Growth of larval and juvenile Diaphus theta (Pisces: Myctophidae) in the transitional waters of the western North Pacific

Diaphus theta is one of the most common myctophid fish species in the subarctic and transitional waters of the North Pacific. The growth of larval and juvenile D. theta was investigated using sagittal otolith increment analysis of specimens caught in transitional waters of the western North Pacific. Samples taken over a 24-h period demonstrated that otoliths exhibited daily growth cycles, allowing accurate determination of age. Calcification of the incremental zone of otoliths took place only at night, suggesting that the formation cycle of the increment of juvenile D. theta was different from that of shallow-water fishes and would be related to their diel vertical migration. The relationships between standard length (SL) and daily growth increment (D) were expressed as linear equations: SL = 2.65 + 0.141D (r ² = 0.942) for larvae of 5.1–9.6 mm SL and SL = 3.54 + 0.129D (r ² = 0.933) for juveniles of 13.7–27.6 mm SL. The growth rates were 0.14 mm d⁻¹ in larvae and 0.13 mm d⁻¹ in juveniles; this is slow compared with tropical or subtropical mycto-phid species, in which growth occurs at about twice these rates. The larval period, including the metamorphic stage, was long compared with species at lower latitudes and was estimated to be 71 days. The slow growth rate and long period of larval stage of D. theta would be the life history pattern of high-latitudinal species adapted to a low-temperature habitat. Received: March 23, 2001 / Revised: July 5, 2001 / Accepted: July 19, 2001     

The single pore residue Asp523 in PKD2L1 determines Ca2+ permeation of the PKD1L3/PKD2L1 complex

The polycystic kidney disease 1-like 3 (PKD1L3)-polycystic kidney disease 2-like 1 (PKD2L1) complex functions as a Ca(2+)-permeable, non-selective cation channel that is activated by acid and its subsequent removal; this is called an off-response. In this study, we identified a single aspartic residue in PKD2L1 that is responsible for the Ca(2+) permeation of the PKD1L3/PKD2L1 complex. Calcium imaging analysis using point mutants of negatively charged amino acids present in the putative pore regions of PKD1L3 and PKD2L1 revealed that neutralization of the aspartic residue in PKD2L1 (D523N), which is conserved among PKD2 family members, abolished Ca(2+) permeation, despite robust cell surface expression. In contrast, neutralization of the other negatively charged residues of PKD1L3 (D2049N and E2072Q) and PKD2L1 (D525N and D530N) as well as substitution of Asp(523) with a glutamate residue (D523E) had little effect on Ca(2+) permeation properties. These results demonstrate that Asp(523) in PKD2L1 is a key determinant of Ca(2+) permeation into the PKD1L3/PKD2L1 complex and that PKD2L1 contributes to forming the pore of the PKD1L3/PKD2L1 channel.     

Plasma estradiol concentrations and effect of HCG on plasma estradiol and testosterone in normal subjects and patients with endocrine disorders.

Plasma estradiol concentrations were determined by radioimmunoassay in various endocrine disorders using antiserum to estradiol-17beta succinyl bovine serum albumin. Clinical significance and diagnostic value of plasma estradiol were assessed in hypothalamic-pituitary, adrenal and gonadal disorders. In general, estradiol concentration was correlated well with the degree of sexual maturity and was of great diagnostic use. Plasma estradiol in females mainly originated from the ovary, while the testis is the principal source of estradiol in males. The adrenal gland seemed to play a minor role as a source of estradiol at least in normal males and females. The role of estradiol in gynecomastia and in liver disease was also investigated. More than a half of the cases with gynecomastia had elevated concentrations of plasma estradiol, which probably explains the pathogenesis of this manifestation. Cirrhotic patients showed frequently hyperestrogenemia probably due to delayed disappearance of estradiol. In the study of stimulation with human chorionic gonadotropin (HCG), 3,000 IU daily for three days in ten normal men, the peripheral concentrations of esradiol showed maximum and fourfold increases 24 hours after the 1st injection of HCG. The testosterone levels, on the other hand, increased stepwise and reached a maximum of about two times preinjection levels 24 hours after the 3rd injection. In gonadal disorders, HCG produced various patterns of plasma estradiol and testosterone in accordance with the gonadal conditions and dissociated response patterns of both sex hormones were frequently found. The determination of plasma estradiol was useful in the study of the function of not only the ovary, but also the testis and the simultaneous measurement of plasma estradiol and testosterone after HCG administration presented interesting informations about pathophysiology of gonadal disorders.     

