Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “elevational migration”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 919 records · Page 51Linked to original sources
PubMed2006

Cancer mortality rates among first and second generation migrants in the Netherlands: Convergence toward the rates of the native Dutch population.

This study investigates the difference in cancer mortality rates between migrant groups and the native Dutch population, and determines the extent of convergence of cancer mortality rates according to migrants' generation, age at migration and duration of residence. Data were obtained from the national cause of death and population registries in the period 1995-2000. We used Poisson regression to compare the cancer mortality rates of migrants originating from Turkey, Morocco, Surinam, Netherlands Antilles and Aruba to the rates for the native Dutch. All-cancer mortality among all migrant groups combined was significantly lower when compared to that of the native Dutch population (RR = 0.55, CI: 0.52-0.58). For a large number of cancers, migrants had more than 50% lower risk of death, while elevated risks were found for stomach and liver cancers. Mortality rates for all cancers combined were higher among second generation migrants, among those with younger age at migration, and those with longer duration of residence. This effect was particularly pronounced in lung cancer and colorectal cancer. For most cancers, mortality among second generation migrants remained lower compared to the native Dutch population. Surinamese migrants showed the most consistent pattern of convergence of cancer mortality. The generally low cancer mortality rates among migrants showed some degree of convergence but did not yet reach the levels of the native Dutch population. This convergence implies that current levels of cancer mortality among migrants will gradually increase in future years if no specific preventive measurements are taken.

Adolescent↗
PubMed1997

Effects of the calciotrophic peptides calcitonin and parathyroid hormone on prostate cancer growth and chemotaxis.

BACKGROUND: The most common site of metastases in prostate cancer is the skeleton and occurs in 70-80% of patients with prostate carcinoma. Calciotrophic peptides are important in the growth and development of normal bone matrix. METHODS: Three human prostate carcinoma cells lines, DU-145, PC-3, and LNCaP, were exposed to varying concentrations of parathyroid hormone (PTH) or calcitonin (CT). Cell proliferation and chemotaxis were assessed. RESULTS: Proliferation increased in LNCaP cells in a dose-dependent manner following treatment with PTH. Proliferation was not altered in PC-3 cells in response to PTH. Proliferation was decreased in DU-145 and PC-3 cells and increased in LNCaP cells after treatment with CT. Cell chemotaxis was increased in the presence of PTH in DU-145 and PC-3 cells compared to vehicle-treated controls. CONCLUSIONS: The combined proliferation and chemotaxis data suggest that PTH has a dual role in prostate carcinoma resulting in an increase in the number and migration of selected prostate cancer cells. With CT, chemotaxis was unchanged in the DU-145 and PC-3 cells and significantly elevated in the LNCaP cell line. The calciotrophic hormones, PTH and CT, may play an integral role in the regulation of prostate cell growth and metastases.

Calcitonin↗
PubMed1984

Gastric epithelial cell proliferation in monkeys fed 3,4,3',4'-tetrachlorobiphenyl.

Rhesus monkeys (Macaca mulatta) fed diets containing 1 or 3 mg/kg of 3,4,3',4'-tetrachlorobiphenyl (3,4-TCB), became moribund after 7-14 weeks. In the body of the stomach the mucosa was thick and cystic gastric glands penetrated the muscularis mucosae. The zymogenic and parietal cells were replaced by or converted into mucus-secreting cells. Autoradiographs of animals labelled with [3H]thymidine showed that in control monkeys gastric epithelial cell proliferation was limited to the isthmus and neck regions of the glands throughout the stomach. In the 3,4-TCB-fed animals most DNA synthesis also occurred in these regions, but [3H]thymidine labelled cells were also seen in the bases of the glands. The labelling indices were not elevated, and therefore the submucosal glands and cysts in this lesion may develop by a failure of the newly formed, downward migrating cells to differentiate and lose their proliferative capacity.

Animals↗
PubMed1992

Soluble interferon-alpha receptor molecules are present in body fluids.

