• Development and Reproduction
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• v.20 no.3
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• pp.247-254
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• 2016

Cytological changes of the epithelial cells according to the developmenatal phases of the seminal vesicle related to the spermatogenic stages in the testicular lobules during spermagenesis in male Neptunea (Barbitonia) cumingii (Gastropoda: Buccinidae) were investigated monthly by electron microscopical and histological observations. N. (B) cumingii is dioecious, and an internal fertilization species. The male genital organ is located near the tentacles. The spermatozoon is approximatley $50{\mu}m$ in length. The axoneme of the tail flagellum consists of nine pairs of microtubles at the periphery and one pair at the center. The process of germ cell development during spermatogenesis can be divided into five succesive stages: (1) spermatogonia, (2) primary spermatocytes, (3) secondary spermatocytes, (4) spermatids, and (5) spermatozoa. A considerable amount of spermatozoa make their appearance in the testicular lobules (or acini) and some of them are tranported from the testis towards the seminal vesicles until late July. In this study, the developmental phases of the epithelial cells of the seminal vesicles of N. (B.) cumingii could be classified into four phases: (1) S-I phase (resting), (2) S-IIphase (early accumulating), (3) S-III phase (accumulating), and (4) S-IV phase (spent). However, in case of N. (B.) arthritica cumingii, the developmental phases of the seminal vesicle were devided into three phases: (1) resting, (2) accumulating and (3) spent. Granular bodies in the inner layer of the seminal vesicles are involved in resorption of digestion of residual spermatozoa.

• BMB Reports
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• v.33 no.2
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• pp.138-146
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• 2000

In eukaryotes, chromosomes undergo a series of complex and coordinated movements during cell division. The kinesin motor proteins, such as the chicken Chromokinesin, are known to bind DNA and transport chromosomes on spindle microtubles. We previously cloned a family of retrograde C-terminus kinesins in Caenorhabditis elegans that mediate chromosomal movement during embryonic development. Here we report the cloning of a C. elegans klp-12 cDNA, encoding an ortholog of chicken Chromokinesin and mouse KIF4. The KLP-12 protein contains 1609 amino acid and harbors two leucine zipper motifs. The insitu RNA hybridization in embryonic stages shows that the klp-12 gene is expressed during the entire embryonic development. The RNA interference assay reveals that, similar to the role of Chromokinesin, klp-12 functions in chromosome segregation. These results support the notion that during mitosis both types, the anterograde N-terminus kinesins such as KLP-12 and the retrograde C-terminus kinesins, such as KLP-3, KLP-15, KLP-16, and KLP-17, may coordinate chromosome assembly at the metaphase plate and chromosomal segregation towards the spindle poles in C. elegans.

• Applied Microscopy
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• v.25 no.1
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• pp.96-110
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• 1995

In order to clarify the process of spermiogenesis of the large-footed bat, Myotis macrodactylus, the testis and the epididymis obtained from mature male bats were examined by electron microscope. Based on the variety and diagnostic characters of organells, the spermiogenesis of the large-footed bat. Myotis macrodactylus could be divided into a total of nine phases. The results obtained from the present study are as follows. 1. The spermiogenesis of large-footed bat, Myotis macrodactylus was divided according to the level of fine structural differentiation into five phases, Golgi, cap, acrosome, maturation and spermiation phases, respectively; Golgi, cap, acrosome and spermiation phases were further subdivided into steps of early and late phase respectively and maturation phase has only one step. Hence, the spermiogenesis of the large-footed bat has been divided into a total of nine phases. 2. In the change of chromatin with nucleus, the chromatin granules are condensed in the whole part of nucleus at the late Golgi phase and completed at the maturation phase. 3. The sperm tail in the epididymis consists of nine outer doublets and two central singlet microtubles. Nos. 1, 5, 6, 9 of the outer dense fibers were larger than the others (2, 3, 4, 7, 8).

