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 523 records · Page 29Linked to original sources
PubMed2001

Metabolic cooperation between different oncogenes during cell transformation: interaction between activated ras and HPV-16 E7.

The metabolism of tumor cells (tumor metabolome) is characterized by a high concentration of glycolytic enzymes including pyruvate kinase isoenzyme type M2 (M2-PK), a high glutaminolytic capacity, high fructose 1,6-bisphosphate (FBP) levels and a low (ATP+GTP):(CTP+UTP) ratio. The sequence of events required for the establishment of the tumor metabolome is presently unknown. In non-transformed rat kidney (NRK) cells we observed a high glutaminolytic flux rate and a low (ATP+GTP):(CTP+UTP) ratio, whereas FBP levels and M2-PK activity are still extremely low. After stable expression of oncogenic ras in NRK cells a strong upregulation of FBP levels and of M2-PK activity was observed. Elevated FBP levels induce a tetramerization of M2-PK and its migration into the glycolytic enzyme complex. AMP levels increase whereas UTP and CTP levels strongly decrease. Thus, ras expression completes the glycolytic part of tumor metabolism leading to the inhibition of nucleic acid synthesis and cell proliferation. The HPV-16 E7 oncoprotein, which cooperates with ras in cell transformation, directly binds to M2-PK, induces its dimerization and restores nucleic acid synthesis as well as cell proliferation. Apparently, the combination of the different metabolic effects of ras and E7 constructs the perfect tumor metabolome as generally found in tumor cells.

Adenylate Kinase↗
PubMed2002

Structural organization of the estalpha3(1) gene in a Colombian strain of Culex quinquefasciatus differs from that in Cuba.

In Culex mosquitoes (Diptera: Culicidae), the most common mechanism for resistance to organophosphorus (OP) insecticides involves amplification of one or more esterases. Two esterase loci are often involved, with different allelic forms co-amplified. Estalpha3(1) is co-amplified with estbeta1 in a Colombian (COL) strain of Culex quinquefasciatus Say. These two alleles co-migrate on acrylamide gels, often leading to misscoring of the phenotype as elevation of a single estbeta enzyme. By sequencing COL genomic DNA, we determined the estalpha3(1) gene length is 1623 nucleotides. The open reading frame of estalpha3(1) encodes a 540 amino acid protein, as for estalpha2(1) in strain Pel RR from Sri Lanka. The intron/exon boundaries of estalpha3(1) are identical to those of estalpha2(1), suggesting that they are alleles of the same locus. The COL estalpha3(1) gene differs from estaalpha3(2) in strain MRES from Cuba, although they have equivalent electrophoretic mobility, showing that these two strains contain distinct resistance-associated amplicons. Twenty nucleotide differences were scored between the MRES partial 495 bp sequence and that in the COL strain, with two amino acid changes, demonstrating distinct estalpha enzymes. Our sequencing data show 95% identity between the three estalpha genes (each has six introns and seven exons) in OP-resistant Cx. quinquefasciatus. Amplified estalpha3(1) and estbeta1 are at least 10kb apart in temephos-selected COL and 2.7kb apart in Pel RR, whereas these non-amplified genes are only 1.7kb apart in the nonselected parental COL stock, as in Pel SS (susceptible Sri Lankan strain), demonstrating that this region of the genome is susceptible to expansion and contraction.

Amino Acid Sequence↗
PubMed1998

Regulation of the zinc transporter ZnT-1 by dietary zinc.

The understanding of mechanisms controlling zinc absorption and metabolism at the molecular level has advanced recently. Kinetics of zinc transport have been investigated for many years, but only recently have genes coding for proteins thought to be involved in the transport process been cloned. Four putative zinc transporters, known as ZnT-1 through ZnT-4, have now been described. Among these transporters, only ZnT-1 is ubiquitously expressed. In this report, we examine the pattern of ZnT-1 expression in the intestine and analyze the regulation of ZnT-1 by dietary zinc in both the intestine and liver. Immunofluorescence demonstrated that intestinal ZnT-1 was most abundant at the basolateral surface of enterocytes lining the villi of the duodenum and jejunum. By Western blot analysis, intestinal and liver ZnT-1 protein migrated as a 42- and 36-kDa protein, respectively. Dietary zinc supplementation elevated the level of intestinal ZnT-1 mRNA and protein approximately 50% and 10%, respectively, but had no effect in the liver. In response to an acute oral zinc dose, the level of intestinal ZnT-1 mRNA was up-regulated 8-fold, without a corresponding increase in ZnT-1 protein. Conversely, the acute oral dose did not affect liver ZnT-1 mRNA, but resulted in a 5-fold increase in liver ZnT-1 protein. These results represent studies on the expression of intestinal and hepatic ZnT-1 in an intact animal model. The data suggest that ZnT-1 is at least part of the mechanism by which dietary zinc is absorbed and that, despite the zinc responsiveness of the ZnT-1 gene, additional factors may be regulating the steady-state level of ZnT-1 transporter protein.

