 genes (8 up-regulated and 6 down-regulated genes) that showed the significant change of expression as compared with normal colonic mucosa. Specifically, we believe that current study will serve as a fundamental base to offer a bioinformative characteristics of the serrated colonic polyp in future clinical applications.

Morphological Study of the Effects of Olfactory Bulb Transplants after Complete Spinal Cord Transection / 대한해부학회지

In the olfactory bulb, normal and transected olfactory axons are able to enter, regenerate, and reestablish lost synaptic contacts with their targets, throughout the lifetime of the organism. It was expected that studies of olfactory bulb ensheathing glia will provide important advances for the field of neural regeneration. Purpose of this study is to analyze morphologically the effects of olfactory bulb transplants into the cord after complete transection. Forty Sprague-Dawley rats were used in this study. Spinal cord of the rats were transected after laminectomy followed by insertion of chopped olfactory bulb tissues immediately and 3 weeks after the operation. In this study, transplants of olfactory bulb were successfully used to promote functional and structural recovery after complete spinal cord transection. The area of damaged spinal cord was greatly diminished after olfactory bulb transplantation. Nearly normal anterior horn cells were observed immediately distal to the transected region. Tyrosine hydroxylase immunoreactive descending fibers were observed in the distal region beyond transected area.

Metric and Non -metric Characteristics of Korean Eyes Using Satadardized Photographs / 체질인류학회지

The purpose of the present study was focused the anthropometric charateristics of normal Korean eyes, including inclination, height, width, epicanthus and upper eyelid crease. The author measured normal eyes and investigated incidence of epicanthal fold and upper eyelid crease in 774 males and 658 females with photographs. The epicanthus were classified by three types and the upper eyelid crease were classified by four types. The angle of inclination of eyes was larger in females than males and in young ages than old ages. Incidence of the slanting eye over 10 degree was 34.1 % in males and 41.0% in females. Incidence of the epicanthal fold was 57.0%, and there was no difference between males and females. The most common type of the epicanthal fold was type I. Incidence of the upper eyelid crease was 30.9% in males, 47.2% in females. The most common type of the upper eyelid crease was parallel (or floating) type. In conclusion, the anthropometric characteristics of normal Korean or oriental eyes are apart each other and slanting eyes in addition to puffy eyelid, narrow palpebral fissure, presence of epicanthal fold and absence of upper eyelid crease.

The Morphometric and Ultrastructural Study of Enteric Nervous System in Adult and Aged Rat Small Intestine / 대한해부학회지

This study was performed to investigate the morphometric and ultrastructural change in the adult and aged rat small intestine. The myenteric and submucous plexuses were stained by NADH-TR in the ileum of adult Sprague-Dawley rats (3 mo., 300~350 gm) and aged rats (24 mo., 500~550 gm). The neurons of myenteric and sumucous plexuses were divided into 3 groups depending on their cell body morphology. Type 1 cells were polygonal or round with abundant cytoplasm. Type 2 cells were spindle shaped and type 3 cells were small and round with scanty cytoplasm. The nerve cell numbers and sizes were measured using an image analyzer (VIDAS, Carl Zeiss, Co., Ltd.). Ultrastructural changes were observed by JEM-1200 EXII (JEOL Co., Ltd.) electron microscope. The result obtained are as followed: 1. In adult rats, majority of neuron population were type 3 and neuron density (total numbers/1 mm2) was more higher in submucous plexus than in the myenteric plexus. 2. Statistically significant loss of type 1 and type 2 neurons were in myenteric and submucous plexus of aged rat small intestine. 3. All types of neuron sizes were increased in aged myenteric and submucous plexuses. 4. Lipofusin granules were prominent in the cytoplasm of aged rat. Cell organelles were not shown degenerative change. These results suggest that type 1 and type 2 nerve cells which is originated from autonomic nerves were lost in aged rat small intestine. Ultrastructurally lipofusin granules were prominent in the cytoplasm of aged rat and the cell organelles were not degenerated.

Studies on the changes of c-fos protein in spinal cord and neurotransmitter in dorsal root ganglion of the rat with an experimental peripheral neuropathy

