Origin of Maxillopoda

The Maxillopoda Dahl (1956) was defined primarily by a 5–6–5 body plan; that is, a head supporting five pairs and a thorax six pairs of appendages, and an abdomen of five segments, the first of which may bear a pair of genital limbs and the last of which, the telson, bears caudal rami. Representatives as diverse as ostracods, cirripeds, orstenocarids and skaracarids appear in the Cambrian, so we are dealing with a radiation that in the most part took place over 500 million years ago. A progenetic origin of the maxillopodans, from an ur-malacostracan stock, has been proposed (Newman, W. A. 1983. Crustacean phylogeny—Crustacean Issues, Vol. 1, pp. 105–119). However, new information, including the recently discovered Cambrian forms Skaracarida and Orstenocarida, the structure of spermatozoa, and preliminary results from the sequencing of ribosomal RNA, suggests that the Maxillopoda are more deeply rooted in the crustaceans than previously supposed, likely closer to the ur-crustacean than to the ur-malacostracan.     

Substance P-related antagonists inhibit vasopressin and bombesin but not 5′-3-O-(thio) triphosphate-stimulated inositol phosphate production in swiss 3T3 cells

The substance P (SP) analogues [DArg¹, DPhe⁵, DTrp^7,9, Leu¹¹] SP (AntD) and [Arg⁶, DTrp^7,9, MePhe⁸] SP (6–11) (AntG) inhibit the action of many different neuropeptides including SP. These analogues might be useful in the treatment of small cell lung cancer but their mechanism of action is unclear. Here, we analyzed the effect of AntD and AntG on neuropeptide vs. guanosine 5′-3-O-(thio) triphosphate (GTPγS) stimulated inositol phosphate generation in permeabilized Swiss 3T3 cells. AntD inhibited vasopressin and bombesin stimulated inositol phosphate formation (IC₅₀ of 0.75 μM and 2 μM, respectively). Similarly, AntG inhibited vasopressin-stimulated inositol phosphate generation with an IC₅₀ of 1 μM. Strikingly, neither AntD up to 10 μM nor AntG up to 20 μM was able to inhibit GTPγS-stimulated inositol phosphate generation. Dose-response curves of neuropeptide-induced inositol phosphate generation were dramatically displaced to the right by either 10 μM AntD or 20 μM AntG. However, neither antagonist affected the dose response of GTPγS-stimulated inositol phosphate generation. Furthermore, 20 μM AntD had no effect on AIF^?₄-induced inositol phosphates in COS-1 cells transfected with G_αq. AntD inhibited [³H]vasopressin binding competitively in intact Swiss 3T3 cells and both AntD and AntG inhibited [³H]vasopressin binding in Swiss 3T3 and rat liver membranes. Scatchard analysis revealed that AntD inhibited vasopressin binding by reducing receptor affinity without affecting receptor number in both intact and membrane preparations of Swiss 3T3 cells. The results strongly suggest that SP analogues AntD and AntG block the action of the Ca²⁺ mobilizing neuropeptides at the receptor level, rather than inhibiting G protein-stimulated inositol phosphate production. © 1995 Wiley-Liss, Inc.     

Isolation of infectious pancreatic necrosis virus (serotype Ab) from diverse species of estuarine fish

Two significant fish kills occurred in the Pamlico River estuary (North Carolina, USA), one in December 1981 and January 1982, and the other in June 1982. The first involved only the southern flounder(Paralichthys lethostigma). Histopathologic examination of morbid and moribund flounder revealed extensive sloughing and necrosis of the mucosa of the pyloric caeca and intestine, and inflammation of the submucosa of the pyloric caeca. Brain and internal organ homogenates from morbid and moribund flounder were assayed on CHSE-214 cells, and a virus was isolated. Virus titers ranged from8.4 · 10² to 6.3 · 10⁷ TCID₅₀ per gram of tissue. Cross-plaque neutralization assays indicated that the southern flounder virus was infectious pancreatic necrosis virus serotype Ab. Immersion challenge showed the isolate is only slightly virulent for fry of brook trout(Salvelinus fontinalis). The second fish kill involved the southern flounder and six other species: hogchoker(Trinectes maculatus), Atlantic silverside(Menidia menidia), spot(Leiostomus xanthurus), Atlantic croaker(Micropogon undulatus), silver perch(Bairdiella chrysura), and striped mullet(Mugil cephalus). Virus was isolated from southern founder, hogchoker, Atlantic silverside, and spot. Neutralization assays indicated that the four isolates were nearly identical; however, the diversity of species affected suggests that the virus might not have been the specific cause of mortality.     

