Identifications of two different mechanisms for sorghum midge resistance through QTL mapping.

Sorghum midge is the one of the most damaging insect pests of grain sorghum production worldwide. At least three different mechanisms are involved in midge resistance. The genetic bases of these mechanisms, however, are poorly understood. In this study, for the first time, quantitative trait loci associated with two of the mechanisms of midge resistance, antixenosis and antibiosis, were identified in an RI (recombinant inbred) population from the cross of sorghum lines ICSV745 x 90562. Two genetic regions located on separate linkage groups were found to be associated with antixenosis and explained 12% and 15%, respectively, of the total variation in egg numbers/spikelet laid in a cage experiment. One region was significantly associated with antibiosis and explained 34.5% of the variation of the difference of egg and pupal counts in the RI population. The identification of genes for different mechanisms of midge resistance will be particularly useful for exploring new sources of midge resistance and for gene pyramiding of different mechanisms for increased security in sorghum breeding through marker-assisted selection.

Response by the corpuscles of Stannius to hypotensive stimuli in three divergent ray-finned fishes (Amia calva, Anguilla rostrata, and Catastomus commersoni): cardiovascular and morphological changes.

In accordance with their vital role in cardiovascular physiology () corpuscles of Stannius (CS) from two teleosts and an holostean species showed marked and consistent degranulation and exocytotic responses to hypotensive stimuli. In eels (Anguilla rostrata LeSueur) acute blood withdrawal (hypovolemic hypotension) was followed by a prompt decrease in cardiac output (CO) and dorsal aortic pressure (P(DA)), a compensatory tachycardic response and an increase in systemic vascular resistance (R(SYS)). Isovolemic hypotension induced by papaverine i.v., led to a similar, but more prolonged, decrease in P(DA) but the heart rate (HR) continued to accelerate, thereby counterbalancing the severe and persistent decrease in R(SYS). Both hypovolemic and isovolemic hypotension were followed by a significant depletion of cytoplasmic granules from eel CS even though plasma concentrations of Ca, Mg, Na(+), and K(+) were normal. In an ancient holostean fish, the bowfin, Amia calva and a generalized teleost fish, Catastomus commersoni, the number of cytoplasmic granules decreased by 39% and 54%, respectively, 120 min after the acute withdrawal of 8 ml kg bw(-1) of blood. These findings suggest that a primary role of the CS is to release cytoplasmic granules containing renin or isorenin into the blood circulation, in response to hypotension and/or hypovolemia.

AT(1) receptor blockade with losartan during gestation in Wistar rats leads to an increase in thirst and sodium appetite in their adult female offspring.

We studied the effects of angiotensin II receptor blockade with losartan on thirst and sodium appetite in pregnant Wistar rats and on their adult female offspring. During maternal adaptation to pregnancy, average daily total water intake increased by 63% (P<0.01); NaCl intake by 214% (P<0.001). These changes were not blocked by daily s.c. injections of losartan (50 mg/kg bw i.p.) from gestation day (GD) 2 until GD 19 which implied that maternal AT(1) receptors were not involved in the up regulation of thirst and sodium appetite during pregnancy. Losartan blockade during gestation led to a significant and continued increase in thirst and sodium appetite in the adult female offspring. Daily water intakes were greater in the losartan (LO) group than in the vehicle-injected control group (CO), leading to a total water intake of 1114 +/- 80.6 ml/kg bw compared with 738 +/- 56.7 ml/kg bw (P<0.05) during the 8-day period of observation. Daily sodium intakes were usually 2-3 times greater in the LO group compared with the CO group, amounting to a final cumulative intake of 232 +/- 33 mmol/kg bw compared with 93.8 +/- 16.5 mmol/kg bw (P<0.05) in 8 days. These elevated sodium and water intakes were nearly counterbalanced by the increased renal excretion of water and sodium by fully functional kidneys that were not injured by the drug. Body weights were 10% lower in the LO group at the start but remained unchanged relative to the CO group during the entire 8-day period of observation. Plasma electrolytes, blood hematocrit and carotid MABP in the LO group did not differ from the CO group.