Animal models for human chronic pain syndromes have been developed and widely used for pain research. One of these neuropathic pain models by Kim and Chung (1992) has many advantages for operation and pain elicitation. In this neuropathic model we have examined the c-fos protein, substance P, CGRP immunoreactivity in dorsal root ganglia and dorsal horn. 50 Sprague-Dawley rats were used for this study. L5 and L6 spinal nerves were ligated tightly to produce the neuropathic pain model. After 2, 4, 8, 16, and 24 hours and 1 week of surgery, rats were anesthetized and sacrificed by perfusion. After confirmation of the roots transected by the surgery, the L5 and L6 dorsal root ganglions and spinal cord were removed and processed for immunohistochemistry. All tissue sections were immunohistochemically stained for substance P, CGRP and c-fos using the peroxidase-antiperoxidase (PAP) method. The number of immunostained substance P and CGRP dorsal root ganglion cells and c-fos immunoreactive dorsal horn cells were counted and analyzed statistically with Mann-Whitney U test. The results are as follows. The number of c-fos protein immunoreactive neurons in the superficial layer of dorsal horn were increased markedly 2 hours after operation, and gradually decreased to normal level 1 week after operation. The number of c-fos protein immunoreactive neurons in the deep layer of the dorsal horn gradually increased to a peak 24 hours after operation, then decreased to the normal level 1 week after operation. The number of substance P and CGRP immunoreactive L5 and L6 dorsal root ganglion neurons were decreased markedly 1 week after the pain model operation. In conclusion, after neuropathic pain model operation, c-fos proteins were immediately expressed in the superficial layer of spinal dorsal horn, thereafter c-fos proteins in the deep layer of spinal dorsal horn were expressed. CGRP and substance P immunoreactive neurons in DRG were decreased markedly 1 week after neuropathic pain model operation. These decrements do not coincide with the other chronic pain models, which show great increases in these pain transmitting substances. Therefore, the relationship between pain and c-fos, SP and CGRP should be investigated further.

The Morphological Studies on the Effects of Nerve Growth Factor on the Schwann Cell in the Diabetic Neuropathy in the Rats / 대한해부학회지

Diabetic neuropathy is a broad term that encompasses many destructive syndromes that various kinds of neuronal population is affected in diabetes mellitus. Diabetic neuropathy has been postulated to occur by diverse pathogenetic mechanisms. Recent studies suggest that the reduction of neurotrophic factors is one of the causes of diabetic neuropathy. This study was performed to identify the effect of nerve growth factor on Schwann cell in the streptozotocin-induced diabetic rats morphologically. Sprague-Dawley rats (weighed about 200 gm) were rendered diabetes by injection of streptozotocin (STZ 65 mg/kg) and nerve growth factor was administered for 4 weeks. The result obtained are as followed: 1. Degenerations in cytoplasmic organelles of Schwann cell of the myelinated nerve fibers in diabetic rats were identified. 2. Degenerations in cytoplasmic organelles of the Schwann cell of the unmyelinated nerve fibers in diabetic rats were identified and abnormal axons were appeared. 3. Nerve growth factor had an effect on the recovery of degeneration and it was more effective in myelinated nerve fibers. These results suggest that early administration of nerve growth factor have the effect of protection of diabetic neuropathy by morphological study.

Physiologic Characteristics and its Clinical Significances in the Patients with Pelvic Outlet Obstruction

Current study was designed to assess the functional etiology of patients with pelvic outlet obstruction. Moreover, physiologic characteristics and theirs clinical significances were evaluated in the patients with ramified diagnosis. METHODS: 172 patients with pelvic outlet obstruction were performed 328 numbers of physiologic studies. These included cinedefecography (n=172), anal manometry (n=87), colonic transit time study (n=38), and anal EMG/PNTML (n=31). On the basis of physiologic findings, patient groups were categorized as rectocele (group I), nonrelaxing puborectalis syndrome (group II), anal dyschezia (group III), and rectoanal intussusception (group IV). The physiologic findings were compared between subgroup patients. RESULTS: Incidence of categorized patients was 51.7% (group I, n=89), 22.7% (group II, n=39), 12.2% (group III, n=21), and 8.7% (group IV, n=15), respectively. The mean age of patients with group III were lower (p<0.05) than that of overall patients. The incidence of female patients was higher in group I and the incidence of male patients was higher in group II (p<0.0001). In cinedefecography, patients with group II showed smaller anorectal angle at strain (p<0.001), at dynamic change between rest and strain (p=0.002). In anal manometry, patients with group III showed higher mean resting pressures (p=0.001), higher maximum resting pressures (p<0.001), higher mean squeeze pressures, and higher maximal voluntary contraction (p=0.003) than those of patients with other group. In neurologic study, mean value of PNTML was 2.32 +/- 0.34 (range, 1.60~3.66) msec in overall patients. The size of rectocele was increased in proportion to patient's age (r=0.229, p<0.05), number of delivery (r=0.393, p=0.001), and degree of perineal descent (r=0.231, p<0.05). The degree of perineal descent was increased in proportion to patient's age (r=0.249, p<0.05). CONCLUSIONS: Present series provided the diagnostic ramification of pelvic outlet obstruction by using the anorectal physiologic investigations. In addition to the function of puborectalis muscle, evacuation dynamics of anorectum should be emphasized. These findings could provide the fundamental information for guideline of future therapy in the patients with obstructed defecation.