Soluble forms of the interferon-alpha receptor (sIFN-alpha R) were identified in human serum and urine by Western blotting with monoclonal antibodies (MAb) directed against IFN-alpha R, and by immunoprecipitation (Iptn) of a covalently cross-linked complex of IFN-alpha R and [125I]IFN-alpha with anti IFN-alpha MAb. Elevated levels of sIFN-alpha R were found in sera of hairy cell leukemia patients. The soluble receptor from serum migrated as a 55 kDa protein in SDS-PAGE, and, as expected, the cross-linked product migrated as a 75 kDa protein. The soluble receptor from urine was found to be a protein of mol. wt. 45 kDa and its cross-linked complex migrated as a 65 kDa protein. The calculated mol. wt. of the entire extracellular domain of the IFN-alpha R prior to post-translational modifications is 47,000. Since there are 12 potential glycosylation points in this extracellular domain, its actual mol. wt. may be as high as 70,000 Da. It is therefore concluded that sIFN-alpha R molecules, corresponding to truncated forms of the extracellular domain of the cell surface IFN-alpha R, are present in human serum and in normal human urine.

Animals↗
PubMed1998

Regulation of Wnt5a expression in human mammary cells by protein kinase C activity and the cytoskeleton.

The Wnts can be classified into two classes based on their ability to transform cells. The Wnt5a class can antagonize the effects of transforming Wnts partly through effects on cell migration. To understand the mechanisms of regulation of Wnt5a, we investigated its expression in human normal and breast cancer cell lines. Elevation of Wnt5a in HB2, a normal breast epithelial cell line, was linearly correlated with cell density, but this did not occur in cancer cell lines. We examined intracellular events responsible for the regulation of Wnt5a by cell to cell contacts, using various metabolic agents known to affect signal transduction pathways. Agents that selectively blocked protein kinase C (calphostin C) or protein tyrosine kinases (genistein) reduced the level of Wnt5a expression markedly. Protein kinase C activation by phorbol 12-myristate 13-acetate up-regulated Wnt5a partly through prolongation of Wnt5a mRNA half-life. Cytoskeleton reorganization following cytochalasin D treatment caused an induction of Wnt5a, which was associated with changes in cell morphology. Calphostin C did not block these effects, showing that protein kinase C is acting upstream of cytoskeletal modulation. However, the cancer cell lines treated with cytochalasin D showed no changes in cell morphology or Wnt5a induction, suggesting disruption of this regulatory pathway in cancer.

Breast↗
PubMed1978

Acquired immunity to the trematode Fasciola hepatica in rats.

Following a primary infection of 5 metacercariae (mc) of Fasciola hepatica, rats became immune to challenge with 30 mc. Immunity was less consistently demonstrated following challenge infection with 5 mc. The levels of precipitating and miracidial immobilizing antibodies, and antibodies detected by an indirect fluorescent antibody test, were monitored during the course of a primary infection of 5 mc and challenge infection of 30 mc. Following primary infection, peaks in the antibody response were associated with the invasion and migration of juvenile flukes in the liver parenchyma. Antibody titres fell when flukes entered the bile duct. There was a slight elevation in the titre of all antibodies following challenge, but, apart from those detected by the fluorescent antibody test, this elevation was not as marked as in control animals. It is suggested that flukes become isolated from, or have diminished contact with, the immune system once they enter the bile duct. This might explain why adult flukes survive in immune hosts whereas challenge metacercariae are destroyed.

Animals↗
PubMed2005

The Akt/PKB pathway: molecular target for cancer drug discovery.

The serine/threonine kinase Akt/PKB pathway presents an exciting new target for molecular therapeutics, as it functions as a cardinal nodal point for transducing extracellular (growth factor and insulin) and intracellular (receptor tyrosine kinases, Ras and Src) oncogenic signals. In addition, alterations of the Akt pathway have been detected in a number of human malignancies. Ectopic expression of Akt, especially constitutively activated Akt, is sufficient to induce oncogenic transformation of cells and tumor formation in transgenic mice as well as chemoresistance. Akt has a wide range of downstream targets that regulate tumor-associated cell processes such as cell growth, cell cycle progression, survival, migration, epithelial-mesenchymal transition and angiogenesis. Blockage of Akt signaling results in apoptosis and growth inhibition of tumor cells with elevated Akt. The observed dependence of certain tumors on Akt signaling for survival and growth has wide implications for cancer therapy, offering the potential for preferential tumor cell killing. In the last several years, through combinatorial chemistry, high-throughput and virtual screening, and traditional medicinal chemistry, a number of inhibitors of the Akt pathway have been identified. This review focuses on ongoing translational efforts to therapeutically target the Akt pathway.

Antineoplastic Agents↗
PubMed1984

Cyclic AMP-dependent protein phosphorylation and insulin secretion in intact islets of Langerhans.

