The prickly pear (Opuntia ficus-indica [Cactaceae]) in South Africa: Utilization of the naturalized weed,and of the cultivated plants

In spite of successful biological control efforts, vast areas of South Africa remain infested with the spiny prickly pear weed, Opuntia ficus-indica. These remnant populations, which vary from sparse to dense and which are more or less stable, are confined mainly to the eastern Cape. They provide a popular fruit and a limited source of income for certain sectors of the population in these areas. In terms of existing legislation, there are, however, restrictions on the large-scale utilization of these fruit. A novel method for mass-rearing the cochineal insect, Dactylopius coccus, for the commercial production of a red dye (carminic acid) has been developed. The cultivated spineless prickly pear has recently been enjoying renewed attention from researchers and growers alike. Whereas it has traditionally been cultivated mainly as a droughtresistant fodder crop, and is still popular as such, it is now increasingly recognised as a fruit, in its own right, with considerable promise as a commercial crop for local and export markets. There is also a need to encourage the use of very young cladodes (nopalitos) as a highly nutritious vegetable for human consumption in South Africa.     

Malaria Parasite-Infected Erythrocytes Secrete PfCK1, the Plasmodium Homologue of the Pleiotropic Protein Kinase Casein Kinase 1

Casein kinase 1 (CK1) is a pleiotropic protein kinase implicated in several fundamental processes of eukaryotic cell biology. Plasmodium falciparum encodes a single CK1 isoform, PfCK1, that is expressed at all stages of the parasite’s life cycle. We have previously shown that the pfck1 gene cannot be disrupted, but that the locus can be modified if no loss-of-function is incurred, suggesting an important role for this kinase in intra-erythrocytic asexual proliferation. Here, we report on the use of parasite lines expressing GFP- or His-tagged PfCK1 from the endogenous locus to investigate (i) the dynamics of PfCK1 localisation during the asexual cycle in red blood cells, and (ii) potential interactors of PfCK1, so as to gain insight into the involvement of the enzyme in specific cellular processes. Immunofluorescence analysis reveals a dynamic localisation of PfCK1, with evidence for a pool of the enzyme being directed to the membrane of the host erythrocyte in the early stages of infection, followed by a predominantly intra-parasite localisation in trophozoites and schizonts and association with micronemes in merozoites. Furthermore, we present strong evidence that a pool of enzymatically active PfCK1 is secreted into the culture supernatant, demonstrating that PfCK1 is an ectokinase. Our interactome experiments and ensuing kinase assays using recombinant PfCK1 to phosphorylate putative interactors in vitro suggest an involvement of PfCK1 in many cellular processes such as mRNA splicing, protein trafficking, ribosomal, and host cell invasion.     

Biotransformation of 2,2-Dimethyl-1,3-Propanediol to 3-Hydroxypivalic Acid by Acetobacter Acetii DSMZ3508 and Related Bacteria

Acetobacter acetii DSMZ3508 and related bacteria converted 2,2-dimethyl-1,3-propanediol into 3-hydroxypivalic acid (2,2-dimethyl-3-hydroxypropionic acid; 3HP) during submerged cultivation in mineral salt medium. The maximum yield of 3-hydroxypivalic acid was 24.4% of the fed substrate after 18 days. Cultivation parameters, as pH, cell density, optimal substrate concentration, and oxygen supply for the bioconversion process were determined.     

Spinoreticular neurons that receive group III input are inhibited by MLR stimulation.

In decerebrate paralyzed cats, we examined the responses of 18 spinoreticular neurons to electrical stimulation of the mesencephalic locomotor region. The activity of each of the spinoreticular neurons was recorded extracellularly from laminae IV through VI of the L(7) and S(1) spinal cord. In addition, each of the 18 spinoreticular neurons received group III afferent input from the tibial nerve. Spinoreticular projections were established for each of 18 neurons by antidromic invasion of the ventro lateral medulla at the P11 though P14 levels. The onset latencies and current thresholds for antidromic invasion from the ventro lateral medulla averaged 15.0 +/- 3.8 ms and 117 +/- 11 microA, respectively. Electrical stimulation of the mesencephalic locomotor region attenuated the spontaneous activity or the responses of each of the spinoreticular neurons to tibial nerve stimulation at currents that recruited group III afferents. Our data support the notion that thin-fiber muscle afferent input to the ventrolateral medulla is gated by a central command to exercise.     

Effects of nonapeptide antagonists on oxytocin- and arginine-vasopressin-induced analgesia in mice

Several peptides, including arginine-vasopressin (AVP), neurotensin, and substance P, produce analgesia that is not mediated by opiate systems. Using the hot plate test, we studied the analgesic effects of intracisternal (i.c.) administration of various doses of the nonapeptide oxytocin (OXY) in Swiss-Webster mice. We found that OXY (1-4 micrograms) significantly increased the latency of animals to jump or lick their paws after placement on a hot plate. This effect was not blocked by naloxone pretreatment, which suggests that it is not opiate dependent. Using the hot plate test, we confirmed that AVP (1 and 4 micrograms) also produces analgesia. We then studied the analgesia produced by OXY and by AVP using 3 nonapeptide analogues with antagonist properties: [Pen1, LpMePhe2, Thr4, Orn8]OXY (PLMPTO-OXY) that has anti-oxytocic properties in the uterine contraction assay, d(CH2)5Tyr(Me)AVP(dTM-AVP) which antagonizes the antidiuretic properties of AVP and d(CH2)5D-Ile2,Abu4-AVP (dIA-AVP) which antagonizes the vasopressor effects of AVP. Simultaneous administration of PLMPTO-OXY completely blocked the analgesia produced by OXY whereas the antidiuretic antagonist dIA-AVP partially blocked OXY-induced analgesia and dTM-AVP had no effect. None of the antagonists used blocked AVP-induced analgesia. We concluded that the neural systems mediating the analgesic effects of i.c. OXY differ from those for AVP.