Corpuscles of Stannius secrete renin or an isorenin that regulates cardiovascular function in freshwater North American eels, Anguilla rostrata LeSueur.

Dorsal aortic blood flow (DABF) and caudal venous blood flow (CVBF) were measured in free-swimming conscious freshwater (FW) North American eels (Anguilla rostrata) with Doppler-flow probes. DABF and CVBF increased in a dose-dependent manner following iv doses of [Asn(1), Val(5), Gly(9)]-angiotensin I (ANG I), [Asn(1), Val(5)]-angiotensin II (ANG II), and [Val(4)]-angiotensin III (ANG III) ranging from 5 to 50 ng x kg bw(-1). A minimum effective dose for ANG I and ANG II was 5 ng x kg bw(-1); that for ANG III was 10 ng x kg bw(-1). DABF and CVBF rates increased during the first 2 min and remained elevated for 20-50 min. Flow responses similar to those of ANG II in form and magnitude followed iv injections of extracts of corpuscles of Stannius (CS-EXT). Increases in DABF and CVBF following injections of ANG I, human renin substrate (hRS), and CS-EXT were all blocked by the angiotensin-converting enzyme inhibitor Captopril. Increases in DABF and CVBF which followed injections of hRS and CS-EXT were blocked completely by pepstatin A. [Sar(1), Val(5)]-ANG II (Sarile) blocked completely the DABF and CVBF responses to ANG II and CS-EXT, but the mammalian receptor antagonists losartan (AT1) and PD123319 (AT2) only partially blocked them. These findings support strongly the hypothesis that the corpuscles of Stannius secrete renin or isorenin and that the renin-angiotensin system regulates cardiovascular function in freshwater eels and other bony fishes that possess them.

Mycobacterium avium subspecies paratuberculosis triggers intestinal pathophysiologic changes in beige/scid mice.

We investigated whether infection of beige/scid mice with Mycobacterium avium subspecies paratuberculosis can induce intestinal pathophysiologic changes. Six-week-old beige/scid mice were inoculated intraperitoneally with M. paratuberculosis, then were killed 32 weeks after inoculation when the small intestine was evaluated for physiologic and morphologic abnormalities. All infected mice developed clinical disease. The lamina propria of the intestine from infected mice was mildly infiltrated with mononuclear cells containing acid-fast bacteria, and had significantly increased villus width. In vitro physiologic studies in Ussing chambers indicated that M. paratuberculosis infection caused significant abnormalities in intestinal transport parameters. Baseline short circuit current and potential difference were abnormally high in tissues from infected, compared with control mice, indicative of increased ion secretion. Baseline conductance was significantly decreased in infected mice, suggesting that intestinal tissue from infected mice was less permeable to ions. The change in short circuit current following transmural electrical and glucose stimulation was significantly reduced in intestines from infected mice, suggesting that inflamed intestine had neural and/or epithelial cell damage. We conclude that infection of beige/scid mice with M. paratuberculosis triggers significant intestinal pathophysiologic changes consistent with chronic inflammation. These functional abnormalities may contribute to the pathogenesis of the wasting syndrome seen in bovids with paratuberculosis. This animal model provides evidence that T cell-independent mechanisms are sufficient to cause mucosal pathophysiologic changes and inflammation in response to a specific pathogen, and may be of relevance to inflammatory bowel disease in humans.

Mecamylamine blocks the [Asp1,Val5]-ANG II-induced attenuation of salt gland activity in Pekin ducks.