Animals↗
PubMed2006

Inhibition of S/G2 phase CDK4 reduces mitotic fidelity.

Cyclin-dependent kinase 4 (CDK4)/cyclin D has a key role in regulating progression through late G(1) into S phase of the cell cycle. CDK4-cyclin D complexes then persist through the latter phases of the cell cycle, although little is known about their potential roles. We have developed small molecule inhibitors that are highly selective for CDK4 and have used these to define a role for CDK4-cyclin D in G(2) phase. The addition of the CDK4 inhibitor or small interfering RNA knockdown of cyclin D3, the cyclin D partner, delayed progression through G(2) phase and mitosis. The G(2) phase delay was independent of ATM/ATR and p38 MAPK but associated with elevated Wee1. The mitotic delay was because of failure of chromosomes to migrate to the metaphase plate. However, cells eventually exited mitosis, with a resultant increase in cells with multiple or micronuclei. Inhibiting CDK4 delayed the expression of the chromosomal passenger proteins survivin and borealin, although this was unlikely to account for the mitotic phenotype. These data provide evidence for a novel function for CDK4-cyclin D3 activity in S and G(2) phase that is critical for G(2)/M progression and the fidelity of mitosis.

Animals↗
PubMed2006

An antiangiogenic neurokinin-B/thromboxane A2 regulatory axis.

Establishment of angiogenic circuits that orchestrate blood vessel development and remodeling requires an exquisite balance between the activities of pro- and antiangiogenic factors. However, the logic that permits complex signal integration by vascular endothelium is poorly understood. We demonstrate that a "neuropeptide," neurokinin-B (NK-B), reversibly inhibits endothelial cell vascular network assembly and opposes angiogenesis in the chicken chorioallantoic membrane. Disruption of endogenous NK-B signaling promoted angiogenesis. Mechanistic analyses defined a multicomponent pathway in which NK-B signaling converges upon cellular processes essential for angiogenesis. NK-B-mediated ablation of Ca2+ oscillations and elevation of 3'-5' [corrected] cyclic adenosine monophosphate (cAMP) reduced cellular proliferation, migration, and vascular endothelial growth factor receptor expression and induced the antiangiogenic protein calreticulin. Whereas NK-B initiated certain responses, other activities required additional stimuli that increase cAMP. Although NK-B is a neurotransmitter/ neuromodulator and NK-B overexpression characterizes the pregnancy-associated disorder preeclampsia, NK-B had not been linked to vascular remodeling. These results establish a conserved mechanism in which NK-B instigates multiple activities that collectively oppose vascular remodeling.

1-Methyl-3-isobutylxanthine↗
PubMed1998

Expression of calcitonin receptors in mouse preimplantation embryos and their function in the regulation of blastocyst differentiation by calcitonin.

Calcitonin secretion in the pregnant uterus is tightly regulated by the ovarian hormones, estrogen and progesterone, which limit its expression to a brief period preceding blastocyst implantation. The binding of calcitonin to a G protein-coupled receptor activates adenylate cyclase and elevates cytosolic Ca2+ levels. The acceleration of preimplantation embryonic development that is known to occur upon elevation of intracellular Ca2+ prompted an investigation into calcitonin regulation of blastocyst differentiation. Using reverse transcription and the polymerase chain reaction to estimate the relative abundance of calcitonin receptor mRNA, a 25-fold accumulation of the splice variant, CR-1a, was observed in embryos between the 1-cell and 8-cell stages. Cytosolic free Ca2+ levels were rapidly elevated in embryos at the 4-cell to blastocyst stages after exposure to 10 nM calcitonin. Blastocysts treated for 30 minutes with 10 nM calcitonin differentiated in vitro at an accelerated rate, as assessed by the translocation of alpha5beta1 integrin to the apical surface of trophoblast cells, the corresponding elevation of fibronectin-binding activity and the timing of trophoblast cell migration. Chelation of cytosolic free Ca2+ with BAPTA-AM, but not inhibition of protein kinase A activity by H-89, attenuated the effects of calcitonin on blastocyst development. These findings support the concept that calcitonin secretion within the progesterone-primed uterus and the coordinate expression of CR-1a by preimplantation embryos regulates blastocyst differentiation through receptor-mediated Ca2+ signaling.