• Korean Journal of Weed Science
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• v.12 no.3
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• pp.261-270
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• 1992

Many herbicides that are applied at the soil before weed emergence inhibit plant growth soon after weed germination occurs. Plant growth has been known as an irreversible increase in size as a result of the processes of cell divison and cell enlargement. Herbicides can influence primary growth in which most new plant tissues emerges from meristmatic region by affecting either or both of these processes. Herbicides which have sites of action during interphase($G_1$, S, $G_2$) of cell cycle and cause a subsequent reduction in the observed frequency of mitotic figures can be classified as an inhibitor of mitotic entry. Those herbicides that affect the mitotic sequence(mitosis) by influencing the development of the spindle apparatus or by influencing new cell plate formation should be classified as causing disruption of the mitotic sequence. Sulfonylureas, imidazolinones, chloroacetamides and some others inhibit plant growth by inhibiting the entry of cell into mitosis. The carbamate herbicides asulam, carbetamide, chlorpropham and propham etc. reported to disrupt the mitotic sequence, especially affecting on spindle function, and the dinitroaniline herbicides trifluralin, nitralin, pendimethalin, dinitramine and oryzalin etc. reported to disrupt the mitotic sequence, particularly causing disappearence of microtubles from treated cells due to inhibition of polymerization process. An inhibition of cell enlargement can be made by membrane demage, metabolic changes within cells, or changes in processes necessary for cell yielding. Several herbicides such as diallate, triallate, alachlor, metolachlor and EPTC etc. reported to inhibit cell enlargement, while 2, 4-D has been known to disrupt cell enlargement. One potential danger inherent in the use of soil acting herbicides is that build-up of residues could occur from year to year. In practice, the sort of build-up that would be disastrous is unikely to occur for substances applied at the correct soil concentration. Crop injury caused by soil applied herbicides can be minimized by (1) following the guidance of safe use of herbicides, particularly correct dose at correct time in right crop, (2) by use of safeners which protect crops against injury without protecting any weed ; interactions between herbicides and safeners(antagonists) at target sites do occur probably from the following mechanisms (1) competition for binding site, (2) circumvention of the target site, and (3) compensation of target site, and another mechanism of safener action can be explained by enhancement of glutathione and glutathione related enzyme activity as shown in the protection of rice from pretilachlor injury by safener fenclorim, (3) development of herbicide resistant crops ; development of herbicide-resistant weed biotypes can be explained by either gene pool theory or selection theory which are two most accepted explanations, and on this basis it is likely to develop herbicide-resistant crops of commercial use. Carry-over problems do occur following repeated use of the same herbicide in an extended period of monocropping, and by errors in initial application which lead to accidental and irregular overdosing, and by climatic influence on rates of loss. These problems are usually related to the marked sensitivity of the particular crops to the specific herbicide residues, e.g. wheat/pronamide, barley/napropamid, sugarbeet/ chlorsulfuron, quinclorac/tomato. Relatively-short-residual product, succeeding culture of insensitive crop to specific herbicide, and greater reliance on postemergence herbicide treatments should be alternatives for farmer practices to prevent these problems.

• Journal of Embryo Transfer
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• v.19 no.3
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• pp.283-289
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• 2004

This study was conducted to determine the effects of incubation time after cooling on mouse meiotic spindle and chromosome alignment and the optimal incubation time for their restoration. Oocytes at the metaphase II were obtained from superovulated mice. Control oocytes were held at 37$^{\circ}C$ during the experiment. Oocytes were rapidly cooled to $0^{\circ}C$, held for 30 minutes, warmed and incubated at 37$^{\circ}C$ for 5, 15, 30, 60 and 120 minutes, respectively. The morphological features of spindle and chromosomes in oocytes were evaluated by immunofluorescent staining. Meiotic spindle of control oocytes exhibited a normal-looking bipolar configuration(barrel-shaped) and highly fluorescent microtubles. The chromosomes were clustered in a discrete bundles at metaphase plate. Disassembly of meiotic spindle and chromosome dispersion were occurred immediately after chilling of oocyte. Fluorescence intensity index(FIS), normal chromosomes aligned and normal spindle configuration were compared according to incubation time at 37$^{\circ}C$. Restoration of a barrel-shaped spindle and normal chromosome alignment was occurring after 5 minutes incubation at 37$^{\circ}C$, improved as a incubation time increased, and decreased gradually after 120 minutes incubation(P<0.05). The optimal incubation time for restoration of meiotic spindle and chromosomes in cooled oocytes was 60 minutes.