An intravenous injection of 2 microg of [Asp1,Val5]-ANG II attenuated fluid secretion by the nasal salt glands of Pekin ducks. Ganglionic blockade with mecamylamine stopped salt gland secretion. Flow was reestablished by intravenous methacholine bromide during ganglionic blockade. A second injection of 2 microg of [Asp1, Val5]-ANG II failed to attenuate secretion during ganglionic blockade, showing that the peptide acts via the central nervous system and postganglionic parasympathetic nerves that supply the salt glands. Sympathetic nerves are located in the walls of blood vessels within the salt glands, and adrenergic fibers with "varicosities" supply extensively the secretory tubules. [Asp1, Val5]-ANG II decreased salt gland secretion both before and after alpha1-adrenergic blockade with prazosin, showing that the lowered activity was not caused by the release of norepinephrine from nerve endings and/or duck adrenal chromaffin cells. beta-Adrenergic blockade with propranolol also failed to prevent the attenuation of secretion in response to an intravenous injection of 2 microg of [Asp1,Val5]-ANG II, which showed that epinephrine did not mediate the response to the peptide.

Mating competitiveness of irradiated flies for screwworm fly eradication campaigns.

Should the screwworm fly invade Australia, the sterile insect technique (as used successfully overseas) is currently the only feasible method of eradication. Used in conjunction with chemical control methods, it relies on large numbers of factory-reared, sterilized males competing successfully with wild males for the wild females. However, laboratory and field studies have shown that the processes of mass rearing, irradiation and distribution seriously impair the competitiveness of the sterilized flies. This study collates and analyses the relatively sparse information on the relative mating competitiveness of sterilized screwworm flies, from both controlled experiments and large-scale field studies. A population dynamics example then demonstrates that competitiveness will be a key parameter in the effectiveness and economic feasibility of any future eradication campaign.

Corpuscles of Stannius and stanniocalcin-like immunoreactivity in the white sucker (Catostomus commersoni): evidence for a new cell-type.

The distribution of stanniocalcin immunoreactivity was examined in the corpuscles of Stannius of the white sucker (Catostomus commersoni) by using a chum salmon stanniocalcin antiserum, Western blotting, and light and electron microscopy. The white sucker possesses at least two stanniocalcin-immunoreactive corpuscles in the most posterior portions of the kidneys. Immunocytochemistry and ultrastructure revealed two cell-types in the corpuscle parenchyma, only one of which was immunoreactive. The nonimmunoreactive cells contained dense-cored vesicles and long processes that extended between the immunoreactive cells and terminated at perivascular spaces. When corpuscle extracts were subjected to electrophoresis and Western blotting, three nonreduced stanniocalcin-like immunoreactive bands (approximately 56, 61, and 64 kDa) were observed. However, in the presence of a reductant, a diffuse band migrating in the range of 28 to 32 kDa was noted. The results of this study on the white sucker demonstrate the presence of a dimeric stanniocalcin-like molecule and present evidence of a previously uncharacterized cell-type in the corpuscles of Stannius.

Tetrapod-type [Asp1] angiotensin is present in a holostean fish, Amia calva.

The renin-angiotensin system has been identified in various vertebrates, from elasmobranchs to mammals. Tetrapod (amphibians to mammals) angiotensin (ANG) has Asp at the N-terminus, but Asp is replaced by Asn in elasmobranch and teleost fish. ANG I has been isolated from incubates of plasma and kidney extracts of the bowfin Amia calva, a holostean fish, using the eel vasopressor activity as an assay system; its sequence was found to be H-Asp-Arg-Val-Tyr-Val-His-Pro-Phe-Asn-Leu-OH after sequence analysis, mass spectrometry, and comparison with the synthetic peptide. This sequence is identical to bullfrog ANG I. [Asn1] ANG I was not detected. Thus the bowfin is the first fish species which contains only [Asp1] ANG I. The bowfin ANG I and II were no more vasopressor than eel peptides in the bowfin, indicating that bowfin ANG II receptors do not distinguish between [Asp1] and [Asn1] peptides. In the rat, bowfin ANG I and rat [Ile5, His9] ANG I have equipressor activities when examined in different animals, but the vasopressor activity of bowfin ANG I decreased following rat ANG I in the same animals, although the activity of rat ANG I was unaffected after bowfin ANG I. The present study directly demonstrates the presence of the renin-angiotensin system in a holostean fish and showed that its ANG II receptors have not yet fully coevolved with the homologous [Asp1] peptide.

