Peter G. Bradford

THE BLACKBOARD LEARNING SYSTEM: THE BE ALL AND END ALL IN EDUCATIONAL INSTRUCTION?*

Blackboard Inc. provides powerful and easy-to-use systems for educational instruction, communication, and assessment. In the last three years, Blackboard Inc. has marketed two major product lines: the Blackboard Commerce Suite and the Blackboard Academic Suite. The core of the Academic suite is the Blackboard Learning System, the course management system for classroom and online educational assistance. Other course management systems and learning management systems exist, including Angel/LMS, eCollege, GNU General Public License/Linux, and LearningSpace, as well as open-source learning systems such as The Sakai Project, Open SourcePortfolio Initiative, Moodle, and uPortal. Despite the drive toward new portal commodities, the Blackboard Learning System has become the dominant e-learning software company. Is this necessarily good for higher educational learning? Members of the United University Professions Technology Issues Committee debate the issue as well as present specific applications of the Blackboard Learning System in distance learning, hybrid courses, and as didactic supplements to other electronic environment enhancement systems.

Stimulation of Phospholipase A2 and Secretion of Catecholamines from Brain Synaptosomes by Potassium and A23187

Abstract: Potassium depolarization of rat brain synaptosomes (containing incorporated l‐acyl‐2‐[14C]arachidonyl‐phosphatidylcholine) stimulated endogenous phospholipase A1 (EC 3.1.1.32) and A2 (EC 3.1.1.4), as determined by the formation of [14C]lysophosphatidylcholine, [14C]arachidonate, and [14C]prostaglandins, and also stimulated the secretion of [3H]catecholamines. The phospholipase A2 stimulation, dependent on calcium, was elicited in resting synaptosomes by A23187 and was demonstrated with incorporated 1‐acyl‐2‐[l4C]oleoyl‐phosphatidylcholine but not with incorporated [I4C]phosphatidylethanolamine or [l4C]phosphatidylserine. Inhibitors of phospholipase A2 [p‐bromophenacylbromide (10 μM), trifluoperazine (3 μM), and quinacrine (3 μM) reduced the potassium‐stimulated [3H]catecholamine release from synaptosomes to 78, 39. and 55%, respectively, of depolarized controls. The addition of lysophosphatidylcholine increased the release of [3H]norepinephrine to levels observed with potassium depolarization, whereas lysophosphatidylethanolamine, lysophosphatidylserine, and sodium dodecyl sulfate were much less effective. Potassium stimulation of synaptosomes increased the endogenous levels of free arachidonic acid and prostaglandins E2 and F2α. Indomethacin and aspirin decreased the amounts of prostaglandins formed, allowed the accumulation of free arachidonic acid, and diminished the potassium‐stimulated release of [3H]dopamine. p‐Bromophenacylbromide inhibited the formation of prostaglandin F2α. Addition of prostaglandin E2 inhibited, whereas prostaglandin F2α enhanced the release of [3H]norepinephrine. These results suggest that calcium influx induced by synaptosomal depolarization activates endogenous phospholipase A2, with subsequent formation of lysophosphatidylcholine and prostaglandins, both of which may modulate neurosecretion.

Pertussis toxin inhibits chemotactic factor-induced phospholipase C stimulation and lysosomal enzyme secretion in rabbit neutrophils

Pertussis toxin suppressed [32P]polyphosphoinositide breakdown and lysosomal enzyme secretion induced by fMet‐Leu‐Phe in rabbit neutrophils. Likewise, fMet‐Leu‐Phe‐ or leukotriene B4‐evoked (3H]inositol trisphosphate accumulation was inhibited by the toxin. These findings, taken together with evidence that pertussis toxin specifically causes inactivation of the guanine nucleotide binding protein (Ni), suggests that guanine nucleotide binding proteins may mediate coupling between calcium‐mobilising receptors and phospholipase C‐mediated reactions in rabbit neutrophils.

Curcumin and obesity

Turmeric has been long recognized for its anti‐inflammatory and health‐promoting properties. Curcumin is one of the principal anti‐inflammatory and healthful components of turmeric comprising 2–8% of most turmeric preparations. Experimental evidence supports the activity of curcumin in promoting weight loss and reducing the incidence of obesity‐related diseases. With the discovery that obesity is characterized by chronic low‐grade metabolic inflammation, phytochemicals like curcumin which have anti‐inflammatory activity are being intensely investigated. Recent scientific research reveals that curcumin directly interacts with white adipose tissue to suppress chronic inflammation. In adipose tissue, curcumin inhibits macrophage infiltration and nuclear factor κB (NF‐κB) activation induced by inflammatory agents. Curcumin reduces the expression of the potent proinflammatory adipokines tumor necrosis factor‐α (TNFα), monocyte chemoattractant protein‐1 (MCP‐1), and plasminogen activator inhibitor type‐1 (PAI‐1), and it induces the expression of adiponectin, the principal anti‐inflammatory agent secreted by adipocytes. Curcumin also has effects to inhibit adipocyte differentiation and to promote antioxidant activities. Through these diverse mechanisms curcumin reduces obesity and curtails the adverse health effects of obesity.

Specific binding sites for [3H]inositol(1,3,4,5)tetrakisphosphate on membranes of HL-60 cells.

