Differential bone morphogenetic protein expression by pluripotent bone marrow stromal stem cells.
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Biomedical subjects
Publications and source records attributed to B Harvey.
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In 1996 there were 65,024 notifications to the National Notifiable Diseases Surveillance System. The record high number of Ross River virus infection notifications was of particular note. The highest rates were recorded in Western Australia, where an outbreak was documented in the South West, and in Queensland. Most cases occurred in the late summer and early autumn months. The number of measles cases has continued to fall markedly following the outbreak in 1993 and 1994. Rubella notifications also fell in 1996. The number of cases of pertussis remained at a similar level to that recorded in recent years, the highest notification rate being recorded for children under the age of one year. A peak in late 1996 marked a resurgence in the pertussis epidemic which has continued into 1997. Notifications of Haemophilus influenzae type b continued to decline reaching a record low rate of 0.3 notifications per 100,000 population. For the enteric diseases, the number of cases of campylobacteriosis rose, with an annual adjusted notification rate of 100.4 per 100,000 population; more notifications were received for this disease than for any other in 1996. The number of hepatitis A cases also rose relative to 1995. This is a reversal of the trend observed in recent years when the notification rate fell. The number of cases of salmonellosis and shigellosis remained stable. Notifications for chlamydial infection and gonococcal infection rose relative to 1995, whilst those for syphilis fell.
This is the fifth annual report of the National Mycobacterial Surveillance System (NMSS), for new and relapsed cases of tuberculosis notified to State and Territory health authorities in 1995. Cases of atypical mycobacterial infection notified to the scheme are also briefly summarised. The notification rate for new cases of tuberculosis was 5.47 per 100,000 population, and for relapsed cases 0.28 per 100,000. These rates have remained stable for a number of years in Australia, and are low compared with rates in other countries. Some identifiable groups in the Australian community continue to experience higher rates of tuberculosis, including members of indigenous communities and some groups born overseas. Surveillance through the NMSS has a major role to play in the control of tuberculosis.
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Chronic ethanol abuse during pregnancy can cause fetal injury. A contributing factor in this fetal injury may be the effect of ethanol on the placenta. Ethanol treatment increases human chorionic gonadotropin (hCG) production by cultured human placental trophoblasts. In this study, we show that ethanol treatment reduces total DNA and total protein while stimulating hCG production in term trophoblasts. Ethanol treatment inhibits growth in rapidly proliferating trophoblastic cells from a first trimester placenta and JEG-3 choriocarcinoma cells. In both cell types, the normal increases in total DNA were inhibited in an ethanol dose-dependent manner. Normal increases in total protein were inhibited as well. In contrast, hCG production, an indicator of differentiation, was stimulated by ethanol treatment. Treatment of JEG-3 cells with antimitogenic agents, methotrexate (MTX) or cytosine arabinoside (Ara-C), inhibited cell growth as indicated by decreased total DNA and total protein accumulation. Similar to that with ethanol treatment, inhibition of cell proliferation was accompanied by increases in hCG production. Taken together, these data suggest that one mechanism by which ethanol increases hCG production in human placental trophoblasts may involve alterations in cellular growth and/or differentiation; such alterations may also occur in other proliferating cells in the growing fetus.
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Chronic treatment of rats with lithium chloride was examined in order to determine its effects on hypothalamic monoamine and metabolite content, basal thyrotropin (TSH) secretion and thyroid function. The hypothalamic concentrations of noradrenaline (NA), dopamine (DA) and its metabolites, dihydroxyphenylacetic acid. (DOPAC) and homovanillic acid (HVA) in the lithium treated rats remained unaltered when compared to control levels. NA turnover and the NA metabolite, 3-methoxy-4-hydroxyphenylglycol (total MHPG), were significantly lower (p < 0.01), whereas both serotonin (5-HT) and its metabolite, 5-hydroxyindole-3-acetic acid (5-HIAA), were significantly higher (p < 0.01 and p < 0.02, respectively) in the lithium treated rat hypothalami than in controls. Chronic lithium treatment significantly elevated basal TSH levels (p < 0.05). This effect was antagonized by methyl p-hydroxybenzoate (methylparaben, p < 0.01), which did not itself affect basal TSH levels. Free serum T3 and T4 levels were not significantly affected by chronic lithium treatment, although T4 tended to be slightly lower than control levels. The monoamine changes observed in the hypothalamus of lithium treated rats did not appear to account for the elevated TSH levels observed in these rats since NA activity which is generally regarded as stimulatory was decreased and 5-HT which has an inhibitory effect on TSH secretion, was increased. The elevated TSH levels may have been due to a reduced negative feedback inhibition of TSH release by the mildly reduced circulating T4 levels caused by chronic lithium treatment.(ABSTRACT TRUNCATED AT 250 WORDS)