Effects of ANG II and III and angiotensin receptor blockers on nasal salt gland secretion and arterial blood pressure in conscious Pekin ducks (Anas platyrhynchos).

The vertebrate renin-angiotensin system controls cardiovascular, renal and osmoregulatory functions. Angiotensin II (ANG II) is the most potent hormone of the RAS but in some vertebrate animals angiotensin III (Val4-ANG III) may be a hormone. We studied the effects of some angiotensins and mammalian ANG II receptor antagonists on nasal salt gland function and arterial blood pressure in conscious white Pekin ducks. Nasal salt gland fluid secretion (NFS) was induced by a 10 ml.kg-1 bw i.v. injection of a NaCl solution (1000 mosmol.kg-1 H2O) and maintained by a continuous i.v. infusion of the same solution at a rate of 0.97 ml.min-1. There was a positive linear correlation between nasal fluid [Na+] and osmolality, between [Na+] and [K+], and also between the rate of NFS and [Na+] and [K+]. [Asp1, Val5]-ANG II (1 nmol.kg-1 i.v.) inhibited NFS but did not change ionic concentrations. Val4-ANG III (1 or 5 nmol.kg-1) and ANG I (1-7) (20 nmol.kg-1) had no effect on NFS. [Sar1, Ile8]-ANG II (SARILE) acted as an ANG II receptor agonist and resulted in a prolonged and complete inhibition of NFS. The AT1 receptor antagonist, losartan (DuP 753) and the AT2 receptor antagonist, PD 123319 both failed to block the inhibitory effect of [Asp1, Val5]-ANG II on the nasal salt glands. [Asp1, Val5]-ANG II (2 nmol.kg-1 i.v.) increased mean arterial blood pressure (MABP), whereas the same dose of [Asn1, Val5]-ANG II (teleost) had only 30% of the pressor potency of the avian ANG II. Neither 1 nor 5 nmol.kg-1 of Val4-ANG III i.v. nor 20 nmol.kg-1 of ANG I (1-7) had any measurable effect on MABP. SARILE blocked completely the pressor response to [Asp1, Val5]-ANG II but the AT1 antagonists losartan and CGP 48933 and the AT2 antagonist PD 123319 all failed to block the pressor response to [Asp1, Val5]-ANG II. These results have substantiated an important role of the nasal salt gland in potassium regulation and highlighted a pharmacological dimorphism of saralasin, namely agonist and antagonist to angiotensin II-mediated inhibition of nasal salt gland function and pressor response, respectively. Using specific nonpeptidergic angiotensin II receptor antagonists, we have confirmed the distinct pharmacology of the avian angiotensin II receptors in a nongallinaceous species and the absence of significant angiotensin I (1-7) and angiotensin II effects on the cardiovascular system and nasal salt gland.

Angiotensin II and cardiovascular regulation in a freshwater teleost, Anguilla rostrata LeSueur.

Cardiac output (CO), dorsal aortic blood flow (BFDA) and blood pressure (PDA), and heart rate (HR) were recorded simultaneously in conscious freshwater eels. Physiological doses of [Asn1,Val5]angiotensin II (ANG II; 25-150 ng/kg iv) were used to investigate its effects on the blood flow [CO, BFDA, and estimated branchial shunting (BS)] and systemic vascular resistance (RSys) components of the pressor response and possible mechanism(s) of action. CO was increased mainly by an elevated stroke volume (SV) due to positive inotropy and/or Frank-Starling principle in a dose-related manner. An intact baroreceptor reflex attenuated the blood flow increase by 25% via the inhibitory cardiac vagal innervation. The elevation in estimated BS was a passive response to the increased CO, since the proportion of CO perfusing the pathway remained constant. PDA showed a similar dose-dependent increase in response to ANG II but the peak PDA preceded the peak CO responses at all doses; RSys was only transiently elevated at peak PDA. The increase in blood flow was an important contributor to the vasopressor responses. Alpha-Adrenergic blockade partially inhibited the pressor effect of ANG II (100 ng/kg) primarily by attenuating the increase in blood flow (50-70%). The data provide evidence for an ANG II-mediated cardiovascular control in teleosts directly and indirectly via catecholamine release.