Effects on insulin release, cyclic AMP content and protein phosphorylation of agents modifying cyclic AMP levels have been tested in intact rat islets of Langerhans. Insulin release induced by glucose was potentiated by dibutyryl cyclic AMP, glucagon, cholera toxin and 3-isobutyl-1-methylxanthine (IBMX); the calmodulin antagonist trifluoperazine reversed these potentiatory effects. Inhibition by trifluoperazine of IBMX-potentiated release was, however, confined to concentrations of IBMX below 50 microM; higher concentrations, up to 1 mM, were resistant to inhibition by trifluoperazine. IBMX-potentiated insulin release was also inhibited by 2-deoxyadenosine, an inhibitor of adenylate cyclase. In the absence of glucose, IBMX at concentrations up to 1 mM did not stimulate insulin release and in the presence of 3.3 mM-glucose IBMX was effective only at a concentration of 1 mM; under the latter conditions trifluoperazine again did not inhibit insulin secretion. The maximum effect on insulin release was achieved with 25 microM-IBMX. Islet [cyclic AMP] was increased by IBMX, with the maximum rise occurring with 100 microM-IBMX. The increase in [cyclic AMP] elicited by IBMX was more rapid than that induced by cholera toxin. Trifluoperazine did not significantly affect islet cyclic AMP levels under any of the conditions tested. When islets were incubated with [32P]Pi, radioactivity was incorporated into islet ATP predominantly in the gamma-position. The rate of equilibration of label was dependent on medium Pi and glucose concentration and at optimal concentrations of these 100% equilibration of internal [32P]ATP with external [32P]Pi required a period of 3h. Radioactivity was incorporated into islet protein and, in response to an increase in islet [cyclic AMP], the major effect was on a protein of Mr 15 000 on sodium dodecyl sulphate/polyacrylamide gels. The extent of phosphorylation of the Mr-15 000 protein was correlated with the level of cyclic AMP: phosphorylation in response to IBMX was inhibited by 2-deoxyadenosine but not by trifluoperazine. Fractionation of islets suggested that the Mr-15 000 protein was of nuclear origin: the protein co-migrated with histone H3 on acetic acid/urea/Triton gels. In the islet cytosol a number of proteins were phosphorylated in response to elevation of islet [cyclic AMP]: the major species had Mr values of 18 000, 25 000, 34 000, 38 000 and 48 000. Culture of islets with IBMX increased the rate of [3H]-thymidine incorporation.(ABSTRACT TRUNCATED AT 400 WORDS)

1-Methyl-3-isobutylxanthine↗
PubMed2005

Role of the chemokine receptor CCR4 and its ligand thymus- and activation-regulated chemokine/CCL17 for lymphocyte recruitment in cutaneous lupus erythematosus.

Skin-infiltrating T lymphocytes are thought to play a major role in the pathogenesis of cutaneous lupus erythematosus (CLE). In this study, we investigated the role of the chemokine receptor 4 (CCR4) and its ligand thymus- and activation-regulated chemokine (TARC/CCL17) for the recruitment of T cells in inflamed skin of patients with CLE. We found significant numbers of CCR4+ T lymphocytes in the skin of all patients with CLE. Interestingly, a subset of patients with disseminated scarring skin involvement were characterized by both lesional and circulating CD8+ T cells expressing CCR4. Destruction of epidermal and adnexal structures was histomorphologically associated with CCR4+ cytotoxic T cells invading basal layers of the epidermis where keratinocytes showed apoptotic death. The CCR4 ligand TARC/CCL17 was strongly expressed in skin lesions and elevated in the serum of CLE patients. The functional relevance of lymphocytic CCR4 expression could be confirmed by TARC/CCL17-specific in vitro migration assays. Our investigations suggest that CCR4 and TARC/CCL17 play a role in the pathophysiology of CLE. In particular, cytotoxic CD8+ T cells expressing CCR4 appear to be involved in scarring subtypes of CLE.

Adult↗
PubMed1998

The equine herpesvirus 1 IR6 protein that colocalizes with nuclear lamins is involved in nucleocapsid egress and migrates from cell to cell independently of virus infection.