Membranes of HL-60 cells were shown to possess saturable binding sites for [3H]inositol(1,3,4,5)tetrakisphosphate, with nanomolar affinity (KD = 90 nM) and a density of 250 fmol/mg protein. The specificity of the binding sites for Ins(1,3,4,5)P4 was assessed by competition studies utilising a variety of inositol polyphosphates; results indicated that both the presence and the correct grouping of the phosphates were important for high affinity recognition. The apparent affinity of the binding sites for Ins(1,3,4,5)P4 was over 200-fold greater than for Ins(1,4,5)P3. The possibility is discussed that this binding site represents the receptor which mediates the action of Ins(1,3,4,5)P4 as a putative intracellular second messenger.

β-Sitosterol enhances tamoxifen effectiveness on breast cancer cells by affecting ceramide metabolism

The objective of this study was to investigate the effects of the dietary phytosterol beta-sitosterol (SIT) and the antiestrogen drug tamoxifen (TAM) on cell growth and ceramide (CER) metabolism in MCF-7 and MDA-MB-231 human breast cancer cells. The MCF-7 and MDA-MB-231 cell lines were studied as models of estrogen receptor positive and estrogen receptor negative breast cancer cells. Growth of both cell lines as determined using the sulforhodamine B assay was inhibited by treatment with 16 microM SIT but only MCF-7 cell growth was inhibited by treatment with 1 microM TAM. The combination of SIT and TAM further inhibited growth in both cell lines, most significantly in MDA-MB-231 cells. CER is a proapoptotic signal and CER levels were increased in both MCF-7 and MDA-MB-231 cells by individual treatment with SIT and TAM and the combined treatment raised cellular CER content even further. SIT and TAM raised CER levels by different means. SIT potently activated de novo CER synthesis in both MCF-7 and MDA-MB-231 cells by stimulating serine palmitoyltransferase activity; whereas TAM promoted CER accumulation in both cell types by inhibiting CER glycosylation. These results suggest that the combination regimen of dietary SIT and TAM chemotherapy may be beneficial in the management of breast cancer patients.

Modulation of signal transduction in cancer cells by phytosterols

Phytosterols are biofactors found enriched in plant foods such as seeds, grains, and legumes. Their dietary consumption is associated with numerous health benefits. Epidemiologic and experimental animal studies indicate that phytosterols are cancer chemopreventive agents particularly against cancers of the colon, breast, and prostate. Phytosterols impede oncogenesis and prevent cancer cell proliferation and survival. The molecular mechanisms underlying these beneficial actions involve effects on signal transduction processes which regulate cell growth and apoptosis. Phytosterols increase sphingomyelin turnover, ceramide formation, and liver X receptor activation. In concert, these actions slow cell cycle progression, inhibit cell proliferation, and activate caspase cascades and apoptosis in cancer cells.

Estrogen Regulation of Apoptosis in Osteoblasts

Dysregulated apoptosis is a critical failure associated with prominent degenerative diseases including osteoporosis. In bone, estrogen deficiency has been associated with accelerated osteoblast apoptosis and susceptibility to osteoporotic fractures. Hormone therapy continues to be an effective option for preventing osteoporosis and bone fractures. Induction of apoptosis in G-292 human osteoblastic cells by exposure to etoposide or the inflammatory cytokine TNF-alpha promoted acute caspase-3/7 activity and this increased activity was inhibited by pretreatment with estradiol. Etoposide also increased the expression of a battery of apoptosis-promoting genes and this expression was also inhibited by estradiol. Among the apoptotic genes whose expression was inhibited by estradiol was ITPR1, which encodes the type 1 InsP3R. InsP3Rs are intracellular calcium channels and key proapoptotic mediators. Estradiol via estrogen receptor beta1 suppresses ITPR1 gene transcription in G-292 cells. These analyses suggest that an underlying basis of the beneficial activity of estrogens in combating osteoporosis may involve the prevention of apoptosis in osteoblasts and that a key event in this process is the repression of apoptotic gene expression and inhibition of caspase-3/7.

L-Arginine and Nitric Oxide in CNS Function and Neurodegenerative Diseases

One of the main functions of L-arginine (ARG) is the synthesis of nitric oxide (NO). NO is an important regulator of physiological processes in the central nervous system (CNS). NO promotes optimal cerebral blood flow, consolidates memory processes, facilitates long-term potentiation, maintains sleep-wake cycles, and assists in normal olfaction. However, at pathological levels, NO adversely affects brain function producing nitroxidative stress and promoting development of neurodegenerative diseases such as Alzheimers disease, Parkinsons disease and other disorders of the CNS. This review summarizes current knowledge of the role of NO in the CNS and the role of diet in regulating the levels of NO.

Non‐antimicrobial and Antimicrobial Tetracyclines Inhibit IL‐6 Expression in Murine Osteoblasts

Previous results from our laboratory have indicated that intracellular calcium is a critical determinant of the osteoblast secretory capacity. 3,4 Since tetracycline is well known for its ability to bind divalent cations, such as calcium and zinc, and to affect intracellular calcium concentrations, 5 we evaluated the abilities of doxycycline and chemically modified tetracyclines, which lack antimicrobial activity, to affect osteoblast IL-6 secretion from MC3T3-EI osteoblastic cells.