Angiotensin I- and II- and norepinephrine-mediated pressor responses in an ancient holostean fish, the bowfin (Amia calva).

Dorsal aortic blood pressure (PSYS, systolic; PDIAS, diastolic; and PDA, mean) and heart rate (HR) were measured in resting freshwater bowfins (n = 6), Amia calva L., before and after i.v. injections of 50, 100, 200, 500, and 1000 ng.kg-1 of synthetic [Asn1, Val5]-angiotensin II (ANG II). Baseline PSYS, PDIAS, and PDA were 27.7 +/- 2.8, 22.4 +/- 1.8, and 24.5 +/- 2 mm Hg, respectively. Bowfins were only moderately responsive to ANG II in a stepwise manner and the increase in blood pressure became significant only at the two highest doses; lower doses tended only to increase arterial pressure. Pressor responses due to 200 and 500 ng.kg-1 decayed over a greater time period compared with other doses. alpha-Adrenergic blockade abolished 70% of the ANG II-mediated pressor responses. Eel, salmon, and goosefish angiotensin I (ANG I; 500 ng.kg-1) elicited similar vasopressor responses (magnitude and time course) which were eliminated by prior angiotensin converting enzyme inhibition (captopril; 2-10 mg.kg-1). Bullfrog ANG I evoked a pressor effect, only at a higher dose (5000 ng.kg-1). Consecutive norepinephrine (NE) injections (100, 200, 500, and 1000 ng.kg-1) increased PSYS, PDIAS, and PDA in a dose-dependent manner which was dependent on alpha-adrenoceptors since phentolamine (1-3 mg.kg-1) abolished 80% of the pressor action of NE. PSYS was elevated by 100 ng.kg-1 of NE but PDIAS and PDA were significantly increased only at 200 ng.kg-1 ANG II and NE had no measurable chronotropic effect and resting HR (27.2 +/- 0.8 beats.min-1) was unchanged. Captopril and phentolamine treatments produced rapid hypotension and bradycardia (25-30%) which lasted from 15 to 30 and 20 to 40 min, respectively. The rising and decreasing phases of the NE-mediated pressor responses had shorter durations than ANG II effects. Tachyphylaxis occurred with the high doses of ANG II and NE. The data show that in the ancient bowfin, which evidently lacks renal juxtaglomerular cells, the cardiovascular system can be regulated by the renin-angiotensin system and NE.

Cardiovascular effects of arginine vasotocin, atrial natriuretic peptide, and epinephrine in freshwater eels.

The effects of 150 ng/kg iv injections of arginine vasotocin (AVT), eel atrial natriuretic peptide (ANP), and epinephrine (Epi) on the cardiovascular dynamics of resting freshwater eels, Anguilla rostrata were studied. Injection of AVT into the caudal vein significantly increased cardiac output (CO) from 15.3 to 23.6 ml.min-1.kg-1 primarily by increasing stroke volume. Mean dorsal aortic pressure (PDA) also increased. Estimated branchial shunting (2.54 ml.min-1.kg-1) was elevated by 130% because of an increased proportion of CO, indicating a vasoconstriction of the branchial arterioarterial pathway. In contrast, Epi reduced the fraction of CO perfusing the arteriovenous pathway. Epi also produced a positive chronotropic effect, increased CO and systemic vasoconstriction, resulting in a vasopressor response. These changes occurred earlier than those of AVT and ANP. Pressor responses triggered by AVT and Epi preceded the increases in CO. Injections of 150 and 200 ng/kg ANP caused a reduction in PDA due to a decrease in CO (and SV) but failed to modulate systemic resistance. The change in CO was the primary contributor to the pressor (and depressor) responses elicited by the three hormones.