The Study of the Effect of Nerve Growth Factor on Intestinal Peristalsis in Streptozotocin-Induced Diabetic Rats / 대한해부학회지

Recently, it has been postulated that diabetic autonomic neuropathy is caused by reduction in availability of nerve growth factor (NGF) in enteric nervous system. This experiments were performed to determine the changes of the distribution of enteric neuropeptide by diabetes and these changes could be prevented by administration of NGF. Sprague Dawley rats (200~250gm) were made diabetic by a single intraperitoneal injection of streptozotocin 65 mg/kg in saline. Recombinant human NGF (Sigma, Co., Ltd.) were administered at a dose of 500ng/kg subcutaneously every day for consecutive 4 weeks after streptozotocin administration. After 4 weeks, rats were anesthetized with ether and perfused with 4% paraformaldehyde. ileum was dissected and prepared by whole mount preparation method. Prepared segments were immunostained for substance p, calcitonin gene-related peptide, vasoactive intestinal peptide, and galanin by PAP technique. For the observation of the interstitial cells of Cajal, segments were immersed in Champy-Maillet solution for 2 days Results obtained were as follows: 1. In myenteric plexus of diabetic rats, substance P-like and VIP-like immunoreactivity were not changed compared with that of the control group. CGRP-like and galanin-like immunoreactivity were decreased in diabetic group and immunoreactive cells for CGRP and galanin were also decreased 18.1% (P<0.01) and 43.7% (P<0.01) respectively. 2. In NGF administerd diabetic group, immunoreactivity of substance p, VIP, galanin in myenteric plexus were slightly increased and immunoreactive cells for substancre p, VIP, galanin were almost the same as that of the control group. However, immunoreactive cells for CGRP of myenteric plexus were not changed by NGF. 3. In submucous plexus of diabetic rats, immunoreactivity of all four neuropeptides(substance p, CGRP, VIP, galanin) were decreased compared with that of the control group. Immunoreactive cells for substance p, CGRP, VIP, and galanin were also decreased in 38.8%, 77.6%, 33.0%, and 35.7%, respectively (P<0.01). 4. In NGF administered diabetic group, immunoreactivities of substance p, VIP and galanin in submucous plexus were increased and the immunoreactive cells were increased significantly compared to diabetic group. However, immunoreactive cells for CGRP of submucous plexus were not changed by NGF. 5. Interstitial cells of Cajal of diabetic group were decreased 7.4% ovoidal cells (A type) and 28.3% round cells (B type) In NGF administered group, the morphology and the number of ICC were not different to the control group. With the above results, it could be assumed that NGF prevent the damage of neurotransmitter and ICC in enteric nervous system.

The Immunohistochemical and Morphometric Study of the Effect of Nerve Growth Factor on Spinal Ganglia in Streptozotocin-Induced Diabetic Rats / 대한해부학회지

Recently diabetic neuropathy has been postulated to occur from reduced availability of neurotrophic factor. This experiment was performed to identify the effect of nerve growth factor on dorsal root ganglia (DRG) in the strepto-zotocin-induced diabetic rat using morphometry and immunohistochemistry. The results obtained are as follows : 1. Unlike in the diabetic group where the type A and B cells were significantly decreased in their total numbers and sizes, these cells were normal in NGF-administered diabetic group. 2. Numbers of cells immunoreactive with SP and CGRP were also significantly decreased in the diabetic group. However, the NGF-administered diabetic group did not show any reduction in the number of these cells. 3. Mean sizes of cells immunoreactive with SP and CGRP cells were reduced in the diabetic group by 18.1% and 26.6% respectively (P<0.01). On the other hand, in NGF-administered diabetic group, mean sizes of SP-immunoreactive cells were increased (10.5%) which was not statiatically significant, and those of CGRP-immunoreactive cells were decreased (18%) compared to the control group (P<0.01). 4. In the diabetic group, many of nerve cell bodies showed some degenerative characteristics including neuron-satellite cell interface of irregular shape, the presence of a number of vacuoles and dense bodies, and nucleus of irregular contour. However, NGF-administered diabetic group exhibited neuron-satellite cell interface of regular form, many neurofilaments and neurotubules, and normal intracellular organelles. These results suggest that administration of NGF protects spinal ganglion cells from morphometric and morphological changes which are associated with a streptozotocin -induced diabetic neuropathy.

The Effects of Nerve Growth Factor on Satellite Cell of the Dorsal Rott Ganglia in Streptozotocin-induced Diabetic Rats / 대한해부학회지

Diabetic neuropathy is an axonal degenerative disease characterized by progressive axonal atrophy and reduced axonal transport. We were interested in the potential neuroprotective effects of nerve growth factor against diabetic neuropathies. To this aim we studied the effect of nerve growth factor on satellite cells, which might play a trophic role toward the related neuron, of the dorsal root ganglion in the streptozotocin-induced diabetic rats by electron in microscope . Diabetes was induced in rats by the streptozotocin. And recombinant human NGF was administrated everyday for 10 consecutive weeks. The results obtained are as follows : 1.In the diabetic induced group, the satellite cells revealed irregular nuclei.The neuron-satellite cell interface was more irregular and plicated than that of control. Large vacuoles and dense bodies were observed and no defects were in the ribosomes and rough endoplasmic reticulum. In the vacuoles, medium electron dense, fiber -like materials were occasionally observed. 2. In the experimental group of diabetic rats treated with NGF for 10 weeks, nucleus was round and the neuron-satellite interface was more regular. Vacuoles and dense bodies were less seen than diabetic rats. In the cytoplasm, many microtubules were observed. In these studies, we considered that streptozotocin induces changes of the satellite cell structure and NGF might improve cellular changes of the satellite cell exposed with streptozotocin.