Animals↗
PubMed2001

Alterations in metastatic properties of hepatocellular carcinoma cell following H-ras oncogene transfection.

AIM: To demonstrate the relationship between H-ras oncogene and hepatocellular carcinoma (HCC) metastasis. METHODS: Activated H-ras oncogene was transfected into SMMC 7721, a cell line derived from human HCC, by calcium phosphate transfection method. Some metastasis-related parameters were detected in vitro, including adhesion assay, migration assay, expression of collagenase IV(c IV ase) and epidermal growth factor receptor (EGFR). RESULTS: The abilities of H-ras-transfected cell clones in adhesion to laminin (LN) or fibronectin (FN), migration, c IV ase secretion increased markedly, and the expression of EGFR elevated moderately. More importantly, these alterations were consistent positively with the expression of p21, the protein product of H-ras oncogene. CONCLUSION: H-ras oncogene could induce the metastatic phenotype of HCC cell in vitro to raise its metastatic potential.

Carcinoma, Hepatocellular↗
PubMed2000

A new small molecule C5a receptor antagonist inhibits the reverse-passive Arthus reaction and endotoxic shock in rats.

C5a is implicated as a pathogenic factor in a wide range of immunoinflammatory diseases, including sepsis and immune complex disease. Agents that antagonize the effects of C5a could be useful in these diseases. We have developed some novel C5a antagonists and have determined the acute anti-inflammatory properties of a new small molecule C5a receptor antagonist against C5a- and LPS-induced neutrophil adhesion and cytokine expression, as well as against some hallmarks of the reverse Arthus reaction in rats. We found that a single i.v. dose (1 mg/kg) of this antagonist inhibited both C5a- and LPS-induced neutropenia and elevated levels of circulating TNF-alpha, as well as polymorphonuclear leukocyte migration, increased TNF-alpha levels and vascular leakage at the site of immune complex deposition. These results indicate potent anti-inflammatory activities of a new C5a receptor antagonist and provide more evidence for a key early role for C5a in sepsis and the reverse Arthus reaction. The results support a role for antagonists of C5a receptors in the therapeutic intervention of immunoinflammatory disease states such as sepsis and immune complex disease.

Animals↗
PubMed2001

Fas-mediated apoptosis causes elimination of virus-specific cytotoxic T cells in the virus-infected liver.

Immunity to allogeneic MHC Ags is weak in rodent livers, raising questions as to the mechanisms that might control responses in this organ. Infection with an adenovirus vector reveals that T cell-mediated immunity to nonself-Ags in the liver is self-limiting. Virus-induced liver injury decreases and coincides with disappearance of virus-specific CTL, concomitant to an increase of apoptotic T cells early after infection. But whereas death in CD4 cells is independent of Fas, perforin, and TNF-alpha, that of CD8 cells requires Fas and not perforin or TNF-alpha pathways. Fas ligand is expressed on liver-infiltrating cells, pointing to death by fratricide that causes almost complete disappearance of virus-specific CTL 4 wk after infection. CTL elimination is virus dose dependent, and high doses induced high alanine aminotransferase values, elevated expression of Fas ligand on CD8 cells, and increased CD8 cell migration into the infected liver.

Adenoviridae Infections↗
PubMed1999

Effect of pulse pressure on vascular smooth muscle cell migration: the role of urokinase and matrix metalloproteinase.