Effect of short- and medium-term toxicity of doxorubicin on spermatogenesis in adult Wistar rats

Doxorubicin (DXR) is a widely used chemotherapeutic anticancer agent that has potent activity against several solid and non-solid human malignant tumors, including childhood malignancies. However, DXR has serious toxic effects on tissues with rapid cell cycles, such as myeloid and lymphatic tissues, intestinal mucosa, testes and ovaries. In the present study, the short- and medium-term toxic effects of DXR on the reproductive system of male Wistar rats were evaluated using morphometric and stereological tools to quantify damage to the seminiferous epithelium. Adult male Wistar rats were treated with dose of 7.5?mg/kg of DXR and were sacrificed at seven, 14, 21 and 28?days after treatment. The testes were fixed in glutaraldehyde solution, routinely processed and embedded in plastic for evaluation under a light microscope. A significant reduction in testis weight was found as a result of massive germ cell apoptosis. Differences in comparison to the control group were found in the relative frequency of all stages of the seminiferous epithelium cycle, with significant differences for stages VIII–XI. Apoptosis significantly decreased the number of pachytene spermatocytes in the stages evaluated (I, II–III and VIII) at seven and 14?days. At 21 and 28?days after treatment, the testes exhibited the massive loss of germ cells that resulted in a missing cell layer. Moreover, reductions in the height of seminiferous tubules, tubular diameter and tubular compartment as well as an increase in the intertubular compartment were found in the period studied.     

Ser162-Dependent inactivation of overproduced sucrose-phosphate synthase protein of maize leaf in transgenic rice plants

To investigate the role of Ser162 in phosphorylation-dependent regulation of maize sucrose-phosphate synthase (SPS) activities in rice, transgenic rice plants expressing wild-type or mutagenized maize SPS were produced. Our results indicate that Ser162 was responsible for overproduction-induced inactivation of SPS protein and for light/ dark modulation of this protein in vivo.     

Sphingosine-1-Phosphate Induces Dose-Dependent Chemotaxis or Fugetaxis of T-ALL Blasts through S1P1 Activation

Sphingosine-1-phosphate (S1P) is a bioactive sphingolipid involved in several physiological processes including cell migration and differentiation. S1P signaling is mediated through five G protein-coupled receptors (S1P1-S1P5). S1P1 is crucial to the exit of T-lymphocytes from the thymus and peripheral lymphoid organs through a gradient of S1P. We have previously observed that T-ALL and T-LBL blasts express S1P1. Herein we analyzed the role of S1P receptors in the migratory pattern of human T-cell neoplastic blasts. S1P-triggered cell migration was directly related to S1P1 expression. T-ALL blasts expressing low levels of S1P1 mRNA (HPB-ALL) did not migrate toward S1P, whereas those expressing higher levels of S1P1 (MOLT-4, JURKAT and CEM) did migrate. The S1P ligand induced T-ALL cells chemotaxis in concentrations up to 500 nM and induced fugetaxis in higher concentrations (1000–10000 nM) through interactions with S1P1. When S1P1 was specifically blocked by the W146 compound, S1P-induced migration at lower concentrations was reduced, whereas higher concentrations induced cell migration. Furthermore, we observed that S1P/S1P1 interactions induced ERK and AKT phosphorylation, and modulation of Rac1 activity. Responding T-ALL blasts also expressed S1P3 mRNA but blockage of this receptor did not modify migratory responses. Our results indicate that S1P is involved in the migration of T-ALL/LBL blasts, which is dependent on S1P1 expression. Moreover, S1P concentrations in the given microenvironment might induce dose-dependent chemotaxis or fugetaxis of T-ALL blasts.     

Aurora kinases: structure, functions and their association with cancer

Background: Aurora kinases are a recently discovered family of kinases (A, B & C) consisting of highly conserved serine\threonine protein kinases found to be involved in multiple mitotic events: regulation of spindle assembly checkpoint pathway, function of centrosomes and cytoskeleton, and cytokinesis. Aberrant expression of Aurora kinases may lead to cancer. For this reason the Aurora kinases are potential targets in the treatment of cancer. In this review we discuss the biology of these kinases: structure, function, regulation and association with cancer. Methods and Results: A literature search. Conclusion: Many of the multiple functions of mitosis are mediated by the Aurora kinases. Their aberrant expression can lead to the deregulation of cell division and cancer. For this reason, the Aurora kinases are currently one of the most interesting targets for cancer therapy. Some Aurora kinase inhibitors in the clinic have proven effectively on a wide range of tumor types. The clinical data are very encouraging and promising for development of novel class of structurally different Aurora kinase inhibitors. Hopefully the Aurora kinases will be potentially useful in drug targeted cancer treatment.