Chronic treatment of rats with LiCl is known to induce a decrease in cAMP, while this decrease has also been found to occur together with both a simultaneous increase in total cortical phosphodiesterase (PDE; EC 3.1.4.17) activity and a concomitant increase in cGMP. These studies have implicated an involvement of PDE in lithium (Li+) action and it has been suggested that cGMP and the cGMP-stimulated PDE may be instrumental in the observed effects of Li+ on cAMP. In this study, three isozymes of PDE were isolated and identified from rat cortex and their activity determined, together with simultaneous measurement of cAMP and cGMP, after chronic treatment with oral LiCl (0.35% m/m). Li+ treatment exerted profound effects on cyclic nucleotides in the cortex, inducing significant suppression of cAMP while increasing cGMP levels. However, the ion only induced a slight but insignificant increase in the activities of the three PDE isozymes. To confirm these observations, methylparaben (MPB), a drug demonstrating both an ability to induce a selective stimulation of cAMP-specific PDE and also to lower intracellular levels of cGMP, was co-administration orally (0.4% m/m) with Li+ over the same period. This combination emphasized certain actions of Li+ not noted with Li+ alone. MPB inhibited the Li(+)-induced increase in cGMP, yet did not prevent the ion from decreasing cAMP. However, the combination of Li+ and MPB engendered a synergistic 100% increase in the activity of the membrane-bound, cAMP-specific PDE, PDE IV. This combination also produced a significant suppression of cAMP, while no reduction in cGMP was observed.(ABSTRACT TRUNCATED AT 250 WORDS)
A memorial service providing bereavement support in a palliative care unit is evaluated. Results indicate that respondents found it to be a positive experience, particularly in relation to its formality and content. One-fifth of respondents experienced distress during the service, but this was evaluated as appropriate, being related to personal thoughts, feelings of loss and sadness, and remembrance.
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We have compared the response of proton and water transport to oxytocin treatment in isolated frog skin and urinary bladder epithelia to provide further insights into the nature of water flow and H+ flux across individual apical and basolateral cell membranes. In isolated spontaneous sodium-transporting frog skin epithelia, lowering the pH of the apical solution from 7.4 to 6.4, 5.5, or 4.5 produced a fall in pHi in principal cells which was completely blocked by amiloride (50 microM), indicating that apical Na+ channels are permeable to protons. When sodium transport was blocked by amiloride, the H+ permeability of the apical membranes of principal cells was negligible but increased dramatically after treatment with antidiuretic hormone (ADH). In the latter condition, lowering the pH of the apical solution caused a voltage-dependent intracellular acidification, accompanied by membrane depolarization, and an increase in membrane conductance and transepithelial current. These effects were inhibited by adding Hg2+ (100 microM) or dicyclohexylcarbodiimide (DCCD, 10(-5) M) to the apical bath. Net titratable H+ flux across frog skin was increased from 30 +/- 8 to 115 +/- 18 neq.h-1.cm-2 (n = 8) after oxytocin treatment (at apical pH 5.5 and serosal pH 7.4) and was completely inhibited by DCCD (10(-5) M). The basolateral membranes of the principal cells in frog skin epithelium were found to be spontaneously permeable to H+ and passive electrogenic H+ transport across this membrane was not affected by oxytocin. Lowering the pH of the basolateral bathing solution (pHb) produced an intracellular acidification and membrane depolarization (and an increase in conductance when the normal dominant K+ conductance of this membrane was abolished by Ba2+ 1 mM). These effects of low pHb were blocked by micromolar concentrations of heavy metals (Zn2+, Ni2+, Co2+, Cd2+, and Hg2+). Lowering pHb in the presence of oxytocin (50 mU/ml) produced a transepithelial current (3 microA.cm-2 at pHb 5.5) which was blocked by 100 microM of Hg2+, Zn2+, or Ni2+ at the basolateral side, and by DCCD (10(-5) M) or Hg2+ (100 microM) from the apical side. The net hydroosmotic water flux (JH2O) induced by oxytocin in frog bladder sacs was blocked by inhibitors of H(+)-adenosine triphosphatase (ATPase). Diethylstilbestrol (DES 10(-5) M), oligomycin (10(-8) M), and DCCD (10(-5) M) prevented JH2O when present in the lumen. These effects cannot be attributed to inhibition of metabolism since cyanide (10(-4) M), or 2-deoxyglucose (10(-3) M) had no effect on JH2O.(ABSTRACT TRUNCATED AT 400 WORDS)
Although the federal government has long had an interest in the health of children, action in support of this interest has been limited, fragmented, and inequitable. While health problems are increasing and becoming more complex and while policy leaders, business groups, and the public recognize that action is necessary, no response has been forthcoming. Development of a policy with measurable goals is needed. Resources must be allocated and data collected to periodically evaluate progress toward goals and to appropriately redirect resources.
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