Plasminogen activator (PA) expression plays an important role in smooth muscle cell (SMC) migration and may therefore contribute to mechanical force-induced arterialization of vein grafts. The aim of this study was to determine whether pulse pressure due to pulsatile flow modulates SMC migration via urokinase (u-PA)-dependent mechanisms. Using a perfused transcapillary culture system, human umbilical vein SMC were exposed to pulse pressures (0-56 mmHg), in the absence or presence of human umbilical vein endothelial cells (EC) by varying pulsatile flow rates (0 ml/min to 25 ml/min). SMC cultured in the absence of EC increased their migration following exposure to increased pulse pressure (248+/-14%). Both u-PA and matrix metallo-proteinase 1 (MMP-1) expression was significantly elevated in SMC exposed to pressure as compared to static controls. The role of proteases in the pulse pressure-induced enhancement of SMC migration was confirmed following pretreatment with aprotinin, an anti u-PA antibody and metalloproteinase inhibitors (181+/-14% for aprotinin vs. 256+/-25% for control, 108+/-4% for anti-u-PA antibody vs. 233+/-17% for non-immune IgG, and 114+/-9% for BB-94, 105+/-7% for BB-3103 vs. 222+/-5% for control). Using SMC derived from u-PA gene knock-out mice, the SMC migratory response to increased pulse pressure was completely inhibited despite a significant increase in MMP expression in these cells. These results suggest that pulse pressure due to pulsatile flow induces SMC migration in vitro via u-PA and MMP-dependent mechanisms. Moreover, u-PA gene deletion results in blunting of pressure-induced SMC migration despite the endogenous upregulation of metalloproteinase. Modulation of u-PA expression by pressure may thus represent an important mechanism whereby hemodynamic forces regulate smooth muscle cell migration.

Animals↗
PubMed2000

The incidence and significance of pseudoparaproteins in a community hospital.

Pseudoparaproteins were observed in 129 (10.5%) of 1,229 high resolution protein electrophoretic fractionations of serum (N = 847), urine (N = 368), or cerebrospinal fluid (N = 14) performed in this laboratory during a 12-month period. The pseudoparaproteins identified in serum electrophoretic patterns included fibrinogen, C-reactive protein, hemoglobin-haptoglobin complex, elevated beta-globulins (transferrin and C3), lysozyme (muramidase), and an extended migration artifact. In the electrophoretic patterns of urine, the pseudoparaproteins consisted of nonspecific gamma zone bands of varying intensity. Gamma zone trace protein in the cerebrospinal fluid was often of sufficient intensity to cause potential confusion with oligoclonal bands. Awareness of the characteristic electrophoretic migration positions of these pseudoparaproteins helps to avoid unnecessary ancillary testing and expense.

Adult↗
PubMed1990

The potential coronal migration of periodontal ligament tissue following experimental regeneration.

The aim of the present study was to determine if the periodontal ligament cells can migrate onto curretted root surfaces following an experimental regeneration procedure. Buccal mucoperiosteal flaps were elevated in all three premolar regions in 5 mongrel dogs. The buccal bone was reduced to approximately 7 mm from its original level on 30 roots. Before the elevated flaps were replaced and sutured, Gore-Tex filters were adjusted to cover exposed root surfaces. No membranes were placed over 10 root surfaces, which served as controls. After 7 weeks of healing, the animals were sacrificed and all the roots were examined for histological evaluation of contralateral experimental and control teeth. With polychrome staining, the new periodontal ligament fibers of the curetted root surfaces were dyed methyl blue and the adjacent gingival collagen fibers were dyed red. On the experimental surface, coronal migration of periodontal ligament cells and connective tissue attachment were identified over long distances of curetted root surface. Periodontal ligament spaces were more prevalent in experimental sites than in control root surfaces. The results of the experiment suggest that the periodontal ligament cells actually migrated onto the curetted root surfaces when a periodontal space was created by physical barriers.

Animals↗
PubMed1989

[Characteristics of T and B components of the immune system in miscarriage of different etiology].

A total of 70 females with threatened abortions induced by hormonal, infectious or unclear factors and 63 second trimester underwent clinical, hormonal and immunological investigations. In all females with threatened abortion, the study revealed the variance in immunological data in accordance with the term of pregnancy and cause of its incompetence. The lesser degree of immunological impairment was documented in the females whose pregnancy was complicated by hormonal disorders, whereas females with a history of infections in the early pregnancy demonstrated more profound immunological shifts. In those patients whose pregnancy was lost in the first trimester and the cause of the wastage remained unclear, the authors noted elevated T and decreased B lymphocytes, as well as dramatically reduced leukocyte migration inhibition factor.