Cancer mortality among immigrant populations in Ontario, 1969 through 1973.

Ontario is home to a sizeable, recently established immigrant population whose cancer mortality has until now remained unexamined. The province''s six largest immigrant groups (British, Italian, German, Dutch, Polish and Soviet) were investigated to compare their cancer mortality experience with that prevailing in Ontario and in their countries of birth for the period 1969 through 1973. Standardized mortality ratios (SMRs) were computed from data from Statistics Canada and the World Health Organization (for 1971) for five sites of cancer. The rates of death from stomach cancer were significantly higher for the immigrant groups (except the Germans) than for the Canadian-born (SMRs 158.6 to 256.1) and were significantly lower for the immigrants (except the Dutch) than for the populations of their countries of birth (SMRs 26.5 to 72.9). The rates of death from colorectal cancer and cancer of the breast tended to be lower among the immigrants. Most male immigrants had high rates of death from lung cancer relative to the Canadian-born, whereas their female counterparts had relatively low rates. For most of the immigrant groups the rates of death from prostate cancer closely resembled those prevailing in the country of birth. Displacement of cancer mortality experience towards that in Ontario was most evident for Polish immigrants. It may have been too soon to see trends among the more recent immigrants (Italian, German and Dutch), who, for the most part, had not yet reached the age of highest cancer risk. Ontario should provide a valuable resource for further studies of lifestyle and environmental determinants of cancer.     

Inactivation of polioviruses and coxsackieviruses in surface water.

Inactivation rates of polioviruses 1 and 3 and coxsackieviruses A-13 and B-1 were determined in situ in the Rio Grande in southern New Mexico, using membrane dialysis chambers. Inactivation of the viruses was exponential, and the rates of inactivation were apparently affected principally by the water temperature. Stability of the viruses in river water differed, with poliovirus 1 and coxsackie B-1 being most stable. Typically 1-log reductions of infectivity at water temperatures ranging between 23 and 27 degrees C required 25 h for poliovirus 1, 19 h for poliovirus 3, and 7 h for coxsackie virus A-13. At water temperatures of 4 to 8 degrees C, the log reduction times for poliovirus 1 and coxsackievirus B-1 were 46 and 58 h, respectively. Results obtained with labeled poliovirus 1 and coxsackievirus B-1 and with infectious ribonucleic acid indicate that inactivation was due to damage to viral ribonucleic acid. Virus-inactivation rates were also affected by heat sterilization of river water, indicating the presence of a heat-labile or volatile inactivating factor. The inactivating factor in Rio Grande water was apparently present at a constant concentration over a 1-year period.     

Structural and compositional changes associated with chlorine inactivation of polioviruses.

Chlorine inactivation of polioviruses resulted in the loss of viral ribonucleic acid, converting the viruses from 156S particles to 80S particles. However, it was found that virus inactivation occurred before the ribonucleic acid was released from the virions. Extraction of ribonucleic acid from partially inactivated virus suspensions indicated that chlorine inactivation was due to degradation of the ribonucleic acid before release and that ribonucleic acid loss was a secondary event. The empty 80S capsids had the same isoelectric point and ability to attach to host cells as infective virions. Thus, no major capsid conformational changes occurred during chlorine inactivation.     

The binding of [3H]adenosine to synaptosomal and other preparations from the mammalian brain.

1. A high-affinity adenosine-binding site with Kd(adenosine) 0.5-1.3 microM was demonstrated in particulate and synaptosomal fractions isolated from the cerebral cortex of guinea pig, rat and ox. 2. Binding of [3H]adenosine to this site was inhibited by theophylline and by 2-chloroadenosine, but not by four other adenosine analogues. 3. Endogenous adenosine, found to be present in some preparations at approx. 1 pmol/mg of protein, diminished the binding capacity of the preparations for [3H]adenosine. 4. Addition of the adenosine deaminase inhibitor erythro-9-[1-(1-hydroxyethyl)heptyl]-adenine revealed the presence of a second lower affinity binding site with Kd (adenosine) 5-9 microM and a higher maximal adenosine-binding capacity. The inhibitor partially blocked binding to the high-affinity site in preparations from which adenosine deaminase had been removed by washing. 5. To preparations of particulate fractions maintained under iso-osmotic conditions, adenosine attachment was non-saturable and temperature-dependent, indicating the existence of an active uptake process. 6. The location and binding constant of the high-affinity adenosine-binding site suggest that it corresponds to the receptor site for adenosine-activated adenylate cyclase.