Corpuscles of Stannius and blood flow regulation in freshwater North American eels, Anguilla rostrata LeSueur.

Cardiac output (CO), heart rate (HR), stroke volume (SV), dorsal aortic blood flow (DABF), dorsal aortic blood pressure (PDA) and plasma electrolytes were monitored in stanniectomized and sham-operated freshwater eels over a 3-week period; branchial shunting and systemic resistance (RSYS) were estimated. DABF was significantly reduced by 45% from 11.72 +/- 0.48 (control) to 6.55 +/- 0.41 (n = 6; day 21) ml.min-1.kg-1 within 3 weeks after the removal of the corpuscles of Stannius. This large reduction in blood flow was due to a 25% decrease in CO and a 100% increase in estimated branchial shunting which preceded the fall in CO. CO was decreased from 16.07 +/- 0.31 (control) to 11.91 +/- 1 (n = 6; day 21) ml.min-1.kg-1 through a reduction in SV; there was no significant change in HR. Estimated branchial shunting, a relative measure of branchial arterio-venous blood flow, corresponded to 2.53 +/- 0.18 ml.min-1.kg-1 (control; n = 12), which represents 16% of baseline CO. Ventral and dorsal aortic pulse flows also decreased following stanniectomy. The decrease in DABF occurred in conjunction with a reduction in PDA which was measured for 12 days in a separate group of eels. Baseline PDA (3.03 +/- 0.1 kPa) significantly decreased by 15% to 2.55 +/- 0.13 kPa 4 days after stanniectomy. However, this fall in PDA was transient and accompanied by an elevation in derived RSYS. These results support the hypothesis that the corpuscles of Stannius are closely linked to cardiovascular regulation in freshwater eels. Electrolyte changes (hypercalcemia, hypomagnesia, hyperkalemia and hyponatremia) were temporally coupled to the changes in blood flows. Impaired cardiovascular function and altered patterns of blood flow to osmoregulatory organs such as the gills, kidney and skin may have led to some or all of the electrolyte disturbances which followed stanniectomy.

Physiological doses of [Ile5]- and [Val5]-Angiotensin II fail to increase plasma catecholamines at the peak pressor response in rats.

Pressor responses to [Ile5]-Angiotensin II and [Val5]-Angiotensin II were measured following single intravenous doses of 0.0075, 0.075, 0.375, 0.75 and 7.5 micrograms/kg b.w. in anesthetised rats. [Val5]-Angiotensin II was significantly (10 per cent) more potent than [Ile5]-angiotensin II when log dose was plotted against the increase in carotid arterial pressure. Doses of 0.075 microgram/kg b.w. or more of each of the two peptides gave a full pressor response within 30 seconds. However, only at the highest and, probably, nonphysiological dose of [Ile5]-Angiotensin II (7.5 micrograms/kg b.w.) was there a significant increase in noradrenaline and adrenaline concentrations measured using a radioenzymatic assay. [Val5]-Angiotensin II was more potent than [Ile5]-Angiotensin II insofar as plasma noradrenaline increased significantly (p < 0.05) following doses of 0.75 and 7.5 micrograms/kg b.w.; adrenaline at the higher dose only. Plasma dopamine was unresponsive to both peptides.

Angiotensin-I- and -III-mediated cardiovascular responses in the freshwater North American eel, Anguilla rostrata: effect of Phe8 deletion.