Abortion, Threatened↗
PubMed1983

Evidence for anti-inflammatory activities of oral synthetic retinoids: experimental findings and clinical experience.

Oral retinoids obviously influence dermal components such as cutaneous capillaries and dermal inflammatory cells in addition to their well-known action on keratinizing epithelia. On this basis, they act as an anti-inflammatory drug. In particular, they reduce the elevated skin temperature, inhibit the motility of neutrophils and eosinophils and their migration into the epidermis, decrease DNA synthesis of human lymphocytes by blocking their response to lectins and stimulate Langerhans cells, monocytes and macrophages in various in vitro and in vivo models. These data indicate that oral retinoids may not only normalize disorders of keratinization but also exert distinct therapeutic effects on various skin diseases with dermal inflammatory involvement regardless of their particular aetiology. In some respects, retinoids resemble corticosteroids, acting as a modified hormone. Preliminary clinical experiences with oral retinoid treatment in skin diseases such as cutaneous disseminated LE, bullous pemphigoid, Duhring's disease, pemphigus, Behçet's disease and necrotizing vasculitis with eosinophilia support these data. Monotherapy or combined administration of oral retinoids with corticosteroids in low doses seems therapeutically beneficial in these disorders.

Acitretin↗
PubMed2004

Lysophosphatidic Acid Stimulates Ovarian Cancer Cell Migration via a Ras-MEK Kinase 1 Pathway.

Lysophosphatidic acid (LPA) is present at high concentrations in ascites and plasma of ovarian cancer patients. Studies conducted in experimental models demonstrate that LPA promotes ovarian cancer invasion/metastasis by up-regulating protease expression, elevating protease activity, and enhancing angiogenic factor expression. In this study, we investigated the effect of LPA on ovarian cancer migration, an essential component of cancer cell invasion. LPA stimulates both chemotaxis and chemokinesis of ovarian cancer cells and LPA-stimulated cell migration is G(I) dependent. Moreover, constitutively active H-Ras enhances ovarian cancer cell migration, whereas dominant negative H-Ras blocks LPA-stimulated cell migration, suggesting that Ras works downstream of G(i) to mediate LPA-stimulated cell migration. Interestingly, H-Ras mutants that specifically activate Raf-1, Ral-GDS, or phosphatidylinositol 3'-kinase are unable to significantly enhance ovarian cancer cell migration, suggesting that a Ras downstream effector distinct from Raf-1, Ral-GDS, and phosphatidylinositol 3'-kinase is responsible for LPA-stimulated cell migration. In this article, we demonstrate that LPA activates mitogen-activated protein kinase kinase 1 (MEKK1) in a G(i)-Ras-dependent manner and that MEKK1 activity is essential for LPA-stimulated ovarian cancer cell migration. Inhibitors that block MEKK1 downstream pathways, including MEK1/2, MKK4/7, and nuclear factor-kappa B pathways, do not significantly alter LPA-stimulated cell migration. Instead, LPA induces the redistribution of focal adhesion kinase to focal contact regions of the cytoplasm membrane, and this event is abolished by pertussis toxin, dominant negative H-Ras, or dominant negative MEKK1. Our studies thus suggest that the G(i)-Ras-MEKK1 signaling pathway mediates LPA-stimulated ovarian cancer cell migration by facilitating focal adhesion kinase redistribution to focal contacts.

Cell Movement↗
PubMed1999

Changes in the levels of mRNAs for GH/prolactin/somatolactin family and Pit-1/GHF-1 in the pituitaries of pre-spawning chum salmon.