• Applied Microscopy
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• v.27 no.3
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• pp.225-234
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• 1997

Vincristine, a kind of anticancerous drugs, interferes with development of microtubles and synthesis of nucleic acid and proteins in cells, and destructs cytoplasmic membrane so that mitosis of cancer cells is inhibited. Unfortunately these anticancerous effects by vioneristime are not limited to specific cancer cells, so several side effects are produced. This study was performed to explore the effects of vincristine on the fine structure of cytoplasmic organelles and cartilagenous matrix in proximal epiphyseal plate of the tibia in rat. The results were as follows: 1. Cisternae of rough endoplasmic reticulum (RER) were fragmented and sacculated, and membrane-bound ribocomes of RER were detached at 3 and 6 hours after vincristine treatment. Severely dilated, fagmented and sacculated cisternae of RER were found at 12 hours after vincristine treatment, and at 24 hours after vincristine treatment a few cisternae were framented and sacculated. At 72 hours after vincristine treatment cisternae of RER were parallely well arraged. 2. Golgi complex was atrophied at 3, 6, and 12 hours after vincristine treatment, while at 72 hours after vincristine treatment the cisternae of Golgi complex were made of 5-6 layers. 3. Mitochondria with disorganized mitochondrial cristae and outer membrane-losed mitochondria were found at 3 hours after vincristine treatment. At 6 and 12 hours after vincristine treatment mitochondria had possessed disorganized cristae, and a few mitochondria with disorganized cristae were. observed at 24 hours after vincristine treatment. While at 72 hours after vincristine treatment mitochondria were shown distinct cristae and double membranes. 4. Phagosome were begun to observe at 3 hourse after vincristine treatment, and at 24 hourse after vincristine treatment many phagosomes were found, while at 72 hours after vincristine treatment a few phagosomes were observed. 5. In the cartilagenous matrix large-sized matrix granules were decreased and collagen fibrils were dispersed at 3, 6, and 12 hours after vincristine treatment, while at 72 hours after vincristine treatment many large-sized matrix granules and numerous matrix it is suggested that although vincristine may induce the degenerative changes of the chondrocyte, resulting in changes of components of the cartilagenous matirx, these toxic effects may be regressed with time.

• Applied Microscopy
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• v.30 no.1
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• pp.45-59
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• 2000

Cis-platin is a widely used anticancer drug against certain solid tumors such as malignant ovarian tumor, malignant carcinoma of head and neck, bladder cancer and cervical cancer of uterus, and its major mechanism of action is inhibition of DNA synthesis of the tumor cell. To investigate the inhibitory effects of cis-platin on the ciliogensis of the ciliated cells in the mucosa of oviduct, the author pursued the alterations of $\alpha-tubulin$, which is the main constituent of the microtubles in cilia, after cis-platin treatment. To eliminate the possible variations due to ovarian cycle, female Spargue-Dawley rats ($150\sim200gm$ in B.W.) were pretreated with estradiol benzoate (20 mg/kg, once a day, for 4 consecutive days). Animals were administrated with cis-platin (6 mg/kg, i.p.) and sacrificed at 1day, 3days, 5days and 7days after treatment, respectively. Immunohistochemistry for $\alpha-tubulin$ using mouse anti-rat $\alpha-tubulin$ monoclonal antibody as primary antibody was done. Immunogold electronmicroscopy for intracellular distributions of $\alpha-tubulin$ was also performed with same primary antibody and Goat anti- mouse IgM which is preconjugated with gold particles of 15 nm as secondary antibody. The results obtained were as follows; 1. Strong immunoreactivity of $\alpha-tubulin$ was observed in ciliated cells of oviducts at 1, 3 and 5 days after estradiol pretreatment. 2. Weak immunoreactivity of $\alpha-tubulin$ was observed in ciliated cells of oviducts at 1 and 3 days after cis-platin treatment but it was recovered to strong immunoreactivity in 5 days 3. In immunogold electronmicroscopy, density of gold particles for $\alpha-tubulin$ reactions was decreased in apical cytoplasm, but few changes were observed in basal body or cilia at 1 and 3 days after cis-platin treatment. From these above results, it is indicated that synthesis of $\alpha-tubulin$ in ciliated cells of rat oviduct is inhibited by cis-platin treatment.