Cardiovascular responses to synthetic eel [Asn1, Val5, Gly9]-ANG-I, ANG-III (2-8), and ANG-I (1-7) were measured in conscious and resting freshwater North American eels. Indwelling Doppler flow probes were placed on the ventral and dorsal aortas, a pressure catheter in the lienomesenteric artery, and a peptide delivery catheter in the caudal vein. Twenty-five and 150 ng.kg-1 ANG-III increased baseline cardiac output (CO) (15.23 +/- 0.31 ml.min-1.kg-1; n = 5) by 23 and 47%, respectively, by increasing stroke volume (SV) but not heart rate (HR). ANG-I (150 ng.kg-1) also elevated CO (62%) by increasing both SV (44%) and HR (14%). Estimated branchial shunting (BS) was increased by 150 ng.kg-1 ANG-I and -III suggesting that more blood perfused the arteriovenous pathway in the gills. Dorsal aortic blood pressure (PDA) (3.08 +/- 0.12 kPa) was elevated by 150 ng.kg-1 ANG-I (67%) and -III (52%). Pressor responses temporally preceded the blood flow increases and there was a significant increase in systemic vascular resistance (RSYS) at the peak pressor responses. At the peak flow responses, increased CO was solely responsible for the increase in PDA; RSYS had returned to baseline values. Pressor responses to ANG-III decayed more rapidly (18.6 min) compared with those of ANG-I and -II (36 min). ANG-I (1-7) had no measurable effect on cardiovascular function indicating that the carboxyl-terminal 8-phenylalanine is an absolute requirement for the hormonal activity of angiotensin in fishes.

The role of restricted food intake in the pathogenesis of cachexia in severe combined immunodeficient beige mice infected with Mycobacterium paratuberculosis.

A paired feeding experiment was conducted to investigate if reduced food intake is a reason for the body weight loss previously observed in severe combined immunodeficient beige (SCID bg) mice infected with Mycobacterium paratuberculosis. Mice were paired on the basis of age, litter and sex. One of each pair was injected intraperitoneally with 10(5) viable M. paratuberculosis organisms. The remainder served as uninfected pairfed mates. Each uninfected mouse was restricted to the amount of food (per gram body weight) that its infected paired mate ate in the previous 24 hour period starting at four weeks postinfection until 12 weeks postinfection when the mice were necropsied. The mean body weights of the two groups were not significantly different (p < 0.05) at the start of the experiment (infected 27.6 +/- 2.1 g, pairfed 27.3 +/- 3.4 g) but the pairfed group weighed less after 12 weeks of restricted food intake. Mycobacterium paratuberculosis was isolated from the spleen, liver, gut and fecal pellets of the infected but not the uninfected mice. Acid-fast bacilli were seen histologically in the liver, spleen and intestines of the infected mice only. Analysis of carcass compositions indicated that both infected and pairfed mice lost dry matter. Despite the loss in dry matter, the infected mice appeared to have maintained their body weights due to an increased retention of body water (presumably due to edema of inflammation). These results suggest that infection of SCID bg mice with M. paratuberculosis causes a reduction in their food intake (presumably due to reduced appetite) which, in turn, contributes to a loss in dry matter. We suggest that this loss in dry matter is one of the initial events that eventually lead to cachexia, and that it precedes the body weight loss that inevitably occurs in SCID bg mice chronically affected with M. paratuberculosis.

Fractional reabsorption of calcium, magnesium and phosphate in the kidneys of freshwater North American eels (Anguilla rostrata LeSueur) following removal of the corpuscles of Stannius.