Changes in the levels of pituitary mRNAs encoding GH, prolactin (PRL) and somatolactin (SL) were determined in pre-spawning chum salmon (Oncorhynchus keta) caught at a few key points along their homing pathway in 1994 and 1995. Furthermore, we analyzed relationships between expression of pituitary-specific POU homeodomain transcription factor (Pit-1/GHF-1) and GH/PRL/SL family genes. In 1994, seawater (SW) fish and matured fresh-water (FW) fish were sequentially captured at two points along their homing pathway, the coast and the hatchery. In addition to these two points, maturing FW fish were captured at the intermediate of the two points in 1995. The levels of hormonal mRNAs were determined by a quantitative dot blot analysis using single-stranded sense DNA as the standard. Relative levels of Pit-1/GHF-1 mRNAs were estimated by Northern blot analysis. In 1994, the levels of GH/PRL/SL family mRNAs except for PRL mRNA in the male FW fish were 1.8-4 times higher than those in the SW fish. In 1995, the level of PRL mRNA was somewhat sharply elevated in the maturing FW fish soon after entry into the FW environment, while that of SL mRNA was gradually increased during upstream migration from the coast to the hatchery. The levels of 3 kb Pit-1/GHF-1 mRNA in the FW fish were higher than those in the SW fish in both 1994 and 1995. The present results indicate that expression of genes for the GH/PRL/SL family and Pit-1/GHF-1 is coincidentally enhanced in homing chum salmon. Moreover, the present study suggests that expression of the SL gene is elevated with sexual maturation, whereas that of PRL gene is elevated with osmotic change during the final stages of spawning migration.

Animals↗
PubMed2006

Opposing roles for Akt1 and Akt2 in Rac/Pak signaling and cell migration.

The Akt/PKB isoforms have different roles in animals, with Akt2 primarily regulating metabolic signaling and Akt1 regulating growth and survival. Here we show distinct roles for Akt1 and Akt2 in mouse embryo fibroblast cell migration and regulation of the cytoskeleton. Akt1-deficient cells responded poorly to platelet-derived growth factor while Akt2-deficient cells had a dramatically enhanced response, resulting in a substantial increase in dorsal ruffling. Swapping domains between Akt1 and Akt2 demonstrated that the N-terminal region containing the pleckstrin homology domain and a linker region distinguishes the two isoforms, while the catalytic domains are interchangeable. Akt2 knock-out cells also migrated faster than wild-type cells, especially through extracellular matrix (ECM), while Akt1 knock-out cells migrated more slowly than wild-type cells. Consistently, Akt2 knock-out cells had elevated Pak1 and Rac activities, suggesting that Akt2 inhibits Rac and Pak1. Both Akt2 and Akt1 associated in complexes with Pak1, but only Akt2 inhibited Pak1 in kinase assays, suggesting an underlying molecular basis for the different cellular phenotypes. Together these data provide evidence for an unexpected functional link between Akt2 and Pak1 that opposes the actions of Akt1 on cell migration.

Animals↗
PubMed1985

Qualitative and quantitative differences in hLH species in the first and second LH release induced by continuous stimulation with synthetic LHRH in normal menstrual cycle as assessed by isoelectrofocusing.

It is known that continuous stimulation with LHRH induces a biphasic release of LH. The two pools theory is generally accepted in interpreting this phenomenon. The present study was conducted in order to elicit qualitative differences in LH included in the two pools. Five hundred micrograms synthetic LHRH was infused for 2h in 10 women in various phases of the menstrual cycle and 5 h blood sampling was performed during and after the infusion. Biphasic release of LH was demonstrated in all the cases investigated. The responsiveness to LHRH was most predominant in the midcycle, followed by the luteal phase. Pools of plasma samples at 30-105 min and 150-225 min of the LHRH infusion (plasma pools I and II; corresponding to the initial and the second LH release, respectively) were subjected to isoelectrofocusing (IEF) fractionation, pH range of 3.5-10. LH in plasma was classified in terms of isoelectric point (pI); i.e. A(pI = 9.13), B(8.60), C(8.16), D(7.67), E(7.24), and F(LH species migrating in the acidic pH area). Percentage of high alkaline LH species was significantly elevated in plasma pool I of the midcycle. No phasic difference was observed in the IEF profiles in plasma pool II. Consistent and significant increase and decrease in the percentage of acidic and high alkaline LH species, respectively, were observed throughout the menstrual cycle when the IEF profiles of plasma pool II were compared with those of pool I. The ratio of biological to immunological LH activities (B/I ratio) was markedly depressed in acidic LH species. The highest B/I ratios were obtained in the LH species migrating in the mid-alkaline region. The acidic LH species might represent the young generation of LH molecules prior to acquisition of biological potency. LH species migrating in the mid-alkaline region might be mature and bio-potent forms of the hormone. High alkaline LH species might represent LH molecules over-processed and having lost a degree of biological potency during a prolonged period of storage.

Adult↗