The equine herpesvirus 1 (EHV-1) IR6 protein forms typical rod-like structures in infected cells, influences virus growth at elevated temperatures, and determines the virulence of EHV-1 Rac strains (Osterrieder et al., Virology 226:243-251, 1996). Experiments to further elucidate the functions and properties of the IR6 protein were conducted. It was shown that the IR6 protein of wild-type RacL11 virus colocalizes with nuclear lamins very late in infection as demonstrated by confocal laser scan microscopy and coimmunoprecipitation experiments. In contrast, the mutated IR6 protein encoded by the RacM24 strain did not colocalize with the lamin proteins at any time postinfection (p.i.). Electron microscopical examinations of ultrathin sections were performed on cells infected at 37 and 40 degreesC, the latter being a temperature at which the IR6-negative RacH virus and the RacM24 virus are greatly impaired in virus replication. These analyses revealed that nucleocapsid formation is efficient at 40 degreesC irrespective of the virus strain. However, whereas cytoplasmic virus particles were readily observed at 16 h p.i. in cells infected with the wild-type EHV-1 RacL11 or an IR6-recombinant RacH virus (HIR6-1) at 40 degreesC, virtually no capsid translocation to the cytoplasm was obvious in RacH- or RacM24-infected cells at the elevated temperature, demonstrating that the IR6 protein is involved in nucleocapsid egress. Transient transfection assays using RacL11 or RacM24 IR6 plasmid DNA and COS7 or Rk13 cells, infection studies using a gB-negative RacL11 mutant (L11DeltagB) which is deficient in direct cell-to-cell spread, and studies using lysates of IR6-transfected cells demonstrated that the wild-type IR6 protein is transported from cell to cell in the absence of virus infection and can enter cells by a yet unknown mechanism.

Animals↗
PubMed2006

Roles of myofibroblasts in prostaglandin E2-stimulated intestinal epithelial proliferation and angiogenesis.

Prostaglandins (PG) are produced throughout the gastrointestinal tract and are critical mediators for a complex array of physiologic and pathophysiologic processes in the intestine. Intestinal myofibroblasts, which express cyclooxygenase (COX) and generate PGE(2), play important roles in intestinal epithelial proliferation, differentiation, inflammation, and neoplasia through secreting growth factors and cytokines. Here, we show that PGE(2) activated human intestinal subepithelial myofibroblasts (18Co) through Gs protein-coupled E-prostanoid receptors and the cyclic AMP/protein kinase A pathway. 18Co cells and primary colonic myofibroblast isolates expressed a number of growth factors; several of them were dramatically regulated by PGE(2). An epidermal growth factor-like growth factor, amphiregulin (AR), which was not expressed by untreated cells, was strongly induced by PGE(2). Expression of vascular endothelial growth factor A (VEGFA) was rapidly increased by PGE(2) exposure. Hepatocyte growth factor (HGF) was elevated in PGE(2)-treated myofibroblasts at both mRNA and protein levels. Thus, PGE(2)-activated myofibroblasts promoted the proliferation and migration of intestinal epithelial cells, which were attenuated by neutralizing antibodies to AR and HGF, respectively. Moreover, in the presence of PGE(2), myofibroblasts strongly stimulated the migration and tubular formation of vascular endothelial cells. Neutralizing antibody to VEGFA inhibited the observed stimulation of migration. These results suggest that myofibroblast-generated growth factors are important mediators for PGE(2)-induced intestinal epithelial proliferation and angiogenesis, which play critical roles in intestinal homeostasis, inflammation, and neoplasia.

Cell Culture Techniques↗
PubMed1991

Increased multimeric mitochondrial DNA in the brain of scrapie-infected hamsters.

We observed a marked increase in multimeric mitochondrial DNA (mtDNA) in brains of scrapie-infected hamsters compared with those of uninfected hamsters. Homogenized brain tissue was subjected to subcellular fractionation to isolate scrapie-associated fibrils and tubulofilamentous structures. Nucleic acids were extracted from the scrapie-associated fibril/tubulofilament fraction which also contained mitochondria. Agarose gel electrophoresis revealed a band corresponding to the size of circular hamster mtDNA in both infected and uninfected samples, but slower migrating bands were observed only in samples from scrapie-infected brain. We showed by molecular cloning, nucleotide sequencing, and Southern blotting that the slower migrating bands are mtDNA. These findings confirm the recent demonstration by differential hybridization that multimeric mtDNA occurs in hamster scrapie brain. Elevated levels of multimeric circular mtDNA have been reported previously in various tumors and cultured cell lines.

Animals↗
PubMed1976

Levels of prostaglandins in the small intestine of rats during primary and secondary infection with Nippostrongylus brasiliensis.