Renal function was observed in freshwater North American eels (Anguilla rostrata LeSueur) 2 weeks after the removal of the corpuscles of Stannius. There was a positive linear correlation between glomerular filtration rates and urine flow rates in both sham-operated and stanniectomized eels but there was no difference in slope or elevation between the two groups nor did urine flow rates ever exceed glomerular filtration rates. Osmolar clearance and free-water clearance were unchanged following stanniectomy. Plasma Ca2+ and K+ concentrations increased and plasma Mg2+, phosphate, Na+ and Cl- concentrations decreased following stanniectomy. Plasma ultrafilterable Ca increased and ultrafilterable Mg decreased after stanniectomy but neither changed relative to its total plasma concentration. Stanniectomy was followed by a decreased renal tubular reabsorption of Mg2+ relative to the amount filtered (CMg/CIn); the same applies to CNa/CIn. Even though the filtered load of Ca increased in conjunction with the predictable hypercalcemia, there was no change in the fraction of filtered Ca reabsorbed. Net tubular secretion of phosphate was observed in both sham-operated and stanniectomized eels together with a slight increase in Cphos/CIn following stanniectomy. Some or all of these changes in plasma electrolytes and/or the modified renal transport of Na+, Mg2+ and possibly phosphate may be caused by the changes in cardiovascular function that were recently shown to follow stanniectomy.

Angiotensin II-mediated catecholamine release during the pressor response in rats.

Angiotensin II (ANG II)-mediated catecholamine release and its possible contribution to the pressor response was assessed in baroreceptor-denervated rats. Neonatal male Sprague-Dawley rats were injected with the sympatholytic drug, guanethidine monosulphate (50 mg/kg s.c., 6 days/week) for 40 days. Plasma catecholamine concentrations were measured using a 3H-radioenzymatic assay as follows: (a) before and 30 s after the injection of saline or ANG II (79.3 pmol/kg i.v.), at the peak of the pressor response, then 50 s and 80 s thereafter, in guanethidine-treated (GUAN) and saline-injected (SHAM) rats, and (b) before and after adrenalectomy (ADX), following the same time-sequence for ANG II as in (a). Peak pressor responses to graded doses of ANG II (6.6, 26.4, 53.0 and 79.3 pmol/kg i.v.) were measured in GUAN+ADX and ADX rats. Destruction of peripheral sympathetic nerves was confirmed by measurements of plasma noradrenaline (NA), adrenaline (AD) and dopamine (DA) concentrations and by changes in pressor responses and heart rates following i.v. doses of tyramine. ANG II induced significantly (P < 0.05) greater pressor responses in GUAN+ADX rats than in ADX rats, especially after the 53.0 and 79.3 pmol/kg doses. Plasma AD concentrations increased within seconds after the pressor response to ANG II in both GUAN and SHAM rats but there was no change in plasma NA or DA concentrations (P < 0.05). ANG-II-mediated AD release from the adrenal medulla may contribute to the overall pressor action of the peptide. The vasculature became more sensitive to ANG II at a time when NA and DA depletion occurred following sympathectomy and/or adrenalectomy. This heightened sensitivity to ANG II was not due to a decrease in circulating ANG II in sympathectomized rats because even though plasma renin activity fell from 6.54 +/- 0.52 to 3.77 +/- 0.26 ng ANG I/ml per h it remained within the normal range.

Comparison of the predicted impact of a screwworm fly outbreak in Australia using a growth index model and a life-cycle model.

The spatial population dynamics of an Old World screwworm fly, Chrysomya bezziana Villeneuve (OWS), outbreak in Australia have been modelled in two ways. The first model uses weekly growth indices derived from climatic data to predict the adult female population. The second is a detailed cohort life-cycle model. Due to technical and time constraints, the growth index model is preferred as the biological component of a much larger bioeconomic model because of its smaller program size and faster execution. In deciding whether adoption of the growth index model would be at the expense of scientific accuracy, the life-cycle model was developed as a yardstick. We showed that the growth index model was a practical and adequate substitution for the OWS life-cycle model and a novel spatial/temporal modelling approach with generic qualities. We elaborate on the previously reported growth index model, describe the life-cycle model and compare the results of both models. In the event of an OWS incursion in northern or eastern Australia, given average climatic conditions, both models predict that most of the suitable range (some 2.3M km2) will be colonized within 4-5 years if an eradication campaign is not attempted. Much of its permanent range would be in tropical and subtropical extensive grazing regions. Where computer or funding resources are restrictive, models incorporating growth indices may prove adequate for spatial population studies of some species.