The level of PGE is increased 10-fold in intestinal tissues during primary infection of the rat with Nippostrongylus brasiliensis. Peak levels (ca. 7,000 pg/cm) were assayed in the jejunal site of infection on day 7 of infection and similar levels were recorded in 'post-infection' (ileal) segments at this time. The level of PGE in 'post-infection' segments showed further increase to 12,000 pg/cm on day 10. The level of PGE also increased in 'pre-infection' (duodenal) but this was delayed by 4-5 days. The level of PGF also increased during primary infection (from about 100 to 950 pg/cm) but this occurred after expulsion. Increase in the level of PGE occurred earlier (at 3-4 days) during secondary challenge given 19 days after primary infection, but the PGE levels followed the primary response when challenge was given 10 weeks after primary infection. It is suggested that PGE plays a dual role in parasite immunity. (1) PGE may directly affect metabolism of the parasite. In this event it is also suggested that protective antibodies cause the release of PG. (2) Elevated levels of PGE act indirectly by affecting gastrointestinal function which alters the microenvironment at the site of infection. The duodenal migration of parasites may be due to this effect of PGE.

Ancylostomatoidea↗
PubMed2001

Human pituitary tumor-transforming gene induces angiogenesis.

Angiogenesis is a key determinant and rate-limiting step in tumor progression and metastatic spread. As pituitary tumor-transforming gene (PTTG) induces basic fibroblast growth factor (bFGF), we tested angiogenesis induced by conditioned medium (CM) derived from NIH-3T3 transfectants overexpressing wild-type human PTTG (WT-hPTTG-CM). We also examined the relationship between PTTG expression and tumor vascularity in a series of human tumors. CM from Wt-hPTTG transfectants induced proliferation, migration, and tube formation of human umbilical vein endothelial cells in vitro. The bFGF concentration in WT-hPTTG-CM was elevated (10.5 +/- 0.56) compared with CM from nontransfected NIH-3T3 cells (3.3 +/- 0.56 pg/mL), and addition of anti-bFGF antibody to CM abrogated these angiogenesis markers (P < 0.01). In vivo, concentrated WT-hPTTG-CM induced chick chorioallantoic membrane spoke-wheel-like appearances. Moreover, CM derived from hPTTG transfectants harboring a point mutation on the C-terminus proline-rich region of PTTG induced weaker angiogenic activity than WT-hPTTG-CM (P < 0.01). Thus, human PTTG induces an angiogenic phenotype in both in vitro and in vivo angiogenesis models, and high PTTG messenger ribonucleic acid is associated with an angiogenic phenotype in human tumors. These PTTG-directed angiogenic actions may be mediated through bFGF, which also contributes to tumor growth.

3T3 Cells↗
PubMed1999

Circulating intercellular adhesion molecule-1 in chronic liver disease and hepatocellular carcinoma.

BACKGROUND: Intercellular adhesion molecule-1 (ICAM-1) is important in the migration and adhesion of immune cells from the circulation to their targets. A circulating form of ICAM-1 (cICAM-1) is elevated in the serum of patients with hepatitis and various cancers. Our aim was to determine the clinical significance of cICAM-1 in chronic liver diseases and hepatocellular carcinoma (HCC). METHODS: We measured the serum cICAM-1 levels in 91 patients with HCC, 47 with liver cirrhosis, 41 with chronic viral hepatitis and 32 healthy controls using an enzyme-linked immunosorbent assay. Ninety-eight patients had serial follow-up. RESULTS: The cICAM-1 levels in patients with HCC (737 +/- 212 ng/ml) and liver cirrhosis (593 +/- 145 ng/ml) were significantly higher than those in patients with chronic viral hepatitis (488 +/- 127 ng/ml) and controls (318 +/- 64 ng/ml). HCC patients had higher cICAM-1 levels than all the other groups. cICAM-1 levels in patients with chronic viral hepatitis correlated with serum alanine aminotransferase, prothrombin time and indocyanine green retention ratio. In HCC patients, alpha-fetoprotein levels and tumor size paralleled cICAM-1 concentrations. Furthermore, HCC patients with distant metastases had higher cICAM-1 levels than those without distant metastases, and levels of cICAM-1 in patients with stage IV HCC were higher than those in HCC patients with stages I, II or III disease. During a seven-year follow-up, 14 patients with chronic hepatitis developed liver cirrhosis when their cICAM-1 levels increased significantly. In 47 HCC patients, cICAM-1 levels decreased after tumor resection or transcatheter arterial embolization, and increased when the tumor recurred. cICAM-1 levels increased gradually in 14 patients with advanced HCC without specific therapy. CONCLUSIONS: CICAM-1 levels are increased in patients with chronic hepatitis, liver cirrhosis and HCC. This reflects the severity and progression of chronic liver disease and HCC. Sequential measurements of cICAM-1 seem more valuable than a single-point assessment in evaluating the progress of liver disease.

Adult↗
PubMed1988

[The topography of P300 in neuropsychiatric pharmacotherapy. III. Cognitive P300 fields in an organic psychosyndrome (Wilson's disease) before and during treatment with D-penicillamine].

Beside senile dementia of Alzheimer's type (SDAT) there are also dementive syndromes due to a disturbance in metabolism. In a case with a disturbance of copper metabolism (Wilson's disease) a similar P300-pattern was found as described in SDAT with signs of a frontal amplitude elevation. Under therapy with d-penicillamine the frontal P300-positivity moved from frontal to parietal structures. Combined with this migration was an amelioration in cognitive function. This single-case study underlines the significance of P300-topography in the evaluation of therapy effects in dementive disorders.

Adult↗
PubMed1985

The intracellular accumulation of UDP-N-acetylhexosamines is concomitant with the inability of human colon cancer cells to differentiate.

The relationship between the intracellular concentration of various nucleotides as measured by high-performance liquid chromatography analysis, and the differentiation of 2 human colon cancer cell lines was studied. HT-29 cells were induced to undergo both structural and functional enterocytic differentiation (as determined by electron microscopy and the presence of brush-border specific enzymes, respectively) by changing the carbon source or adding Na butyrate to standard tissue culture media. This differentiation occurred after the cells reached confluency when they were cultured in galactose, uridine, inosine, or without nucleosides (all in the absence of glucose) and in the presence of glucose plus Na butyrate. Cells cultured in 25 mM fructose or glucose +/- nucleosides did not differentiate. In all culture conditions where HT-29 cells did not differentite, the intracellular concentrations of 2 compounds which co-migrated with UDP-N-acetylglucosamine and UDP-N-acetylgalactosamine rose approximately equal to 10-fold at confluency and remained elevated throughout the stationary phase, whereas their concentrations remained constant and low after confluency in cells that underwent differentiation. This indicated that the accumulation of these compounds is associated with the inability of these cells to differentiate since other nucleotides and nucleotide sugars did not change in a similar fashion. Purification of the presumed UDP-N-acetylhexosamines, followed by the identification of the products from their chemical and enzymatic hydrolysis, confirmed the identity of these two peaks. Nucleotide analysis of Caco-2 cells, which undergo enterocytic differentiation after they reach confluency even when cultured on glucose, revealed the same pattern of UDP-N-acetylhexosamine levels as differentiated HT-29 cells, with its concentration remaining relatively constant and very low, even after the cells were confluent. The significance of the accumulation of UDP-N-acetylhexosamines in cells unable to differentiate is discussed.

Adenocarcinoma↗
PubMed1976

Migration of Oncomelania quadrasi observed by the mark and release method in a wet bank of a stream in Leyte, Philippines.

The migration and population size of Oncomelania quandrasi were studied at two sites in a submerged bank of a stream in Leyte Philippines. The snails collected by filter paper in an experimental area were marked with manicure and released in the same area. Collection was repeated every 4 days in the same area for 5 more times and snails without mark were marked with manicure of different colors at each time. The immigration and emigration rates and population were calculated from the collection data. One experimental site with an area of 5.86 m2 was established at the edge of the water pathway, 3 sides of which were surrounded by wooden planks except that side facing the water pathway to determine the migration between the bank and water pathway. The other experimental site was 7.54 m2 in area, located in a submerged place close to high land and was left open in all sides. The ranges of the population, immigration and emigration rates during a 4 day period were 3845 to 7638, 0 to 0.4448 and 0.2263 to 0.8911, respectively in the former site. The results in the latter area were 1336 to 2468, 0.1261 to 0.6725 and 0.1349 to 1.2340, respectively. It was observed that the replacement of individual snails in a habitat was largely due to migration which in turn was influenced much by the change of water level in the bank. The emigration increased with the elevation of water level. On the other hand, the immigration increased with the lowering of water.

Animals↗